All Topics (with details-not just images,tx,etiologies, more!) Flashcards

Use this if you want to study more details like epidimology, location, clinical manifestations) (1726 cards)

1
Q
A
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2
Q

What are the two types of Odontogenic Cysts?

A

Inflammatory
or
Developmental

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3
Q

List the type of Inflammatory cysts

(4)

A
  • Periapical (radicular)
  • Residual periapical
  • Buccal bifurcation
  • Paradental
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4
Q

List the types of Developmental Cysts?

(9)

A

‐ Dentigerous
‐ Eruption
‐ Gingival cyst of newborn
‐ Gingival cyst of adult
‐ Lateral periodontal
‐ Glandular odontogenic
‐ Odontogenic keratocyst
‐ Orthokeratinized odontogenic
‐ Calcifying Odontogenic

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5
Q

All of the following are histologically the same because they are all what?

-Periapical (radicular)
‐ Residual periapical
‐ Buccal bifurcation
‐ Paradental

‐ Dentigerous
‐ Eruption
‐ Gingival cyst of newborn
‐ Gingival cyst of adult

A

squamous epithelial lined cysts

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6
Q

What are the sources of epithelium
within the jaw bone ?

(6 sources)

A

▪ Epithelial rests of Malessez
▪ Reduced enamel epithelium
▪ Fissural cysts – when 2 pieces of bone come together
▪ Odontogenic cysts
▪ Epithelial component of odontogenic tumors
▪ Salivary gland inclusions – rare, incorporated in development

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7
Q

radicular cyst, inflammatory cyst are other names for

A

Periapical Cysts

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8
Q

▪ The most common cyst of the jaws

A

Periapical Cysts

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9
Q

Periapical Cysts

Demographic and location

A

▪ Any age (peak in 3rd ‐ 6th decades, rare in 1st decade)
▪ No sex predilection
▪ MX > MD (anterior MX most common)

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10
Q

Tooth vitality and Periapical Cysts

A
  • Involved tooth usually non‐vital/non‐responsive with thermal and electric pulp testing
  • Should test vitality of tooth if see radiolucency in apex\
  • If tooth vital, and still see radiolucency ► should do biopsy
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11
Q

Periapical Cyst

(Radiographic)

A
  • Usually appears as well‐circumscribed periapical radiolucency with widening of the PDL space and/or loss of lamina dura
  • Typically small (< 1 cm) but can grow to large dimensions if left untreated
  • Radiographic findings can NOT be used for definitive diagnosis
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12
Q

Why the Radiographic findings of Periapical Cyst can NOT be used for definitive diagnosis?

A

‐ similar appearance with:

  • periapical granuloma
  • odontogenic tumors
  • early COD {Cemento Osseous Dysplasia}
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13
Q

Lateral radicular cyst appears on the lateral surface of the root of a non‐vital/non‐responsive tooth
‐ A differential for which cyst?

A

lateral periodontal cyst

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14
Q

What is this radiographic finding?

A

Periapical Cysts

►Would need to test both teeth for vitality.

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15
Q

What is this radiographic finding?

A

Periapical Cyst

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16
Q

What is this radiographic & clinical findings?

A

Periapical cyst

shows inflammation at site
abscess developed fistula tract thru
soft tissue. Pt will have pain until
pressure is released

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17
Q

The wall of which cyst?

A

Periapical Cyst

Open clear areas = Cholesterol clefts where fat
used to be. Multinucleated cells (purple dots)
trying to break down cholesterol

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18
Q

What is this and what is it associated with?

A

keratin pearl – can be associated w/SCC

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19
Q

What are these radiographic findings?

A

Residual Cysts

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20
Q

What is the radiographic finding?

A

Residual Cyst

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21
Q

Periapical Cyst

treatment

A
  • endodontic therapy or extraction of involved teeth
  • larger lesions may require biopsy along with endodontic therapy
  • lesions which fail to resolve should be biopsied
  • follow-up at 1-2 years
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22
Q

Residual Cyst

Etiology

A
  • After tooth extracted, not properly cleaned ► the residual cells of the cyst lining and inflammatory cells continue to proliferate
  • Has to be at site where tooth was previously removed
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23
Q

Residual Cyst

Radigraphically

A
  • well defined round to oval radiolucency in the site of a previous extraction
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24
Q

Residual Cyst

Histologically is identical to which cyst?

A
  • identical to the radicular cyst (periapical cyst)
  • Should biopsy to rule out other causes
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25
What is the radiographic finding?
Paradental Cyst
26
What is the radiographic finding?
Paradental Cyst
27
Residual Cyst _Treatment_
-Removal * Enucleation if small * Marsupialization if large * Note:* * Enucleation* means: removal of an organ or other mass intact from its supporting tissues *Marsupialization* means: surgical technique of cutting a slit into an abscess or cyst to empty its contents and suturing the edges of the slit to form a continuous surface from the exterior surface to the interior surface of the cyst or abscess. Promotes Decompressing and shrinkage.
28
**Paradental Cyst** _Etiology_
Some controversy over this designation ‐ some think they are inflammatory cyst ‐ some think they are developmental cysts ▪ Etiology: _remains unclear_
29
**Paradental Cyst** _Radiographically_
* Radiolucent area noted * most frequently, along the distal aspect of an impacted or partially erupted third molar
30
What is the radiographic finding?
**Buccal Bifurcation Cyst** *as seen in occlusal radiographs*
31
What is the radiographic finding?
**Buccal Bifurcation Cyst** *as seen in occlusal radiographs*
32
Which cyst has been associated w/ enamel extensions into furcation areas of the involved teeth?
**Paradental Cyst**
33
**Paradental Cyst** _Treatment_
**Extraction** of the _tooth along with the lesion_
34
**Buccal Bifurcation Cyst** is similar to what Cyst ?
_Similar to **a paradental cyst**_ ‐ **EXCEPT**: location is _central on the buccal of mandibular first molars_
35
**Buccal Bifurcation Cyst** _Etiology_
unclear
36
**Buccal Bifurcation Cyst** is most commonly seen with eruption of what tooth?
The eruption of ***the permanent first molar***
37
**Buccal Bifurcation Cyst** _Clinically_
seen as * swelling * tenderness of soft tissue over involved area
38
dentigerous cyst or follicle ?
_dentigerous cys_t b/c **\*attachment at CEJ**
39
What is the radiographic finding?
**Dentigerous Cyst**
40
What are these radiographic findings?
**dentigerous cyst**
41
What are these radiographic findings?
**dentigerous cyst**
42
What is the radiographic finding?
**dentigerous cyst**
43
What is this gross finding?
Grossly image of ## Footnote **Dentigerous Cyst**
44
Dentigerous Cyst Treatment
* **Decompression**: Try to open window in the jawand put tube into cyst lumen and have pt irrigate a few times a day for a few weeks ► release pressure and allows bone to grow back ► **cyst will shrink** * If get rid of whole area surgically► c_an risk_ _fracturing the jaw_
45
Which Radiograph type is best to see **Buccal Bifurcation Cyst?**
▪ Radiolucency best seen with **an occlusal radiograph**
46
Buccal Bifurcation Cyst _Treatment_
▪ **Enucleation** **of cyst**; tooth extraction unnecessary ▪ Some cases _resolve w/o surgery_ ▪ Some resolve _w/ daily irrigation_ of buccal pocket with saline/hydrogen peroxide
47
**Dentigerous Cyst** also known as ?
**Follicular Cyst**
48
What is **most common type of developmental odontogenic** **cysts?** 20% of all epithelial lined cysts of the jaw
**Dentigerous Cyst**
49
What is the clinical finding?
**Eruption Cyst**
50
What is the clinical finding?
**Eruption Cyst**
51
**Dentigerous Cyst** _Origin_ & _Etiology_
*_Originates_*: by **the separation** of the _follicle_ from the _crown of an unerupted tooth_ *_Pathogenesis_*: **accumulation of fluid** between the tooth and the _reduced enamel epithelium_
52
Dentigerous Cyst _Clinically_
▪ Small cysts typically asymptomatic and picked up on routine radiographic exam ▪ Large lesions may show expansion of bone ▪ Cysts may become infected, especially if partially erupted tooth
53
Dentigerous Cyst _Demographics_ & _Location_
* Mostly **mandibular 3rd molars** (rarely unerupted deciduous teeth) * Most commonly present in **2nd and 3rd decades**
54
What is a key characteristic of **Dentigerous Cyst** _location_?
* **Attached to the tooth at the CEJ**
55
Small Dentigerous Cyst are hard to differentiate radiographically from ---?
**enlarged/hyperplastic follicle** Rule of thumb: * If 4‐5mm or more of radiolucency ► _dentigerous cyst_ * If \<4mm of radiolucency► can be _hyperplastic follicle_
56
What is the clinical finding?
Cysts of the Newborn: Palatal cysts
57
Gingival cyst of the newborn/ Dental lamina cysts/Cysts of the Newborn-gingival
58
What is the Soft tissue counterpart of a dentigerous cyst?
Eruption Cyst
59
**Eruption Cyst** also known as
_eruption hematoma_
60
**Eruption Cyst** Etiology
* Results from accumulation of fluid in the follicular space when the tooth has erupted over the alveolar bone **\*NOT in bone\***
61
What is the clinical finding?
**Gingival Cyst of the Adult**
62
What is the clinical finding?
Gingival Cyst of the Adult
63
What is the clinical finding?
Gingival Cyst of the Adult notice the _bluish hue_
64
**Eruption Cyst** _Demographic_ & _Location_
▪ Usually seen in **1st decade** *(children)* ▪ Most often involves **1st permanent molar** and **maxillary incisors**
65
**Eruption Cyst** Clinically
Frequently _normal mucosal color_, BUT surface trauma (ex. chewing) may result in bleeding into the cystic space► may look **purple or blue** ▪ Usually **soft** or **fluctuant**(like a balloon) _upon palpation_
66
**Eruption Cyst** _Treatment_
* Unless symptomatic, no treatment required, cysts resolve upon eruption of teeth
67
**Cysts of the Newborn** can either be --- or ---
**Palatal cysts** or **Gingival cyst**
68
**Palatal cysts** _Types_ _&_ _Location_
**‐ Bohn’s nodules:** scattered over HP (hard palate), often junction of HP and SP (soft palate) **‐ Epstein’s pearls:** along median palatal raphe
69
Which is here is **Lateral Periodontal Cyst** **Lateral Radicular Cyst** **Lateral Odontogenic Kertocyst**
* Could be differential for lateral Odontogenic keratocyst, except this does not grow in size * Lateral radicular cysts from an accessory canal if tooth is non vital * or it could be Lateral Periodontal Cyst if tooth is vital!
70
What is the radiographical finding?
**Lateral Periodontal Cyst**
71
What is the radiographical finding?
**Lateral Periodontal Cyst**
72
What is the histological finding?
**Lateral Periodontal Cyst** see the _alternating thin to thick epithelium_ ***a characteristic of these cysts***
73
What is the histological finding?
**Lateral Periodontal Cyst**
74
Cysts of the Newborn: **Palatal cysts** _Demographics_
* Seen in 60‐80% of neonates
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Cysts of the Newborn: **Palatal cysts** _Clinically_
* 1‐3 mm cream to white papules (keratin filled cysts) ## Footnote **\*NOT in bone\***
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Cysts of the Newborn: Palatal cysts Treatment
**No treatment is required** ‐ Resolve (degenerate or rupture) on their own in a few months ‐ Once baby eats solid foods, will go away
77
What is the radiographical finding?
**Botryoid Odontogenic Cyst** well circumscribed, between 2 teeth (similar to lateral odontogenic cyst), multilocular
78
What is the radiographical finding?
**Botryoid Odontogenic Cyst**
79
Cysts of the Newborn: **Gingival cyst of the Newborn** Also known as
**Dental lamina cysts**
80
Gingival cyst of the newborn _demographics & Location_
* Found superficially on the **alveolar ridge mucosa** * **MX** \> MD * Rarely seen after 3 mos. of age
81
**Gingival cyst of the newborn** _Treatment_
▪ No treatment is necessary ▪ Spontaneously resolve (degenerate or rupture)
82
**Gingival cyst of the newborn** _Clinically_
* 1‐3 mm creamy white papule (keratin filled cysts) * \*NOT in bone\*
83
What is the soft tissue counterpart of the **lateral periodontal cyst ?**
**Gingival Cyst of the Adult**
84
What is the radiographical finding?
**“Primordial” Cyst** Assuming histologically it is *different from OKC*
85
Gingival Cyst of the Adult _Origin_
Derived from dental lamina rests **‐ Rests of Serres**
86
**Gingival Cyst of the Adult** _Demogrophic & Location_
**▪Uncommon lesion** ▪ 60‐75% **mandibular canine/premolar area** ‐ most common location on the _facial or buccal aspect_ ▪ **5th and 6th decade** most common
87
**Gingival Cyst of the Adult** _Clinically_
* Painless, dome‐like swellings up to 5 mm in diamete * Often with a bluish or grayish hue
88
**Gingival Cyst of the Adult** has _similar histology_ to which cyst?
**lateral periodontal cyst**
89
**Gingival Cyst of the Adult** _Treatment_
* **simple surgical excision** * _Unlikely_ to recur/come back
90
What are the site distribution of OKC?
Most of OKC in posterior region
91
**Lateral Periodontal Cyst** represents the intrabony counterpart of which cyst?
**gingival cyst of the adult?**
92
Lateral Periodontal Cyst _Origins_
* Developmental cyst believed to arise from **dental lamina rests**
93
**Lateral Periodontal cyst** is diagonsed when cysts occur in the _lateral periodontal region_ and after what have been excluded?
* **an inflammatory origin cysts** or t**he diagnosis of odontogenickeratocyst** _have been excluded_
94
**Lateral Periodontal Cyst** _Charcterstics_ and _tooth vitality_
▪ Commonly **asymptomatic** and _found on routine radiographic exam_ ▪ Associated teeth tests **vital/responsive with electric pulp test**
95
if you see a radilucency Lateral to a teeth how would you know if it's Lateral Periodontal Cyst or Lateral Radicular Cyst or Lateral OKc
‐ **If pulp alive**► **lateral periodontal cyst** or ***Lateral Okc ( if huge lesion)*** ‐ If pulp dead► **lateral radicular cyst**
96
**Lateral Periodontal Cyst** _Demographic_ and _Location_
▪ Most likely found after age 30 ▪ Males\>Females **▪ ~65% mandibular canine/premolar area** ‐ Can also be seen _between canine and lateral incisor_
97
What is the radiographical finding?
**Odontogenic Keratocyst OKC**
98
What is the radiographical finding?
**Odontogenic Keratocyst OKC**
99
What is the radiographical finding?
**Odontogenic Keratocyst OKC**
100
What is the radiographical finding?
**Odontogenic Keratocyst OKC**
101
What is the radiographical finding?
similar to *lateral periodontal cyst* but is actually **OKC**
102
What is the histological finding?
Odontogenic Keratocyst Histology Notice the daughter cysts
103
**Lateral Periodontal Cyst** _Radiographically_
Present as **well circumscribed**, **unilocular** _radiolucencies between 2 teeth,_ located **lateral to tooth root** ▪ Most often **0.5‐1.0 cm** in diameter ▪ Radiographic features are **NOT** diagnostic
104
What is this radiographic finding?
✎A patient who has **Nevoid Basal Cell Carcinoma Syndrome** ✎We can see **multiple cystics** areas and lesions in _the jaws, maxillary and mandible_ ✎**Both 3rd molar displaced** in the maxilla because of the cyst
105
What is this radiographic finding?
✎**Multiple lesions**, impacted 3rd molar in mandible and displaced 3rd molar up into the sinus, ✎These too many lesions hard to manage the issue with a surgery ✎This large area on the left mandible – good example of why we do decompression because if you just remove this lesion and the entire area is left open, this would be an area risk for fracture
106
What is this called which can be seen with Nevoid Basal Cell Carcinoma Syndrome
✎An example of the **pitting** that can be seen **palmar and plantar** ~ This is a side of a hand ✎This is an early stage of basal carcinoma which never goes on (like it is aborted)
107
What are these **findings** that is associated with ## Footnote **Nevoid Basal Cell Carcinoma Syndrome?**
* **thousands of basal cell carcinoma** is developing on the skin -very difficult to manage with surgery, ~ That’s why they remove the larger ones, the deeper ones ~ They leave the one that’s less as an issue until they get to a larger size to be removed
108
Lateral Periodontal Cyst _Treatment_
* consists of **conservative enucleation**
109
What cyst is a **variant of lateral periodontal cyst?**
**Botryoid Odontogenic Cyst**
110
**Botryoid Odontogenic Cyst** _Grossly_ and _Microscopically_
shows **a grape‐like cluster** of small individual cysts
111
**Botryoid Odontogenic Cyst** _Radiographically_
▪ Either unilocular or multilocular on radiographs, depending on size of the lesion ▪ Cyst lining similar to lateral periodontal cyst
112
**Glandular Odontogenic Cyst** _Charcterstics_
* **A rare odontogenic cyst** which exhibits features of _glandular differentiation within the epithelium_ * Presumably **represents the pluripotentiality of odontogenic epithelium**
113
Glandular Odontogenic Cyst _Demographics_
▪ Wide age range from 2nd to 9th decades **‐** *_mean age 49_* **▪ ~ 80% of cases in mandible ▪ Anterior lesions** ‐ More common ‐ _May cross the midline_
114
**Glandular Odontogenic Cyst** _Radiographically_
▪ Uni‐ or (more often) multilocular radiolucency ▪ **Well‐defined** with **a sclerotic border**
115
**Glandular Odontogenic Cyst** reccurance rate
(~ 25% recurrence rate) Can be locally aggressive
116
Glandular Odontogenic Cyst _Clinically_
▪ Usually asymptomatic unless inflamed
117
What is this radiographic finding?
``` **Calcifying Odontogenic Cyst (COC)** ``` * _in the mandible_ and you can see it **well circumscribed radiolucency** * a little bit of blunt root resorption in this area * _No calcifications_ in this one yet ►so this is still **unilocular radiolucency**
118
What are the _clinical_ and _radiographic_ findings here? What is this lesion?
* Clinical finding for this patient was **Obliteration of the vestibule space**, because the mandible is showing expansion * radiographically:we see radiolucency going as far as the first molar * This is a **mixed radiolucent radiopaque lesion** in developing calcifications. * This is an example of **Calcifying** **Odontogenic Cyst (COC)**
119
**“Primordial” Cyst** why it is _controversial!_
* **Mixed up with OkC** * Originally meant to describe cyst which **develops in bone at a site where a tooth was meant to develop (usually a third molar)** * If this lesion exists, **it is truly rare and would have histology distinct from OKC** * * In the current literature, reference has been almost _nonexistent_
120
“Primordial” Cyst is **not** a true -------
* lesion, *was actually some other type of cyst* * * it is now thought that most of the reported Primordial cysts were actually **OKCs**
121
**Odontogenic Keratocyst** **OKC** _Also known as_
**keratocystic odontogenic tumor (KOT)** -2005 WHO _but now it's back to **OKC**_
122
**Odontogenic Keratocyst (OKC)** _Etiology_
* **Growth and expansion** of this lesion due not only to osmotic effects/pressure, but to _unusual gene expressions_
123
Which **unusal gene expression** causes _growth and expansion of OKC_ ?
* _Expresses **Ki‐67**_ (high rate of cell proliferation) * O_verexpression of **Bcl‐2**_ (antipoptotic protein) * _Overexpression of **MMP’s 2 and 9**_ (thought to allow growth into connective tissue) * _Mutation of **PTCH**_, a tumor suppressor gene * when PTCH is non‐functional → cell proliferation
124
**Odontogenic Keratocyst (OKC)** _Demographic & Location_
* ~ **60%** present in **2nd and 3rd decade**, but can occur at any age * **Mandible** affected in 60‐80% of cases * tendency to occur in **posterior mandible and ramus** * **25‐40% of cases involve an unerupted tooth** * ‐ **5%** of patients have **_multiple cysts_**
125
**Odontogenic Keratocyst (OKC)** differes from **Meloblastoma** **in its growth pattern**
**Odontogenic Keratocyst (OKC) :**grows in anterior to posterior manner before causing cortical expansion *while* **Meloblastoma:** causes **cortical expansion _early_**
126
Which cyst make up **~10‐15%** of all **odontogenic cysts?**
**Odontogenic Keratocyst (OKC)**
127
5% of **Odontogenic Keratocyst (OKC)** are associated with _which syndrome?_
**nevoid basal cell carcinoma syndrome**(*_**Gorlin syndrome**)_*
128
Odontogenic Keratocyst _Reccurance Rate_
* **HIGH Recurrence Rate** * **Benign**, but _locally aggressive biologic behavior_ * _Solitary OKCs have_ ~**10% recurrence rate with appropriate treatment** * _Multiple OKCs hav_e ~ **30% recurrence rate**
129
**Odontogenic Keratocyst** **(OKC)** _Reccurance Rate Order_ from **highest** to **lowest** reccurance rate
**Syndrome OKC \> Multiple OKC \> Solitary OKC \> Conventional odontogenic cysts**
130
**Odontogenic Keratocyst** **OKC** _Radiographically_
* Usually **a well‐circumscribed** *_radiolucency_* with **smooth, often** **corticated margins** ▪ Cysts may be ‐ **Unilocular** (most common) ‐ **Multilocular** (larger lesions)
131
**Odontogenic Keratocyst** **OKC** _clinically_
▪ **Small cysts** are typically **asymptomatic** and picked up on routine radiographic exam ▪ **Larger cysts** may or may not be asymptomatic ▪ \*Cysts tend to grow in an antero‐posterior direction prior to lateral growth ►_therefore cysts are usually quite large when they start to expand the cortical plate_
132
**Odontogenic Keratocyst** **OKC** Has similar Radiographic findings with ?
* dentigerous cyst * ameloblastoma * and others
133
**Odontogenic Keratocyst OKC** _Treatment_
▪ **Marsupialization** (decompression) ▪ **Peripheral ostectomy** ‐ Carnoy’s solution ▪ **Resection** ▪ **Medications targeted to PTCH** ▪ ***Long term follow‐up***
134
**Nevoid Basal Cell Carcinoma Syndrome** is also known as ----- ?
**Basal Cell Nevus or Bifid Rib Syndrome** or **Gorlin syndrome**
135
Which cyst is assoicated with Nevoid Basal Cell Carcinoma Syndrome ?
**Odontogenic Keratocyst “OKC”**
136
**Nevoid Basal Cell Carcinoma Syndrome** **(Gorlin syndrome)** _modes of inheritanc_e
**_Autosomal dominant_ inheritance**
137
Which **_Gene mutation and pathway_** _associated with_ **Nevoid Basal Cell Carcinoma Syndrome** **(Gorlin syndrome)**
* _Mutation_ of **PTCH** (tumor suppressor gene) * in the **Sonic Hedge Hog pathway**
138
**Nevoid Basal Cell Carcinoma Syndrome** _Prognosis_
■ Prognosis _depends on progression of skin tumors_
139
**Nevoid Basal Cell Carcinoma Syndrome** _Treatment_
✎Surgery (typically MOHS) ✎Sometimes curette them ✎ Radiation therapy (RT) is typically not the first line of therapy with small lesions RT ✎Cryotherapy which means they just use a little liquid nitrogen and freeze them ✎Photodynamic therapy with photosensitizer and topical medications ■ New medication: **Vismodegib _inhibits sonic hedgehog pathway by binding smoothened (SMO)_** * *suppressive rather than curative cause it seems to work for short time and after ~7-8 months ..may also helps _suppress growth of OKC_*
140
Why **Basal Cell Carcinoma** is very problematic ?
It’s not the lesion themselves causing metastasis that’s the issue, it’s the lesion growing deeply and in affecting adjacent structures that really is the issue with basal carcinoma
141
What is the **Most common type of skin cancer?**
**Basal Cell Carcinoma (BCC)**
142
**Basal Cell Carcinoma (BCC**) _Demographics_
* 2-3 million cases a year * About 3 out of 4 skin cancers are basal cell carcinomas
143
Basal Cell Carcinoma _Growth_ and _location_ | (BCC)
- Develop in the **lowest layer of the epidermis**, called the **basal Laye**r - Develops on sun-exposed areas: _cumulative DNA Damage_ **- Slow-growing** • If not treated, basal cell c**ancer can grow into nearby areas and invade the bone or other tissues beneath the skin**
144
Basal Cell Carcinoma _Progrssion_ | (BCC)
within 5 years of being diagnosed with BCC►**35%-50%** of people _develop a new skin cancer_
145
**Calcifying Odontogenic Cyst** **​COC** also known as ?
* **Calcifying Cystic Odontogenic Tumor** * **_Gorlin Cyst_ ( don't confuse it with Gorlin syndrome)** * **Ghost Cell Tumor** *
146
**Calcifying Odontogenic Cyst (COC)** can present in **3 types**
1. **■ Cystic Unilocular COC** * COC with odontoma (~ 20%) * Extraosseous/peripheral – present in _older patients_ 2. **■ Solid COC (odontogenic ghost cell tumor)** * Often demonstrate _a more aggressive behavior_ * WHO once considered them all CCOT now back to COC 3. ■ **Odontogenic ghost cell carcinoma** * _very rare lesion_
147
**Collision Tumors** is a term used to describe lesions involving Calcifying Odontogenic Cyst (COC), what does that mean?
* where you see **_both features_ of ameloblastoma with COC** or **adenomatoid odontogenic tumor with COC**
148
**Calcifying Odontogenic Cyst (COC)** _may occur in association_ _with_ **which tumors or cysts?**
* **Odontomas** (a benign tumour linked to tooth development) * **Ameloblastomas** (rare, noncancerous (benign) tumor) * **Adenomatoid odontogenic tumor** (rare tumor of epithelial origin that is benign, painless, noninvasive, and slow-growing)
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**Calcifying Odontogenic Cyst (COC)** _Demographics & Location_
■ Peak in _second decade_, most **before age of 40** ■ Frequently presents **anterior to molars** ■ ~ **20% extraosseous (peripheral)**, found in **older age group** (~ 50 years of age) ■ Female \> Male ■ **~ 70% occur in MX** ■ One third are associated with **unerupted teeth**, usually a **canine**
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Calcifying Odontogenic Cyst _Radiographically_ | (COC)
■ Usually **a well-circumscribed unilocular radiolucency,** _infrequent multilocular cases_ ■ **One third to one half** show _radiopaque structures within the radiolucency_ ■ When you see **calcifications** within a lesion, you don't use the term uni or multi locular anymore, but they are called **_mixed radiolucent/radiopaque lesions_** ■ May cause **resorption or displacement of roots** **■** **_One third_** are associated with **unerupted** **Canine**
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The hallmark of Calcifying Odontogenic Cyst COC Histology is
**_Ghost cells_** They have that sort of polygonal shape or roundish shape with the pink that looks like the cytoplasm, but in the location where the nucleus would have then, there's an empty spot
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Histologically speaking, Calcifying Odontogenic Cyst COC, basically looks similar to what epithelium?
**_ameloblastic epithelium_**
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**Calcifying Odontogenic Cyst COC** _Treatment_
■**Enucleation with peripheral ostectomy** ~ Very similar to odontogenic keratosis ■ **Follow up is long term** because s_ome of the solid tumors have a more aggressive behavior_ **■ Peripheral lesions are treated with excision**
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When COC is associated with another tumor, ameloblastoma, how would you treat?
■ the treatment is based on **the more aggressive tumor** **~** So you would treat the _ameloblastoma_. ~You wouldn't treat conservatively the COC though
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**Odontogenic ghost cell carcinoma** _Prognosis_
**(5 year survival ~ 70%).** * It is _rare_ and shows _cytologic atypia histologically_ * It has an _unpredictable biologic behavior_
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**Fissural Cysts** | (6)
❑ Nasolabial cyst ❑ Globulomaxillary cyst (historic) ❑ Nasopalatine (incisive canal) cyst ❑ Incisive papilla cyst ❑ Median palatal cyst ❑ Median mandibular cyst (historic)
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**Nasolabial Cyst** also known as
aka Nasoalveolar cyst
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where a number of the visual cysts would develop
(1) That's the nasopalatine, which is sort of up in the labial nasal fold and it's in the soft tissue. (2) Sort of where the nasal alveolar cyst would occur. (3) Where the globular maxillary cyst would occur between the canine and the lateral sometimes between the lateral and the first premolar (4) The nasopalatine in the cyst of the nasopalatine papilla (5) Is the median palatal
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**Nasolabial Cyst** _Etiology_
■ Thought to be caused by: * either **epithelial remnants of the nasolacrimal duct** * or **cells left after fusion of the maxillary, medial and lateral nasal processe**s during _development of the midface_
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**Nasolabial Cyst** _Location_
_Rare_ **soft tissue cyst of the upper lip**, lateral to the midline (right under the ala of the nose) \*NOT in bone\* ■ Clinically see a swelling which can cause elevation of the ala of the nose ■ Intraorally see a swelling in the maxillary vestibule lateral to the midline (usually sort of in the canine area or just a little bit distal to the canine area) ■ Pain is uncommon, unless cyst becomes infected
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**Nasolabial Cyst** _Clinically & Intraoray_
■Clinically we see a **swelling** which _can cause elevation of the ala of the nose_ ■ Intraorally see **a swelling in the maxillary vestibule lateral to the midline** (usually sort of in the canine area or just a little bit distal to the canine area) ■ **Pain is uncommon,** _unless cyst becomes infected_
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**Nasolabial Cyst** _Demographics_
■ Peak in **4th and 5th decades** ■ **3 to 4 times** _more common in **females**_ ■ ~ **10%** of cases are **bilateral**
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**Nasolabial Cyst** _Treatment_
* **Surgical Excision** via i**ntraoral approach**, * usually do not recur ~ **very low risk of occurrence**
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What is this clinical finding?
Nasolabial Cyst The lesion here just below the nose and you can tell that it's sort of raising the edge of the nose slightly
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What is this clinical finding?
**Nasolabial Cyst** the lesion raising the edge of the nose slightly
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_Nasolabial Cys_t has a a **respiratory type epithelium** and so it's very similar to what you would see in ?
either in the **sinus** or in the **nasopalatine ducts**
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Is this ## Footnote **Globulomaxillary Cyst** **lateral granulomas** **OKCs** **COCs**
* we can see the **displacement of the root** * A **teardrop or pear shaped** radiolucency between the lateral and the canine * **Well circumscribed** maybe leaving **a little sclerotic edge** up here * ended up being in **a odontogenic keratocyst (OKC)**
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Is this Globulomaxillary Cyst , lateral granuloma or OKC?
~ it is kind of **a teardrop or pear shaped size** ~Little less well differentiated in this particular instance but again **unilocular radiolucency between the roots of two teeth** This one ended up being an **OKC**
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"Globulomaxillary Cyst" _Origin_ _controvesy_ why the name in quotations?
* it's in quotations, because really there is no such thing as a globulomaxillary cyst * because it was thought that this was remnants _after fusion of the globular portion of the nasal process with the maxillary process,_ and now we know that **these two processes are always united from the start and that there is no fusion** * When biopsied these cysts are **odontogenic in origin**
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what does it mean for **Globulomaxillary Cyst** to be **odontogenic in origin**?
✎This is term used to **describe a cyst in a particular anatomic location** _it is not a diagnosis_ ✎An odontogenic cyst (inflammatory cyst, lateral periodontal or even sometimes OKC) that forms in the area **between the maxillary lateral incisor and the canine roots** ~ It's really associated with a_n anatomic location **not** with any particular cyst._ ✎So it can be any of the odontogenic lesions such as **lateral granulomas or cysts, OKCs, COCs, etc.**
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**Globulomaxillary Cyst** _Radiographically_
## Footnote ✎Presents as a **“inverted pear”** shaped **well-circumscribed radiolucency** ✎Frequently causes **displacement of the roots**
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What are two different ways nasopalatine duct cyst arise?
* *A**. It can either be _the cyst totally within bone_ * *B**. It can actually cause _widening of the orifice and causing the soft tissue expansion in this way_
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Most common non-odontogenic cyst of the oral cavity
**Nasopalatine Duct Cyst**
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**Nasopalatine Duct Cyst** also known as
**incisive canal cyst** **nasopalatine canal cyst**
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**Nasopalatine Duct Cyst** _Origin_
* arise **from epithelial remnants of the nasopalatine duct** which, _embryologically, connects the oral and the nasal cavities_
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What is this radiographic finding?
**Nasopalatine Duct Cyst** ## Footnote ✎This person is edentulous ✎ **an inverted pear shape** ✎The nasal spine is superimposed on your radiolucency ► **a heart shape**
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What is this radiographic finding?
**Nasopalatine Duct Cyst** ✎Between the roots of the two teeth, a well circumscribed radiolucency, not showing any changes to the adjacent structures ✎could be an enlargement of the incisive canal due to variation in size ~ **early lesions can be hard to diagnose** ✎**the treatment in such cases**: a follow up with another radiograph in six months to see if there's been any change in size **✎ No surgical intervention until you see the cyst expanding**
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What is this oral finding?
This is showing you the how the papilla can be enlarged if it's only in soft tissue or if there's a partial soft tissue partial bone expansion *Nasopalatine Duct Cyst*
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**Nasopalatine Duct Cyst** _Demographic_ and _Location_
* Peak presentation in the **4th to 6th decades**, _but can occur at any age_ ~ *because it takes a little bit of time for the cyst to grow within the bone* * commonly found on the **anterior palate** ~ typically in the _nasal area of the papilla._
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What is this radiographic finding?
**Median Palatine Cyst**
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Nasopalatine Duct Cyst _Clinically_
■ present with **swelling** o_f the anterior palate_ (in the nasal area of the papilla) ■ Most are **asymptomatic**, but _they may have pain or drainage_
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Is this Median Mandibular Cyst Or something else
Remember ## Footnote _Median Mandibular Cyst_ is a term used to describe a cyst in a **anterior mandible** not a definitive diagnosis So, this turned out to be an early ameloblastoma. It wasn’t a cyst The lesion radiolucency in the anterior mandible and again
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**Nasopalatine Duct Cyst** _Radiographically_
■ a **well-circumscribed unilocular** **radiolucency** on _the midline of the anterior hard palate_ _between and apical to the central incisors_ ■ The radiolucency often have an oval or inverted pear shape with a sclerotic border ■ Superimposition with the nasal septum can create an appearance of the classic **“heart” shape**
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**Cysts of the incisive papilla** **Incisive papilla cyst**
Is a **soft tissue cyst** (no bone involvement) located in the same area as the **Nasopalatine Duct Cyst** _on the midline of the anterior hard palate between and apical to the central incisors_ . They may be symptomatic or asymptomatic and usually are not seen radiographically. some consider them to be uncommon variants of the nasopalatine duct cysts
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**Nasopalatine Duct Cyst** _Treatment_
* **surgical excision** * **recurrence is rare**
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What is this radiographic finding?
**Surgical Ciliated Cyst of the Maxilla** In this premolar shot (middle image) you can see a **well-circumscribed lesion** ✎Because the maxillary sinus is **radiolucent**, it almost looks like this is **radiopaque** but it's not ✎ If you did a CBCT you would see that **it's an empty space within the bone of the maxilla.** It's not actually radiopaque
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**Median Palatine Cyst** **is** **_a variant of which cyst?_**
**nasopalatine duct cyst** * it represents a more **posteriorly** placed nasopalatine duct cyst * ~ It's probably due to some sort of anatomic variation in the patients; that their palatine duct is just placed more posteriorly * So **instead of being between the roots of these two teeth, it's placed more posteriorly**
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**Median Mandibular Cyst**
* **A controversial cysts** whose existence is questioned ~ similar to **the globulomaxillary cyst** ■ Originally *thought to arise from the fusion of the “halves” of the mandible, but current embryology finds that the mandible forms from a single bilobed process, therefore, no epithelial remnants would be found* ■ Now, it is thought that cysts in this area represent **odontogenic cysts or tumors** * **Median Mandibular Cyst is a** term used **to describe a cyst in a particular anatomic location not a definitive diagnosis** * ~ It is other lesions that occur in that particular location * **The Anterior Mandible**
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**Surgical Ciliated Cyst of the Maxilla** _Etiology_
■ Occurs after trauma or sinus surgery (iatrogenic - reactive not neoplastic)
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**Surgical Ciliated Cyst of the Maxilla** _Formation_
■a portion of the sinus lining is **separated** from the sinus and forms an epithelial lined cavity in bone ■ Cavity f**ills with mucin** produced by the _mucous cells of the cyst lining_ ■ These cysts **enlarge** as the _intraluminal pressure increases_, causing **destruction of bone**
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**Surgical Ciliated Cyst of the Maxilla** _occurs frequently_ **after** **which procedures?**
* after **a Caldwell-Luc procedure** * *sometimes with **difficult maxillary extractions***
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In which country **Surgical Ciliated Cyst of the Maxilla** are reported with higher frequency ?
**Japan**
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What are **pesudocysts?**
* **They have no epithelial lining.** * They’re called cysts by convention just because that's what everybody is used to * **They're not true cysts.**
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pesudocysts List (5)
* Aneurysmal Bone Cyst * Antral Pseudocyst * Simple Bone Cyst * Osteoporotic Bone Marrow Defect * Stafne Bone Cyst
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**Aneurysmal Bone Cyst** Demographics
■ Most common site in the body is **long bones *or* vertebrae** _■ In the jaw_s, most frequently seen in the **1st and 2nd decade** **■ MD \> MX** ## Footnote *it's a pesudocyst*
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**Aneurysmal Bone Cyst** _Clinically_
* swelling, frequently a rather rapid swelling * often with **pain** and/or **paresthesia** (signs which can be suggestive of the presence of _a malignant or aggressive lesion_)
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**Aneurysmal Bone Cyst** Etiology
* Etiology is **unclear**, may result from **trauma** or a **vascular malformation** * most agree that it is a _**reactive** and ***not*** a neoplastic lesion_
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**Aneurysmal Bone Cyst** _Radiographically_
■ **a radiolucency** which can be either **unilocular or multilocular** in appearance ■ **Borders are variable**, *often irregular in shape* and may be **ill-defined** (again, giving the suggestion of malignancy) ■ **Teeth may be displaced** ■ we may see **cortical expansion and thinning** ~ the cortex itself can become quite thin
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What does this person have?
- you might think that he has an odontogenic infection but he didn't. You can see that there's a pretty significant swelling on the left side of his face This is a **Aneurysmal Bone Cysts**
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What is this radiographic finding?
Aneurysmal Bone Cyst you can see that there is kind of a **multilocular radiolucency** in this particular area
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What is this radiographic finding?
**Aneurysmal Bone Cyst** ## Footnote ✎ There's a **radiolucency** involving _the second molar_ that's going as far anterior as the first molar and back to the third molar ✎ There is a little bit of **spiking root resorption** and _that's one of the signs that we associate with malignancy_ ✎ It's a little bit **ill-defined** *~ hard to say exactly where it begins and ends*
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What is this gross finding?
**Aneurysmal Bone Cyst** ✎ It looks like **a blood soaked sponge** ✎ There’s these **open sinusoidal spaces** and then fibrous connective tissue surrounding them. *✎The sinusoidal spaces can vary in size; some of them are fairly small and others are large*
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**Aneurysmal Bone Cyst** _Treatment_
■ Treatment is **surgical enucleation and curettage** ■ **lesions can recur** ~ Usually the recurrence is because you didn't get the entire thing out the first time around ■ Some surgeons follow **enucleation** with **cryotherapy** ■ **Irradiation** is _contraindicated_
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Is **bleeding a concern** during surgical removal of **Aneurysmal Bone Cyst?**
■ No, **vascularity is predominantly “low flow”**, therefore not as much concern for bleeding upon surgical removal ■ As compared with **central hemangioma** where there is a concen for bleeding
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**Antral Pseudocyst**
They are different than **surgical ciliated cyst** in their lining, etiology, location and appearance!
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What is this radiographic finding?
**Antral Pseudocyst** * a **Dome-shape** **swelling** on the floor of the sinus. * _They can sometimes_ be **fairly subtle** **Antral Pseduocyst** are **NOT Mucoceles** **Mucoceles** would have more of **meniscus-like appearance**where it would come up to**the edge of the sinus**
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As opposed of surgical ciliated cysts, **Antral psuedocysts are not ----** *( in term of their lining)*
_Not epithelial lined spaces_
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What are these radiographic findings?
**Aneurysmal Bone Cyst** ## Footnote ✎ A **dome shape swelling on the floor of the sinus** that’s associated with some _sort of inflammation of tooth of t_he **premolar** caused inflammation underneath the apex of the bone (right) and then that leads to accumulation of fluid which causes the sinus lining to elevate off the bone and fill with fluid ✎ After root canal therapy and once the infection gets under control, these will typically resolve on their own
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As opposed of surgical ciliated cysts, **Antral psuedocysts are not ----** *( in term of location)*
Not within the bone **but are in the sinus**
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As opposed of surgical ciliated cysts, **Antral psuedocysts Develop as ----** ## Footnote ***( in term of etiology)***
develop a**s an accumulation of an inflammatory exudate** (often serum) _between the sinus epithelial lining and the bone_ -It develops because of an **inflammatory event in the jaw,** usually the **maxilla**, often from the roots of the maxillary teeth that cause inflammation
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As opposed of surgical ciliated cysts, **Antral psuedocysts appear as ----** ## Footnote *( in term of Radiology)*
Appears as **a dome shaped elevation** _of the floor of the sinus_
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**Simple Bone Cyst** also known as
aka **traumatic bone cyst**
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What is this radiographic finding?
**Simple Bone Cyst** ## Footnote ✎**A well-circumscribed with cortication** in the **body of the mandible**, affecting _the posterior aspect (premolars and the molars )_ ✎Note the **scalloping** that happens up **between the roots**. It doesn't cause root resorption and actually the lesion will grow up between the roots of the teeth
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What is this radiographic finding?
**Simple Bone Cyst** * **A well-circumscribed**showing **the scalloping up between the roots of the teeth radiolucency**
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What is this radiographic finding?
**Simple Bone Cyst** ## Footnote ✎Big lesion example: It’s going back to the molar area here. ✎You can see that the lesion extends _over to the canine on the other side_ ✎Most lesions are usually **in the anterior mandible**
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**Simple Bone Cyst** _Charcterstics_
* **A benign**, empty or fluid filled, cavity in bone which is devoid of an epithelial lining – **a pseudocyst** * Thought to be **reactive**, NOT *neoplastic*
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**Simple Bone Cyst** _Etiology_
_Etiology_ **ununcertain**, theories include: * **trauma** * **ischemic necrosis of medullary space** * **cystic degeneration of a primary bone lesion**
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**Simple Bone Cyst** _Demographics_
* In jaws, most likely in the **2nd decade** * Almost **exclusively the mandible** * **Twice** as common in **males**
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**Simple Bone Cyst** _Radiographically_
* a **well-circumscribed radiolucency** with **an irregular outline** * Tendency to **“scallop” around and between roots** *_(highly suggestive_*, but *_not diagnostic of this lesion_*)
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**Simple Bone Cyst** _Treatment_
* **exploration** and **curettage** of space to create bleeding. Clot will organize and allow bone repair * **Recurrence** is **_rare_**
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What is this radiographic finding?
* You can see there's a little bit of radiolucency. * There happened to actually still be teeth in the area, but * when it was _biopsied_ it showed that it was a * **hematopoietic** or **osteopoietic bone marrow defect**
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**Stafne Bone Cyst** _Charcterstics_
■ An **asymptomatic** focal _concavity_ of the cortical bone on the _lingual aspect of the MD_ ■ A *pseudocyst*, not a true cyst
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**Osteoporotic Bone Marrow Defect** _Demographic_
■ _Uncommon finding_ ■ \> 75% of cases are in **females** ■ ~ 70% occur in the **posterior MD**, often in _an edentulous area_ it's a *pesydocyst*
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**Osteoporotic Bone Marrow Defect** _Etiology_
* **Etiology unclear** * may be **hyperplasia of marrow** due to need for RBCs or * **abnormal regeneration of bone** after **an extraction or persistence of fetal marrow**
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**Osteoporotic Bone Marrow Defect** _Charcteristics_
* it's a pesydocyst * a **radiolucency** in an area typically where tooth has been removed. Instead of filling in with bone, it fills in with marrow. * When we biopsy it, you’re seeing the hematopoietic elements. (fat, early stages of (the -blasts of) red cells, white cells. * We see basic **bone forming marrow** **content**
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What is this radiographic finding?
**Stafne Bone Cyst** _This is the classic look._ - a **well-circumscribed corticated radiolucency** - **below the inferior alveolar nerve**, away from the teeth. - They can be either **oval**, like this, or **round** in appearance
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What is this radiographic finding?
**Stafne Bone Cyst** Less common location Check if the teeth were vital with vitality test Get a CBCT in that area to see what was going on first and then once you saw the CBCT you'd be able to make the diagnosis.
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Osteoporotic Bone Marrow Defect
**Hematopoietic bone marrow defect**
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**Osteoporotic Bone Marrow Defect** _Clincalally_
■ Typically **asymptomatic** and found on _routine_ radiographic exam
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**Osteoporotic Bone Marrow Defect** _Radiographically_
* **Irregularly shaped radiolucency** with _either_ **a well-defined or ill-defined border** (It can be in the _differential diagnosis with malignancy_)
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**Osteoporotic Bone Marrow Defect** _Treatment_
■ **Must biopsy** to make a definitive diagnosis ■ **No further treatment is then necessary** ~ You don't have to remove it; you can just leave it as it is
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**Stafne Bone Cyst** also known as
**static bone cyst, Stafne defect**
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**Stafne Bone Cyst** _Demographics and Location_
* Most commonly found near **the angle of the mandible** **below the inferior alveolar nerve** (but also _seen in the anterior MD)_ * **\> 80% in Males** * usually noted **only in adults**
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**Stafne Bone Cyst** _Radiographically_
Oval round well-circumcribed radilucency Below the Inferior Alveolar Nerve
235
**Stafne Bone Cyst** _Etiology_
* Believed to be **developmental** in origin, *but usually noted only in **_adults_***
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**Stafne Bone Cyst** _Treatment_
* lesions in the posterior MD are usually pathognomonic * **no further treatment is necessary**
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**Dermoid Cyst** _Charcterstics_
* **Benign** developmental cystic lesion * Considered a form of teratoma Remember: _Teratomas_ have **all four embryologic** **layers** and so you can see these cysts that have **teeth, bone, hair, muscle, and nerves.** **Dermoid cyst** is sort of a lesser version of a teratoma in that **it just has dermis, rather than all the other layers**
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**Dermoid Cyst** _Clinically_
* Depending on whether the cyst is above or below the mylohyoid muscle►the lesion will cause **swelling into the oral cavity elevating the tongue** or **under the chin in the submandibular area**, _respectively_ * Usually **found on the midline** * **Painless** and **slow growing,** _if not infected_ * _Upon palpation, cyst feels **doughy or rubbery**_ * _Usually **roundish to oval-ish swelling**_
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**Dermoid Cyst** _demographic and locations_
* Most common in the 1st and 2nd decade ( young pts) * Can be found anywhere, but in the oral cavity they are ususally located i**n the anterior floor of the mouth (FOM) -** *usually* ***on the midline***
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**Dermoid Cyst** _Treatment_
* **surgical excision** * _recurrence_ is ***rare***
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_Dermoid Cyst_ a **dome shaped swelling**in _the floor of the mouth._ If these were left long enough, they could _cause issues with swallowing_
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What is this clinical finding?
**Dermoid Cyst** ## Footnote ✎This is **a larger lesion on the floor of the mouth**, causing elevation of the tongue ✎If you let this go/grow, it would be similar to **Ludwig’s angina** where you would basically **eventually obstruct the airway** ✎**The difference** is this is **very slow growing** while **Ludwig’s happens** rather quickly. with **fever and other symptoms.**
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What is this clinical finding?
**Dermoid Cyst** * This is showing you when they occur below the **mylohyoid muscle.** * You get **an elevation under the chin.** * This is **a fairly small on**e but they can get much larger
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**Epidermoid Cyst** also known as
**infundibular cyst** **epidermal inclusion cyst** **“sebaceous” cyst** (laymen’s term, not really sebaceous) ~
245
**Epidermoid Cyst** _Charcterstics_
* A very common skin cyst
246
**The epidermoid cyst** is similar to which cyst?
similar to the dermoid cyst, except we don't see those **adnexal structures**
247
**Epidermoid Cyst** _Etiology_
* Often occur after _***inflammation*** of a hair follicl_e
248
**Epidermoid Cyst** _Demographics and Location_
■ **_Males_** \> *Females* ■ **Young adults** _more likely to have cysts of the_ **fa**ce ■ **Older adults** _have cysts of the_ **back**
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**Epidermoid Cyst** Associated with which **syndrome**?
Associated with **Gardner’s syndrome** **Gardner syndrome** is associated with **polyps in the intestine**. **Gardner syndrome** is associated with **epidermoid cysts.**
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What is this clinical finding?
Epidermoid Cyst **A dome-shaped swelling.** There’s **no change** in the overlying skin color, no redness, no pain
251
**Epidermoid Cyst** _Clinically_
■ **Subcutaneous** ***nodular***, ***firm to fluctuant,* _papule_** ~ It tends to be **a subcutaneous, dome-shaped nodule that can be either firm to fluctuant**, _depending on how much stuff is within the lumen_
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What is the key difference between _a dermoid and epidermoid cyst?_
* The key difference between a dermoid and * epidermoid cyst, **is that there's no adnexal structures in an epidermoid cyst. _There are adnexal structures in a_** **_dermoid cyst._** * The adnexal structures are: **sebaceous glands, sweat glands, hair follicles, etc.**
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**Epidermoid Cyst** _Treatment_
■ Treatment is **_excision_** ■ _Recurrence_ is ***rare***
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What is this clinical finding?
Thyroglossal Duct Cyst This is **NOT** a goiter. It looks like an enlargement of the thyroid, but this ended up being just a cyst, so they had a thyroglossal duct cyst
255
Thyroglossal Duct Cyst _Etiology/Origin_
* _A developmental cyst_ that develops **from epithelial remnants of a tract which forms when the thyroid anlage descends into the neck** _from an area that later forms **the foramen caecum**_ * Follows a path that goes **anterior to the hyoid bone and ends below the thyroid cartilage**
256
Thyroglossal Duct Cyst Clinically
■ Cysts are typically **painless fluctuant swellings,** _unless infected_ ■ **If the cyst remains attached to the hyoid bone or the tongue ►** i_t will move up and down when swallowing or protruding the tongue_ ■ **~ 1/3 will present with a fistulous tract** ~ _so they'll be draining._
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Thyroglossal Duct Cyst Treatment
■ **surgical excision** ■ _recurrence_ are ***not uncommon*** ■ *Rare cases* of **thyroid carcinoma** developing in these cysts have been reported
258
Thyroglossal Duct Cyst Demographics and locations
■ **60-80% of cysts** are _below the hyoid bone_ ■ **Most commonly present in the first 2 decades** (~ 50% prior to 20 years of age) ■ Cyst classically **forms at the midline** ■ _The most common developmental cyst of the neck_
259
What is **the most common** ## Footnote **developmental cyst of the neck?**
Thyroglossal Duct Cyst
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Branchial Cleft Cyst Also known as
**cervical lymphoepithelial cysts**
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What is this clinical finding?
Branchial Cleft Cyst **a small one in a child.** You can see that there's a small cystic lesion here on the neck
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What is this clinical finding?
**Branchial Cleft Cyst** Then you can see it in an older person; this is getting to be maybe 4-5 centimeters at least in size. He left his for a little bit longer
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**Branchial Cleft Cyst** _Demographic and location_
■ Most commonly presents in the **3rd to 5th decades** ■Located on the **lateral aspect of the neck**, usually **anterior to the sternocleidomastoid muscle** ■**2/3** of the reported lesions have been **on the left side** ■Although cyst are uncommon in the parotid gland, can see multiple lymphoepithelial cysts bilaterally in **HIV positive patients** ■These cases present as painless uni- or bilateral swellings of the parotid glands
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Branchial Cleft Cyst _Clinically_
* presents as a **soft fluctuant swelling** ranging from **1 to 10 cm** _in diameter_
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Branchial Cleft Cyst _Etiology_
Etiology is _disputed_ * Some think it is _from_ **remnants of the branchial cleft** * Others think it is _cystic change of parotid gland epithelium_ which **became entrapped in a cervical lymph node during development**
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What is this clinical finding?
**Oral Lymphoepithelial Cyst** **A pale dome-shape swelling in the floor of the mouth. ​**because the lesion is so close to the surface; you're seeing _little capillaries of the mucosa lining the lesion_
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Branchial Cleft Cyst & HPV patients
We can see _multiple Branchial Ceft cysts_ bilaterally on the parotid gland Painless swelling bilaterally or unilaterally on the parotid gland
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**Branchial Cleft Cyst** _Treatment_
surgical excision, recurrence is rare
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Oral Lymphoepithelial Cyst _Demographics and Location_
■ **Uncommon lesion** ■ **The Most frequent location is _the floor of the mouth (FOM)_** (\> 50%)
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**Oral Lymphoepithelial Cyst** _Clinically_
■ Usually **less than 1 cm** _in diameter_ ■ May feel **firm or soft** _on palpation_ ■ Typically **creamy to yellow** _in color_ ■ **Painless** _unless infected_
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**Oral Lymphoepithelial Cyst** _Treatment_
* **Surgical Excision** * _Reccurance_ is ***Rare***
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What is the relationship between lesion's **agrressivness**, **rate of reccurance** and **follow up duration ?**
the more aggressive the biologic behavior, the higher risk of recurrence, and the longer the follow up needed for the patient
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What is the spectrum of benign and malignant lesions
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Which lesions are considered benigns
Things that have a very low rate of recurrence when you do a conservative excision or a nucleation ►they're going to be very benign and they're not going to be likely to be recurrent: ▪ **Odontoma and radicular cysts** are way down here near the benign side ▪ **AOT** (Adenomatoid Odontogenic Tumor) is benign. ▪ **COCs** (Calcifying odontogenic cyst) are benign. ▪ **OKCs** (Odontogenic keratocyst) ‐ they’re benign. ▪ Even **Ameloblastomas** are benign
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which lesions are on the malignant side?
But eventually you get over to the side over here where you can have something like an ***Ameloblastic carcinoma*** ‐ truly malignant --\> W*e know that it can metastasize and it can lead to death* ▪ Lesions like **Ameloblastomas and CEOTs** will need to be _managed more aggressively._ (**Not just curettage, aka surgical scraping or cleaning**) o You have **a resection ‐ either a portion of the mandible is removed or a segment of the mandible is removed.**
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What are the **3 Classification of benign tumors?**
1. **Epithelial** 2. **Mesenchymal** 3. **Mixed**
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What are the list of Epithelial Benign Tumors? (5)
**▪ Ameloblastoma ▪ Adenomatoid odontogenic tumor ▪ Calcifying epithelial odontogenic tumor ▪ Squamous odontogenic tumor** ▪ **Odontogenic keratocyst** (aka Keratocystic odontogenic tumor)
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What are the list of ***Mesenchymal*** Benign Tumors? (5)
**▪ Odontogenic myxoma ▪ Central Odontogenic fibroma ▪ Cementifying fibroma ▪ Cementoblastoma ▪ Granular cell odontogenic tumor**
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What are the list of ***Mixed*** Benign tumors? 5
**▪ Odontoma** (complex and compound) **▪ Ameloblastic fibroma/odontoma ▪ Primordial odontogenic tumor ▪ Dentinogenic ghost cell tumor ▪ Calcifying cystic odontogenic tumor**(aka COC, ghost cell tumor)
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**Ameloblastoma** _Charcterstics_
* **An epithelial odontogenic neoplasm (**Tumor of Epithelial Origin) * with a close histologic **resemblance to the enamel organ**
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**Ameloblastoma** _Origin_
**_Potential sources of epithelium include:_** **o Enamel organ** – look like they’re about to deposit a substance but never do **o Odontogenic rests (Malassez, Serres)** **o Reduced enamel epithelium** **o Epithelial lining of odontogenic cysts** ‐ can actually have an ameloblastoma arise within a dentigerous cyst
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Ameloblastoma _Radiographically_
**-Osteolytic tumor** **(radiolucent – no hard tissue formed)** - **Well-circumscribed uni**- or **multilocular radiolucency** - Often with **sclerotic** or **corticated borders** - May see **blunt root** **resorption** and **displacement of teeth** - Frequently seen **in association with unerupted teeth**
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**Ameloblastoma** Clinically
* Rather **slow growing tumor** * Larger lesions present as ***painless*** ***expansion*** or ***swelling*** of bone * Smaller ones are ***asymptomatic***, can be seen on routine imaging * **Buccal and lingual cortical expansion is common** * May perforate cortical plate and invade surrounding soft tissue * Can arise in a dentigerous cyst (see transition from stratified * squamous to ameloblastic epithelium)
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**Ameloblastoma** _Types_
Conventional/multicystic/solid/ (~ 80%) * **Unicystic** (~6-15%) need entire specimen (excision) to know * **Desmoplastic** * **Peripheral** * **Malignant**
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**Ameloblastoma** _Demographics_
▪ **11‐18% of non‐cystic lesions** of the _maxillofacial bones_ ▪ **4th and 5th decade most common,** but occurs over a broad age range *(rare in first decade*) o Usually starts 2nd decade, can go up to 80‐90s. **Late 30s/early 40s are usually the peak** **▪ \> 80% occur in the mandibl**e _(most in molar/ramus area)_
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What is **_the second_** **most common** **odontogenic neoplasm**?
**Ameloblastoma** _(after odontoma)_ o although ***odontomas*** are more _like hamartomas_
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Which tumor can arise in **a dentigerous cyst?**
**Ameloblastoma** (we see transition from stratified squamous to ameloblastic epithelium)
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**ameloblastoma** _location_
▪ Almost 80% or a little over 80% (of ameloblasts) are down in the mandible. ▪ And the vast majority are in the posterior mandible ▪ Do occur in maxilla but at lower rate
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What is this radiographic finding?
**Unilocular and unicystic** ‐ An example of **a unilocular ameloblastoma** that is not associated with an impacted tooth ▪ Is between roots of two teeth, may be confused with lateral periodontal cyst. **Well‐circumscribed radiolucency**
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What is this radiographic finding?
▪ Typical appearance for **ameloblastoma** **Multilocular**, **very well‐circumscribed,** _associated with impacted tooth_. Can see bowing of _inferior aspect of mandible_ _lateral oblique radiograph.was used here_
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What is this radiographic & clinical finding?
**Ameloblastoma** **clinically:** Have expansion of the buccal plate, obliterating the vestibule in this area. **Radiographically:** Root resorption of molar, unilocular radiolucency in mandible
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What is this radiographic finding?
**Ameloblastoma** * **Small lesion** distal to impacted tooth. * **Unilocular radiolucency** with _elevation of alveolar ridge + some expansion of soft tissue_
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What is this radiographic finding?
**Ameloblastoma** ▪ **Well‐circumscribed radiolucency** with **a sclerotic or corticated margin**. ▪ If you had a CBCT, it would probably show you that there was a thin septa in this area of residual bone trabeculae. ▪ **Fracture could be caused by very large cysts.** ▪ **Resolve by decompressing unless with odontogenic tumor** – need to remove the mandible **1cm+** on either side of lesion
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**Ameloblastoma** _Etiology_
▪ Over expression of **Bcl‐2 (**anti‐apoptotic protein) ▪ **Expression of fibroblast growth factor (FGF)** ▪ **Over expression of matrix metalloproteinases (MMPs 9 and 20**) – like in OKC, allowing tumor to grow into surrounding area ▪ Surprisingly, _no significant increase in Ki‐67 expression_ (cell proliferation marker) **– ameloblastomas do NOT turn over rapidly**
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**Case** **16yo female** Describe the lesion and what is the diagnosis?
▪Left mandible, **multilocular radiolucency associated with impacted tooth** ▪ It's **well circumscribed,** edge may be a little **bit sclerotic or corticated** ▪ It has _displaced an impacted tooth down_ towards the inferior aspect of the mandible ▪ Appears to be expanding the cortex of the mandible in areas ▪ There's **blunt resorption of the teeth adjacen**t (PMs and molar) **Ameloblastoma**
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Case ## Footnote ▪ **Well‐circumscribed radiolucency, no impacted tooth** ▪ But notice that **it’s coming up to posterior aspect of first molar** ▪ _Surgery done to remove lesion, left inferior aspect of mandible_ Follow‐up image: **conservative surgery but still removed bone up to mesial aspect**. _Less conservative would be removing entire mandible_ ▪ Concern with that is **paresthesia** (from removing the nerve as well)
**Conventional/Solid Ameloblastoma**
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**Unicystic ameloblastoma** _types_ Subgroup of ameloblastomas
▪ **Unicystic** (Simple or luminal) * lumina- confined to the surface lining of the cystic space ▪ **Plexiform** (intraluminal) * intralumina-one or more areas of the ameloblastic epithelial lining, proliferate into the lumen of the cystic space ▪ **Mural** – hard to distinguish from conventional, so pathologists think they should NOT be treated the same as unicystic (which would be a more conservative treatment) ▪ **Ameloblastoma arising in a cyst** ‐ can usually be treated in a similar way ***as unicystic ameloblastoma.***
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What is this radiographic finding?
**Unicystic Ameloblastoma** but could be **Dentigerous Cyst** based on clinical presentation! So radiograph is not diagonstic
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What is this radiographic finding?
Desmoplastic Ameloblastoma * **Spherical growth**. Within it, has both radiodense and radiolucent areas (is * **mixed radiolucent‐radiopaqu**e)– similar appearance to *_benign fibro‐osseous lesions._* * **Well‐circumscribed, corticated**.
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**Conventional/Solid Ameloblastoma** _Treatment_
* **Resection** (treatment depends on extent of the lesion and anatomy of involved bone) * **Segmental** * **Composite** * **Long term (decades) follow up** is needed for these patients
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**Peripheral Ameloblastoma**
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**Unicystic Ameloblastoma** _Demographcics and Locations_
▪ **Younger initial presentation** (~ 50% in ***2nd decade***) ▪ **90% in MD (mandibular)** ▪ Typically _asymptomatic and found on routine radiographic exam_
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**Unicystic Ameloblastoma** _Radiographically_
* Commonly **a well‐circumscribed radiolucency** that _surrounds the crown of an unerupted tooth_ * Commonly accompanied by **_root resoprtion_**
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**Unicystic Ameloblastoma** _radiographically_ can be confused **with which cyst?**
* Radiographically can be confused with **dentigerous cyst** * **Presence of root resorption** should _increase your suspicion of ameloblastoma_
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**Unicystic Ameloblastoma** _Treatment_
* Treatment is typically **enucleation and curettage** * Reports of lower rate of recurrence (10‐20%) than conventional ameloblastoma (50‐90%) with similar treatment * Some recommend decompression prior to surgery * Use of **Carnoy's solution** ***after enucleation- resulted in a recurrence rate _lower_***
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**Desmoplastic Ameloblastoma** _Location_
* **Anterior jaws** (particularly **maxilla**)
307
**case**
Calcifying Epithelial Odontogenic Tumor (CEOT) **Clinically:** we see **a little expansion** on _inferior aspect of mandible + lingual_ too Radiographically: we see **well‐circumscribed**, **a little corticated/sclerotic edge**, **impacted tooth** ▪ we can see bowing of inferior aspect of mandible ▪ Within areas of radiolucency, see areas of opacity **(calcified lesions = classic CEOT)** ▪ _When smaller► could have looked ***unilocular***_
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**Desmoplastic Ameloblastoma** _Radiographically_
* looks **“fibro‐osseous”** due to **mixed radiolucentradiopaque** **appearance** * Mineralization of **dense collagen** * **Well‐circumscribed**, _corticated_.
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What is this radiographic finding?
**Calcifying Epithelial Odontogenic Tumor(CEOT)** * **flecks of calcifications.** * **Calcifications** all around crown is common
310
What is this radiographic finding?
**Calcifying Epithelial Odontogenic Tumor(CEOT)** * **Multilocular radiolucency with calcifications**. * **an expansion** *up to PMs and back to 2nd molar* * as well as **bowing of mandible.**
311
What is this radiographic finding?
**Calcifying Epithelial Odontogenic Tumor(CEOT**) * ***Fewer calcifications here***, **well‐circumscribed and corticated, impacted** tooth. * **periosteal reaction** _causing elevation_ at the bottom of image!
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**Calcifying Epithelial Odontogenic Tumor(CEOT)** * **well‐circumscribed radiolucency with calcifications** *_in lower anteriors_*
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**Peripheral Ameloblastoma** _Origin and Charcterstics_
* Thought to arise from **epithelial rests or basal cells in the gingiva** * *Uncommon* * **Does not invade underlying bone** * *Histology is the same as _conventional type_*
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**Peripheral Ameloblastoma** _location_
* Found on **gingiva or alveolar mucosa (**\*that's why it's named *peripheral* or extraosseous)
315
What are the two types of **“Malignant” Ameloblastomas ?**
1. **Malignant ameloblastoma** 2. **Ameloblastic carcinoma**
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Adenomatoid odontogenic tumor (AOT) _Origin_
* thought to arise from ***remnants of the dental lamina in the gubernacular cord /canal***
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What is **Ameloblastic carcinoma?**
* **a primary lesion** has _atypical poorly‐differentiated_ * _neoplastic_(malignant) histology * **may metastasize**
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What is the DD?
**well‐circumscribed radiolucency at crown of an impacted canine** _Hard to tell if attaches at CEJ._ If further down, *less likely **a dentigerous cyst*** and more likely **AOT, ameloblastoma, or OKC**
319
What is this radiographic finding?
we see **calcifications** forming, with both radiolucent and radiolucent areas. *▪ Dentingerous cyst, ameloblastoma, and OKC are NO LONGER in the* **differential diagnosis.** **_This is clearly AOT_** **_(_Adenomatoid odontogenic tumor)**
320
What is this clinical finding?
Adenomatoid odontogenic tumor (AOT) **Swelling in maxillary vestibule**
321
What is this clinical finding?
**Adenomatoid odontogenic tumor** **(AOT)** fibrous capsule of AOT is at least partially encapsulated. Easy to remove; “popped right out”.
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What is this clinical finding?
**Adenomatoid odontogenic tumor** **(AOT)** An expansion _into lingual area_ as well as _into vestibule_
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What is this radiographic finding?
_Adenomatoid odontogenic tumor_ _(AOT)_ **Snowflake‐like calcifications** within ***mixed, well‐circumscribed radiolucency***
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What is this radiographic finding?
Adenomatoid odontogenic tumor (AOT) * **Teardrop shape / inverted pear** _between roots of teeth_. * **Well-circumscribed, corticated margin** & **snowflake‐like calcifications** *within*
325
What is a **malignant ameloblastoma?**
▪ Malignant ameloblastoma o Primary lesion and metastasis have normal welldifferentiated ameloblastic (benign) histology o Most commonly to lung
326
**CALCIFYING EPITHELIAL ODONTOGENIC TUMOR** **CEOT** also known as ?
**Pindborg Tumor**
327
Calcifying Epithelial Odontogenic Tumor (CEOT)
▪ Uncommon (~1% of odontogenic tumors) ▪ Does not have inductive effect
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**Calcifying Epithelial Odontogenic Tumor** **(CEOT)** _Demographics and Location_
o **2nd to 10th decade**s, peak **~ 4th decade** o **MD (mandibular) 2 : 1 MX (maxillary)** o Usually ***posterior mandible***
329
Calcifying Epithelial Odontogenic Tumor (CEOT) Clinically
* Presents as **painless slowly expanding swellings** * sessile swellings **of the gingiva or alveolus** *( 2 times more on mandible than maxilla* * **Peripheral lesion** may be seen, but are **rare**
330
**Calcifying Epithelial Odontogenic Tumor** **(CEOT)** _Radiographically_
* *May be **unilocular***, but **most commonly as a multilocular lesion** * ***May be entirely radiolucent*** or ***a mixed radiolucent-radiopaque lesion*** * **Often associated with an unerupted tooth** * *MD third molar most common* * **Calcifications** in the lesion, if present, are typically *prominent around the crown of the impacted tooth.*
331
What is this radiographic finding?
In addition to *fracture*, there is **semilunar loss of bone around the molars ►** (SOT) **Squamous Odontogenic Tumor**
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What is this radiographic finding?
**SOT** **Squamous Odontogenic Tumor** * ***Semilunar** loss of bone*. * **Alveolar bone** is gone due to **impacted canine** that is visible
333
**Calcifying Epithelial Odontogenic Tumor** **(CEOT)** have clinical presentation _similar to what lesion?_
* CEOT clinically is similar to **ameloblastoma** * Also**, CEOT** has potential _to be locally invasive_, if in the right anatomic location, *but has **a less aggressive biologic behavior** compared to **ameloblastoma***
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**Calcifying Epithelial Odontogenic Tumor** **(CEOT)** _Treatment_
▪ **Enucleation** _with peripheral ostectom_y ▪ **Resection** _with rim of normal bone_ ▪ _Recurrence_ rate is ***~12%*** ▪ **~ 2%** demonstrate *malignant transformation*
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What is this radiographic finding?
Central odontogenic fibroma (COF) * **well‐circumscribed radiolucency** *posterior to molar*
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What is this radiographic finding?
Central odontogenic fibroma (COF) round mass of opacity due to FCT. **Ground glass‐like appearance**
337
**Adenomatoid odontogenic tumor** **(AOT)** _Demographics and Location_
▪ 2/3 **anterior jaws** ▪ 2/3 **females** ▪ 2/3 associated with **an impacted canine** ▪ 2/3 **MX** ▪ 2/3 **2nd decade** – kids and teenagers\ That's why it's known as **the tumor of two thirds** ▪ ~ 3‐7% of all odontogenic tumors *New research showing more in **_ant md_** though*
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**Adenomatoid odontogenic tumor** **(AOT)** _Clinical charcterstics_
* Frequently ***_asymptomatic_***, discovered upon routine radiographic exam or when lesion becomes large enough to expand bone * Tumor of *Epithelial Origin*
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**Adenomatoid odontogenic tumor** **(AOT)** _Radiographically_
▪ ***~ 75%*** are **well‐circumscribed unilocular radiolucency** involving the **crown of an unerupted tooth** o ***less often,*** they are **found between the roots of teeth** **▪** ***Mixed radiolucent/radiopaque appearance*** is likened to **“snowflake” calcifications** *▪ May be totally radiopaque in some cases* **▪ Divergence of roots** _is frequently seen_
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If an **Adenomatoid odontogenic tumor (AOT)** is not showing any calcifications yet, it’s in the differential diagnosis with ------ ?
**a dentigerous cyst.**
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What is this radiographic finding?
**Odontogenic Myxoma** * Classic example of **enlargement of the mandible** caused by **multilocular radiolucency.** * Enlarged into oral cavity ‐ **alveolar ridge elevated**
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What is this radiographic finding?
**Odontogenic Myxoma**
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Case
**Clinically**: obliteration of vestibule on patient’s left mandible **Radiographically**:lesion running from posterior by third molar all the way anterior to canine. Well‐circumscribed, multilocular radiolucency is scalloping up between teeth, causing some root divergence **Grossly**: gelatinous appearance of myxoma makes it hard to remove **After treatment:** post‐surgery; had excised all the way to right 2nd PM This is **Odontogenic Myxoma**
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**Adenomatoid odontogenic tumor** **(AOT)** _Treatment_
* Treatment is usually **_enucleation_** * _recurrence_ is ***rare***
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**CEMENTOBLASTOMA (True Cementoma)** * First molar has **tumor attached to the root.** * Mostly **radiopaque but has some less radiodense areas within** = *_classic for cementoblastoma._* * **Radiolucent halo** around region.
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What is this gross and histological finding?
**Cementoblastoma** **Grossly** continuous growth from tumor to the root of the tooth. Brownish areas were more vascular. **Histologically:** tubular dentin in tooth, attached to mass of tissue with calcifications
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**Squamous Odontogenic Tumor** **(SOT)** _Demographics and Location_
▪ Typically _involves alveolar ridge_ **▪ Anterior \> Posterior jaws** ▪ Seen from 2nd to 7th decade (mean 40 years of age)
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**Squamous Odontogenic Tumor** **(SOT)** Clinical charcterstics
* Tumor of *Epithelial Origin* * ***Rare*** * Usually ***asymptomatic***, but _may present with tooth mobility and slight pain_ * **Multiquadrant** ~ 20-25% * A couple reported cases *in families*
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**Squamous Odontogenic Tumor** **(SOT)** _Radiographically_
* **Well‐circumscribed radiolucency** , often ***a semilunar radiolucency of alveolar ridge*** * Can mimic _periodontal disease_
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**Squamous Odontogenic Tumor** **(SOT**) _Origin_
* Thought to arise ***from epithelial rests (Malassez) in the periodontal ligament space***
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**Squamous Odontogenic Tumor** **(SOT)** _Treatment_
* Treatment is **conservative local excision** * _Recurrence_ is ***rare***
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Compound Odontoma Vs Complex Odontoma
**Compound Odontoma** * Mature normal appearing pulp, enamel and dentin * Organization like teeth, with enamel surrounding dentin which surrounds pulp ( Well developed rudimentary “tooth” forms) * appear as small tooth‐like structures in the Anterior jaws (esp. MX) **Complex Odontoma** * Mature pulp, enamel and dentin * No organization, mass of dentin and enamel matrix and pulp tissue (\*\*Poorly developed mass of calcified deposits) * appear as masses of radiopaque material with * variable densities in the Posterior jaws (esp. MD)
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What is this radiographic finding?
Classic appearance of **Odontoma** * **multiple tooth‐like shapes** *aggregated together* * Typically with some sort of **radiolucent halo around them**
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What is this radiographic finding?
**Compound Odontoma** _little teeth‐like structures_ blocking canine eruption
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What is this radiographic finding?
**Complex Odontoma** * _2‐2.5cm mass overlaying the molar_. * ***radiolucent rim/halo*** that is **mixed**, *mostly* **radiopaque**
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**Squamous Odontogenic Tumor** **SOT** Histologically may be mistaken for what other lesions?
* **Ameloblastoma** * **Squamous cell carcinoma (SCCa)**
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**Central odontogenic fibroma (COF)** also known as ?
* *Odontogenic Fibroma (central) **
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**Central odontogenic fibroma** **(COF)** _Origin_
- Tumors of Mesenchymal Origin - Some believe represents **the counterpart to the peripheral ossifying (odontogenic) fibroma** *(in soft tissue)*
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Case
Primordial Odontogenic Tumor (POT) **unilocular radiolucency**
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**Central odontogenic fibroma** **(COF)** _Location_
* **MX ≈ MD** * lesions in **MX** tend to be **anterior to first molar** * those in **MD** **anterior ≈ posterior** * **1/3** associated with an **unerupted tooth**
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**Central odontogenic fibroma (COF)** _Clinically_
*_-Small lesion_* tend to be **asymptomatic** -*_Larger lesions_* can cause **cortical expansion and tooth mobility**
362
**Central odontogenic fibroma** **(COF)** _Radiographically_
* *Small lesions* tend to be **well-circumscribed unilocular radiolucencies** * **often periradicular** * can mimic periapical granulomas and cysts * *Larger lesions* tend to be **well-circumscribed multilocular radiolucencies** * ***Borders*** are usually **sclerotic** * **Root resorption** or **divergence** may be seen * ***~ 10- 15%*** will show **radiopaque flecks** _within the radiolucency_
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What is this radiographic finding?
**Ameloblastic Fibroma (AF)** 1‐3 potential locules, no impacted tooth associated
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**Central odontogenic fibroma** **(COF)** _Treatment_
* **Enucleation** with **curettage** or **excision** * usually d**on’t recur**
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What is this radiographic finding?
**Ameloblastic Fibro-odontoma (AFO)** * _well‐circumscribed radiolucency_ * ***corticated edg***e + **calcification**
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What is this radiographic finding?
**Ameloblastic Fibro-odontoma (AFO)** has expansion into oral cavity. Flecks of calcification in lesion with impacted tooth = odontoma
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What is the Microscopic *_Differential Diagnosis_* of **Central odontogenic fibroma (COF)**?
**o Desmoplastic fibroma** ‐ *a more aggressive lesion* o **Fibromyxoma *‐*** *variant of odontogenic myxoma with abundant collagen* **o Hyperplastic tooth follicle** *‐ typically loose immature stroma, but when hyperplastic can have abundant collagen*
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**Odontogenic Myxoma** _Origin_
* Tumors of *Mesenchymal Origin* * Thought to arise from ***the tooth follicle or dental papilla***
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**Odontogenic Myxoma** _Demographics and Location_
* **~3-5%** of all odontogenic tumors * Wide age range, but **3rd decade most common** * Found anywhere in the ***MD or MX***
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**Odontogenic Myxoma** _Radiographically_
* *Small lesions* present as **asymptomatic radiolucencies** found upon routine exam * *Larger lesions* can cause **painless expansion of bone** * All are **radiolucent lesions**, but the appearance can vary from **well‐ circumscribed to irregular and diffuse** * ***Unilocular*** to, **more commonly, multilocular** _(“soap bubble” or “honeycomb”) radiolucency_ * **Borders** are often **scalloped**, can see sc_alloping around the roots of teeth_ * But can cause **displacement of teeth and resorption of the roots of teet**
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What is this radiographic finding?
**Ameloblastic Fibrosarcoma** in the mandible developed after two years from AF
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**Odontogenic Myxoma** _Grossly_
* the tumor is described as **loose**, **soft** and **gelatinous**
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**Odontogenic Myxoma** _Treatment_
* **Surgical excision** or **resection** * Because the lesion is not encapsulated and has a gelatinous loose consistency► it is difficult to remove completely * this is thought to be why myxoma **has a fairly high recurrence rate** * _**Maxillary posterior lesions** should be treated more aggressively_
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**CEMENTOBLASTOMA** _Origin_ | (True Cementoma)
* Tumor of *Mesenchymal* origin * **Benign tumor** of *cementoblasts*
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CEMENTOBLASTOMA _Demographics and Location_ | (True Cementoma)
* Typically present in **2nd and 3rd decade** (~75% prior to the age of 30) * **75% MD** * ▪ ~ 90% in **molar/premolar region** *
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**CEMENTOBLASTOMA (True Cementoma)** _Clinically_
* **2/3** of cases have **pain and swelling** * Can cause **cortical expansion *_if large enough_***
377
**CEMENTOBLASTOMA (True Cementoma)** _Radiographically_
* **Radiopaque mass** _fused to_ *the root of the affected tooth* * Usually has a **thin radiolucent halo or rim** _surrounding the radiopacity_
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CEMENTOBLASTOMA _Treatment_ | (True Cementoma)
* **surgical extraction** _of the involved tooth with attached tumor_ * **Root amputation (with attached tumor) and endo** is an option *_for smaller lesions_* * _Recurrence_ is ***unlikely***
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**Cementoblastoma** has similar histologic presentation to what?
**osteoblastoma** Difference is Osteoblastoma is **NOT** a_ttached to the root of a tooth_ (whereas cementoblastoma must be)
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What are **Odontogenic Tumors of Mixed Origin** (Epithelial and Mesenchymal)
They are tumors in which the _odontogenic epithelial componen_t causes **induction** of the _mesenchymal component_ **to produce a product** **Examples:** * Odontomas * Ameloblastic fibroma * (and Ameloblastic fibrosarcoma) * Ameloblastic fibro-odontoma
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**Odontoma** _Origin_
* Odontogenic Tumors of Mixed Origin (Epithelial and Mesenchymal * They are **_hamartomas_** *rather* than _true neoplasms_ * They are **_masses of enamel and dentin_** *with variable amounts* ***of*** **_pulp and cementum_**
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What is **the most common odontogenic “tumor”**?
**Odontoma**
383
**Odontoma** _Demographics and Locations_
▪ **First 2 decade** *_most common_* (mean age of ***14***) Location is based on *the type of Odontoma* * **Compound Odontoma** * _Anterior jaws (esp. MX)_ * \*\***Well developed rudimentary “tooth” forms** * **Complex Odontoma** * _Posterior jaws (esp. MD_) * **\*\*Poorly developed mass of calcified deposits**
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Odontoma _Charcterstics_
* Often associated with _an unerupted tooth_ * Lesions **may prevent eruption of teeth** * Usually ***small* in size,** but ***rare cases of \> 6cm reported*** * *large lesions* **can cause bone expansion**
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**Odontoma** _Radiographically_
▪ Radiographically see **a radiopaque structure(s)** *surrounded by* **a radiolucent rim** ▪ As with any calcified lesion, those found *early in development* may appear _totally or *predominantly radiolucent*_ ▪ **Compound odontomas** *appear as* **small tooth‐like structures** ▪ **Complex odontomas** *look like* **masses of radiopaque material** *with* **variable densities**
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**Odontoma** _Treatment_
▪ **Simple excision** or **enucleation** ▪ **Unlikely** *to* **recur**
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**Primordial odontogenic tumor (POT)** **Origin**
* Tumor of mixed origin * Very rare! first reported in 2014 -**less than 30 cases so far**
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**Primordial odontogenic tumor (POT)** _Demographics and Location_
* Most common in **1st and 2nd decades** * Mean age **12.5 years** * **MD:MX 6:1**
389
**Primordial Odontogenic Tumor (POT)** _Clinical Charcterstics_
- **Asymptomatic** found on routine imaging - Can cause **tooth displacement** and **cortical expansion**
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**Primordial Odontogenic Tumor (POT)** _Radiographically_
* **Well-defined radiolucency** _associated with_ **an impacted tooth** * Most commonly **a third molar**
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**Primordial Odontogenic Tumor (POT)** _Treatment_
* **conservative excision/enucleation** * So far ***no recurrence***
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Ameloblastic fibroma (AF) and ameloblastic fibro-odontoma (AFO) _Charcterstics_
* _Uncommon_ ***benign* mixed** odontogenic neoplasms. * **Considered together b**ecause it is thought they are _variations of the same process_
393
**Ameloblastic fibroma (AF) and ameloblastic fibro-odontoma (AFO)** _demographics and location_
* Typically presents in **first 2 decades** * mean is 12 years of age * **~ 70%** occur in **the posterior mandible** * **~ 75%** associated with **unerupted teeth**
394
**Ameloblastic Fibroma (AF)** _clinical and radiographic presentations_
* **Small lesions** are **asymptomatic** and found on routine exam * **Large lesions** _can cause bone expansion_ * **Smaller lesions are unilocular Radiolucencies** * **Large ones are multilocular radiolucencies** * **Border** is **well defined and often sclerotic** * ***Untreated***, _can grow to very large size_
395
**Ameloblastic Fibro-odontoma (AFO)** _Clinical and Radiographic features_
- Clinical features similar to **Ameloblastic Fibroma AF** *(Small lesions are asymptomatic and found on routine exam & Large lesions can cause bone expansion)* Radiographically, we see **a mixed radiolucent/radiopaque lesion** _because of the formation of odontomas_
396
**Ameloblastic fibroma (AF) and ameloblastic fibro-odontoma (AFO)** _Treatment_
* **Conservative surgical excision** or **curettage**, _easily_ _removed from surrounding bone_ * _Prognosis_ is **excellent**, _recurrence_ is ***unusual*** * ▪ **Rare cases** reported of **development of ameloblastic fibrosarcoma** _in area of AF or AFO_
397
**Ameloblastic Fibrosarcoma** _Charcterstics & Origin_
* _Malignant counterpar_t of **ameloblastic fibroma** * **Rare lesion** which may arise in the site of a previous AF/AFO or arise de novo
398
**Ameloblastic Fibrosarcoma** _Demographics and location_
* **1.5 times** _more common_ in **males** * ~ **80% MD**
399
**Ameloblastic Fibrosarcoma** _Clinically_
* **Pain**, **swelling** and **rapid growth** are *common presenting signs*
400
**Ameloblastic Fibrosarcoma** _Radiographically_
* presents as an **ill-defined destructive radiolucency** *with* **irregular borders**
401
**Ameloblastic Fibrosarcoma** _Treatment_
- **Radical surgical excision** as the tumor is ***very aggressive*** *and* ***infiltrative*** - _Prognosis_ is *dependent on* **complete removal of tumor**
402
**Odontogenic carcinomas** **List them (5)**
-**Ameloblastic carcinoma** **-Primary intraosseous carcinoma, NOS** **-Sclerosing odontogenic carcinoma** **-Clear cell odontogenic carcinoma** **-Ghost cell odontogenic carcinoma** All fairly rare lesions!
403
What is the Differential Diagnosis D/D of **Multilocular Radiolucency**
**MOCHA** * **M odontogenic **_M_**yxoma** * **O **_O_**dontogenic keratocyst** * **C **_C_**entral giant cell granuloma** * **H Central **_H_**emangioma** * **A _A_meloblastoma** **Others:** * Aneurysmal bone cyst * early CEOT * ameloblastic fibroma AF * central MECa
404
**Key Concepts of Malignant Lesions on Imaging**
**Rapidly growing and infiltrative** –finger-like extensions into surrounding anatomy Remember: in some instances, a benign lesion can mimic a malignant one. Therefore we should be wary of all the information that is available.
405
Key Concept of Malignant Lesions on Imaging
ill-defined invasive borders followed by bone destruction
406
Key Concept of Malignant Lesions on Imaging
Destruction of the cortical boundary (floor of maxillary antrum) with an adjacent soft tissue mass (arrows)
407
Key Concept of Malignant Lesions on Imaging
Tumor invasion along the periodontal membrane space causing irregular thickening of this space
408
Key Concept of Malignant Lesions on Imaging
Multifocal lesions located at root apices and in the papilla of a developing tooth destroying the crypt cortex and displacing the developing tooth in an occlusal direction (arrow)
409
Key Concept of Malignant Lesions on Imaging
Four types of effects on cortical bone and periosteal reaction, from top to the bottom: •**cortical bone destruction** *without* **periosteal reaction** ***•laminated periosteal reaction*** *with* **destruction of the cortical bone and the new periosteal bone** **•destruction of cortical bone** *with* **periosteal reaction at the periphery** *forming* **Codman's triangles** **•a spiculatedor sunray** _type of periosteal reaction_
410
**Key Concept of Malignant Lesions on Imaging**
Bone destruction around existing teeth, producing an appearance of teeth floating in space.
411
What is this radiographic finding?
**Chondrosarcoma** * its consistent widening as opposed to seen in periodontitis and inflammatory disease
412
Case CC of loose teeth wanted extractions and a denture
**Chondrosarcoma** * Ill defined lesion of anterior maxilla * Areas of radiolucency * Classic area of moth‐eaten look * Circular area of radiolucency with trabecular * pattern * Patient left without surgery, not heeding medical advice Then patient came back ▪ Someone was willing to do the dentures for her ▪ CC‐ denture was not fitting ▪ Expansion of cortical plate ▪ Hyperkeratotic because of denture rubbing ▪ Still has malignancy ▪ Advise for surgery ▪ Refused again Then the lesion kept on Lesion still growing ▪ Metastasize to lungs ▪ Admitted to breathing issues ▪ About 5 ½ years from initial dx to pt passing away
413
What is this clinical finding?
**Chondrosarcoma** * Alveolar process and floor of mouth affected * **Limitations of movement of the tongue**
414
Case * 83 year old female with nodular areas under denture on anterior mandibular ridge * ▪ c/c of her denture rocking
Can see in the anterior region there’s an elevation histology shows it's not chondrosarcoma because it contained **_Cutright lesion_** **papule or nodule on alveolar ridge** * Osseous and/or chondromatous metaplasia within the soft tissue of the gingiva o **Lesion is NOT central in bone or connected to bone** *_▪ NOT a malignant lesion_* o Thought to be **reactive metaplasia due to a poorly fitting denture**
415
**Chondroma** & **Chondrosarcoma**
* *Chondroma –** benign * *Chondrosarcoma**‐ malignant * Both are listed here _because_ * _a benign cartilaginous tumor central In the jaw is extremely rare_ (or may not exist) * _Lesions tend to recur many times_ and **eventually metastasize *( Basically chondromas are not really benign)***
416
**Chondrosarcoma** _Charcterstics_
* **Malignant tumor** that _forms cartilage_ * **10%** of all primary bone tumors, but ***rare in the jaws***
417
What is this clinical finding?
**Osteosarcoma** ## Footnote ▪ Swelling on left side of face ▪ Difficult opening
418
What is this clinical finding?
**Osteosarcoma** * See something in the operculum * Infection in third molar?
419
What is this radiographic finding?
**Osteosarcoma** * AP Plain Film * Most of jaw was missing * Radiolucency affecting entire ramus and condyle
420
What is this radiographic finding?
**Osteosarcoma** * Classic _sunburst pattern_ * **Fuzzy appearance** _on outer edges of cortex_
421
What is this radiographic finding?
**Osteosarcoma** * _cloudy bone formation_ on surface of cortex on facial and lingual aspect
422
What is this clinical finding?
**Osteosarcoma** a patient with swelling with side of face
423
What is this radiographic finding?
**Osteosarcoma** ▪ _Lytic lesion_ ▪ *Slightly* **ill defined** ▪ **Loss of bone** in the _inferior aspect of mandible_
424
**Chondrosarcoma** Clinical presentations
* Patient’s chief complaint is **painless swelling,** *may be associated with tooth mobility* * **Symmetric widening of the PDL space** * Can be _initial presentation with chondrosarcoma and osteosarcoma_ * **Along radicular surface of the tooth** there is the _same rate of widening all the way down the tooth_ * ***In contrast to periodontal disease***, where there is _a triangular shaped loss of space_
425
**Chondrosarcoma** Radiographically
* **Poorly defined radiolucency**, often with ***scattered radiopaque foci*** * Radiopaque foci can be seen since the cartilage in the tumor can ossify
426
**Chondrosarcoma** _Treatment_
* **Radical surgical excision** _on initial treatment_ * _Maxillectomy/Mandibulectomy_ * If anterior region they remove the entire anterior portion of the jaw * These lesions *don’t respond to radiation or chemotherapy* * ***Although used as adjuncts for lesions that can’t be treated surgically*** * *For example **a posterior sinus** **lesion** _since that is the base of the skull_* * *These patients have **poorer prognosis** than those with more accessible sites such as the mandible* * **Prognosis is poorer** *than for osteosarcoma* (which contrasts with the prognosis in extragnathicsites) * **Treatment failure** (and ***mortality***) is usually **due to uncontrolled local disease** *not metastasis*
427
Why any diagnosis of **chondroma** in the jaws **should be viewed with suspicion?**
* **Since 20% of chondrosarcomas of the jaw are initially misdiagnosed as chondromas** ► any diagnosis of chondromain the jaws should be viewed with suspicion * **All cartilaginous tumors arising in the jaws should be excised widely** * (\>60% of cartilaginous tumors of the jaw recur and ~7% metastasize to the lung and/or bone )
428
**Osteosarcoma** _Demographics & Location_MD \> MX, Male \> Female
* **Most common malignant bone tumor in the jaws** is _metastatic disease_ * **Most commonly primary** (meaning started at this location) **malignant bone tumor in patients under 40 years old** * 2nd most common overall after *multiple myeloma* * _Mean age at presentation for jaw lesions_ is **33 years old,** *10‐15 years older than that for long bones* *
429
**Osteosarcoma** _Clinically & Radiographically_
* **Swelling and pain** are the common presenting symptoms **(25% have “toothache”)** * Can also have ***loosening of teeth,** **paresthesia of lip** and **nasal obstruction*** * **Symmetric widening of the PDL** is often _an early radiographic change_ * Lesions vary from ***dense sclerotic, mixed sclerotic*** *and* ***radiolucent*** *to* ***all radiolucent***
430
**Osteosarcoma** _Treatment_
* _Important to distinguish from chondrosarcoma as treatments are different_ * **_Osteosarcoma_** is currently treated with **pre-op multi-agent chemotherapy followed by surgery** * ***Radiation therapy*** alone is ***insufficient*** for cure * **_Favorable jaw site – MD symphysis_** * **_Worst site – MX sinus_** * **5 year survival is ~ 20%** (***_up to 80% if caught early_*** and *_treated with radical resection)_*
431
What is this clinical finding?
**Langerhans Cell Disease** Infant with _Acute disseminated type_ ▪ See lesions on head/ear
432
What is this clinical finding?
Langerhans Cell Disease we see _lesions on maxilla_
433
What is this clinical finding?
**Langerhans Cell Disease** ▪ Older child ▪ Chronic disseminated form ▪ Alveolar ridge involvement ▪ Lot of bone loss and mobility ▪ Painful to brush
434
What are these clinical findings?
**Langerhans Cell Disease** Torus and molar involvement
435
What is this clinical finding?
**Eosinophilic Granulations** Erythematous area
436
What is this radiographic finding?
▪ Child with _disseminated form_ ▪ **Punched out radiolucency** in the skull
437
What is this clinical finding?
▪ Child with **bone loss** surround the teeth **▪ Floating teeth** _disseminated form_
438
What is this radiographic finding?
▪ Floating teeth ▪ Only attached by soft tissue due to extensive bone loss _disseminated form_
439
What is this radiographic finding?
**Eosinophilic granuloma**
440
**Peripheral (juxtacortical) Osteosarcoma** _Location_
* **Arise on the surface of the bone** (vs. medullary site for usual forms of osteosarcoma) * Usually **long bones**
441
What are the two types of **Peripheral (juxtacortical) Osteosarcoma ?**
**parosteal** – *_well differentiated_*, but will **recur** with less than an en bloc or radical surgery **periosteal** – _higher grade_ with prominent **cartilaginous** component
442
**_Parosteal_ Peripheral Osteosarcoma** _Charcterstics_
o **Mushroom like growth** on bone surface o **No** *elevation of periosteum* o **No** *new bone formation* o **Low grade**
443
**Periosteal Peripheral Osteosarcoma** Charcterstics
o Usually **sessile** **growth** on bone surface o **Elevation of periosteum** o **New bone fills in** space under periosteum o **Prognosis is _better_** *than medullary osteosarcoma* ***but worse than**parosteal type*
444
**Langerhans Cell Disease** also known as ?
* **Histiocytosis X (old name**) * **Langerhans cell granuloma** * **Eosinophilic granuloma** * **_Langerhans cell histiocytosis_**
445
**Langerhans cell histiocytosis** _Etiology_
Etiology unclear o Demonstration that LCH cells are **clonal**, along with the recent discovery of **activating BRAF mutations in LCH cells**, ►**strongly suggests that LCH is a neoplastic disease**
446
**Langerhans cell histiocytosis** _Demographics & Location_
* **Males**\>\>\> Females * More than half of cases seen **under the age of 10** * **Jaw** affected in **10 ‐20% of cases**
447
What is this radiographical finding?
* **Punched out** radiolucency * **Lytic** radiolucency *without cortication* MM Multiple Myeloma
448
What is this radiographical finding?
* more punched out radiolucency in iliac crest in the image * Bone marrow biopsy usually done in this area since it’s frequently involved multiple Myeloma MM
449
What is this radiographical finding?
Multiple Myeloma ## Footnote ▪ Radiolucency without sclerotic border ▪ Multiple and separated
450
What is this clinical finding
Swelling of gingiva ## Footnote **▪ Plasmacytoma**
451
**Langerhans Cell Histiocytosis** _Clinically & Radiographically_
**_Clinically:_** Common sites: **skull, rib, vertebrae, and mandible** ▪ Often have associated **pain or tenderness** **_Radiographically:_** ▪ In jaws we see loss of alveolar bone in molar area o Mimics severe periodontitis
452
Types of Langerhans Cell Disease List 3
**▪ Acute disseminated form (Letterer‐Siwe disease) ▪ Chronic disseminated form (Hand‐Schuller‐Christian Disease, ▪ Eosinophilic Granuloma (chronic localized)**
453
**Acute disseminated form** (Letterer‐Siwe disease) charcterstics
* **Multisystem** (bone, skin, liver spleen and lymph nodes) * **Infants** * **high mortality** * **rapidly progressive**
454
**Chronic disseminated form (Hand‐Schuller‐Christian Disease, Multifocal Eosinophilic Granuloma)** _Charcterstics_
* **Unisystem** (frequently *bone*, but _also skin and viscera)_ * **Children** * ***fairly* high mortality** * ***more* chronic progression**
455
What is this gross finding?
**Ewing Sarcoma** ## Footnote ▪ Long bone ▪ Large expansion
456
What is this radiographical finding?
**Ewing Sarcoma** * an _expansion of tissu_e * **Dissolution of bone** in that area
457
**Eosinophilic Granuloma (chronic localized)** _Charcterstics_
* **Solitary or multiple bone lesions** *without visceral involvement* * **Adults** * **very low mortality** * Some reports of **association with smoking marijuana** * In these cases ***the lungs are involved***
458
The site of invovelement of Langerhans Cell Disease depends on ?
Site of involvement depends on clinical form * Neoplastic proliferation of Langerhans cells * Langerhans cells * Dendritic mononuclear cells normally *found in the epidermis and mucosa* * Antigen presenting cells to T lymphocytes
459
What is this radiographical finding?
Metastatic Carcinoma to Jaw Bones ▪ A. Metastatic breast carcinoma surrounding the apical half of the second and third molar roots and extending inferiorly. It has destroyed the inferior border of the mandible.
460
What is this radiographical finding?
Metastatic Carcinoma to Jaw Bones B. Bilateral metastatic lesions from the lung destroying the mandibular rami.
461
What is this radiographical finding?
**Metastatic Carcinoma to Jaw Bones** D. Destruction of the left mandibular condyle (arrows) from a thyroid metastatic lesion
462
What is this radiographical finding?
**Metastatic Carcinoma to Jaw Bones** A. Partial panoramic image of prostate metastatic lesions involving the body and ramus; note the sclerotic bone reaction (arrows).
463
What is this radiographical finding?
**Metastatic Carcinoma to Jaw Bones** B. Occlusal image of prostate lesions causing sclerosis and spiculated periosteal reaction (arrows)
464
What is this radiographical finding?
Metastatic Carcinoma to Jaw Bones C. Periapical image of a metastatic lesion of breast carcinoma; note the irregular widening of the periodontal membrane spaces and patchy sclerotic bone reaction, especially around the roots of the molars
465
**Chronic disseminated form** (Hand-Schuller-Christian Disease, Multifocal Eosinophilic Granuloma) What is its classic Triad?
* **Exophthalmus** * **Diabetes insipidus** * **Lytic defects of bone**
466
**Chronic disseminated form** *_of Langharan Disease_* Clinically and radiographically
Clinically: * we see _mobility of teeth_ Radiographically: * picture of child with **“teeth floating in air”** * **Sharply punched out radiolucent lesion**s, *ill- defined radiolucency in some cases*
467
**Eosinophilic Granuloma** _Charcterstics & Demographics_
* **Elderly men** often present with **lung lesions** *_(increased incidence with smoking)_* * **Localized lesions,** usually affecting **one bone** * If found to be a*n accessible solitary lesion,* **treatment** is usually **curettage and possibly low dose RT** * in some instances it can be **initial presentation of systemic disease** – but that would _typically be in children or young adults_
468
Langerhans Cell Histiocytosis Histology It contain **rod shape called**
**Birbeck granules**
469
What is the differential diagnosis for **Alveolar Bone Loss in Children?**
**o Juvenile periodontitis** **o Langerhans cell histiocytosis** **o Papillon‐Lefevre syndrome** **o Cyclic neutropenia/agranulocytosis** **o Burkitt’s Lymphoma**
470
**Multiple Myeloma** _charcterstics_
**Monoclonal Expansion of malignant plasma cells** * Plasma cells make a lot of immunoglobulin ► So we will see a lot of immunoglobulin
471
**Multiple Myeloma** _Demographics and Location_
* Most common in **40‐70 year old** * Means 63 years old * Bones most commonly involved include **ribs, vertebrae and skull** * **70‐90%** will have ***_jaw involvement at some point_***
472
**Multiple Myeloma** _Clinically_
* Present with **bone pain (\>70%)** and **pathologic fractures** * ***Anemia, thrombocytopenia and neutropenia*** _due to crowding out of normal cells within bone marrow by proliferating malignant cells_ * _50‐60%_ have **Bence‐Jones proteins in urine** (light chains, usually kappa)
473
▪ Solitary plasmacytoma Vs Extramedullary plasmacytoma Vs Multiple myeloma – multifocal disseminated disease
**▪ Solitary plasmacytoma** * *Individual lesion **in bone*** * When affecting oral cavity, ~95% of the cases are ramus and angle of the mandible * In many cases p_rogress to more systemic disease_ **Extramedullary plasmacytoma** * *individual **soft tissue** lesion* (not central In bone) **Multiple myeloma** * ***multifocal*** *disseminated disease*
474
**Multiple Myeloma** Radiographically
* **“punched out” radiolucencies** (no sclerotic margin) often _with an irregular outline_
475
**Multiple Myeloma** Lab findings
* **Elevated M spike in serum** * *Elevation of immunoglobulin in serum* (**hyperglobulinemia**) most **commonly IgG** * *Deposition of amyloid in tissues* (**macroglossia**)
476
**Multiple Myeloma** _Treatmet_
Treatment can include : * **chemotherapy** _with or without Radtiaion Therapy_ * bone marrow transplant * interferon * antibodies made against tumor cells * thalidomide * Even with treatment, many patients do not survive more than 18‐24 months, however treatment modalities are improving * Older patients are treated less aggressively
477
**Ewing Sarcoma,** Ewing’s family of sarcomas _Charcterstics_
▪ Highly malignant, undifferentiated, small round cell tumor/small blue cell tumor o The cell of origin is in question, may be of neural crest origin
478
**Ewing Sarcoma** _Demographics and Location_
* ​**Primarily a disease of children and adolescents (**90% of patients are between 5 and 30 years old) ▪ **\>60% males** ▪ * _Twice as common_ **in mandible** * **Caucasians\>\>\>\>Blacks and Asians** * Make up **~6% of primary malignant bone tumors** * In the jaws, the ratio of primary tumor to metastasis is 14 to 1 * **50%** of cases i**n the femur and pelvic bones** * **~1%** occur in the **jaw bones**
479
**Ewing Sarcoma** _Clinically_
* Patients often present with **pain, swelling, fever and elevated ESR** (similar to signs of inflammation) * May be misdiagnosed as **an infection or osteomyelitis** * **Paresthesia** and **loosening of teeth** are _common findings with jaw lesions_
480
**Ewing Sarcoma** _Radographically_
* **an irregular lytic lesion** *with* i**ll‐defined margins** * **Root resorption** _may be seen_ * May see **thickening of the periosteum** with a characteristic **“onion skinning” pattern** (like with peripheral periostitis) * seen more in long bones
481
**Ewing Sarcoma** Treatment
* **Combined therapy with multi‐agent chemotherapy, radiation therapy and surgery** has led to 40% ‐ 80% survival rates * **Gnathic Ewing sarcoma** has *_a lower mortality rat_*_e_ than all other primary sites
482
What are the most common carcinomas that metastasize to the jaw
The most common carcinomas to jaw: **B**reast **L**ung **T**hyroid and **C**olon **K**idney **P**rostate ▪ “B. L. T. and Cold Kosher Pickle”
483
Malignant tumors of jaw _Review_
Metastatic tumors to the jaw are more common than primary lesions ## Footnote ● Think osteosarcoma, chondrosarcoma, or osteoblastic metastasis (breast or prostate) if lesion radiographically looks malignant and has radiopaque internal pattern ● Ewing’s sarcoma is clinically accompanied by signs of inflammation ●Multiple myeloma characteristically presents as multiple, well‐ defined, punched‐out radiolucencies ● Bone affected by Non‐Hodgkin’s lymphoma radiographically appears to be dissolving ● Langerhans cell histiocytosis characteristically presents as scooped‐ out radiolucencies at the mid‐root level ● Remember to include metastatic carcinoma to jaw as a radiographic differential diagnosis for malignant lesions
484
485
What are Gastrointestinal Diseases what are example of them?
Inflammatory bowel diseases associated with oral findings **▪ Crohn disease ▪ Ulcerative colitis ▪ Pyostomatitis vegetans ▪ Celiac Disease**
486
**Crohn Disease Regional Ileitis** What areas does affect? What are the symptoms?
What areas does affect? ● Primarily affecting distal small intestine and proximal colon What are the symptoms? ● Symptoms include **abdominal cramping, pain, bloating, diarrhea**, and **nauseas** (*similar amongst the GI diseases*) ● Patients often have **weight loss and malnutrition** ● **20%** have **abrupt onset of symptoms** *resembling* **_acute appendicitis_** *or* **_bowel perforation_**
487
**Crohn Disease Regional Ileitis** When it is diagnosed? Etiology? Prevalence? What are the oral implactions?
When it is diagnosed? ● Usually initially *diagnosed* **in adolescents** Etiology? **●** *Etiology* **unknown‐ immunologically mediated?** o Theory of being _too clean as a child and having a negative response as we grow older since we’re not used to normal bacteria_ Prevalence? ● *Prevalence* i**ncreasing, reason unknown** What are the oral implactions? ●Oral lesions can be first sign of disease
488
**Crohn Disease Histopathology**
● **Superficial or deep ulceration** *with adjacent granulation tissue* extending into deep submucosa or below ● **A transmural granulomatous inflammation** o Sarcoid‐like, non‐caseating, poorly formed granulomas, in all tissue layers (50‐70% of cases) usually adjacent to blood vessels or lymphatics ● **Transmural inflammation with lymphoid aggregates** throughout bowel wall
489
Crohn Disease Oral Findings
* **Recurrent oral ulcerations** _can mimic those seen with_ **recurrent aphthous lesions** * **Diffuse or nodular swelling** of _the oral and perioral tissues_ * Can look like ***epulis fissuratum*** * **Deep linear granulomatous‐appearing ulcerations** (often in the buccal vestibule area) * ***_Cobblestone mucosal appearance_*** * **Polypoid tag‐like lesions** on _vestibular and retromolar mucosa_ * **Enlargement of lips** _caused by granulomatous inflammation:_ **orofacial granulomatosis**
490
**Crohn Disease** _Treatment_
* Current strategies aim for _deep and long‐lasting remission, with the goal of preventing complications_, such as *surgery, and blocking disease progression* * **_Immunosuppressant_** such as _cyclosporine_ * In more severe cases; * *high dose corticosteroids and** * **chemotherapeutics to induce a remission** * **Nutritional supplements** _(iron, folate)_ * Because _they are unable to absorb nutrients_ * If medical means do not keep patient under control► **surgical removal of a portion or all of the intestine** * When _intestinal symptoms are under control_►**oral ulcerations resolve**
491
Which systemic disease manifests like this?
Crohn Disease * Patients can also get **angular cheilitis** * Above the **Linear ulceration,** can see **a flap like structure** which is **the hyperplastic margin**
492
Which systemic disease has this oral manifestation?
* we see the **ulceration** and **hyperplastic tissue** surrounding it.
493
Which systemic disease has this oral manifestation?
**Crohn Disease** _Nodular appearance_ of **buccal mucosa**
494
Which systemic disease has this oral manifestation?
_Crohn Disease_ we see **more nodules**
495
Which systemic disease has this oral manifestation?
Crohn Disease _Linear granulomatous ulcerations_ But they are **not** *the aphthous ulcerations* **but the more linear type**
496
How different is **Ulcerative Collitis** from **Crohn Disease**?
Unlike Crohn’s, lesions extend in a continuous fashion proximally from the rectum (no skip lesions) and histologically don’t have granulomas
497
Pseudomembranous Ulcerative Colitis Causes?
Bactrial Overgrowth in the pseduomemberane (C.difficile Overgrowth) Causes: * **Clindamycin** prolonged use ~2 weeks _can cause the C. difficile overgrowth._ * _Always_ ***warn patients if you prescribe clindamycin about possible side effects*** and stop usage _since do not want them to develop untreatable strains_
498
Ulcerative Colitis 1. What are the symptoms 2. What type of Cancer risk it presents?
What are the symptoms * A chronic inflammatory disease of the colon (mucosa and submucosa) presenting with **diarrhea, rectal bleeding, abdominal pain, weight loss and fever** What type of Cancer risk it presents? * Increased risk of **colon cancer**
499
Pyostomatitis vegetans _Treatment_
● Treatment is n**ot well standardized**, fairly rare disease and good double blind studies rare ● Can **use topical corticosteroids** ● Werchniak et al had **good results with topical tacrolimus** ● **Sulfasalazine** or **Prednisone** *_for GI lesions_* ● If GI symptoms are under control► oral lesions will resolve
500
Oral Manifestations of which systemic disease?
Pyostomatitis Vegetans
501
Oral Manifestations of which systemic disease?
Pyostomatitis vegetans
502
Oral Manifestations of which systemic disease?
**Pyostomatitis vegetans** *Snail track appearance*
503
**Ulcerative Colitis** _Oral Lesions_
● In some cases, patients get **recurrent oral ulcerations** (can have _aphthous‐like lesions_) ● **Papillary mucosal projections** with _deep linear ulcers_ and _fissures_ ● **Intraepithelial pustules of the mucosa** (_pyostomatitis vegetans_)
504
**Ulcerative Colitis** _Management_
● Use of _anti‐inflammatory medications_ **o Sulfasalazine or Prednisone** ● If medical means do not succeed► then **removal of part or all of colon**
505
What is the difference between Inflammatory Bowel Disease IBD & Irritable Bowel Syndrome IBS
**● IBD** o Classified as a **_disease_** o Can cause **destructive inflammation and permanent harm to the intestines** o The disease can be _seen during diagnostic imaging_ o **Increased risk for colon cancer** ● IBS o Classified as a **_syndrome_**, a group of symptoms o Dose _**not cause** inflammation; rarely requires hospitalization or surgery_ o There is _**no sign of abnormality** during an exam of the colon_ ▪ Usually because it’s only _periodic_ o **No increased risk form colon cancer or IBD**
506
**Pyostomatitis Vegetans** what is it? Demographics? Symptoms onset?
**What is it?** * Thought to be an unusual presentation of inflammatory bowel disease, especially ulcerative colitis (sometimes with Crohn’s)\ **Demographics** * In only a rare subset of patients * Typically present before 30 years of age **Symptoms onset** * **~25%** of cases seen in **absence of GI symptoms** * May see oral symptoms **before** the GI symptoms
507
Pyostomatitis Vegetans _Oral Symptoms_ and _Most common sites in the mouth?_
**Oral Symptoms** ● **Recurrent oral ulcerations** _concurrent with, or prior to ***GI symptoms***_ ● Oral mucosa is **erythematous** and **thickened** with **multiple cream/yellow‐colored pustules**and**superficial erosions** ● *Linear* **“snail track**” _oral pustules_ **Most common sites in the mouth?** ● Most common sites include **buccal and labial mucosa, soft palate,** *and* **ventral tongue**
508
**Celiac (Sprue) Disease** What is it? Which gene is involved? Symptoms?
What is it? ● **Chronic disease** (diffuse enteritis) of **the small intestine** _which improves upon **withdrawal of gluten proteins**_ Which gene is involved? ● \>90% express **HLA‐B8** _histocompatibility antigen_ Symptoms? ● Patients present with **diarrhea, gas, weight loss, fatigue, impaired nutrient absorption, etc**
509
Oral manifestation of which Systemic Disease?
**Amyloidosis** Nodular “waxy” depositions in skin **deposition on the eyelid**
510
Which systemic disease has this oral manifestation?
Amyloidosis orange, red, yellow tinge
511
Which systemic disease has this oral manifestation?
Amyloidosis Macroglossis and crenation of tongue (indentation near the teeth area) _skin deposits_ on the comissure,
512
Which systemic disease has this oral manifestation?
**Amyloidosis** _macroglossia_
513
Which systemic disease has this oral manifestation?
**Amyloidosis** _Amyloid deposition_ on the tongue is amyloid, you have papule and nodule like area, can see the **crenation** of the tooth
514
Which systemic disease has this oral manifestation?
Amyloidosis Submucosal amyloid deposit
515
Which systemic disease has this oral manifestation?
**Amyloidosis** _Amyloid deposition_ with **ulceration** and **petechiae**
516
Which systemic disease has these oral manifestations?
Amyloidosis ▪ different color compared to normal tongue with amyloid
517
Patients with **Celiac (Sprue) Disease** have risk of _developing which cancer?_
● 10‐15% risk of **GI lymphoma**
518
Celiac (Sprue) Disease _Oral Symptoms_
● 10‐15% risk of GI lymphoma ● Oral symptoms include aphthous‐like ulceration of mucosa ● Patients can have enamel defects and pitting
519
**Amyloidosis** What is it? From what does it form? Seen with what disease?
**What is it?** * _Protein deposits in tissue_ * Paucicellular eosinophilic deposits amorphous eosinophilic deposit **From what does it form?** * Form **fibrillar β‐pleated sheets** within the tissue Seen with what disease? * **multiple myeloma**
520
**Amyloidosis** what are its Types and what they are associated with?
1. **▪ _Primary amyloidosis_** is associated with **multiple myeloma** 2. **Reactive systemic amyloidosis** 3. **Hemodialysis** associated **amyloidosis kidney dysfunction** 4. **Hereditary amyloidosis** **(Familial Mediterranean Fever)**, present with **polyneuropathies, cardiac arrhythmias, renal failure, CHF** 5. **Localized dermal amyloidosis**
521
**Primary amyloidosis** is associated with **which cancer?**
**multiple myeloma**
522
Hemodialysis associated amyloidosis leads to ------
kidney dysfunction
523
**Amyloidosis** **Organ Limited** _Clinically_
* **Rare in oral cavity** * Amyloid _nodule_, **asymptomatic** submucosal deposit * **Not** associated with ***systemic symptoms***
524
**Primary or Muliple Myeloma associated Amyloidosis** Systemic _Demographics & Clinical presentations_
* Older adults **\> 65yrs** * **Male** predilection * Amyloid deposits _lead to_ **_macroglossia, carpal tunnel_ syndrome, hepatomegaly, dry mouth** * **Skin lesions:** Waxy papules and plaques, **smooth surface (eyelid area, retroauricular, neck, lips), orangy, red appearance**
525
**Secondary Amyloidosis** systemic _Etiology & Effects_
* Due to _chronic inflammatory process_ * *(osteomyelitis, TB,** **sarcoidosis)** * Affects **liver, kidney, spleen, adrenals** *but not heart* * can affect multiple organs, _heart is usually spared_
526
**Hemodialysis associated Amyloidosis** _Etiology & Effects_
## Footnote o **Accumulation of normal protein** (beta‐2 microglobulin) in plasma _o Deposits in bones and joint_s **o Carpal tunnel syndrome, cervical spine pain** o **Tongue deposits** can have **macroglossia**
527
**Amyloidosis** _Clinical Presentations_
* **Deposition of an extracellular proteinaceous materia**l‐often **immunoglobulins** * all types have common feature of a _β‐pleated sheet molecular configuration_ * **Macroglossia** * **can be massive and exhibit dental indentations** (**crenation**) with _yellowish peripheral nodules_ * **Gingiva**: _usually normal in color,_ but *may be bluish, spongy and enlarged* * **Xerostomia** _if deposits in salivary glands_ * **Mucosal petechiae** can be seen
528
Amyloidosis _Mangement_
* **Medical work‐up** *to determine* **type of amyloidosis** * T**reat underlying disease** when possible * **No treatment available for most types** * **Chemo drugs** _(Colchicine, Prednisone, Melphalan, Thalidomide, Cyclophosphamide)_ for **multiple myeloma** * **Serum electrophoresis** – monoclonal gammopathy very complicated and time consuming treatment * **Renal transplant** for _dialysis‐associated type_ * *Death* **due to cardiac failure, arrhythmias or renal failure** *_is not uncommon_* within a few year of dx
529
Diabetes Mellitus
Endocrine Disease * a group of metabolic disorders with one common manifestation**: hyperglycemia** * Basic problem is either _a decreased production of insulin_ or _tissue resistance to insulin_
530
Diabetes Mellitus _Pathophysiology_
▪ **Insulin** is hormone produced by ***beta cells of the pancreatic islets of Langerhans*** ▪ It is _required for the uptake of glucose by body cells_ ▪ **Insulin binds specific receptors which trigger** the _intracellular events necessary for glucose uptake_
531
Diabetes Mellitus Types
Type 1 Type 2
532
Diabetes Mellitus Type I _Definition_ _Demographics_ _Symptoms_ _Etiology_
_Definition_ insulin‐dependent diabetes mellitus (IDDM) _Demographics_ 5‐10% of cases **_Juvenile onset (avg age 14)_** _Symptoms_ * Severe **absolute lack of insulin** * **Hyperglycemia** and **ketoacidosis** * **Blood glucose levels of 200‐400 mg/dl** (70‐120 normal) * **Ketoacidosis** from using *protein* and *fat* for energy instead of glucose body _can’t use glucose_ * **Thin body habitus** _Etiology_ * **Autoimmune disease** * Thought to be possible viral infection as trigger to Islet cell antibody destruction of beta cells
533
**Diabetes Mellitus** Type II _Definition_ _Demographics_ _Symptoms_ _Etiology_
_Definition_ * non‐insulin‐dependent diabetes mellitus (NIDDM) _Demographics_ * **About 90% of cases** * Onset in **older, obese adults (80‐90%)**; _ketoacidosis is rare_ _Symptoms_ * _Patients produce some insuli_n, can typically be treated with oral medication * **“insulin resistance”**‐ insulin levels appear WNL or elevated _Etiology_ * **Decreased number of insulin receptors or defective receptors** * *Genetic abnormalities, multifactorial* * _Growing percent_ of the **US population** as well as around the world
534
**Diabetes Mellitus** _Complications_
▪ **Decreased neutrophil chemotaxis** ►_do not fight off infections as well as you should_ ▪ **Peripheral vascular disease**►microangiopathy o Results in **ischemia**: kidney failure, gangrenous complications of lower limbs, retinal involvement leading to blindness o Amputations, CVA or MI o **Ketoacidosis** may lead to *_diabetic coma_*
535
**Diabetes Mellitus** _Oral Findings_ **_Most often associated with Type I_** *but may be seen with Type II*
* **Periodontal disease**‐ more frequent occurrence, more rapid progression * **Poor healing** _post oral surgery/extractions_ * **Enlargement and erythema of the attached gingiva** * **Increased risk of infections** * Candidiasis * **Xerostomia**‐ 1/3 of pts complain of dryness * **Diabetic Sialadenosi**s‐ both type I and type II * **Mucormycosis**‐ in uncontrolled disease and the tissue becomes necrotic because it is not getting any blood supply * **Dental Caries**o **Benign migratory glossitis** * Increased prevalence in type I
536
**Diabetes Mellitus** **TYPE I** _Management_
* **Insulin injections** * **Insulin shock**‐ _if blood glucose falls *below 40 mg/d*l_ * Treat with **dextrose**
537
**Diabetes Mellitus** **TYPE II** _Management_
* **Dietary modification** and **weight loss** * **Oral hypoglycemic agents** * ex. tolbutamide, glyburide, metformin * *Drugs may cause* **a lichenoid drug reaction**
538
Oral Manifestation of which systemic disease
**Diabetes Mellitus** Gingivitis = puffy red papillae here between the central and lateral incisors
539
Oral Manifestation of which systemic disease ?
**Diabetes mellitus** Anterior papillae are very puffy and red and fill of pus Posterior gingiva are very hyperplastic
540
Oral Manifestation of which systemic disease ?
Hyperplastic gingiva
541
Oral Manifestation of which systemic disease ?
Diabetes Mellitus Sialadenosis
542
Oral Manifestation of which systemic disease ?
Diabetes Mellitus diabetic patient who developed *Mucormycosis* Notice it is causing _necrosis_ in the palate
543
Which systemic disease has this oral manifestation?
**Lichenoid mucositis looks like lichen planus** -same reticular white pattern, but there are areas of erosion and some ulceration as well -some diabetic medications can lead to this
544
**Hyperthyroidism** _Treatment_
* Treatment includes: * **Surgery** – complete or partial removal of thyroid gland * **Medications** * _Propylthiouracil_ and _methimazole_ block normal use of iodine by thyroid gland * **Radioactive iodine 131I** * Treatment often results in **hypothyroidism**
545
Which systemic disease has this oral manifestation?
**Hyperthyroidism** * enlargement of the neck * characteristic stare
546
Hyperthyroidism what is its most common form?
**Graves’ Disease is the most common form** o An autoimmune disease attacks thyroid (TSH receptor) o Leads to _elevated release of thyroxine_ o Most often a diffuse thyroid enlargement **(goiter)**
547
**In Hyperthyroidism, what happens to** **T4** (thyroxine) and **TSH** values
* **Serum T4** (thyroxine) is **_elevated_** and * **TSH is _decreased_**
548
Hyperthyroidism _Demographics_
▪ **5‐10X** more common in **females** ‐ 2% of women ▪ **3rd ‐ 4th** _decade of life_
549
**Hypothyroidism** _Treatment_
▪ Treatment is **thyroid hormone replacement** ▪ Prognosis is **generally good** ▪ If children are not treated in a timely fashion ► **permanent CNS damage can occur (mental retardation)**
550
Which systemic disease has this oral manifestation?
hypothyroidism woman who had hypothyroidism, lips are thickened, thick creases in the face
551
Which systemic disease has this oral manifestation?
hypothyroidism, in child, still has deciduous teeth even though its an older child Radiographically we see the teeth have not erupted in the oral cavity
552
Which systemic disease has this oral manifestation?
**Hypothyroidism** **Macroglossia** and **crenation** (scalloping) of the lateral tongue
553
Before and after tx of which systemic disease?
hypothyroidism
554
Hyperthyroidism What patients might complain of? What are the symptoms?
**What patients might complain of?** * nervousness * heart palpitations * heat intolerance * muscle weakness * emotionally labile **What are the symptoms?** * weight loss, excessive perspiration, tachycardia, tremors, eyelid retraction and exophthalmos * **20‐40%** have **ocular involvement** o Early in the disease‐ **characteristic stare with eyelid retraction and lid lag** o **Exophthalmos or proptosis** ▪ **Oral findings** in children can include **early eruption of teeth**
555
Benign and malignant tumors of thyroid and pituitary gland can cause which systemic disease
**hyperthyroidism**
556
**Hypothyroidism** What happens in Hypothyroidism? What it is called in children & adults? How it is diagnosed?
_What happens in Hypothyroidism?_ * Decreased levels of thyroid hormone _What it is called in children & adults?_ * **cretinism** in children * **myxedema** in adults _How it is diagnosed?_ * Diagnosed by **measuring T4** (free thyroxine) in serum
557
Hypothyroidism Primary and secondary etiologies and T4,TSH profile?
**▪ Primary Hypothyroidism** ‐ due to abnormality in thyroid gland o **T4** *_low_*, **TSH** *_elevated_* **▪ Secondary Hypothyroidism (less common)** ‐ pituitary gland doesn’t produce adequate amounts of TSH o **T4** *_low_*, **TSH** *_low_* or borderline
558
**Hashimoto’s thyroiditis** or **thyroid surgery** are main causes in adults of which systemic disease?
**Hypothyroidism**
559
Hypothyroidism _Symptoms_ _Oral findings_
_Symptoms_ * Symptoms include lethargy, dry skin, thinning hair, swelling (edema) of face and extremities, huskiness of voice, weakness and fatigue * ▪ Infants have failure to thrive _Symptoms_ o **Thickened lips** and **macroglossia** due to _accumulation of glycosaminoglycans (GAGs)_ o In children can see **failure of tooth eruption** even though teeth have normal development (enamel pitting can be seen)
560
An Oral Manifestaion of which systemic disease?
Hyperparathyroidism in young children
561
**Primary Hyperparathyroidism** Charcterstics
o _Uncontrolled_ PTH production o 80‐90% caused by **parathyroid adenoma** o ~15% caused by hyperplasia o ~ 2% caused by parathyroid carcinoma
562
**Secondary Hyperthirydoism** _Charcterstics_
o PTH continuously produced in response to chronic low serum calcium (usually associated with chronic renal disease)
563
**Hyperparathyroidism** _Classic triad_ _of_
**bones, stones, and groans (& moans)** * **Bones** – Changes in the bones: * Subperiosteal resorption of distal phalanges (early in disease) * Loss of lamina dura around roots (early in disease) * Loss/blurring of trabecular density in bone with resultant “ground glass” appearance in radiographs * Brown tumor * **Stones** – renal calculi (especially with primary disease) due to elevated serum calcium basically kidney stones * **Groans** – duodenal ulcers * **Moans** – changes in mental status mild dementia
564
Which systemic disease has this oral manifestation?
**Pseudohypoparathyroidism** pulp chambers are very elongated
565
Which systemic disease has this oral manifestation?
**Pseudohypoparathyroidism** issues with eruption, no pulp stones present
566
**Hyperparathyroidism**
Can be *Primary* or *Secondary* * Reduced amounts of PTH * Parathormone normally stimulates osteoclasts in bone and resorption in kidney, to bring serum levels of calcium back to normal with decreased parathyroid function, serum calcium levels drop → hypocalcemia * Lab findings ‐ PTH ↓, calcium ↓, phosphate↑, and normal renal function * Postive Chvostek’s sign ( sign of low Calcium) Females 2 to 4 times more than males
567
**Hyperparathyroidism** _Bones Manfestiation_
* **Subperiosteal resorption** of distal phalanges (early in disease) * **Loss of lamina dura** around roots (early in disease) * **Loss/blurring of trabecular density** _in bone with resultant_ * **“ground glass”** appearance in radiographs * **Brown tumor** * **Steitis fibrosa cystica**
568
What systemic disease causes this oral symptoms?
Hereditary Hypophosphatemia/vitamin D‐resistant rickets teeth look fairly normal, have a draining abscess with ulcers and perilous
569
What systemic disease causes this oral symptoms?
Hereditary Hypophosphatemia/vitamin D‐resistant rickets teeth look fairly normal, have a draining abscess with ulcers and perilous
570
**Hereditary Hypophosphatemia** _Histology_
 Enlarged pulp horns o Can extend up to DEJ  Abnormal globular dentin o Dentin may exhibit clefting  Enamel clefts  Bacteria noted in enamel, dentin and pulp o Pulpal involvement leads to necrosis and development of the periapical pathology
571
What is the most severe bone manifestation in people with hyperparathyroidism
**Steitis fibrosa cystica** Where we see **central degeneration** and **fibrosis** of **longstanding brown tumors**
572
What are the manifestation of **_Brown tumor_** in Hyperparathyroidism
* **uni‐ or multilocular Radiolucency** (pelvis, ribs, mandible) * seen with _persistent disease_ * histology of **giant cell lesion** (**like CGCG**)
573
Hyperparathyroidism Treatment
It is typically **surgical removal** of _a portion or all of the parathyroid glands_
574
**Hypoparathyroidism** _Etiology_
▪ Can be due to **inadvertent surgical removal** when **thyroid gland** is _excised_ or to _autoimmine destruction._ ▪ **DiGeorge syndrome** (anomaly) and **endocrine‐candidiasis syndrome** can show this.
575
What is _a Chvostek’s sign?_
* The Chvostek sign is a clinical finding associated with hypocalcemia, or low levels of calcium in the blood. * This clinical sign refers to a twitch of the facial muscles that occurs when gently tapping an individual's when the facial nerve below the zygomatic process
576
**Hypoparathyroidism** in young children
* If develops in young children **tooth development can be affected** ​ * **_pitting enamel hypoplasia_** and **_failure of eruption_** * **Persistent oral candidiasis** in a young patient may be a sign of the onset of **endocrine‐candidiasis syndrome** *(check for other endocrine abnormalities)*
577
**Hyperparathyroidism** _Management_
* Oral vitamin D precursor * vitamin D2 (or ergocalciferol) * Dietary supplements of calcium * Teriparatide (a portion of PTH) injections twice daily
578
**Pseudohypoparathyroidism** Also known as? _What is it?_ _How it appears clinically_ _What is its lab findings?_
_Also known as?_ Albright hereditary osteodystrophy _What is it?_ ▪ **Normal parathyroid** and **PTH**, but activation of target cells is **dysfunctional** _How it appears clinically?_ ▪ Clinically, patient appears to have hypoparathyroidism o Based on **elevated serum levels of PTH seen with hypocalcemia,hyperphosphatemia** and **normal renal function** Lab findings **PTH ↑, calcium ↓, phosphate** ↑
579
**Pseudohypoparathyroidism** Types What causes it Type of inheritance & mutation
*_Types_* Two broad disorders multiple subtypes **Type I and Type II** *_What causes it_* **Abnormal biochemical pathway**s that result in lack of target cell activation despite **normal levels of PTH** *_Type of inheritance_* Can be _autosomal dominant inheritance_ – **defective PTH** **receptor on the target cells**
580
**Pseudohypoparathyroidism** _Management_
- Vitamin D and calcium supplements - Serum and urinary calcium are monitored
581
**Pseudohypoparathyroidism** _Oral Findings_
* *- Generalized enamel hypoplasia** - **Widened pulp chambers** with **pulpal calcifications (“dagger” shaped pulp stones)** - _Oligodontia_ - _Delayed eruption_ - _Blunting of root apices_
582
Hereditary Hypophosphatemia Also known as? What type of inheritance? What mutation causes it?
**Also known as?** vitamin D‐resistant rickets looks like they have rickets. **What type of inheritance?** ▪ Most cases are X‐linked inheritance (males) **What mutation causes it?** o Mutation in PHEX ‐ zinc metalloproteinase gene ▪ phosphate regulating gene with endopeptidase activity on the X chromosome ▪ Mutation affects **metabolism of vitamin D precursors to the active metabolite** o Therefore _low or no absorption of calcium_ ▪ _Decreased capacity for reabsorption of phosphate from the renal tubules_
583
**Hereditary Hypophosphatemia/vitamin D‐resistant rickets** Clincal Findings _Lab findings_
_Clinical Findings_ ▪ Clinical features similar to those of rickets, but resistant to treatment with vitamin D o **Short stature** (upper body fairly normal, lower body shortened) o **Lower limbs short and bowed** ▪ _Similar to Vitamin D‐dependent rickets except no hypocalcification of teeth_ ▪ **Teeth have enlarged pulp chambers and elongated pulp horns** (extend to DEJ) ▪ With **minor attrition of occlusal cusps, pulp is exposed to the oral cavity** ▪ Exposures are often very small and when note periapical radiolucencies, it appears that otherwise normal teeth have periapical pathology _Lab findings:_ **↓ serum phosphate**
584
Hypophosphatasia What is it? Type of inheritance? Clincal findings? Lab Findings?
**What is it?** Rare metabolic bone disease **Type of inheritance:** **_Autosomal recessive_** inheritance, generally the younger the age of onset the more severe the expression **Clincal findings:**  Bone abnormalities resemble rickets  Often presents with premature loss of primary teeth o not from periodontal disease, thought that marked reduction, or lack, of cementum allows exfoliation **Lab findings:** ↓ alkaline phosphatase, ↑ blood and urinary phosphoethanolamine
585
Hypophosphatasia Types 4
 Perinatal  Infantile  Childhood  Adult
586
Hypophosphatasia _Perinatal_
o Most severe manifestations o Death in a few hours secondary to respiratory failure o Marked hypocalcification of skeleton
587
Hypophosphatasia _Infantile_
o Diagnosed ~4‐6 months due to failure to grow o Skeletal malformations  shortened bowed limbs, rib and skull abnormalities o Nephrocalcinosis, nephrolithiasis  Can have premature exfoliation of teeth
588
Hypophosphatasia _Childhood_
o Diagnosed at later age, variable clinical expression o Early sign is **premature loss of primary teeth, may be the only teeth affected** o **Large pulp chambers** *and* **alveolar bone loss** o P**remature fusion of cranial fontanels** can lead to _increase intracranial pressure and brain damage_
589
Hypophosphatasia _Adult_
o Mild presentation o **Premature loss of primary or permanent dentition**; patient may be **edentulous** o **Stress fractures in _feet_** o Increased number of fractures assoc. with minor trauma
590
**Acromegaly** vs **Gigantism**
**Acromegaly** – excess production of growth hormone **after** closure of the epiphyseal plates **Gigantism** – excess production of growth hormone **before** closure of the epiphyseal plates
591
Acromegaly Etiology Clinical signs Oral Findings
Etiology ▪ Usually due to _a pituitary adenoma_ Clinical signs ▪ _Renewed growth of small bones_ of the hands and feet as well as membranous bones of the skull and jaws ▪ Soft tissues are also affected Oral Findings ▪ Mandibular ***prognathism***, ***macroglossia***, and **diastema formation**
592
Which systemic disease has these clinical manifestations?
**Acromegaly**
593
_Addison’s Disease_ **also known as** **etiology** **when do clinical symptoms appear?**
**also known as** Hypoadrenocorticism **etiology** ``` Insufficient production of corticosteroid hormones due to destruction of adrenal cortex (autoimmune, infection, tumors, etc.) ``` **when do clinical symptoms appear?** ▪ Need ~90% destruction of gland before clinical symptoms
594
Which systemic disease manfiest like this?
**Addison’s Disease**
595
Which systemic disease manfiest like this?
**Addison’s Disease**
596
Addison’s Disease /Hypoadrenocorticism Clincal symptoms Lab findings
_Clincal symptoms_ * diffuse hyperpigmentation of skin (bronzing), fatigue, * irritability, depression, weakness, etc. * Oral mucosa shows **diffuse** *or* **patchy macular pigmentations flattened pigmentations** _Lab findings_ failure of cortisol to rise in response to a rapid ACTH stimulation
597
Which systemic disease is associated with this symptom?
_Pellagra_ Deficience in Vitamine B3 (Niacin)
598
Pellagra Deficience in Vitamine B3 (Niacin) Dermititis of the skin
599
Which systemic disease manifests like this?
Pellagra Deficience in Vitamine B3 (Niacin) erythema of the tongue
600
**Vitamin B3 (Niacin)** _Deficiency known as_ _Classid Triad_ _Oral symptoms_
**Deficiency** pellagra **Classic triad** **D**ermatitis, **D**ementia, **D**iarrhea **Oral symptoms** _stomatitis_ and _glossitis_
601
**Plummer‐Vinson Syndrome** Why it is a concern?
**Why it is a concern?** Premalignant process o ↑ incidence of oral and esophageal SCCa
602
Which systemic diseaswe associated with these oral manifestations?
**PLUMMER‐VINSON SYNDROME** denuded tongue and angular chelitis
603
Which systemic diseaswe associated with these oral manifestations?
_PLUMMER‐VINSON SYNDROME_ **Angular chelitis** (top) hard to get rid of them **Atrophic Glossitis** (bottom) red beefy tongue
604
How blood looks with
**Top photo**: in Iron Deficiency Anemia, Plummer‐Vinson Syndrome, small area that is pale in the center **Bottom photo** : normal smear, center is not pale
605
**Vitamin C** **Deficiency** _Known as_
scurvy
606
**Iron Deficiency Anemia** _Charcterstics of the_ Anemia _Symptoms_
**Charctersics of Anemia** a _hypochromic_, _microcytic_ anemia *decrease in color, smaller than normal* **Symptoms** fatigue, light headedness, lack of energy .
607
Iron Deficiency Anemia Oral Symptoms
* **Angular cheilitis** (corner of the mouth ulceration) * **Dysphagia** (difficulty swallowing) * **Atrophic glossitis** (bald tongue, loss of papilla) beefy colored tongue * **Glossodynia** (burning tongue)
608
Smear blood of Pernicious Anemia vs normal blood smear
not biconcave
609
Iron Deficiency Anemia _Treatment_
Treated with iron supplements, extreme cases with blood infusions
610
Which systemic disease manifests like this?
**Pernicious Anemia** glossitis, denuded papillae
611
This is a before and after of which systemic disease?
**Pernicious Anemia** ## Footnote denuded tongue and then the papillae is back again after the treatment. You have to get injections for the rest of your life
612
Plummer‐Vinson Syndrome What is it ( assiosited with what difficiency)? Demographics?
**What is it ( assiosited with what difficiency)?** * Iron deficiency anemia with **glossitis** and **esophageal strictures** * _Similar signs and symptoms_ as iron deficiency **Demographics** * Mostly women 30‐50 years old * Northern European heritage more common
613
Which systemic disease has this oral manifestation?
Uremic Stomatitis
614
**Plummer‐Vinson Syndrome** *Iron Deficiency Anemia* _Treatment_
* Treated with iron supplements * Need long term follow up for eval of SCCa
615
Before and after treatment of which systemic disease?
**Uremic Stomatitis** Before and After Tx with Dialysis changes on ventral and lateral side of the tongue, better outcome after dialysis
616
Which systemic disease has these oral manifestations?
Reiter’s Syndrome (Reactive arthritis) This not actually a geogrpahic tongue!
617
Which systemic disease has these oral manifestations?
Reiter’s Syndrome (Reactive arthritis) Top: erythema on the palate and areas of ulceration Bottom: classic look of geographic tongue, but it is not geo tongue. They are symptoms of Reiter’s
618
**Infective endocarditis**
▪ Janeway lesions o Seen on palms of hands and soles of feet (tiny micro emboli that are causing lesions on the hands and feet) ▪ **Erythematous macule or petechiae** ▪ _Painless_ ▪ **Septic micro emboli**
619
Which systemic disease has these clinical manifestations
Infective Endocardiatios Janeway lesions These are **Septic Emboli**
620
Which systemic disease is this?
Hyperparathyroidism Here we see we see * _a granular appearance of the max and mand bone everywhere,_ it is **not localized**. * There is a **loss of bone density** and **the loss of definition of cortical bone.** * Here we see a **loss of definition of lamina dura** as well _because it is now granular, and is not as clear._
621
Which systemic disease shows radiographically like this ?
**Hyperparathyroidism**; this is the **brown tumor** which is sometimes **well or ill defined,** **multi or unilocular radiolucency** with **granular septation.** If you have a patient that is younger than 15-20 years old that has **a central giant cell granuloma** ► you have to check that patient for hyperparathyroidism, because it could be a brown tumor.
622
Which systemic disease shows radiographically like this ?
This is another medical CT scan. You see the granular appearance of the maxilla, skull, and well-defined multilocular radiolucency with granulation. We call this a brown tumor because it is associated with **hyperparathyroidism.** **( s**ystemic endocrine diseases)
623
Which systemic disease shows radiographically like this ?
Hyperparathyroidism ## Footnote On our intraoral radiographs, we see **loss of definition of lamina dura** because the bone now has **a granular appearance** which extends to the lamina dura. The teeth are usually normal, but there is a loss of lamina dura around the teeth. These teeth are not mobile.
624
Which systemic disease shows radiographically like this?
a medical CT scan of a patient with **secondary hyperparathyroidism.** We see a **lack of cortical bone** – no normal cortical bone. Inside the skull we have **a granular appearance**, with **radiolucent and radiopaque dots**, we call this **a salt and pepper dots**. This is why we call this a salt and pepper appearance, _there is no normal cortical bone._ *( systemic endocrine diseases)*
625
**Pernicious Anemia** Type of Anemia? What difficiency? Causes?
_Type of Anemia?_ **_Megaloblastic_** Anemia _What difficiency?_ **Vitamin B12 difficiency** _Causes?_ * Poor absorption of vitamin B12 (extrinsic factor, cobalamin) * These patients _lack intrinsic factor,_ usually **due to autoimmune destruction of parietal cells** * ***Intrinsic factor*** produced by parietal cells in the stomach is **needed for absorption of B12**
626
Pernicious Anemia Symptoms
* Have **burning sensation of** *tongue, lips and buccal mucosa* * One of the things you need to rule out in patients with burning mouth syndrome * **50‐60% of patients** have **tongue symptoms,** see **atrophy** (papilla denuded) and **erythema**
627
Which systemic disease shows radiographically like this?
we have 2 Pas of patients **with pseudohypoparathyroidism**. * hypoplasia of enamel, tooth material * hypoplastic tooth bud ( hypoplastic means arrested development) * delayed eruption, * external root resorption.
628
Pernicious Anemia _Treatment_
* monthly IM injections of **cyanocobalamin** * **cannot take ​**_**B12 orally**, you need injections_
629
**Pernicious Anemia** CLASSIC TRIAD
1 – **Generalized weakness** 2 – **Painful tongue** 3 – **Numbness or tingling of the extremities**
630
**UREMIC STOMATITIS** _What is it?_ _What causes the oral lesions?_
What is it? * Uncommon complication of renal failure * Patients have markedly **elevated levels of urea** _in their blood stream_ **What causes the oral lesions?** * Cause of oral lesions is unclear, may be urease produced by normal flora degrades urea in saliva liberating free ammonia which damages mucosa
631
**UREMIC STOMATITIS** _Clinical Presentation_
Most cases in patients with **acute renal failure** ▪ Abrupt onset of **white plaques or crusts** o _Bad taste_ and _burning_ also possible o **May be** *painful* ▪ Usually on the **buccal mucosa, tongue and floor of mouth** o If localized to the tongue can mimic ***oral hairy leukoplakia*** ▪ May detect **an odor of ammonia or urine** on the patients breath
632
**Uremic Stomatitis** _Treatment_
▪ Usually clears within a few days _after renal dialysis has begun_ ▪ **Mildly acidic mouth rinses** seem to clear oral lesions *(ex. diluted hydrogen peroxide)* ▪ **Palliative treatment *_for pain_*** includes _ice chips or a topical anesthetic_
633
Reiter’s Syndrome also known as? Corrlate with which antigen? Associated with what?
_also known as?_ **Reactive arthritis** _Corrlate with which antigen?_ Correlation with **HLA B27 (\> 70%)** _Associated with what?_ Typically seen after patient has either **a bacterial dysentery or an STD** sometimes **chlamydia**
634
**Reiter’s Syndrome (Reactive Arthritis)** _Etiology_ _Demographic_ _Clinical Presentation_
_Etiology_ * Thought to be due to **an abnormal immune response to the infection** _Demographic_ * Almost **exclusively** seen ***in males*** _in their twenties_ _Clinical Presentation_ * Oral lesions (~ 20% of cases) include **painless oral ulcerations**, **erosions/erythema of mucosa**, as well as erosions of the tongue which can mimic geographic tongue (both clinically and histologically)
635
**Reiter’s Syndrome** Classic Triad
Reiter’s Syndrome **Classic Triad** ▪ 1 – Polyarthritis (lasting more than one month) ▪ 2 – Conjunctivitis or uveitis ▪ 3 – Urethritis
636
**Hyperparathyroidism** Radiographic features
▪ **Stones, bones, moans, and groans** ▪ **Radiolucent appearance** (_generalized osteopenia_) What we see in the bones is one of the earliest radiographic features that we see = sudden erosions in the phalanges in the bones of the hands followed by mineralization of the skeleton including max and mand, skull base. As a result, you have generalized osteopenia. **10% of these patients have brown tumors** ▪ **Brown tumors:** Brown tumors are the same as central giant cell granulomas. When they are associated with hyperparathyroidism, we call them brown tumors. ▪ **Punctate or nodular calcifications** in the joints and kidneys =stones ▪ **Entire calvaria** has _a granular appearance_ classically known as the **“salt and pepper”** skull as a result of the generalized osteopenia, we have this granular appearance in the skull
637
**Hypoparathyroidism** _Radiographic features_
What is Hypoparathyroidism: ## Footnote _Insufficient secretion of PTH o Damage or removal of the parathyroid glands during thyroid surgery_ Principal radiographic change: calcification of the basal ganglia Sometimes we have **pseudohypoparathyroidism.** This happens when we have a normal amount of PTH, but there is something wrong with the response of the target tissue. So, we have normal PTH but abnormal response to PTH. **dental enamel hypoplasia, external root resorption, delayed eruption, or root dilaceration**
638
Hyperpituitarism What is it? What is its types
_What is it?_ * Hyperfunction of the anterior lobe of the pituitary gland caused by a benign functioning tumor of the anterior lobe * it's a systemic endocrine disease _What is its types ?_ ▪ Types based _on age of onset_ * **Gigantism** happens in ***children***, **generalized overgrowth of most long bones, hard and soft tissue**. These patients are usually very tall. Proportion in these patients may be normal, but very large appearance. * **Acromegaly** Increased hyperfunction in **adult patients**. In these patients, the epiphysis of the long bones already closed, **you can see in the mand or max.** One of the observable features is **enlargement of the whole mandible/skull/sinuses/soft tissue.** Patients usually present with _“My hat is not fitting anymore, my denture is not fitting anymore”_
639
**Hyperparathyroidism** _What is it?_ _What are its types?_
_What is it?_ * **Excess of circulating parathyroid hormone important in formation of osseous structures** * Increase bone remodeling but tips the balance of osteoblastic and osteoclastic activity in favor or osteoclastic resorption * it's a systemic endocrine disease _What are its types?_ **o Primary hyperparathyroidism Type** 1 ▪ Uncontrolled parathyroid hormone production by parathyroid neoplasm (adenoma \>\> hyperplasia \> adenocarcinoma) **o Secondary hyperparathyroidism Type 2** ▪ Continuous parathyroid hormone production in response to chronic low serum calcium levels ▪ Renal osteodystrophy
640
Which systemic disease is this?
Hyperparathyroidism Here we see we see * _a granular appearance of the max and mand bone everywhere,_ it is **not localized**. * There is a **loss of bone density** and **the loss of definition of cortical bone.** * Here we see a **loss of definition of lamina dura** as well _because it is now granular, and is not as clear._
641
Which systemic disease shows radiographically like this ?
**Hyperparathyroidism**; this is the **brown tumor** which is sometimes **well or ill defined,** **multi or unilocular radiolucency** with **granular septation.** If you have a patient that is younger than 15-20 years old that has **a central giant cell granuloma** ► you have to check that patient for hyperparathyroidism, because it could be a brown tumor.
642
Which systemic disease shows radiographically like this ?
This is another medical CT scan. You see the granular appearance of the maxilla, skull, and well-defined multilocular radiolucency with granulation. We call this a brown tumor because it is associated with **hyperparathyroidism.** **( s**ystemic endocrine diseases)
643
Which systemic disease shows radiographically like this ?
Hyperparathyroidism ## Footnote On our intraoral radiographs, we see **loss of definition of lamina dura** because the bone now has **a granular appearance** which extends to the lamina dura. The teeth are usually normal, but there is a loss of lamina dura around the teeth. These teeth are not mobile.
644
Which systemic disease shows radiographically like this?
a medical CT scan of a patient with **secondary hyperparathyroidism.** We see a **lack of cortical bone** – no normal cortical bone. Inside the skull we have **a granular appearance**, with **radiolucent and radiopaque dots**, we call this **a salt and pepper dots**. This is why we call this a salt and pepper appearance, _there is no normal cortical bone._ *( systemic endocrine diseases)*
645
Which systemic disease shows radiographically like this?
we have 2 Pas of patients **with pseudohypoparathyroidism**. * hypoplasia of enamel, tooth material * hypoplastic tooth bud ( hypoplastic means arrested development) * delayed eruption, * external root resorption.
646
Which systemic disease shows radiographically like this?
Acromegaly (Hyperpituitarism) * enlargement of the mandibular bone with a high degree of enlargement * a class III appearance * enlargement of sella tursica because of the pituitary gland enlargement
647
**Ranula** Definition Associated with Clinical features Treatment
• **Definition**: mucocele-like lesion that forms unilaterally on the floor of the mouth • may break through the mylohyoid muscle & enter neck space = *“plunging ranula”* • **associated with:** the _ducts of the sublingual & submandibular glands_ **• clinical features:** - must be _on floor of the mouth_ for it to be considered a ***ranula*** - big & have deep blue color if exophytic - sometimes can grow downward/deep & won’t see blue as much **• treatment**: surgical excision
648
**Hyperparathyroidism** Radiographic features
▪ **Stones, bones, moans, and groans** ▪ **Radiolucent appearance** (_generalized osteopenia_) What we see in the bones is one of the earliest radiographic features that we see = sudden erosions in the phalanges in the bones of the hands followed by mineralization of the skeleton including max and mand, skull base. As a result, you have generalized osteopenia. **10% of these patients have brown tumors** ▪ **Brown tumors:** Brown tumors are the same as central giant cell granulomas. When they are associated with hyperparathyroidism, we call them brown tumors. ▪ **Punctate or nodular calcifications** in the joints and kidneys =stones ▪ **Entire calvaria** has _a granular appearance_ classically known as the **“salt and pepper”** skull as a result of the generalized osteopenia, we have this granular appearance in the skull
649
Which systemic disease shows radiographically like this?
_Osteoporosis_ * **reduction in bone density,** * **larger bone marrow spaces.** We **need more tests to confirm osteoporosis** besides dental radiographs.
650
**Hypoparathyroidism** _Radiographic features_
What is Hypoparathyroidism: ## Footnote _Insufficient secretion of PTH o Damage or removal of the parathyroid glands during thyroid surgery_ Principal radiographic change: calcification of the basal ganglia Sometimes we have **pseudohypoparathyroidism.** This happens when we have a normal amount of PTH, but there is something wrong with the response of the target tissue. So, we have normal PTH but abnormal response to PTH. **dental enamel hypoplasia, external root resorption, delayed eruption, or root dilaceration**
651
Which systemic disease shows radiographically like this?
medical CT scan with a patient with **osteopetrosis**- very dense. Not a nice definition of the cortical bone. We see decreased in size of skull foramina.
652
Which systemic disease shows radiographically like this?
pt with Osteopetrosis we see **Hypovascular bones** so they are *more prone to osteomyelitis*. This is a sign of sequestrum which is a sign of osteomyelitis.
653
pt with Osteopetrosis * **Generalized increase in bone density,** increased trabeculation, loss of large bone marrow spaces. * These patients are more prone to **osteomyelitis** _because they are Hypovascular_. * We have to be careful in **extractions** because they don’t have the same vascularity as other healthy patients have. * We see an **onion skin appearance** by the white arrow.
654
Hyperpituitarism What is it? What is its types
_What is it?_ * Hyperfunction of the anterior lobe of the pituitary gland caused by a benign functioning tumor of the anterior lobe * it's a systemic endocrine disease _What is its types ?_ ▪ Types based _on age of onset_ * **Gigantism** happens in ***children***, **generalized overgrowth of most long bones, hard and soft tissue**. These patients are usually very tall. Proportion in these patients may be normal, but very large appearance. * **Acromegaly** Increased hyperfunction in **adult patients**. In these patients, the epiphysis of the long bones already closed, **you can see in the mand or max.** One of the observable features is **enlargement of the whole mandible/skull/sinuses/soft tissue.** Patients usually present with _“My hat is not fitting anymore, my denture is not fitting anymore”_
655
**Hyperpituitarism** _Radiographic Features_
**▪ General features** * _Enlargement_ (ballooning) of the **sella turcica** * _Enlargement_ of the **paranasal sinuses** (especially the **frontal sinus**) * _Thickening_ of the outer table of the **skull** **▪ Jaws** * _Enlargement of the **jaws**,_ most notably the **mandible** * **Class III skeletal** as a result of the mandible enlargement with growth centering in the condylar head **▪ Teeth and associated structures** * _Spacing of the teeth, enlargement of tongue_, it could result in spacing of teeth in the anterior region o **Hypercementosis the forces** are higher now * so you may see H**_ypercementosis_** * Hypercementosis is **excessive deposition of non-neoplastic cementum over normal root cementum,** which alters root morphology. This cementum may be either hypocellular or cellular in natur*
656
Which systemic disease has this radiographic manifestation?
Ricket / Osteomalacia hyperplasia or thinning of mineralization of teeth. We can see hyperplasia of enamel in patients.
657
Hypopituitarism What is it? What is it called? How it appears radiographically?
_What is it?_ Reduced secretion of pituitary hormones it's a systemic endocrine disease _What is it called?_ **Dwarfism** _How it appears radiographically?_ ▪ Finding of the jaws o **Normal eruption of primary dentition** but _delayed exfoliation_ o **Small jaws -**\> crowding and malocclusion because there is not enough space for the teeth to erupt
658
Which systemic disease manifest radiographically like this?
**Renal Osteodystrophy 1** *Presentation is variable*. Sometimes you see **denser or granular appearance of bone.** You see _increase here_ but you sometimes will also see loss of definition of lamina dura, sometimes a sclerotic appearance and trabeculation.
659
Which systemic disease manifest radiographically like this?
**Renal Osteodystrophy 2** sometimes you see: * **increase in bone density** * **loss of definition of lamina** * **dura and cortical bone**
660
**Osteoporosis** What is it? Why it happens? What the bone are like?
_What is it?_ ▪ **_Generalized decrease in bone mass_ i**n which the histologic appearance of bone is normal, it is a metabolic bone diseases (MBD) _Why it happens?_ * **Aging process (postmenopausal women)** bone mass usually increases until 30 years of age, and then there is a gradual decrease- about 8% loss in females and 3% loss in males * **Nutritional deficiencies** * **Hormonal imbalance** * **Inactivity** * **Corticosteroid or heparin therapy** _What the bone are like?_ ▪ **More prone to fracture** (distal radius, proximal femur, ribs, and vertebrae)
661
Which systemic disease manifests radiographically like this?
Hypophosphatasia
662
Which systemic disease manifests radiographically like this?
large root canal structures, large root chambers, premature loss of teeth = **hypophosphatasia.**
663
Osteopetrosis What is it? How is the bone is like? What are the effects on other structures? What are the consquences?
_What is it?_ **Defect in the differentiation and function of osteoclast**s, (osteoclasts that are used to resorb bone in the bone modeling process. They are not functioning properly ►so we have an increase in bone density.) It is a metabolic bone diseases (MBD) _How is the bone like?_ Bone is **dense, fragile, and _susceptible to fracture_** _and **infection ►**_we now have a_n osseous structure but small bone marrow spaces_ _What are the effects on other structures?_ It compromised vascular structures and cranial nerves
664
**Osteopetrosis** _What are the consquences?_
* Compression of the cranial nerves as they pass through the narrowed skull foramina -\> **blindness, deafness, vestibular nerve dysfunction, and facial nerve paralysis.** * Compromises hematopoiesis Poor vascularity -\> **osteomyelitis**
665
Which systemic disease manifests radiographically like this?
**Hypophosphatemia** * Periapical lesions with radiolucency but no caries on the crown. * There is loss of definition of cortical bone. * On the teeth, you have: * large pulp chambers * hypoplasia of enamel and dentin * periodontal and periapical lesions.
666
Which systemic disease manifests radiographically like this?
Progressive Systemic Sclerosis (scleroderma) ## Footnote sharp areas of resorption in the bones near muscles attached to the angle of the mandible= masseter and medial pterygoid. You see resorption at the coronoid process at the attachment of the temporal bone as well.
667
Which Systemic disease manifests radiographically like this?
**Progressive Systemic Sclerosis (scleroderma)** * presence of **widening of the PDL space everywhere** around the root of the tooth.
668
Rickets and Osteomalacia _What are they_ _Differences_ _Effects on Bones_
***_What happens?_*** They are metabolic bone diseases (MBD) Inadequate serum and extracellular levels of ***calcium*** and ***phosphate***, ***failure of normal activity of vitamin D.*** There are different levels in the conversion from I,12- dihydroxy vitamin D that can have errors, not just the consumption of vitamin D. ***_Differences_*** **Rickets**: disease affects the growing skeleton in i**nfants and children** **Osteomalacia**: disease affects the **mature skeleton in adults** **Effects on bones:** A softening and weakening of bones
669
Which systemic disease mainfest radiographically like this?
On a **sickle cell anemia** patient, you see: * **loss of this cortical bone area** * **the hair-on-end appearance on the skull**
670
Which systemic disease mainfest radiographically like this?
Sickel Cell Anemia enlargement of bone marrow spaces, less trabeculation, more osteoporotic bone. You see periapical pathology associated with teeth with no obvious reason. You see the radioluscencies around the apex of the mandibular teeth.
671
In Rickets and Osteomalacia, there is Failure of normal activity of vitamin D, what causes it?
o Lack of vitamin D in the diet o Gastrointestinal malabsorption problems o Lack of exposure to UV light o Liver disease o Kidney disease o Defect in the intestinal target cell response
672
Clinical presentation Ricket vs Osteomalacia
_Rickets_ o Growth retardation o Short stature o **Bowing of long bones** of the legs, waddling gait o **Radiograph manifestations in the teeth** (especially \<3 years of age) **and jaws** _Osteomalacia_ o Weak fragile bone structure _o Diffuse skeletal pain_ o Susceptible to fracture with minor injury o _Radiographic manifestations in the jaws_ **are uncommon** o you may see **hyperplasia** *or* **thinning of mineralization of teeth. You can see hyperplasia of enamel in patients.**
673
Which systemic disease mainfest radiographically like this?
**Thalassemia** * **osteopenic bone (***loss bone mass and bones get weaker*) * **radiolucent appearance of bone** * thinning of cortical bone around the mandible and maxilla. * Usually there is **hypoplasia of the paranasal sinuses.**
674
**Renal Osteodystrophy** What is it? what can it lead to?
_What is it?_ **Chronic renal failure** produces **bone changes** by _interfering with the hydroxylation of vitamin D in the kidneys_ -\> _hypocalcemia_ -\> **inhibit the normal calcification of bone and teeth** *(it is a metabolic bone disease)* _what can it lead to?_ (secondary hyperparathyroidism) **level of calcium is low** leads to having **hyperparathyroidism secondary to osteodystrophy**
675
Which systemic disease manifests radiographically like this?
Dwarfism * hypopituitarism* * We see* multiple dental anomalies: **hypodontia, radicular fusion,** fused roots of left lateral incisor and left canine **and impacted permanent teeth.** * (from google)*
676
**Hypophosphatasia** _What is it?_ _What are the types?_
**_What is it?_** * Rare metabolic bone disease due to **lack of tissue-nonspecific alkaline phosphatase** **_What are its types?_** **Four types: prenatal, infantile, childhood, adult** * _The younger the age of onset, the more severe the_ * _manifestations_ * It may have premature loss of these patients because loss of function of the lungs in these patients
677
**Hypophosphatasia** Common factors? Dental manfestations?
Common factors? * _Low levels_ of **tissue-nonspecific alkaline phosphatase** * **High** blood and urinary **phosphoethanolamine** * **Rickets-like skeletal malformations** Dental manfestations? * _Premature shedding_ of **primary incisors** * **Enamel hypoplasia** * _Enlarged_ **pulp chambers** and **root canals**
678
**Hypophosphatemia** _What is it?_ _Clinical Manifestations? Dental Manifestations?_
_What is it?_ * A **rare**, **heterogeneous** group of **inherited** metabolic disorders characterized by **decreased phosphate reabsorption** _in the distal renal tubules_
679
**Hypophosphatemia** Clinical Manifestations? Dental Manifestations?
_Clinical Manifestations_ * **Rickets-like skeletal malformations** _Dental Manifestations_ * **Enlarged pulp chambers** and **root canals** * **Periapical and periodontal abscesses** of no obvious cause * **Enamel hypoplasia**
680
**Progressive Systemic Sclerosis (scleroderma)** What is it? Demographics?
_What is it?_ * **Excessive collagen deposition** resulting in **hardening (sclerosis) of the skin and other tissues** can have involvement of _GI tract, heart, kidney,etc_ _Demographics?_ * Middle aged female
681
Progressive Systemic Sclerosis (scleroderma) _Clinical symptoms_ _Oral Manifestations_
_Clinical Presentation_ * Thickened, leathery quality skin * joint pain * exaggerated response to cold (Raynaud's disease) * heartburn. * more prone for heart problems and respiratory insufficiencies, _Oral Manifestations_ * microstomia (small mouth) * Xerostomia (dry mouth) * telangietasia ("spider veins") * Increased decayed, missing and filled teeth. * higher Gingivitis scores (usually) * Deeper Periodontal Pockets
682
Progressive Systemic Sclerosis (scleroderma) _Treatment_
Treatment for generalized symptoms may involve: * **corticosteroids** * **immunosuppressants, such as methotrexate or Cytoxan** * **nonsteroidal anti-inflammatory drugs** Depending on your symptoms, treatment can also include: * blood pressure medication * medication to aid breathing * physical therapy * light therapy, such as ultraviolet A1 phototherapy * nitroglycerin ointment to treat localized areas of tightening of the skin *(from google)*
683
**Sickle Cell Anemia** _What is it?_ _What causes it?_
_What is it?_ **Chronic hemolytic blood disorder** _What causes it?_ ▪ **Abnormal hemoglobin, resulting in anemia** -\> by increasing the production of red blood cells -\> **requires compensatory hyperplasia of the bone marrow**
684
**Sickel Cell Aniema** Radiographics findings
* loss of this cortical bone area * See the hair-on-end appearance on the skull * enlargement of bone marrow spaces * less trabeculation, more osteoporotic bone * periapical pathology associated with teeth with no obvious reason
685
**Thalassemia** What is it? What causes it?
What is it? * **Defect in hemoglobin synthesis** What causes it? * **RBC with reduced hemoglobin content** and _short life span_
686
**Thalassemia** _Clinical and Radiographic findings_
* **Hyperplasia of the bone marrow** **component** of the bone which results _in fewer trabeculae per unit area and can **change the overall shape of the bone**_ * **Protrusive premaxilla** * **Radiographic appearance** very similar to _Sickle Cell Anemia_
687
Suspect systemic endocrine and metabolic disease if radiographs show what?
generalized decrease in bone density of jaws (thin cortices; granular cancellous bone; loss of lamina dura). * Refer to physician for lab tests to make the diagnosis
688
We can include certain systemic endocrine and metabolic diseases as radiographic differentials in the presence of: o **Localized focus of radiolucency**- think what? o **Mandibular prognathism and incisor flaring**- think what? **o Premature shedding of primary incisors**-think what? o **Enamel hypoplasia, enlarged pulp chambers and periapical abscesses of no obvious cau**se- think what?
o Localized focus of radiolucency► **think brown tumor and hyperparathyroidism** o Mandibular prognathism and incisor flaring► **think acromegaly** o Premature shedding of primary incisors► **think hypophosphatasia** o Enamel hypoplasia, enlarged pulp chambers and periapical abscesses of no obvious cause► **think hypophosphatemia**
689
Palatine Torus/Torus Palatinus
* Tori are incredibly common, a normal of variant * Part of physical exam is to visualize as well as running index finger over the hard palate every time * Sometimes, torus palatinus is quite small and unnoticeable until you touch it (feel a hard bump and it’s just a bony growth) * Sometimes, they are pedunculated; Sometimes, they get so large they become traumatized; vascular supply on surface can sometimes form ulcerations and even get a little bone exposure. * If patient with history of use of bisphosphonates (bone modifying agents given to women who have osteoporosis or osteopenia and to prevent metastesis for certain cancers), he will remove that dead bone, and it will slowly heal. That’s one of the perils of having an enlarged palatine torus
690
What is this clinical finding?
Palatine Torus/Torus Palatinus
691
What is this clinical finding?
Palatine Torus/Torus Palatinus
692
What is this clinical finding?
Mandibular Torus: Torus Mandibularis
693
What is this clinical finding?
Mandibular Torus: Torus Mandibularis
694
What is this clinical finding?
Buccal Exostoses
695
**Mandibular Torus: Torus Mandibularis**
- Sometimes pt’s tori are so large that the sublingual frenum gets stuck underneath - repeated irritation/trauma can create a little white rim on the tori - these tori are rock hard and may grow overtime, but we don’t really understand why people get them
696
What is this clinical finding?
Unencapsulated Lymphoid Aggregates
697
What is this clinical finding?
Lymphoepithelial cyst we see a tiny yellowish cyst. we see the blood vessels on the surface; this is quite characteristic.
698
What is this clinical finding?
**Unencapsulated Lymphoid Aggregates** **Post-tonsillectomy** Can even develop these on area of tonsils. (left pic) Red/salmon is a lymphoid aggregate (unencapsulated lymphoid tissue). This is someone who had a tonsillectomy , and you can see these lymphoid aggregates on posterior pharyngeal wall (salmon color).They move around the area. (right pic) It grew back even in post-tonsillectomy patients.
699
What is this clinical finding?
Fordyce Granules
700
What is this clinical finding?
Fordyce Granules
701
**Buccal Exostoses**
* Sometimes patient develops **exostoses** (another word for **torus**). * Can get buccal exostoses, all just bone. Can pick these up on radiograph, the _bone is a lot denser._ **Why does it happen?** * Maybe it’s related to parafunctional habits – but don’t really understand the * basis for the exostosis. * They’re going to be **bilateral**. If it’s unilateral, we start thinking about other bony diseases *a variant of normal*
702
What is this clinical finding?
**Fimbriated fold/Plica semiluminaris**
703
What is this clinical finding?
**Frenal tag**
704
**Unencapsulated Lymphoid Aggregates**
* the lymphoid aggregates _are part of the foliate papillae_ (they contain some taste buds as well). * **This is lymphoid tissue -**- when you get a cold or upper respiratory tract infection, sometimes these areas can become **hyperplastic** _in response to infection_ – **can become** **a little enlarged.** * These are usually **bilateral.** * *a variant of normal*
705
What is this clinical finding?
Sublingual Varices
706
What is this clinical finding?
Sublingual Varices
707
What is this clinical finding?
Sublingual Varices
708
What is this clinical finding?
Circumvallate papillae
709
What is this clinical finding?
Parotid Papillia (Stenson duct)
710
What is this clinical finding?
Parotid Papillia (Stenson duct)
711
What is **Lymphoepithelial cyst?**
a cystic structure.develops in that area where there are already _unencapsulated lymphoid tissue._ **This is not normal – Pathologic** Sometimes when you get a cyst in this area -- because of lymphoid tissue, you can develop lymphoepithelial cyst – **a tiny yellowish cyst**. we see the blood vessels on the surface; this is quite characteristic.
712
What is this clinical finding?
Linea Alba
713
What is this clinical finding?
Leukoedema
714
**Fordyce Granules**
* Occurs on the buccal labial mucosa, retro molar pad and tonsillar area and lips * They are white or yellow **ectopic sebaceous glands** * They can be present in small or large quantity * Why do we have sebaceous glands in mouth? we dont know, evolutionary advantage? we don’t really understand. * a variant of normal
715
What is this clinical finding?
Palatal Rugae
716
Fimbriated fold/Plica semiluminaris
* Some patients have *_more obvious_* **fimbriated folds or plica semilunaris** in their mouths than others * When you look at the **ventral surface of the tongue**, you’ll sometimes be able to pick these up. * These are **duct opening from a series of salivary glands, minor glands,** but they’re a little bit different than other minor glands in the mouth. * They produce more of a **viscous type of saliva**, and they are **the glands of the Blandin and Nuhn** * a variant of normal
717
What is a Frenal tag?
* Frenal attachments are **thin folds of mucous membrane with enclosed muscle fibers that attach the lips to the alveolar mucosa and underlying periosteum.** * Most often, during the oral examination of the patient the dentist gives very little importance to the frenum, for assessing its morpholology and attachment. * Sometimes occur; essentially normal of varient
718
**Sublingual Varices**
* Tortuous dilated vessels (enlarged engourged veins) on the ventral surface of the tongue, and sometimes stretch onto lateral border * Appears bluish purple in color * More prominent with increasing age; we don't see it in younger pts. * Nothing to be concerned about, a variant of normal
719
**Circumvallate papillae**
* Located in the **posterior region of the tongue**; dividing the body from the base * They are mushroom shaped and arranged in V-shape formation * Although they are usually not apparent in most patients, you may be able to visualize them in some * a variant of normal
720
## Footnote **Parotid Papillia (Stenson duct)**
* **Located in right and left buccal mucosa** at the level of the occlusal plane close to the maxillary first and second molar. * This structure may appear a**s a small dot or have a prominent pink to red papillae presence.** * This is the **parotid papilla**, and It is the opening of the parotid duct which drains saliva from the parotid gland. *A normal of variant*
721
**Linea Alba**
•a white line or keratotic area that present along occlusal plane in some patients * due to some friction In that area. (the buccal mucosa) * It varies in thickness and opacity * Can be seen in some patients who have bruxism * a variant of normal
722
**Leukoedema**
* A bluish and white filmy opalescence of the mucosa is observed * In order to differentiate it from other white lesions à gently stretch the patient’s cheek forward and the leukoedema will disappear or partly fade and appears less apparent * It is commonly found in people of color and some smokers. * a variant of normal
723
Palatal Rugae
* Raised ridges or folds * Located in the anterior palate on either side of the mid-palatine raphe behind the incisive papilla * They vary in number and size * May increase with age * a variant of normal
724
**Irritation Fibromas** Composed of Etiology Clinical features ;Color Location Treatment
* AKA – **Fibroma, Traumatic Fibroma** * Composed of dense, scar-like, fibrous connective tissue * Occurs as a **result of chronic trauma** * **Clinical Features:** *Exophytic lesion* * Usually **less than a centimeter in diameter** * **Color**: lighter pink than surrounding mucosa,the surface can be white sometimes bc it’s rubbing and bumping into other oral structures (like teeth), so they get surface keratinization * **Locations**: buccal mucosa, tongue, lips, gingiva * Very common; **totally _benign soft lesion_** * _**Treatment**:_ _You don’t have to remove them, but the surgical Tx = to excise them_ _bc pts will stop biting them and they’ll heal and stop the irritation_
725
What is this clinical finding?
**Irritation Fibromas**
726
What is this clinical finding?
**Irritation Fibromas**
727
What is this clinical finding?
Chronic Hyperplastic Pulpitis (pulp polyp)
728
**Giant Cell Fibroma**
729
**Chronic Hyperplastic Pulpitis** What is it? Location? Age? Clinical Appearance? Treatment?
• **AKA:** pulp polyp • An e_xcessive proliferation of chronically inflamed dental pulp tissue_ – granulation tissue/ fibrous tissue with inflammatory cells *(like a little fibroma that occurs from pulp tissue​) ( benign soft tissue leasion)* **• Location:** • Teeth with large, open carious lesions • Primary or permanent molars **• Age:** Children & young adults • **Clinical Appearance**: A red or pink nodule of soft tissue protruding from the pulp chamber and fills the entire cavity of the tooth • **Treatment**: RCT or extraction of tooth
730
**Giant Cell Fibroma**
* Very small form of fibrous tumour that show giant cells * Age: relatively rare in paediatric patients. * **Clinically** it is presented as a painless, sessile, or pedunculated growth which is usually confused with other fibrous lesions like ***irritation fibromas or Retrocuspid papilla*** * **Location**: Largely occur on lower gingivae and on palate\
731
What are these clinical findings (what is the name of the syndrome or complex?)
**Tuberous sclerosis complex** we see A lot of gingival enlargement – is this overgrowth from disease or from seizure medication? Multi organ system involvement
732
What is this clinical finding?
**Epulis Fissuratum**
733
**Cowden Syndrome**
* **(multiple hamartoma and neoplasia syndrome)** * • **Autosomal dominant disorder** affecting multiple organ systems * • Caused by mutations in the phosphatase and tensin homolog gene (PTEN, a tumor suppressor gene) * • Oral and perioral findings include * *multiple papules on the lips and gingivae,** * **papillomatosis** (benign fibromatosis) of the buccal, palatal, faucial, and oropharyngeal * _mucosae_ often producing a **“cobblestone” effect**, and the _tongue_ may also present as **pebbly or fissured.** * • **Multiple papillomatous nodules** (histologically inverted follicular keratoses or * trichilemmomas) are often present on the perioral, periorbital, and perinasal skin, the pinnae of the ears, and neck. * • These nodules are often accompanied by **lipomas, hemangiomas, neuromas, vitiligo, café au lait spots, and acromelanosis .** * • A variety of neoplastic changes occur in the organs exhibiting hamartomatous lesions,with **an increased rate of breast and thyroid carcinoma and gastrointestinal malignancy.** * **Squamous cell carcinoma of the tongue** and **basal cell tumors of the perioral skin** have also been reported. * Incredibly rare ( board loves it)
734
What is this clinical finding?
Inflammatory Papillary Hyperplasia of the Palate
735
What is these clinical findings? (what is the name of the syndrome or complex?)
**Cowden Syndrome** *Very rare!*
736
**Tuberous sclerosis complex**
• is an inherited disorder caused by mutations in the tuberous sclerosis complex (**TSC1 or TSC2) genes** • Characterized by **seizures** and **mental retardation** associated with **hamartomatous glial proliferations** and **neuronal deformity** in _the central nervous system._ • **Fine wart-like lesions** (adenoma sebaceum) occur in **a butterfly distribution over the cheeks and forehead**, and histologically similar lesions (vascular fibromas) have been described **intraorally.** • Characteristic **hypoplastic enamel defects** (pitted enamel hypoplasia) occur in 40 to 100% of those affected. • Rhabdomyoma of the heart and other hamartomas of the kidney,
737
**Epulis Fissuratum** _AKA_ _Cause_ _Location_ _Clinical presentation_ _Composed of_ _Treatment_
• **AKA:** denture-induced fibrous hyperplasia, fibrous inflammatory hyperplasia • **Cause**: ill-fitting denture • **Location**: vestibule (maxilla or mandible), along the denture border •**Clinical presentation:** Arranged in elongated folds of tissue into which the denture flange fits; • Surface ulceration within the folds is common • **Composed of** _dense fibrous connective tissue_ • **Treatment**: **surgical excision** (scalpel vs CO2 laser -laser is better) and **reline then remake of denture**
738
What is the clinical finding?
**Pyogenic Granuloma** **We can see the corresponding radiograph;** -although the radiograph suggests generalized bone loss, there is a lot of calculus on the distal of #16 \> it makes sense that this is a pyogenic granuloma
739
What is this clinical finding?
**Pyogenic Granuloma:**
740
Pyogenic Granuloma Histology
They are filled with blood vessels so they’re very very rich in vascularization \> they tend to bleed easily
741
What is this clinical finding?
**A parulis** ***It is not a pyogenic granuloma*** **A parulis** is a _proliferation of granulation tissue at the opening of a sinus tract_ When the infection breaks through the alveolar bone and presents itself, it will sometimes cause this proliferation of granulation tissue
742
**Inflammatory Papillary Hyperplasia of the Palat**e Majority occur with what disease? Associated with what? Clinical appearance Treatment
* **Majority occur with** _denture stomatitis_ * **Associated with** a removable full or partial denture or orthodontic * appliance (Something you see in patients who wear denture all the time, don’t take it out, chronic denture wear) * **Clinical Appearance:** Palatal vault is covered by **multiple erythematous papillary projections** (fibrous connective tissue surfaced by epithelium) --(**papillary** but no papilla, instead it’s bumpy and bosselated) * ***Granular*** or **cobblestone appearance** * **Erythema** is usually _due to superinfection with candida_ * **Treatment:**Treat underlying candidiasis, fix denture. These bumps can be removed, take electrosurgery loop, and scrape off the bumps – heals well
743
What is this clinical finding?
**Peripheral Ossifying or Cementifying Fibroma** ## Footnote Lesion in the image is pedunculated – put a periodontal probe on normal gingiva and glide along underneath it, there’s a stalk
744
**Peripheral Ossifying Fibroma** Histology
* When sessile, when removing it, take scalpel blade and just cut into it * If has a little bone or cementum formation inside it, you can feel the bone with the scalpel
745
What is this clinical finding?
**Peripheral Giant Cell Granuloma**
746
Peripheral Giant Cell Granuloma Histology
Giant cells inside the lesion
747
What are the 3P or 4P?
**• Pyogenic granuloma/pregnancy tumor • Peripheral _ossifying***_or_***cementifying_ fibroma • Peripheral giant cell granuloma • Peripheral fibroma (4P)** _Memorize these well!_ *All benign soft tissue lesions*
748
**Pyogenic Granuloma** What a differential diagonsis to consider if we see it
- if it’s on the gingival tissues, take a radiograph - always consider **SCC** as a differential diagnosis
749
**What is this clinical finding?**
Inflammatory Gingival Enlargement Example of someone with true hyperplastic gingivitis Maybe related to very poor plaque control In this case, either porcelain or porcelain fused to metal full coverage restorations that have very bulky margins, and that may play a role for food to pick up
750
**Pyogenic Granuloma** What is it? Etiology Assossiated with which demographics? Location? Treatment?
* **What is it?** Reactive connective tissue hyperplasia - exuberant granulation tissue; Misnomer – not pyogenic and not a true granuloma * **Etiology:** Response to injury - calculus or overhang restoration * **Assosiated with**? Often occurs in **pregnant women (“pregnancy tumor”)**, also associated with **puberty** * **Treatment**: Excision and removal of irritant (eg calculus, overhanging restorations)
751
What is the Differential diagnosis of gingival enlargement
Acute Myelogenous Leukemia (AML) Wegener’s Granulomatosis Kaposi Sarcoma Plasma Cell Gingivitis **Generalized gingival enlargement – all different cases and diseases**
752
**How to differentiate Pyogenic Granuloma from the other 2Ps ?** (Peripheral ossifying or cementifying fibroma & Peripheral giant cell granuloma)
* They often occur in the gingival, but can occur in multiple areas * that’s the one thing that distinguishes this from the other 2 P’s: pyogenic granuloma can occur on ANY oral site, most commonly on the gingival tissues
753
What is this clinical finding?
Hereditary Gingivofibromatosis
754
**Infantile Hemangioma** **(“strawberry” hemangioma).** Infant with two red, nodular masses on the posterior scalp and neck *Neville Cr*
755
**Pyogenic Granuloma** _Clinical appearance_ _Location_ _Size_ _Developing rate_ _Age:_
* **Clinical appearance** * Usually **ulcerated** * Soft exophytic lesion, either **sessile or pedunculated** * **Deep red to purple in color, bleeds easily** * **Location:** * **Most common – *gingiva*** * Also occurs in **other areas of the oral mucosa ( can happen anywhere)** * **Size**: small to large (millimeters to centimeters) * **Develop** rapidly and then remain static * **Age**: Any age
756
How to recogonize a **capillary Malformation?**
When you apply pressure to it, it evacuates the lesion (disappears!), when you pull away, it refills and you see it again – that tells you it’s a vascular lesion
757
What is this clinical finding?
**Capillary Malformation (Low flow)**
758
How to differentiate between **Venous malformation (low flow)** from **Arteriovenous or arteriolar malformations (High flow)**
Venous malformation (Low flow) **No bruit, non-pulsatile** vs Arteriovenous or arteriolar malformations (High flow) **Bruit and pulsatile** **In other word, Venous lesion = Does not have pulse** **Histopathologically they look different too** **Treatment:** **-**Don't biopsy this unless it's rapidly growing, if it is rapidly growing then suspect ► *angiosarcoma*? ( unlikely) -can be surgically treated by oral surgeons -clamping off the blood vessel and dissecting it out, or putting a sclerosis agent
759
What is this clinical finding?
Venous malformation (low flow) *Many pts can live with this without treatment*
760
**What are these clinical findings ( which syndrome or complex is this)?**
Osler-Weber-Rendu Syndrome
761
What are these clinical findings? (What is the syndrome or complex)?
Sturge-Weber Angiomatosis Sturge-Weber syndrome
762
What are these clinical findings (What is the syndrome or complex)?
**Sturge-Weber Angiomatosis** **Sturge-Weber syndrome** Notice how the vascular malformation is only one side.. Remember: Vascular changes follow trigeminal nerve, so it doesn’t cross midline
763
What is this clinical finding?
**Lymphangioma**
764
What is this clinical finding?
**Cystic Hygroma** a type of Lymphangioma
765
**Peripheral Ossifying or Cementifying Fibroma** _What is it?_ _Clinical appearance_ _Derived from_ _Age_ _Sex_ _Reccurance rate_ _Treatment_
* a reactive benign soft tissue lesion * **Clinical appearance:** Well-demarcated, sessile or pedunculated lesion that appears to originate from _the gingival interdental papilla_ * **Derived from:** cells of the periodontal ligament * **Age**: children and young adults * **Sex**: females more than males * **Recurrence rate** – about 16% * **Treatment**: Surgical excision
766
What is this clinical finding?
**Neuroma** **(Traumatic Neuroma)** Not a benign true neoplasm, it’s reactive lesion This is an edentulous patient, so resorbed bone, so flange of denture is impinging in the area of mental foramen – develop from repeated trauma Sometimes have to cut into nerve, peel the neuroma from nerve, careful not to sever nerve
767
What are these clinical findings (Which syndrome or complex)?
Multiple Endocrine Neoplasia (MEN) Syndrome
768
What is this clinical finding?
neurofibroma -it looks like **lymphoepithelial cyst,** but this is further anterior and not where you would get lymphoid tissue – so it’s not lymphoepithelial cyst, it’s neurofibroma Yellow – nerves typically yellow
769
What is this clinical finding?
neurofibroma
770
**Peripheral Giant Cell Granuloma** _​What is it?_ _Location?_ _Age?_ _Clinical appearance:_ _Radiographic finding?_
* **What is it?** Probably a reactive lesion due to local irritating factors (giant cells develop inside the lesion which is a benign soft tissue lesion) * **Location**: _Gingiva_, usually anterior to the molars * **Age:** Most frequently seen between 40-60 years old * **Clinical appearance:** dusky purple, sessile or pedunculated, smooth-surfaced, dome-shaped papule or nodule. Most lesions are less than 1.5 cm in diameter, though infrequently, may grow as large as 5 cm in greatest dimension * **Radiographic Features:** Usually none, but superficial destruction of the alveolar bone may occur
771
What are these clinical findings (which syndrome or complex)?
**Neurofibromatosis syndrome** **von Recklinghausen’s Disease** * Lisch nodules on iris, pigmented (eye picture) * Neurofibromatosis in mouth (bottom left picture) * Café au lait (bottom right picture)
772
What is the clinical finding?
Schwannoma/ Neurilemoma
773
What is this clinical finding?
Schwannoma/ Neurilemoma
774
Schwannoma/ Neurilemoma _Histology_
**Antoni A and Antoni B.** Streaming fascicles of spindle-shaped Schwann cells characterize Antoni A tissue. These cells often form a palisaded arrangement around central acellular, eosinophilic areas known as **Verocay bodies.** Antoni B tissue is less cellular and less organized; the spindle cells are randomly arranged within a loose, myxomatous stroma.
775
What is this clinical finding?
Granular Cell Tumor
776
What is this clinical finding?
Granular Cell Tumor
777
Granular Cell Tumor Histology
Has pseudoepitheliomatus hyperplasia of epithelium (seen on left picture) Characteristic feature are the granular cells on the right picture Infiltrate down into the muscle layers, that’s when pathologist confirms granular cell tumor
778
_Diagnosis_ and _Treatment_ of the 3Ps
•**Diagnosis**: All 3 “P” lesions usually occur on gingival interdental papillae ( however pyogenic granuloma can occur anywhere) • Since they can look similar clinically, **excisional biopsy necessary to determine diagnosis** • **Treatment**: complete excision and removal of local irritant (scaling and root planing)
779
What is this clinical finding?
**Congenital Epulis**
780
**Gingival Enlargement** Etiology
- Response to chronic inflammation - Hormonal changes (pregnancy/puberty) - Immune-mediated/plasma cell gingivitis - Drug induced - Genetic/ Inherited NOTE: Gingival enlargement is not always ***hyperplastic tissue***
781
What is this clinical finding?
Neuroectodermal tumor of infancy look how they removed it here surgically *is rare, rapidly growing, pigmented neoplasm of neural crest origin. It is generally accepted as a benign tumour despite of its rapid and locally destructive growth.*
782
**Lipoma** _What is it?_ _Location?_ _Cliniclly?_ _Histologically?_ _Treatment?_
* **What is it:** Benign tumor of mature fat cells; Relatively rare * **Location:**Won’t see on gingival tissue, will see _on buccal mucosa, on the tongue, and floor of the mouth_ * **Clinically** appears as _a yellowish mass_ surfaced by thin overlying epithelium, When you feel it, it’s soft * **Histologically**: a well-delineated tumor composed of mature fat cells with a thin capsule * **Treatment**: surgical excision,does not recur
783
What is this clinical finding?
**Lipoma** Usually very orange looking lesion in site where there’s adipose tissue Very obvious, nothing as orange as lipoma
784
**Drug Induced Gingival Enlargement** **What are the famous drugs that are known to cause it?**
* **Phenytoin**: (or Dilantin) – the drug that used to be given to every single * person that had seizures * Calcium-channel blockers * Nifedipine *not as prescribed anymore* * Dilitiazem still prescribe * Amlodipine: is prescribed as one of the first line therapy for hypertension (very commonly prescribed); it doesn’t typically cause gingival overgrowth except in some selected patients, usually those with pretty poor oral hygiene * Cyclosporine A (used for for bone marrow transplant, graft vs host disease, solid organ transplant) * **Cyclosporine is universally recognized as causing gingival hyperplasia** * **Cyclosporine** is largely replaced with **Tacrolimus**, which typically doesn’t cause gingival overgrowth * Cyclosporine A is largely replaced with Tacrolimus, which typically doesn’t cause gingival overgrowth Some drugs have more connective tissue component, others have more epithelial component Not all identical under the microscope * Cyclosporine provides more epithelial change, Dilantin causes more of a connective tissue change
785
What is this clinical finding?
**Vascular leiomyoma** **High-power view showing spindle-shaped cells with bluntended nuclei. Immunohistochemical analysis shows strong positivity for smooth muscle actin (inset).**
786
**What is this clinical finding?**
**Rhabdomyoma** ## Footnote Will see the striated muscle Differential diagnosis… looks like granular cell tumor – don’t know til you remove it If patient presents with relatively slow growing tumor like this, will I get incisional biopsy or excisional biopsy? Hard to say If confident benign tumor and it’s this size and I don’t think it’s vascular (no pulse, can do aspiration), feels firm – try to excise it If it looks different, like you think it’s malignant minor salivary gland neoplasm (won’t find it in this site, but if it’s on hard palate) – incision?
787
What is this clinical finding?
**Leiomyosarcoma**
788
**Hereditary Gingivofibromatosis** _What causes it?_ _How common?_ _what effects on oral cavity?_ _Treatment?_
**What causes it?** * Various genes that are implicate (Putative inherited mutations are in the SOS1 or CAMK4 genes.) Linked to both autosomal dominant and recessive patterns of inheritance ​**How common?** * Very rare **what effects on oral cavity?** * Sometimes gingival overgrowth will completely obliterate the teeth, grow around entire tooth * Enlargement may be present at birth or may become apparent only with the eruption of the deciduous or permanent dentitions. * Tooth migration, prolonged retention of the primary dentition, and diastemata are common, and enlargement may completely cover the crowns of the teeth, resulting in compromised oral function. **Treatment** * Need surgical (usually laser) treatment – just grows back, so have to get it done periodically
789
What are these clinical findings?
Rhabdomyosarcoma In this case, hasn’t broken through epithelium They don’t all break through
790
Infantile Hemangioma _When do they appear?_ _Rate of Development_ _Clinical presentation_ _Treatment_
* **_When do they appear?_** They are rarely present at birth, infants are Born with this in place. * **Rate of development:** the tumor will demonstrate rapid development that occurs at a faster pace than the infant’s overall growth in the first few weeks of life, * **Clinical presentation:** Either superficial or deeper tumors * Superficial tumors of the skin appear raised and bosselated with a bright-red color (“strawberry” hemangioma); They are firm and rubbery to palpation, and the blood, cannot be evacuated by applying pressure. * Deeper tumors may appear only slightly raised with a bluish hue. * May be left with a _pink or magenta macule_ in site where hemangioma occurred after its involute * **Treatment:** Typically will involute with time, Some cases don’t involute, so need to be removed * *It is a vascular Anomaly*
791
What is this clinical finding?
**Fibrosarcoma**
792
**Capillary Malformation** (Low flow)
* a type of vascular anomaly * CMs are commonly known as port wine stains. * They look like a pink, red or purple patch of skin * occur in 1 in 300 newborns.
793
What is this clinical finding?
**Kaposi Sarcoma** Solitary vascular lesion on hard palate – it was so small so he decided to just excise it in this case^
794
What are these clinical findings?
**Kaposi Sarcoma** * Widespread Kaposi, can see cutaneous lesions * Oral images of this patient: on palate, starts with macule on patient’s left posterior palate –macular stage * Then in becomes proliferative – exophytic nodular stage (seen on patient’s right anterior palate,surrounding canine and some incisors) * Can see engorged blood vessels in area on histology slide
795
What is this clinical finding?
**Plasmacytoma in Multiple Myeloma** * They already had **multiple myeloma** then developed plasmacytoma * When you biopsy this, **it’s filled with plasma cells** bc they’re producing the abnormal immunoglobulins, which are the cause of the devastating issues of multiple myeloma
796
**Acute myelogenous leukemia***with* **granulocytic sarcoma** ## Footnote * *Complaining of lump inside of her cheek** * *Notsomuch worried about her gingiva**, despite her overgrowth – leukemic infiltrates that got into gingival tissues * *Left buccal mucosa**, kept biting on it, feeling incredibly fatigued though she was always working out * *Oral surgeon biopsied** her buccal mucosa and read by pathologist as pyogenic granuloma * *Physician** sent her for bloodwork, dental school sent her for bloodwork too
797
What is this clinical finding?
Lymphoma * Well circumscribed ulceration in area * Associated swelling in periphery * White change in the patient’s left area * Been there for 3 weeks * It’s lymphoma
798
What is this clinical finding?
Looks like it could be a salivary gland neoplasm, but it’s not It was another **lymphoma** Manifest in a number of different ways
799
**Case** **40 year old male Completely healthy otherwise Not taking any medications Presents with bump on the tongue** First question: did you do anything that might have led to this? Bite your tongue? “possible I bit my tongue, or it could be when I had a dental procedure, maybe they accidentally cut into the side of my tongue” – then it developed This tells us, is this a reactive lesion? Is it pedunculated or sessile? It’s pedunculated, larger at the top than the base Let’s look at the surface: it’s ulcerated When palpating, it’s only on the surface - don’t feel any submucosal presentation Tongue underneath feels relatively normal This bump is kind of firm and it bleeds like crazy when you touch it When you look at teeth, no area where they’re too sharp
**Do you think it’s a fibroma? No. Why?** Fibroma is covered with normal coloring epithelium – sometimes see a little white change on surface or see tiny traumatic ulcer on surface This is not like that, this is completely ulcerated Not fibroma; fibroma is a chronic bump that patient is aware of **Is it squamous cell carcinoma? Interesting, it is indeed very friable; but no** Sometimes SCC can develop and can be exophytic and don’t have deep invasion, But this is pedunculated, SCC would not be pedunculated History says there could be some kind of trauma, biting, or nick with bur – not squamous cell **Mucocele? No** Would you typically develop mucocele on lateral border of tongue? No Not going to be as many mucoceles in this area, but there are the glands of Blandin and Nuhn, so it’s possible to develop on ventral surface of tongue This bump doesn’t look like a fluid filled bump though, it has surface ulceration, redness ;Mucoceles have intact surface, would not bleed, or be red **Granular cell tumor? No** Granular cell tumor would have normal overlying epithelium (it’s pushing up from underneath) This does not have normal overlying epithelium **Hemangioma reserved for congenita**l; not a vascular malformation either **Neurofibroma? No, not the same surface** **Salivary gland neoplasms? Possible**, there are salivary glands in that area; keep this in differential The one that this is is **pyogenic granuloma**: usually red, ulcerated, and bleeds easily
800
**Osler-Weber-Rendu Syndrome** _AKA_ _What is it and its clinical appearance_ _Type of Herditary and Etiology_ _What can it cause?_ _Location?_
**AKA** • _Hereditary Hemorrhagic Telangiectasia_ **What is it and its clinical appearance** • _disorder of development of the vasculature_ characterized by **telangiectases** and **arteriovenous malformations** in specific locations. These are essentially endothelial cell issue – get tafted area of abnormal blood vessels multiple different organ systems – causes complications **Type of Herditary and Etiology** •Autosomal dominant with mutations i_n at least five gene_s but mutations in two **genes (ENG and ACVRL1/ALK1)** cause approximately 85% of cases. **What can it cause?** • Can cause hemorrhage **Location?** often on fingers, lips,tongue, but always look at the fingers!
801
**Sturge-Weber Angiomatosis** **Sturge-Weber syndrome**
* Rare, non-hereditary developmental condition * **Vascular proliferation** involving tissues of the brain and face * Face: **Unilateral** distribution along one or more segments of the trigeminal nerve ( unilateral means don't cross the midline) known as **port wine stain/ nevus flammeus --** they are deep-purple color. * **Intracranial calcifications**; **neurological disorders** * **Intraoral involvement** _is common_
802
**Lymphangioma** _What is it?_ _Types_ _Locations:_ _Treatment_
**What is it?** • Benign tumor of lymphatic vessels **Types** * Microcystic * Mixed * Cystic hygroma (macrocystic) **Location** * Most frequent extra-oral location: **posterior triangle of the nec**k; * intraoral location: **tongue** **Treatment**: monitor, surgery if needed, _recurrence common_
803
**Neuroma** _AKA_ _What is it?_ _Clinical presentation_ _Location_
**AKA** * _traumatic neuroma_ **What is it?** * Reactive (ie not a true neoplasm) proliferation of nerve tissue after injury, usually extraction or other surgical procedure **Clinical presentation** * They are smooth-surfaced, nonulcerated nodules. * May be painful (30% of cases) and sometimes associated with altered nerve sensations that can range from anesthesia to dysesthesia to overt pain **Location** * mental foramen area, tongue, lower lip
804
Multiple Endocrine Neoplasia (MEN) Syndrome _What is it?_ _Inhertiance type?_ _Which type is associated with multiple mucosal neruoma?_ _What other presentations?_ _Increase risk of which cancer?_
***_What is it?_*** Group of rare conditions ***_Inhertiance type?_*** Autosomal dominant ***_Which type is associated with multiple mucosal neruoma?_*** **Type 2B associated with multiple mucosal neuromas (one of the first visual signs)** ***_What other presentations?_*** • Marfanoid features • Multiple tumors and hyperplasias of endocrine organs (ie pheochromocytoma) *_Increase risk of which cancer?_* **•** Increased risk for **medullary thyroid cancer (prophylactic thyroidectomy)** *_Common board questions_*
805
**Neurofibroma** _What is it?_ _Clinical presentation?_ _Location?_ _Treatment?_ _Mailgnancy?_
**What is it?** * A benign tumor arising from peripheral nerve tissue **Clinical presentation:** * Slow growing, painless lesion * Smooth-surfaced, nodular mass that varies in size * Skin more commonly involved than oral mucosa Location: * **Common oral mucosal sites:** tongue and buccal mucosa * May develop _centrally in bone_ **Treatment**: surgical excision **Malignant transformation** _reported, but rare_
806
**Neurofibromatosis syndrome** _Most common form?_ _intheritance type?_ _Clinical presntation?_ _Malignant transformation?_
_Most common form?_ Several forms, **type I** is **most common (von Recklinghausen’s Disease)** _intheritance type?_ • 85-97% of cases inherited as _autosomal dominant trait,_ c**hromosome 17 (NF1 gene)** **Clinical presentations:** * **Skin nodules** **(neurofibromas)** * **Café au lait** pigmentation on skin * **Lisch nodules** very diagnostic (a pigmented hamartomatou in the iris of the eyes) **Malignant transformation** * reported in 5% of cases (**neurofibrosarcoma**)
807
**Schwannoma/ Neurilemoma** _What is it?_ _Age?_ _Location?_ _Clinical presentation?_ _Treatment?_ malignant transformation ?
**What is it?** • Benign neoplasm of Schwann cell origin • Uncommon lesion: 28-48% occur in the head and neck **Age?** • Most common in young and middleaged adults **Location?** • Most common intraoral location: tongue **Clinical presentation?** • The **solitary** schwannoma is a slow-growing, encapsulated tumor that typically arises in association with a nerve trunk. • May present with pain **• Treatment** • surgical excision **malignant transformation** reported, but rare
808
**Granular Cell Tumor** **What is it?** **Location?** **Age?** **Treatment?**
**What is it?** Benign tumor derived from Schwann cells **Location?** • Oral cavity is the most common location • Vast majority of cases seen on dorsal tongue **Clinical presentation?** * Typically an **asymptomatic sessile nodule that is usually 2 cm or less in size (firm)** * The mass is typically **pink,** but some granular cell tumors appear **yellow**. * The granular cell tumor is usually solitary, although multiple, separate tumors sometimes occur, especially in black patients. * The lesion often has been noted for many months or years, although sometimes the patient is unaware of its presence. **Age**: 40-60, rare in children **Treatment** • Treated by surgical excision (Be careful with excision! no need to get all of it out, just most of it) rarely recurs
809
Congenital Epulis ## Footnote **AKA** **Cell resemble?** **Cell origin?** **Clinical features & location** **Treatment?**
• **AKA**: Congenital epulis of the newborn • **Cells resemble** cells of the granular cell tumor **• Cell of origin** is unknown, not derived from nerve **• Clinical features:** * Sessile or pedunculated mass, usually found on * *the anterior** **gingiva/ alveolar mucosa** * Almost always occurs in baby girls * Present at birth **• Treatment:**Surgical excision, does not recur
810
**Neuroectodermal tumor of infancy** _Location?_ _Rate of development?_ _Treatment?_ _Origin?_ _Clinical presentation?_
**Location?** Often occur as soft tissue mass largely in _anterior maxilla_ **Rate of development?** So fast developing that it envelops and moves the teeth **Treatment?** Needs to be surgically excised **Origin?** Thought to be of **neuroectodermal source** **Clinical presentation?** Pigmented change in tissue
811
Lipoma vs Lipofibroma
* Sometimes lipomas can be mixed with fibrous tissue, can be **lipofibromous** * Two lesions that look almost identical but one is **lipoma**, one is **lipofibroma** * Only difference is that **one has fibrous tissue in it, no other difference**
812
Benign Tumors of Muscle
• **Leiomyoma** • Benign tumor of smooth muscle **• Vascular Leiomyoma** • Benign tumor of smooth muscle walls of blood vessels **• Rhabdomyoma** • Benign tumor of skeletal muscle They are SUPERRR rare If become malignant, they become leiomyosarcoma or rhabdomyosarcoma – malignant even more rare
813
**Leiomyosarcoma**
* a type of rare cancer that grows in the smooth muscles. * So, so rare * Diseases that move rapidly, because they’re malignancies * You might see surface ulcerations, they’re moving so fast, they break through the epithelium
814
**Rhabdomyosarcoma**
* is a type of sarcoma. * **Rhabdomyosarcoma** usually begins in muscles that are attached to bones and that help the body move, but it may begin in many places in the body
815
What is Sarcoma ?
Sarcoma is cancer of soft tissue (such as muscle), connective tissue (such as tendon or cartilage), or bone.
816
Fibrosarcoma _what is it?_ _Age?_ _Rate of growth?_ _Treatment?_ _Survival rates?_
**•What is it?** Malignant tumor of fibroblasts • **Age?** Most common in young adults and children • **Rate of growth?** Slow growing lesion that is usually not painful (Can be slow growing, can be rapidly growing – different criteria determining high or low grade) • **Treatment**: surgical excision, recurrence is common(Aren’t always easy to surgically remove, because already metastasized into other reservoirs, spread into contiguous areas) Aren’t always radiosensitive, don’t always respond to radiation treatment • 5-year **survival rates** range from 40-70%
817
**Vascular Malignant Neoplasms**
**• Angiosarcoma** • Malignant tumor of blood vessels **• Lymphangiosarcoma** • Malignant tumor of lymphatic vessels **• Kaposi’s sarcoma** * Malignant neoplasm associated with endothelial cells * Seen predominantly in poorly controlled HIV infected patient population (not exclusively) * Elderly people can develop Kaposi
818
**Kaposi Sarcoma** _Etiology_ _Types_ _Treatment_
**Etiology**:Caused by **HHV-8 (human herpesvirus 8) /***part of herpes family* **Types:** * **Classic:** late adult life, Italian and Jewish men, skin of lower extremities * **Endemic:** African form * **Iatrogenic immunosuppression-associated:** most often occurs in recipients of organ transplants * **AIDS-related** **Treatment** * Surgical excision, radiation therapy or systemic chemotherapy for multiple nonoral lesions, if it gets large, dose-radiation therapy!
819
**Plasmacytoma in Multiple Myeloma**
Presents as soft tissue lesion It is possible that a patient can present with plasmacytoma that would be the first sign of multiple myeloma (it would be a rare sign, but it can happen)
820
**Lymphoma**
* **Lymphoma** is a general term for a complex group of heterogeneous lymphoreticular malignancies. * **Lymphoma** is the _sixth most common malignancy_ and the **second most common neoplasm of the head and neck after squamous cell carcinoma** and **accounts for 50-59% of head and neck neoplasms in children.** * They constitute approximately 3-5% of all known malignancies and are generally divided into two morphologically distinct types: **Hodgkin’s lymphoma (HL)** and **non-Hodgkin’s lymphoma (NHL).** * These malignancies typically **arise within the lymphatic tissues and can progress to extranodal disease as in NHL.** * **Cervical lymph node involvement can be present in any type of lymphoma**. * HL extends by means of contiguous nodal spread whereas NHL tends to disseminate hematogenously and is typically a systemic diagnosis. * Within the head and neck, **Waldeyer’s ring** is the most common site of involvement, accounting for more than half of all extranodal head and neck lymphomas. * **Oral involvement by lymphoma** may represent _a localized disease process_ but is _more often part of a systemic process that secondarily involves the cervical lymph nodes._ * **Lymphoma** arising within the oral cavity accounts for less than 5% of all oral malignancies, and **approximately 85% of these lesions involve the pharyngeal tonsil** and the **palate** * Extralymphatic sites include the **salivary glands, paranasal sinuses, oral cavity, and larynx.**
821
What is this clinical finding?
Lymphoma * Well circumscribed ulceration in area * Associated swelling in periphery * White change in the patient’s left area * Been there for 3 weeks * It’s lymphoma
822
What is this clinical finding?
Looks like it could be a salivary gland neoplasm, but it’s not It was another **lymphoma** Manifest in a number of different ways
823
**Case** **40 year old male Completely healthy otherwise Not taking any medications Presents with bump on the tongue** First question: did you do anything that might have led to this? Bite your tongue? “possible I bit my tongue, or it could be when I had a dental procedure, maybe they accidentally cut into the side of my tongue” – then it developed This tells us, is this a reactive lesion? Is it pedunculated or sessile? It’s pedunculated, larger at the top than the base Let’s look at the surface: it’s ulcerated When palpating, it’s only on the surface - don’t feel any submucosal presentation Tongue underneath feels relatively normal This bump is kind of firm and it bleeds like crazy when you touch it When you look at teeth, no area where they’re too sharp
**Do you think it’s a fibroma? No. Why?** Fibroma is covered with normal coloring epithelium – sometimes see a little white change on surface or see tiny traumatic ulcer on surface This is not like that, this is completely ulcerated Not fibroma; fibroma is a chronic bump that patient is aware of **Is it squamous cell carcinoma? Interesting, it is indeed very friable; but no** Sometimes SCC can develop and can be exophytic and don’t have deep invasion, But this is pedunculated, SCC would not be pedunculated History says there could be some kind of trauma, biting, or nick with bur – not squamous cell **Mucocele? No** Would you typically develop mucocele on lateral border of tongue? No Not going to be as many mucoceles in this area, but there are the glands of Blandin and Nuhn, so it’s possible to develop on ventral surface of tongue This bump doesn’t look like a fluid filled bump though, it has surface ulceration, redness ;Mucoceles have intact surface, would not bleed, or be red **Granular cell tumor? No** Granular cell tumor would have normal overlying epithelium (it’s pushing up from underneath) This does not have normal overlying epithelium **Hemangioma reserved for congenita**l; not a vascular malformation either **Neurofibroma? No, not the same surface** **Salivary gland neoplasms? Possible**, there are salivary glands in that area; keep this in differential The one that this is is **pyogenic granuloma**: usually red, ulcerated, and bleeds easily
824
ADENOMA
benign tumor of glandular origin
825
Characteristics of a Benign Tumor:
 Encapsulated ‐ distinguishable from surrounding tissues  Freely movable ‐ not fixed  Slow growing  Non tender ‐ patients do not complain of pain
826
BENIGN SALIVARY GLAND TUMORS | (list 3)
 **Pleomorphic adenoma** aka mixed tumor  **Monomorphic adenoma**s o **Canalicular adenoma** o **Basal cell adenoma**  **Warthin tumor** (papillary cystadenoma lymphomatosum)
827
PLEOMORPHIC ADENOMA | (MIXED TUMOR)
* This tumor comes in many forms/shapes * **Most common salivary gland tumor** * **Painless, slowly growing, firm mass** * Adults (30‐50 years old) ; slight female predilection * Sites: * 50% to 77% of **parotid tumors** (most commonly found in parotid-2/3rd to 3/4th of parotid tumors) * Minor SG: **palate\>upper lip\>buccal mucosa\>** other site (most common intraoral site is the **palate**) * Malignant transformation possible in long standing lesions (about 5% cases) ‐\> called Ca ex PA
828
What is this clinical finding?
PLEOMORPHIC ADENOMA | (MIXED TUMOR)
829
What is this clinical finding?
PLEOMORPHIC ADENOMA Classic presentation: includes swelling in the parotid region | (MIXED TUMOR)
830
What is this clinical finding?
PLEOMORPHIC ADENOMA **Palatal presentation**: since salivary glands are only in lateral sides of the palate, **usually swellings are in one side and not the midline.** Lateral swelling is a clue that you are looking at a salivary gland lesion (left pics) On the right pic, it involved midline and crossed over to other side, so there are exceptions. But more commonly found in lateral side of the palate. | (MIXED TUMOR)
831
What is this clinical finding?
PLEOMORPHIC ADENOMA * Upper lip presentation: sometimes swelling can be seen extra orally and intraorally. * Remember the swelling will be movable, not tender, not fixed to underlying structures. | (MIXED TUMOR)
832
What is this clinical finding?
**Untreated pleomorphic adenoma** slow growing, but can grow to enormous sizes
833
**Pleomorphic adenoma** histology
This is a **mixed tumor** with myxoid component (right) and fibrous/epithelial component(left) This type of tumor can produce a lot of different tissues, since the origin is from myoepithelial cells aka plasmacytoid cells, which are pluripotent cells which means they can differentiate into many different lineages of cells such as
834
What is this clinical finding?
Canalicular Adenoma
835
What is this clinical finding?
**Canalicular Adenoma** * ***Mucocele*** might look this way, but what would make it lower on * differential diagnosis is the location of the swelling. Mucocele is mostly seen on lower lip and this pic shows upper lip. Salivary gland tumors and mucoceles * can have the same clinical presentation, so always do a biopsy for formal histopathology diagnosis.
836
**Basal Cell Adenoma**
* **Basaloid appearance of the tumor cells** * **Primarily parotid lesion** * **predominantly in women over 50 years of age**. It is uncommon in young adults.  (Basal cells are located in epithelium that is adjacent to interface with the connective tissue and they are separated from the CT by a basement membrane, stem cells of epithelium are located in basal cell layer)  Basal cells are typically Blue in appearance and cuboidal,
837
What is this clinical finding?
**Basal Cell Adenoma**
838
What is this clinical finding?
PAPILLARY CYSTADENOMA LYMPHOMATOSUM (WARTHIN TUMOR)
839
**MUCOEPIDERMOID CARCINOMA** **Charcterstics?** **Location** **Clinical appearance in minor gland** **Can be mistaken for** **Histopahtology**
** Most common malignancy of salivary glands  Most common malignant SG tumor in children** **Locations**  **Palate**, most common intraoral site  Rare primary intrabony (jaws) tumors  Most common in **parotid**  **Minor SG: palate 2nd** **Clinical appearance in minor gland:** asymptomatic fluctuant swelling; blue or red colored ** Can be mistaken for mucocele**  **Histopathology**: note the cells growing into adjacent tissue, showing infiltration
840
Monomorphic Adenomas What is it? Types? Treatment?
**What is it?** Proliferation of 1 type of cell makes up the tumor. **Types? Includes:** o Canalicular Adenoma o Basal Cell Adenoma **Treatment** for all monomorphic adenomas is surgical excision & diagnosis is done with biopsy
841
What is this clinical finding?
MUCOEPIDERMOID CARCINOMA
842
What is this clinical finding?
MUCOEPIDERMOID CARCINOMA ## Footnote *Request all for biopsies!*
843
What is this radiographical finding?
**CENTRAL MUCOEPIDERMOID CARCINOMA** * _Intrabony presentations_, may have extraoral swelling depending on the stage * Started as small swelling and progressed rapidly:, need to pick it up early! * Patient recovered, but might need radiation, lost salivary glands, needed reconstruction of palate
844
**Canalicular Adenoma**
* Almost exclusively in **minor SG** * Striking predilection for **upper lip (\>75%)** * Nearly always occurs in **older adults** * **Slowly growing, painless mass** * One clue for visualization of soft tissue swellings is increased vascularity with **blue‐ish tint in the area.**
845
What is the clinical finding?
**ACINIC CELL ADENOCARCINOMA**
846
What is the clinical finding?
ACINIC CELL ADENOCARCINOMA blue‐ish tint
847
What is this clinical finding?
Untreated acinic cell adenocarcinoma ## Footnote  Because it is slow growing, and a low grade tumor, the patient is alive and not dead with a tumor this size.  Similar presentation to pleomorphic adenomas, but there is a lot of ulceration on the surface and prominent vascularization in acinic cell adenocarcinoma.
848
Adenoid Cystic Carcinoma
 **High grade salivary gland malignancy** ( very bad cancer to get)  Adults  **Palatal mass; ulcerations**  Spread through **perineural invasion** ‐ tumor wraps itself around nerves and spreads through perineural spaces  **Grows slowly in the beginning and then picks up speed**  **Histology**: Duct like proliferation with cystic spaces
849
What is this clinical finding?
Adenoid Cystic Carcinoma
850
What are these clinical findings?
Adenoid Cystic Carcinoma
851
What are these clinical findings?
Adenoid Cystic Carcinoma
852
Adenoid Cystic Carcinoma
Swiss cheese appearance, cribriform pattern (full of holes aka cystic spaces)
853
Perineural invasion Histology
Perineural invasion: nerve nuble in the center and is wrapped by tumor
854
What is this clinical presentation?
Polymorphous Adenocarcinoma
855
What is this clinical presentation?
Polymorphous Adenocarcinoma
856
What is this clinical finding?
Carcinoma Ex Pleomorphic Adenoma
857
PAPILLARY CYSTADENOMA LYMPHOMATOSUM (WARTHIN TUMOR)
* **finger‐like projections, benign, cystic spaces, aggregates of****lymphocytes)** * Vast majority occur within **the parotid gland** * Very rare intraorally * **Predominantly in men** * Typically between **5th and 8th decades** * _Strong correlation with cigarette smoking_ * **Most common SG tumor to occur bilaterally** (bilateral parotid swelling), but can be unilateral * **Etiology:** Thought to arise within lymph nodes as a result of entrapment of * salivary gland elements early in development * **Clinical Features:** * **swelling that has** more subtle presentation * **Doughy to cystic mass** * In the inferior pole of the gland, adjacent and posterior to the angle of the mandible * **Treatment**: surgical excision, responds very well to it
858
Summary for benign tumors
 **Encapsulated, freely movable, not fixed to underlying structure, not tender, patients do not complain of pain, slow growing**  There is one tumor of the ones discussed that does have a risk of malignant transformation (only 5% and will take many, many years) and that is **Pleomorphic adenoma**
859
MALIGNANT SALIVARY GLAND TUMORS List 5
 Mucoepidermoid carcinoma  Acinic cell carcinoma  Adenoid cystic carcinoma  Carcinoma ex‐mixed tumor/malignant mixed tumor  Polymorphous adenocarcinoma
860
CLINICAL FEATURES OF ADENOCARCINOMAS (malignant gland tumors)
 Infiltrative  Fixed to underlying structures, not moveable  Rapid or slow growth, depending on grade and type of malignant salivary gland tumor  Larger, rapidly growing lesions may cause pain and/or paresthesia  Ulcerated overlying mucosa
861
**MUCOEPIDERMOID CARCINOMA** _What are its compoenents?_ _Within jaw prognosis_ _Treatment_ _Prognosis_ _Therapy by gene?_
**What are its compoenents?** Mixture of mucus‐producing cells and epidermoid or squamous cells May arise **within jaws** from odontogenic epithelium of dentigerous cysts • More common in the **mandible** than maxilla **• Molar‐ramus area** **Treatment**: Usually treated by surgical excision **Prognosis:** • Overall prognosis is _fairly good_ • 10% of patients die, due to local recurrence or metastasis  Low‐grade tumors have good prognosis (\>90% are cured)  High‐grade tumors the prognosis is guarded (Only 30% survive) **Therapy by gene?** *CRTC1–MAML2, CRTC3‐MAML2* gene fusions (targeted therapy)
862
**ACINIC CELL ADENOCARCINOMA**
*  Occurs **predominantly in major SGs,** *  Found in **all age group**s, peak incidence in 5th and 6th grade *  **No gender predilection** *  _Malignancy with serous acinar differentiation_ *  **Most common in the parotid** (since 90% serous acini) *  Variable microscopic appearance *  May even appear **encapsulated**, since it is SLOW growing *  **Better prognosis than salivary gland malignancies**
863
**Adenoid Cystic Carcinoma** Location Growth rate Clinical presentation Treatment Prognosis
**Location**:  Approx. 50% occur within the minor SG ‐ palate most common site **Growth rate**  Usually a slowly growing mass **Clinical presentation**  Pain is a common and important early finding, occasionally occurring before there is noticeable swelling (described at annoying pain)  Tendency to show perineural invasion, corresponds to pain **Treatment**  Excision usually the treatment of choice ‐ but edges of tumor may have perineural invasion and remain undetected ‐ makes tumor dangerous **Prognosis**  5‐year survival rate as high as 70% (maybe 90%)  By 20 years, only 20% ‐ poor long term prognosis
864
Polymorphous Adenocarcinoma _Location_ _Gender_ _Appearance_ _growth patterns_ _Treatment_
* **Location:** * Almost exclusively in the **minor SG** * **60%** on the hard or **soft palate** * **Gender"** * *2/3rds in **females*** * **Appearance**: * Tumor cells have _deceptively uniform appearance_ * **Growth patterns:** * Different growth patterns – polymorphous * _Perineural invasion ‐ common_ ‐ but considered low grade tumor * **Treatment**: Wide surgical excision; overall prognosis relatively good, with 80% cure rate
865
**Carcinoma Ex Pleomorphic Adenoma** _What is it?_ _Mean age?_ _Growth pattern_ _Treatment?_ _Prognosis_
**What is it?** (benign tumors that have underwent malignant transformation‐ takes a lot time, 15 to 20 years) **Mean age** about 15 years greater than benign counterpart **Growth patterns:** Mass present for many years with recent rapid growth with associated pain or ulceration **Treatment**: Best treated by wide excision, with local node dissection and radiation **Prognosis:** guarded, with 50% local recurrence or metastases and dying Prognosis is case to case scenario, may transform to high grade tumor
866
What are the **FREQUENCY OF SALIVARY GLAND TUMORS BY LOCATION** _Lower lip_
**o Mucocele o Mucoepidermoid Ca o Pleomorphic Adenoma**
867
What are the **FREQUENCY OF SALIVARY GLAND TUMORS BY LOCATION** _upper lip_
**o Canalicular Adenoma o Salivary Duct Cyst\* o Pleomorphic Adenoma**
868
What are the **FREQUENCY OF SALIVARY GLAND TUMORS BY LOCATION** _Parotid_
**o Pleomorphic adenoma o Warthin’s tumor o Basal cell adenoma o Mucoepidermoid ca o Acinic cell ca o Adenoid cystic ca o Ca ex mixed tumor**
869
What are the **FREQUENCY OF SALIVARY GLAND TUMORS BY LOCATION** _Palate_
**o Pleomorphic adenoma o Adenoid cystic ca o Mucoepidermoid ca o PLGA o Monomorphic adenoma**
870
**SG Tumors: Summary of Key Points**
 Involve both major and minor glands ** Benign and malignant tumors both have similar clinical presentation**  Most malignant salivary gland tumors do not show histopathologic characteristics associated with malignancy  Most occur in adults  Warthin Tumor seen in parotid, may be bilateral ** Mucoepidermoid carcinoma** o Can occur in children o May occur centrally in bone
871
Inflammatory/Reactive Lesions of the Salivary Glands List 5
* mucocele/mucous cyst * ranula * necrotizing sialometaplasia * sialolithiasis * sialadentitis
872
**Mucocele** _Definition_ _Clinical features_ _Location_ _Histological features_ _Treatment_
**• definition:** a lesion that forms when a salivary gland duct is severed & secretion spills into the adjacent CT • **a pseudocyst** (not lined by epithelium) — mucous builds up in the CT & causes a bump **• clinical features:** * swelling in the tissue that may increase & decrease in size * may have a bluish hue, fluctuant on palpation — fluid filled, soft, compressible **•** **location**: _lower lip most common site_, but may form in any area where there are minor salivary glands **• histologic features:** - a cyst-like space in soft tissue - lined by compressed granulation tissue - lumen filled with mucin, foamy macrophages & inflammatory cells **• treatment:** surgical excision, removal of associated minor salivary glands • may recur if don’t remove all associated injured minor salivary glands
873
What is this clinical finding?
**Mucocele**
874
What is this clinical finding?
**Mucous Cyst**
875
What is this clinical finding?
**Ranula** Notice how it's unilateral on the floor of the mouth
876
What is this clinical finding?
Ranula * Notice how it's unilateral* * on the floor of the mouth*
877
**Necrotizing Sialometaplasia** _Definition_ _Predisposing factors_ _Clinical features_ _Histologic features_ _Treatment_
**• Definition:** locally destructive inflammatory condition — looks malignant but is _benign_ *• salivary gland ischemia* — “heart attack of the palate”; blood flow is interrupted **• predisposing factors:** - local trauma - palatal injection of local anesthesia - previous surgery - many are idiopathic.. • usually a clinical diagnosis based on history & how fast — palate uncommon for SCC **• clinical features:** - initially appears as a non-ulcerated swelling of the palate - often associated with pain or paresthesia - within 2-3 weeks, necrotic tissue sloughs off & becomes a crater-like ulcer - patient may say: “a chunk of the roof of my mouth fell out” **• histologic features:** - necrosis of the salivary glands — coagulative necrosis (green circles in histology —\>) - *salivary gland duct epithelium* is replaced by **squamous epithelium** — appear as islands of squamous epithelium deep in the CT & **resembles SCC** (arrows in histology —\>) • **Treatment**: no treatment, spontaneously resolves within 6 to 10 weeks • _irrigating & debriding the area_ can reintroduce vascularity & help healing
878
What is this clinical finding?
Necrotizing Sialometaplasia
879
**Sialolithiasis** Definition Location Origin Clinical features Radiological features Histological features Treatment
**Definition:** lith = stone ;; sialolith: a salivary gland stone **Location:** occur in both major & minor salivary glands • floor of the mouth is most common location (Wharton’s duct is a common place) *• often causes obstruction of the duct* **Origin:** arise from _desposition of calcium salts around nidus of debris within the duct lumen_ * *clinical features:**- minor glands: hard yellowish structure in soft tissue - may be visible on a radiograph - recurrent swelling (due to the obstruction) - episodic pain & swelling during times of increased salivation - can be palpated if the stone is located toward the terminal portion of the duct * *Radiological features** : may be viewed as a radiopacity on an occlusal x-ray--well defined radiopacity * *Histological features-** concentric rings of calcification, color of it in stain depends on level of calcificatio * *Treatment**: promote passage of stone (massage, sialogogues, increase fluid intake) or surgical removal
880
What is this clinical finding?
Sialolithiasis
881
What is this clinical finding?
**Sialolithiasis** Notice how it can appear radiographically as a well defined radiolucency
882
What is this Radiographical finding?
**Sialolithiasis**
883
**Mucous Cyst** _Definition_ _Clinical features_ _Histological features_ _Treatment_
•_Definition:_ a pseudocyst • microscopicallly appears as an epithelial lined cystic structure that is actually a dilated duct • **clinically you CANNOT tell the difference between a mucocele & mucous cyst** **• clinical features:** - same as a mucocele **• histologic features:** - same as mucocele but will see an epithelial lining (but actually a dilated duct) **treatment**: same as mucocele; surgical excision
884
**Sialadenitis** _definition_ _causes:_ _clinical features:_ _histologic features:_ _Treatment:_
• **definition**: acute or chronic _inflammation in major or minor salivary glands_ **• causes:** • obstruction of a salivary gland duct (sialolith) • infection (mumps [viral], staph aureus [bacterial, most common], candida [fungal]) • decreased salivary flow (Sjogren’s, sarcoidosis) • parotid gland = parotitis **• clinical features:** **- acute:** most common in parotid, swollen & painful gland, erythematous & warm overlying mucosa/skin, purulent discharge, low-grade fever **-** **chronic**: caused by recurrent or persistent ductal obstruction, periodic swelling & pain **• histologic features:** - acute or chronic inflammatory cell infiltrate in the salivary gland - in chronic cases = salivary gland replaced by fibrous CT & fat - **cells: acute = neutrophils** ;; **chronic = lymphocytes, plasma cells, macrophages** **• Treatment:** antibiotics, rehydration, surgical drainage, or surgical removal of gland
885
What is this clinical finding?
**Sialadenitis** Acute: parotid papilla purulent discharge
886
What is this clinical finding?
Sialadenitis Chronic: caused fibrosis
887
Summery of inflmattory salivaory conditions
**Mucocele** * fluctuant swelling * bluish hue * lower lip most common **Ranula** * fluctuant swelling * floor of mouth **Sialolithisis** • major glands: episodic pain & swelling of affected gland • minor glands: asymptomatic/ local swelling or tenderness • if superficial - firm to palpation & yellowish color **Necrotizing Sialometaplasia** • initial painful swelling • later necrotic ulcer • posterior lateral hard palate & soft palate **Sialadenitis** • painful swelling of affected gland • purulent discharge if acute infection
888
Rx Topical Treatments: Cautery
**‐ Debacterol** (sulfonated phenolics; sulfuric acid solution) **o Chemical cautery** o Label: one time application for 5‐10 seconds ‐ NOT recommended to patients with frequent outbreaks
889
What are the Topical Therapy Categories to treat ulcers?
**Topical anesthetic agents** o To numb the pain **‐ Surface protective agents/bioadhesives** o Cover the ulcer if small enough **‐ Anti‐inflammatory/immunomodulatory agents** o Applied to ulcer surface (corticosteroids) **‐ Anti‐microbials** o Some evidence that topical tetracycline may help **‐ Chemical/physical cautery Lasers** ‐ Over‐the‐counter (OTC) versus prescription (Rx **All essentially do the same thing:** o Numbing agent o Mucosal covering agent ‐ Bottomline: **o ALL canker sores will heal on their on with time**
890
Frequent Minor RAS or Major RAS Treatment
**‐ Treatment to reduce pain ‐ vs. ‐ Abortive treatment to reduce healing time ‐ vs. ‐ Suppressive treatment to suppress recurrences ‐ Combination of all** Also Consider * Using Sodium Lauryl Sulfate‐Free Toothpastes * Remove Obvious Possible Causes
891
Infrequent Simple Minor RAS Treatment
**‐ Treatment to reduce pain** Also Consider * using Sodium Lauryl Sulfate‐Free Toothpastes * Remove Obvious Possible Causes * ‐ Repair sharp teeth/restorations * ‐ Remove plaque * ‐ Optimize lubrication
892
Steps in Managing RAS patient
‐ History of RAS ‐ Medical History o Medications o Review of Systems ‐ Social History ‐ Dental History ‐ Diet/Nutritional History ‐ Physical Examination ‐ LaboratoryTests
893
How do we treat this?
‐ Repair sharp teeth/restorations ‐ Remove plaque ‐ Optimize lubrication Ulcer
894
What is this clinical finding?
**Behcet’s Disease** ‐ Recalcitrant oral ulcers associated with Behcet’s Disease ‐ Later developed genital ulcers and other complications ‐ Image: o Sores in the labial mucosa have classic aphthae appearance o Other ulcers are major aphthae: ▪ Larger ▪ Irregular borders ▪ Intense proliferative erythema
895
What is this clinical finding?
**Behcet’s Disease** ‐ Recurrent inflammatory disorder of unknown cause: o Bacterial? ‐ Affects: o Middle Eastern Males o Asian Females ‐ Onset 3rd – 4th decade ‐ HLA‐B51 association Recurrent aphthous ulcers generally precede other signs: o Genital/skin/eye lesions & others (arthritis, Gl lesions, CNS symptoms, vascular lesions) ‐ Diagnosis based upon criteria (point system): no laboratory tests
896
What is this clinical finding?
**Hematinic Deficiencies** ## Footnote **‐ Superficial ulcers** o Not classic aphthous ulcers ‐ Equivocal associations with iron, Vit B1, B2, B6, B12, and folate. ‐ Blood tests are not recommended routinely in all patients with RAS. ‐ Indications for blood work (CBC): o Older patient with recent RAS history o Suspicious medical history/review of systems **o Strict vegetarian patients**
897
What is this clinical finding?
**HIV‐Associated Aphthous** * CD4 counts \<100 cells/mm3 are predisposed to major RAS * ‐ Other sites may be affected: * o Esophagus * o Genitals * o Anus/rectum * ‐ We see this **less frequently since ART** * ‐ Diagnosis is important, particularly if no prior history
898
What are these clinical findings?
**Inflammatory Bowel Diseases** * **Specific lesions:** * o Diffuse labial and buccal swelling * o Cobblestones * o Other specific lesions * ▪ Mucosal tags * ▪ Deep linear ulcerations * o Mucogingivitis * o Granulomatous cheilitis * * **Non‐specific lesions:** * o Aphthous ulcerations * o Pyostomatitis vegetans * o Dental caries * o Gingivitis and periodontitis * o Other non‐specific lesions
899
What is this clinical finding?
**Transient Lingual Papillitis** * ‐ Relatively rare * ‐ Canker sore meets **fungiform papilla** of tongue * Multiple papilla can become inflamed (above image) * **Very painful** * ‐ Ulcer Appearance: * Tiny * Transient * On fungiform papilla of tongue * **‐ Typically resolves in 7‐10 days**
900
What is this clinical finding?
**Herpetiform aphthous stomatitis** * Apppears like **herpesvirus but unrelated to it** * account for **5% of cases (**the least common) **Appearance**: * begin as multiple (up to 100) 1- to 3-mm crops of small, painful clusters of ulcers on an erythematous base. * They coalesce to form larger ulcers that last 2 weeks. * *A bunch of smaller ulcers that coalesce*
901
What is this clinical finding?
**‐ Minor Recurrent Aphthous Ulcers (RAS)‐ Rare Case** _o Keratinized Mucosal Site_ ‐ 11‐year‐old boy ‐ Canine is in process of erupting ‐ Canker sore present on his keratinized mucosa (RARE) **o 99% of canker sores occur on NON-KERATINIZED MUCOSA**
902
What is this clinical finding?
**Minor Recurrent Aphthous Ulcers (RAS)** * **aka‐ “Canker Sores”** * ‐ High prevalence: 5‐25% * ‐ Comprises the overwhelming majority of cases * o 75‐85% of ALL RAS cases * **‐ \<10 mm in diameter** * ‐ Ulcer appearance: * **o Shallow** * **o Round/Oval Shaped** * **o Yellow pseudomembrane** * ▪ Slightly raised margin * ▪ Erythematous Halo * **‐ Typically resolves in 7‐10 days** * o \*May take longer if in a “high‐traffic” site * **‐ No scarring** * ‐ Recurrence rates vary
903
What are the Hallmarks of Aphthous Ulcers
**‐ Hallmarks:** o 1. Central ulceration o 2. Ring of erythema (erythematous border) ▪ Accentuated in right image
904
What is this clinical finding?
**‐ Aphthous Ulcer of the tongue** ‐ Aphthous ulcers can occur on specialized structures of the mouth
905
What is this clinical finding?
``` Aphthous ulcer (“The canker sore”) ``` What would it be like to have a canker sore on your uvula? o Painful to swallow ‐ The location of the canker sore will predict the symptoms
907
Rx Topical Treatments: Corticosteroid Rinse‐
**‐ Dexamethasone elixir 0.5mg/5ml (ETOH base) or solution (H20 base)** ‐ Indicated for difficult to reach lesions to obtain access to all of them o Disp:600ml o Label: swish with 5‐10 ml for 5 minutes up to 0.5mg/5mL 4x/day and expectorate 00s preservalve.) May be used as suppressive therapy in selected patients with close surveillance o Prevent recurrences ‐ May buy an EXTRA DAY of healing time _dr. Kerr prefers the elixir_
911
What is this clinical finding?
**Major Recurrent Aphthous Ulcers (RAS)** * ‐ 10 – 15% of all RAS cases * **‐ \>10 mm in diameter** * ‐ Ulcer Appearance: * **o Deeper** * **o Irregular borders (usually)** * ‐ **Typically resolves in WEEKS or MONTHS** * ‐ May be associated with fever or malaise * o The associated cytokine release can induce a fever * ‐ Predilection for the throat * **‐ Often DOES leave scarring** * ‐ Recurrence rates vary
921
Rx Topical Treatments: Corticosteroids for Ulcers
**‐ Triamcinolone acetonide** in Orabase 0.1% (intermediate) o Disp: 5g tube Dental Past o Label: apply a thin film over ulcer after meals and bedtime APOTHECON o Do not use for more than 2 weeks **‐ Fluocinonide gel or ointment** 0.05% (Potent) o Disp: 15g tube o Label: apply a thin film over o Do not use for more than 2 weeks ‐ Clobetasol ointment 0.05% (Ultra potent) o Disp: 15gtube Label: apply a thin film over ulcer bid
923
Problem with topical tx
Topical Treatments ‐ Drug is easily washed away or rubbed off ‐ Topical anesthetics have a short‐lived effect ‐ Often difficult to apply due to location ‐ Cost may be a disincentive to buy OTC ‐ Once ulcers are established, these treatments are not as effective, therefore abortive treatment early on is preferred
924
What about systemic treatments – taking pills to treat ulcers?
**‐ Prednisone or systemic steroids were the one systemic treatment that Dr. Kerr has has success with in practice** **o 0.5 mg/kg of Prednisone would be prescribed for about 1 week** o Very successful in patients with frequent outbreaks of multiple canker sores ‐ In some limited cases Dr. Kerr has seen some success with: o Colchicine o Pentoxifylline
925
**What is Human herpes virus (HHV)** **what is it's 8 types?**
Large family of double stranded DNA viruses ## Footnote ❏ HHV‐1: HSV‐1‐Herpes simplex virus type 1 (most common in oral cavity) ❏ HHV‐2: HSV‐2‐Herpes simplex virus type 2 ❏ HHV‐3: VZV‐Varicella zoster virus ❏ HHV‐4: EBV‐Epstein Barr virus ❏ HHV‐5: CMV‐Cytomegalovirus ❏ HHV‐6: Sixth disease/Roseola (commonly seen in children, spreads through saliva and respiratory droplets) ❏ HHV‐7: Roseola ❏ HHV‐8: KSHV‐Kaposi sarcoma‐associated herpesvirus
926
**What is the Mode of infection of HHV?**
Primary infection → Latency → Reactivationn → Recurrent infection
927
After the primary infection the HHV‐1/HSV1 stays in ------------
**Sensory ganglia**
928
After the primary infection the HHV‐2/HSV2 stays in ------------
**Sensory ganglia**
929
After the primary infection the HHV‐3/VZV stays in ------------
**Sensory ganglia (dorsal root ganglia)**
930
After the primary infection the HHV‐4/EBV stays in ------------
**B‐Lymphocytes**
931
After the primary infection the **HHV‐5/CMV** stays in ------------
**Myeloid cells, salivary gland cells, endothelium**
932
After the primary infection the HHV‐6 stays in ------------
**CD4+ T‐Lymphocytes**
933
After the primary infection the **HHV‐7** stays in ------------
**CD4+ T‐Lymphocytes**
934
After the primary infection the **HHV‐8** stays in ------------
* *B‐lymphocytes (latency)**, **endothelial cells (Kaposi sarcoma) **
935
**Herpes Simplex Virus** _types_ _&_ _locations_
❏ **Type 1**‐ adapted to _oral, facial, and ocular areas_ (more common in oral cavity) ❏ **Type 2**‐ adapted to _genital area_ ❏ Other sites may also be affected ○ **Herpetic whitlow** (finger) ○ **Herpes gladiatorum** (wrestlers) ○ **Herpes barbae** (beard area)
936
Herpes Simplex Virus primary infection
○ Acute/Primary Herpetic Gingivostomatitis ○ The easy way to remember where the ulcerations occur? ➢ gingiva and oral cavity **gingivo** (=**gingiva** or _fixed_ keratinized mucosa) + **stoma** (= the **movable** part of the oral cavity where the CT is looser, including the **labial and buccal mucosa, and the tongue**).
937
Herpes Simplex Virus Recurrent infection
two manifestations: 1. **Herpes labialis:** occurs on the vermillion border 2. **Intra‐oral herpes**: occurs ONLY on the fixed keratinized mucosa (mucosa that doesn't move around) MEMORIZE THIS
938
What does it mean if a person has a primary infection?
 They don’t have antibodies
939
Who’s the typical group that will get primary herpetic gingivostomatitis?
 Children and young patients
940
What is this infectious disease? Describe it
HSV‐1: Primary Infection it is a raised blister/papule on the vermilion The bottom arrow pointing to a mucosal ulcer w/ tan pseudomembrane.
941
What is this infectious disease? Describe it
**HSV 1- Primary Herpetic Gingivostomatitis** Ulcer with an erythematous halo (top two arrows). We also have ulcerations that are irregular in shape on the gingiva (bottom two arrows). **❏ Clinical Features:** * Cervical lymphadenopathy * Chills * Fever * Nausea * Anorexia * Irritability * Sores in mouth * Ulcerations on fixed and movable mucosa * Variable number of lesions * Ulcers coalesce and form larger irregular ulcerations * Gingiva enlarged and painful * **Resolution in 5‐7 days**
942
What is this infectious diseease? What is its pathogensis ?
**HSV‐1: Primary Infection** _pathogensis_ ❏ Usually young age ❏ Often asymptomatic ❏ Symptomatic = Primary herpetic gingivostomatitis ❏ In adults is usually pharyngotonsillitis (back of throat) ❏ Spread through infected saliva or active lesions ❏ Incubation period = 3‐9 days These photos represent **gingivostomatitis** **multiple irregularly shaped ulcers present on the fixed and movable mucosa, bilaterally**
943
What is this infectious disease? What probably this patient also have?
HSV1: primary herpetic gingivostomatitis there are multiple irregularly shaped ulcers present on the fixed and movable mucosa --\> most likely diagnosis is primary herpetic gingivostomatitis since the patient has fever and malaise.
945
HSV‐ Histopathology
❏ Molding ❏ Margination ❏ Multinucleation ❏ Also Tzanck cells
946
What is a definitive diagnosis for HSV1 Herpes simplex
HSV‐ Cytology‐ Papanicolaou Stain (PAP)
947
How to interpere HSV‐ Laboratory Results based on IGg and IGm a
If you have **positive IgM** *and* **negative IgG** → that means it’s an acute recent infection. Then you have to wait 4‐6 weeks If you do the serology then and get **positive IgG** *and* **negative IgM** → that means the person has **the established infection.**
951
How is Primary HSV (Herpes Simplex) diagnosed?
❏ Clinical diagnosis → based on putting all the features together ❏ Culture (may take 2 weeks) → not worth it ❏ Tissue biopsy → very invasive **❏ Cytologic smear (less invasive)** ○ easiest bc you take a popsicle stick to scrape an ulceration then you put those cells on a slide, you send it to a pathologist after fixing the cells with some alcohol then you can see the virally‐altered cells ❏ Serologic testing→ to look for antibodies 4‐8 days after they were exposed.
955
What is the **treatment** of **Primary Herpetic Gingivostomatitis ?**
* ❏ Supportive/Palliative Treatment * ❏ Fluids, nutrition, rest, avoid spreading to others * ❏ Avoid touching eyes, genitals * ❏ Possible referral to MD if infant is not drinking because of pain * ❏ Medications: 1. Topical anesthetic (OTC vs Rx) 2. Mucosal coating (OTC) 3. Analgesic (OTC vs Rx) 4. Antiviral (Rx)
956
What are the medications used to treat Primary HSV?
**❏ OTC Magic Mouthwash Formulation:** helps the person to actually be able to eat bc they have so many ulcerations ○ 1 Part‐ Diphenhydramine/ Benadryl (anticholinergic) 12.5mg/5mL elixir ○ 1 Part‐ Lidocaine (topical anesthetic) ○ 1 Part‐ Magnesium hydroxide/ Maalox (mucosal coating agent) ○ Disp: 4 oz bottle ○ Label: Rinse with 5mL every 2 hours for 30 sec. then spit out **❏ Rx‐Topical Anesthetic** ○ Lidocaine 2% viscous solution\* (viscous lidocaine) ○ Disp: 100mL bottle ○ Label: Rinse with 10 mL for 2 minutes and spit out \*May diminish the gag reflex therefore better suited for older patients‐ shouldn’t be prescribed to kids. Remember serious sideeffects of seizures and methemoglobinemia in pediatric population. **❏ OTC Analgesic** ○ Acetaminophen (Tylenol) OR ibuprofen (NSAID) suspension/ tablets as directed for body weight ❏ **Rx Antivirals** ○ Generally only indicated for immunocompromised or dehydrated patients ○ Limited evidence for other cases‐ see Cochrane Oral Health Group Review\* (\*Amended recently) ○ Oral acyclovir suspension (Zovirax) is typically used ○ 15 mg/kg up to adult dose of 200mg ○ Rinse and swallow, 5 times a day for 5‐7 days
957
HSV-1 RECURRENT INFECTION
* §**Secondary herpes** * §Mild, self-limiting * §Vermilion border * §Intraorally on **fixed keratinized mucosa** * §7-10 days * **§Unilateral** * § Prevalence‐15‐45% * 90% of adults have the antibodies, but 15‐45% of them can get recurrent herpes. Most of us have the antibodies, but we never exhibited the primary infection or a recurrent infection***.** * **§ 1‐6 outbreaks a year**
958
**Reccurent HSV-1** Latency place is --------
**trigeminal ganglion**
959
What are the Stages of recurrent Hsv-1?
Prodrome►papules►vesicles►ulcer►crust►heals►no scar
960
What is this infectious disease? describe it
**recurrent Hsv-1/Recurrent herpes** It is raised (papule), so it’s in the middle stage
962
What are some of **triggers** of the Recurrent HSV?
* Old age, Allergy * UV light ,Trauma * Physical / emotional stress, Dental treatment * Fatigue, Respiratory illnesses * Heat, Fever * Cold, Menstruation * Pregnancy, Systemic Diseases * Malignancy
963
What is this infectious disease? describe it
Recurrent HSV-1 Punctuate ulceration erythematous border, irregular shape, fixed mucosa, unilateral
964
What is this infectious disease? describe it
Recurrent HSV-1 This is recurrent intraoral herpes. We have punctate (point‐like) ulcerations which sometimes have clusters of coalescing ulcers. That’s the words you wanna use Other features of the ulcers: ○ Erythematous border ○ Irregular shape ○ Fixed mucosa ○ Unilateral
965
What is this infectious disease? describe it
Recurrent HSV-1 **Bilateral** \> THIS IS KEY -differential diagnosis with a Staph infection that occurs periorally with kids -\> impetigo
966
What is this infectious disease? describe it
Recurrent HSV-1 Vesicle stage (unilateral)
967
What is this infectious disease? describe it
Recurrent HSV-1 crust → later crust comes off and then you'll have epithelialization underneath
968
What is this infectious disease? describe it
Recurrent HSV-1 papule bc its raised
969
What is this infectious disease? describe it
**Recurrent HSV-1** healing stage cause you might see this one day
970
What is HSV‐ Recurrent Infection‐ Shedding ?
Asymptomatic shedding can occur in seropositive patients ❏ More common after surgical procedures and in immunocompromised patients ❏ We need to take Universal precautions
978
How to diagnose Recurrent HSV?
**❏** **Clinical**‐ if you see punctate ulcers unilaterally on the palate, it is usually recurrent herpes simplex. ❏ Culture (may take 2 weeks) ‐ takes too long ❏ Tissue biopsy‐ if it wasn't typical **❏ Cytologic smear**‐ the ideal way if you want a definitive diagnosis
979
What is this infectious disease?
**Atypical recurrent HSV** **❏ Immunocompromised host** Atypical recurrent HSV can have this appearance on the movable mucosa too, not just fixed
980
What is this infectious disease?
**HSV Associated Erythema Multiforme** ❏ Skin immune reaction in response to infection ❏HSV implicated in trigger for erythema multiforme where you get target lesions and crusted ulcerations on the lip ❏ need to prescribe :antiviral prophylaxis
981
What is the Treatment Recurrent HSV-1?
_❏ **Depends on severity/frequency**_ _❏ **Preventive/suppressive vs episodic/abortive strategies** Two types of treatment:_ **Preventive/Suppressive: taking antivirals everyday to prevent an outbreak** **Episodic: taking antivirals here and there to abort the process; episodic: abortive. _❏ Drugs used:_** ❏ *Antiviral agents* ❏ *Antiviral‐steroid combination agents* **_❏ Avoid precipitating factors, like use sunscreens – avoid any triggers_**
982
e At which stage should the abortive/ episodic treatment be done to avoid the outbreak?
❏ the **prodrome**, prodrome treatment is abortive \*\*remember this!\*\*
983
RECURRENT HERPES LABIALIS-RX TOPICAL/SYSTEMIC AGENTS
Topical like Acyclovir or Acylovir + steroid combination There are many OTC topical medications
984
suppressive or preventative therapy of Recurrent HSV-1
: taking antivirals everyday to prevent those 6 outbreak/year. There is modest evidence that systemic **acyclovir or valacyclovir** prevents recurrent herpes labialis these drugs tend to only affect virally‐altered cells. They don’t affect the mammalian cells; they’re very safe.
985
Episodic/ Abortive therapy of reccurent HSV1
❏ Episodic‐Occurring, appearing, or changing at usually irregular intervals ❏ Abortive‐Tending to cut short the course of a disease ○ Medication has to be taken during Prodrome ○ When the patient feels a burning, itching, and tingling
986
What are Recurrent Herpes Labialis‐ FDA Approved Topical Treatments?
❏ Rx: **Acyclovir cream 5% (Zovirax)** Disp: 5g tube Label: dab on lesion every 2 hours for 4 days ❏ Rx: **Penciclovir cream 1% (Denavir)** Disp: 5g tube Label: dab on lesion every 2 hours for 4 days ❏ Rx: **Docosanal cream (Abreva) OTC** Disp: 2g tube Label: dab on lesion five times per day for 4 days **Acyclovir and Penciclovir should be taken during the prodrome stage** ❏ Rx: Acyclovir 5%/ hydrocortisone 1% cream (Xerese) Disp: 5g tube Label: dab on lesion 5 times a day for 5 days ❏ Rx: Acyclovir buccal tablets (Sitavig) 50mg Disp: 2 dose pack Label: apply to canine fossa within 1 hour of symptoms (single dose)
987
What are Recurrent Herpes Labialis‐ FDA Approved Systemic Antivirals ?
**❏ Rx: Valacyclovir 1g tablets** Disp: 4 tabs Label: 2 tabs stat PO, then again in 12 hours (ie 2 doses) *Given during prodrome.* **❏ Rx: Famciclovir 500mg tablets** Disp: 3 tabs Label: 3 tabs stat PO
988
What are other Topical Agents for treating Recurrent Herpes Labialis?
❏ Ice ❏ L‐lysine ❏ Bioflavonoids ❏ Evaporants ‐ Desiccants ❏ Emollients ❏ Bioadhesives (Zilactin‐benzyl alcohol, topical pain reliever) ❏ Wound‐healing modification/ occlusive agents
991
HHV3 What is it's primary infection and Secondary infection known as?
❏ Primary infection **○ Varicella/ Chicken pox** ❏ Secondary infection **○ Zoster/ Shingles** ○ May affect oral cavity/ face if reactivation along distribution of V1/2/3
992
What is this infectious disease? describe it
HHV3 Varicella (chickenpox) It is caused by Varicella Zoster Virus Infection a typical macular, papular, vesicular rash – it’s bilateral
993
What is this infectious disease?
**Herpes Zoster/ Shingles** * It is affecting the intraoral region * and the maxillary branch. * Picture on the far right looks like recurrent HSV (cluster of coalescing ulcers) * Looking at the picture on the left you can determine it is NOT a recurrent intraoral herpes **because we have vesicles that opened up and crusted over on** **the skin.** **VZV histopathology is the same as HSV.** **VZV remains latent in the dorsal root ganglion** travels down the sensory nerves to skin upon reactivation. ❏ The reactivation presents as **a painful rash in one or two adjacent dermatomes that does not cross the midline.** ❏ The rash is **maculopapular** and **develops into vesicles.** ❏ One complication of zoster is **post‐herpetic neuralgia**: pain that persists in the area where the rash once was present.
995
What is this infectious disease?
**HHV 5** **Cytomegalovirus Infection** Histopathology look like an owl eyes means the cells are affected- they are **nuclear inclusions and cytoplasmic inclusions.**
996
What is this infectious disease? Desercibe it
HHV 5 Cytomegalovirus Infection When a person is immunocompromised, particularly those who’ve had a transplant or HIV+ patients, only these people will present with ulcerations It's very hard to identify based on photo alone - it's very nonspecific
998
What is this diseases? Which virus is asscoaited with it?
**Nasopharyngeal carcinoma** ❏ Associated w/ HHV‐4 (EBV) ❏ You might be one of the first people to detect this cancer – the first sign is the swelling of the lymph nodes In this case, these are late stages of the disease. *this photo from google*
999
What is this disease? Which virus causes it describe it
**Oral hairy leukoplakia** Epstein‐Barr Virus induced disease ❏ Corrugated white keratotic lesion on the lateral tongue in HIV+ people
1000
What is this infectious disease?
**Infectious mononucleosis** **Epstein‐Barr Virus/EBV‐induced disease** The virus spreads through saliva, which is why it's sometimes called "kissing disease." Mono occurs most often in teens and young adults. However, you can get it at any age. Symptoms of mono include: **Fever** **Sore throat** **Swollen lymph glands** * when you have salivary transfer, your lymph nodes get swollen * people feel fatigue and fever * they have tonsilitis * can lead to the secretion of white or gray‐ green tonsillar exudate * they can get petechiae on the palate too.
1001
**HHV5** is it symptomatics? where does the diseases predominantly found? Latency?
**Cytomegalovirus Infection** ❏ Usually **asymptomatic** ❏ Symptomatic infections are nonspecific: **chills, fever, sore throat** ❏ What’s interesting here: ❏ When the cells are affected, they form these owl eyes – they are **nuclear inclusions and cytoplasmic inclusions.** ❏ Disease states found predominantly in: * **○ pregnancy/neonates** (congenital infection) * **immunocompromised patients,** particularly **transplant and HIV+** **patients** **​** ❏ Latency in **myeloid cells, salivary gland cells and endothelium**
1002
What is this diasese? which viruse causes it
**Burkitt Lymphoma** Epstein‐Barr Virus Infection * Fast growing tumor discovered by Dr. Burkitt * **High grade lymphoma B** **cells**‐ Usually affects the jaws of children. * **It is the fastest growing tumor/cancer**. * There is _translocation of c‐myc_
1003
What is this infectious diasese?
**EBV mucocutaneous ulceration** Very rare *Photos from google*
1004
Which disease has Stary sky pattern histopathology?
**Burkitt Lymphoma** *caused by **EBV***
1005
What is this disease? Describe it
**Kaposi sarcoma** HHV 8 Kaposi sarcoma on the skin: \>1cm Different color, so this is called a **patch**. Erythematous patches present on multiple areas of the face.
1006
Kaposi sarcoma Histopathology
Histopathology shows **malignant endothelial cells proliferating.** There are tiny spaces. Extravasation of RBCs can be seen
1007
What is this disease?
**Kaposi Sarcoma (HHV‐8)** Right photo: we see Patch, slightly raised plaque stage ○ This is different from **hemangioma** because if you press on it, it doesn’t blanch (where all the blood goes away, and it looks white) Left photo: Nodular is when it becomes very exophytic You need to do a biopsy for this because it looks irregular.
1010
What are HPV types that cause **Genital Benign Lesions**?
**6, 11, 16, 18** ***(condyloma – can be malignant)***
1011
What are HPV types that cause **Non‐genital Benign** Involving **Mucosa**?
**6 & 11**
1012
What are HPV types that cause **Non‐genital Benign** Involving the **Skin**?
**2 & 4**
1013
What are HPV types that cause **Malignant & Potentially Malignant Disorders**?
**16, 18**
1014
**HHV‐8** What is it? Assoicated with what? How it evolved? How it is treated?
**Kaposi sarcoma--associated herpesvirus (KSHV)** **❏ Vascular neoplasm of endothelium** ❏ Associated with **immunosuppression** ❏ Usually evolves through 3 stages: **○ Patch►plaque►nodular** * **More commonly seen in patients with HIV infection.** * **Treated** with _topical agents and chemotherapy._
1015
What is HPV Pathogenesis and Incubation period?
Incubation period: **3 weeks – 2yrs** ▪ Basic Explanation: Basal epithelial cell infection ► Genome replicates ► DNA released into stratum corneum ▪ Detailed Explanation: 1. HPV accesses and infects cells of the epithelial basal layer through breaks in the skin or mucosa 2. The virus becomes incorporated in the genome of the infected cell 3. The site of HPV integration into the cellular genome is in the general region of known oncogenes 4. The virus replicates during keratinocyte differentiation in the spinous and granular cell layers 5. A portion of the HPV genome encodes proteins that are capable of inducing cell proliferation and transformation **(E6, E7)**
1016
HPV Pathogenesis – High Risk ▪ Break in the skin ► HPV (dark dots) invades and infects basal cells ▪ HPV incorporates into DNA ► moves up epithelium as it matures ► releases Then 2 things happen 1. or 2.
1. Completely have infection go away or 2 .Stays and forms wart or affects maturation (becomes cancer, depending on strain)
1017
**HPV Genome Organization**
▪ LCR: long control region ▪ P97: promoter protein ▪ E1‐E7: early region genes ▪ L1,L2: late region genes
1021
HHV‐4 Latency? and What are the EBV inducded diseases?
**Epstein‐Barr Virus Infection** Latency in **lymphocytes** §Infectious mononucleosis §Oral hairy leukoplakia §Nasopharyngeal carcinoma §EBV mucocutaneous ulceration §Burkitt lymphoma §Other lymphomas (Hodgkin, post transplant)
1028
what are the charcterstics of HUMAN PAPILLOMA VIRUS (HPV) ?
§Small, non-enveloped **icosahedral DNA virus** that infects **skin or mucosal cells of humans.** **§Circular DNA** §198 types established **§High and low risk types** ## Footnote **‐ HIGH risk = CANCER ‐ LOW risk = WARTS**
1029
What can HPV Epithelial Lesions cause? | (3)
▪ **Benign**: neoplasms of squamous epithelium ▪ **Pre‐malignant**: epithelial dysplasia – can lead to cancer ▪ **Malignant**: squamous cell carcinoma – infiltration of epithelial cells
1034
What are Routes of Transmission for HPV?
▪ **Sexual/non‐sexual direct contact** ▪ **Salivary transfer** ▪ **Contaminated objects (fomite)** – not well established ▪ **Autoinoculation** – child puts finger into mouth ▪ **Perinatal/pre‐natal transmission**
1038
What is the Molecular Mechanism of HPV?
``` **E6 = degrades p53 E7 = inactivates pRb** ``` ## Footnote 1. E2 = attachment location of Integrated HPV 2. transcription of E6 + E7 3. Binding of the viral E7 protein to pRb ► release of E2F and other proteins ► signals for the cell cycle to progress ▪ **As long as the E7 protein stays attached to pRb, uncontrolled cell proliferation will continue** HPV E6 protein is: ‐ A ubiquitin ligase ‐ contributes to oncogenesis by attaching ubiquitin molecules to p53 ► making p53 inactive and subject to proteasomal degradation ▪ **Normal function of p53 = to stop cell division + repair damaged DNA so that damaged cells do not reproduce (apoptosis)** ▪ _When p53 is inactive_, cells with changes in the DNA, such as integrated viral DNA, are not repaired ► destabilizes the cell ► increases the risk of malignant transformation
1039
What is Persistence of HPV
▪ Low‐risk types: clear faster, less likely to become persistent ▪ High‐risk types: clear slowly, more likely to become persistent
1040
What is the Prevalence of Oral (HPV)
Overall: 6.9% (CI 6.7‐8.3) ▪ Gender: **Men (10.1%) \> Women (3.6%) – women clear faster** ▪ Age: **bimodal distributio**n – 30‐34yo and 60‐64yo (she says 30‐34 but Dr. Kerr’s graph shows mid‐20s ▪ High Risk HPV (3.7%) \> Low risk HPV (3.1%) ▪ **HPV‐16 infection most prevalent** (1% or 2.13 million Americans) ▪ Based on NHANES study w/ oral rinse sampling and PCR
1041
What are Risk Factors Associated w/ Prevalence of HPV?
▪ Ever had sex (7.6%) vs never had sex (0.9%) ▪ Male ▪ Increased number of sexual partners (vaginal or oral sex) ▪ Tobacco smoking ▪ HIV infection
1042
Most prevelant HPV TYPE?
HPV 16 = most prevalent
1043
What is the Prevalence in HIV + ?
**Ppl w/ HIV+ and low CD4 T‐cells lvl** = higher risk of HPV **HPV 16+ higher if CD4 \<200**
1044
Compare between SCC in Squamous Cell Carcinoma caused by HPV vs Tobacco and Alcohol
**▪ HPV associated SCCa** ‐ Wild type TP53 ‐ Low pRb _‐ Increased p16_ **▪ Tobacco and Alcohol associated SCCa** _‐ \*Mutated TP53_ – mutated by carcinogens in tobacco and alcohol► cancer ‐ pRB overexpression ‐ Decrease p16
1045
BENIGN ORAL LOW RISK HPV LESIONS (WARTS) How do they appear? Color? Size? Histologic?
§_Appear_ as **single or multiple exophytic papules, either sessile and flat or pedunculated and papillary.** §_Color_ depends upon degree of keratinization, ranging **from white to pink.** §_Size_ of papules **generally \<10mm in diameter.** §_Histologically_, lesions may have **koilocytes.**
1046
What are the types of Benign Oral Low Risk HPV Lesion ? (5)
▪ Squamous papilloma ▪ Verruca vulgaris ▪ Condyloma acuminatum ▪ Focal epithelial hyperplasia ▪ Oral florid papillomatosis
1047
What is this infectious diease?
SQUAMOUS PAPILLOMA Benign Oral Low Risk HPV Lesion **HPV 6+11** “finger‐like projections - The projections are almost feathery - exophytic lesion
1049
**SQUAMOUS PAPILLOMA** _What is it?_ _Gender?_ _Age?_ _Location?_ _Apperance ?_ _Treatment?_
▪ **Benign proliferation of stratified squamous epithelium resulting** ► p*_apillary, verruciform, rugose (ridged or wrinkled) mass_* ▪ **HPV types 6 + 11** – Low risk ▪ **M = F** ▪ **Any age** (more common in 30‐50s) ▪ Any oral mucosal surface (palate most common) ▪ **Soft, painless, usually pedunculated, exophytic lesion w/ numerous finger‐like projections** ▪ **HPV DNA detected in only ~50%** ▪ \*\*should remove from mouth – but WOULD NOT submit for HPV typing
1050
What is this infectious diease?
SQUAMOUS PAPILLOMA Benign Oral Low Risk HPV Lesion **HPV 6+11** “finger‐like projections
1051
What is this infectious disease?
***Oral Verruca Vulgaris*** HPV 2,4,6 Also “finger‐like projections” remember it's *contagious*
1052
**Oral Verruca Vulgaris** What is it? Contagious? Age? Location? Apperance ?
▪ HPV **2**, and others (1,**4,6**,7,11,26,27,29,41,57,65,75‐77) ▪ Benign, HPV‐induced focal hyperplasia of stratified squamous epithelium ▪ **Contagious** – transmitted by direct contact ▪ **Any age** – frequently seen in children ▪ More common **Anterior** \> Posterior part of mouth ▪ **Soft, painless, usually pedunculated, exophytic lesions w/ numerous fingerlike projections** (similar to squamous papilloma) ‐ _How to tell the difference? Under microscope_
1053
What is this infectious disease?
**Condyloma Acuminatum** (Venereal Wart) HPV 6,11 – can be cancerous Genital warts “short, blunt, clusters” Characteristic clustering of multiple lesions
1056
What is this infectious disease?
(Multifocal) Epithelial Hyperplasia/**Heck's Disease** HPV 13,32 **“Flat‐top papules”**
1057
What is this infectious disease?
(Multifocal) Epithelial Hyperplasia/**Heck's Disease** HPV 13,32 **“Flat‐top papules”**
1058
**Condyloma Acuminatum (Venereal Wart)** What is it? Contagious? Transmission? Age? Location? Apperance ?
**HPV Types 6, 11** – _condyloma can turn cancerous_ ▪ Virually induced proliferation of stratified squamous epithelium – usually genital or anal mucosa ▪ **Contagious** – transmitted by direct contact ▪ Incubation period: 1‐3mo ▪ Considered **sexually transmitted disease** (if corroborated by history) ▪ **Oral lesions** – usually **anterior part of mouth** ▪ S**essile, pink, well‐demarcated, non‐tender exophytic mass ▪ Short, blunted surface projections ▪ Larger than papilloma or verruca vulgar** ## Footnote **▪ Characteristic clustering of multiple lesions**
1059
What is this infectious disease?
**Oral Florid Papillomatosis** Very characteristic appearance - diffused, in multiple locations - papillary **"Multifocal, papillary lesions"** -if we biopsied these or had these removed for aesthetic regions, we’d see that the epithelium have become white, long, taller, and bumpy
1061
If you see Condyloma Acuminatum in a child, what is the next step?
-Since this is a sexually transmitted disease, we need to suspect sexcual child abuse and investigate further!
1062
**(Multifocal) Epithelial Hyperplasia/Heck's Disease** What is it? Appearance? Which communities or environment? Demographics age and gender? Histology?
▪ HPV Types **13, 32** and others (1,6,11,16,18,55) ▪ **HPV‐induced localized proliferation of oral squamous epithelium ▪ “Flat‐top papules”** ▪ Endemic in some **Inuit/Alaskan native + Native American** **communities**, **Puerto Rican communities** ▪ _Crowded situations, malnutrition_ ▪ Usually seen in children ▪ May be seen in HIV + individuals ▪ **M = F** ▪ Histology: **focal epithelial acanthos**
1065
**Oral Florid Papillomatosis** What is it? What are its types? What is clinical appearance?
IIt's benign HPV disease ▪ HIV infection ‐ Increased prevalence since advent of HAART therapy ‐ Multiple HPV types ▪ Down syndrome Oral Florid Characteristics: ‐ **Diffuse, multiple locations ‐ Papillary ‐ Bumpy and tall**
1067
**Benign Oral HPV Lesions** HISTOPATHOLOGY
**§Acanthosis §Koilocytosis §Binucleated***and***multinucleated keratinocytes §Dyskeratosis §Mitosoid figures §Basilar hyperplasia**
1068
HPV is thought to cause --% of oropharyngeal cancers in the US
HPV is thought to cause **70%** of oropharyngeal cancers in the US That's why we want to know if high risk HPV– better prognosis
1069
**HPV Testing**
_▪ Pathologists order it_ ▪ Only do testing if pathologist sees cancer **No HPV testing on low‐risk HPV lesions (warts)** ▪ No medical indication for **low‐risk HPV testing** b/c ‐ infection **NOT** associated w/ disease progression ‐ no treatment or therapy change indicated when low‐risk HPV is ID’ed ▪ HPV testing using p16 surrogate on **oropharyngeal squamous cell carcinoma** **(SCC)**
1070
Management of Oral HPV Lesions Solitary Lesions
‐ Usually appear exophytic and papillary ‐ Excision is warranted ‐ Consider possible recurrence
1071
**Oral Molluscum Contagiosum** _Which viruse causes it?_ _Clinical Appaerance?_ _Who get affected?_ _Histopathology?_ Treatment?
▪ **Poxvirus** ▪ Presents as: ‐ pink, dome‐shaped, smooth‐surfaced or umbilicated (like belly‐button) papules ‐ with caseous plug involving skin, lips, buccal mucosa, and palate ▪ Florid cases seen in immunocompromised persons ▪ Children, young adults ▪ Histopathology characterized by: ‐ Large intracytoplasmic inclusion bodies – “Henderson‐Paterson bodies” ‐ Kids can have 6‐9mo and will go away
1072
What is this infectious disease?
**Oral Molluscum Contagiosum** *multiple pink, dome‐shaped, smooth‐surfaced or umbilicated (like belly‐button) papules ‐ with caseous plug*
1073
Management of Oral HPV Lesions ## Footnote **Multiple Lesions**
‐ Use high power evacuation to prevent transmission ‐ Treatment = controversial ‐ Excision/ablation vs Topical vs Intralesional therapy (or combo) ‐ Consider higher rate of recurrence
1074
What is this infectious disease?
**Measles** **\*Characterized by Koplik’s spots** salts/grains
1075
HPV multiple lesions ## Footnote Excision/Ablation
Excision/Ablation ▪ Scalpel ▪ Carbon dioxide laser – be cautious, don’t know what is burned away ▪ Electrosurgery
1076
What is this infectious disease?
**_Hand, foot, and mouth disease_** caused by **Coxsackie Virus** affect children contagious The condition is spread by direct contact with saliva or mucus.
1077
What is this infectious disease?
**Herpangina** casued by **_Coxsackie Virus_** *red macules and vesciles on the soft palate* a sudden viral illness in children. It causes small blisterlike bumps or sores (ulcers) in the mouth
1078
What is this infectious disease
**Acute lymphonodular pharyngitis** Caused by **Coxsackie Virus** *Affects children* Nodules on the soft palate. -distinctive, raised, micronodular lesions occur primarily in the pharynx and related structures and regressed without ulceration.
1079
**HPV multiple lesions** Topical Therapy
▪ Podophyllin resin ▪ Imiquimod (extra‐oral use only) ▪ Cidofovir ▪ Interferon
1080
What is this infectious disease?
Rubella caused by Family: Togavirus; Genus: Rubivirus ``` Forchheimer sign (left) Palatal petechiae (right) ``` | (German Measles)
1081
Topical Podophyllin for what is it used Is it FDA approved Safe or not Durging pregnancy?
▪ Topical cytotoxic agent which arrests mitosis ▪ Genital warts and other papillomas ▪ Not FDA approved for oral warts ▪ Serious adverse reaction if absorbed systemically ▪ Pregnancy category X
1082
Topical Imiquimod
▪ Induces cytokines + chemokines w/ resutlant anti‐virl (HPV) effects Not FDA approved for oral warts
1083
HPV vaccine
**Newest is Gardsail 9** against many types for both men and women ▪ 2 doses recommended for boys/girls age 11‐12 and 6mo later ▪ Recommended for everyone \<26yo (MAX) ▪ NOT recommended for 26+yo unless risk for new infections (less benefit since most already exposed) ▪ Virus like particles (VLP) of L1 capsid protein present in vaccine Results of Vaccination ▪ Drops in infections w/ HPV types that cause most HPV cancers + genital warts in teen girls, young adult women ▪ Among vaccinated women – cervical precancers dropped by 40%
1084
What precentge of people will be infected with HPV in their lifetime?
▪ 80% ppl will be infected in lifetime so better take the vaccine early!
1087
**Measles** Which viruse causes it? How does it spread? Symptoms? Clinical charcterstics? location?
**▪ Paramyxovirus** ▪ Spread through _respiratory droplets_ ▪ **Symptoms**: runny nose, red/watery eyes, cough, fever, rash, desquamation of skin ▪ \***Characterized by Koplik’s spots** ‐ Pathognomonic for measles ‐ Discrete, bluish white punctate mucosal macules ‐ Surrounded by rim of erythema ‐ Represent foci of epithelial necrosis ‐ Often precedes skin manifestations **▪ Most common location for Koplok’s spots:** _Buccal mucosa_ ‐ Lesions may resemble _“grains of salt sprinkled on erythematous background”_
1089
Enterovirus‐Coxsackie Virus What diseases can it cause ? (3) Who do they effect? How they are treated?
**-Herpangina**‐soft palate, red macules ► fragile vesicles (back of throat) ‐ **Hand, foot, and mouth disease** – oral lesions more in anterior regions (aphthous‐like), hand/foot (vesicles) ‐ **Acute lymphonodular pharyngitis** – nodules on the soft palate ▪ Usually seen in children ▪ Self‐limiting
1093
**Rubella (German Measles)** Which viruse causes it? How does it spread? Symptoms? Clinical signs? Assosited with what syndrome? Is there a vaccine? How it is diagnosed?
**▪ Family: Togavirus; Genus: Rubivirus** **▪ Respiratory droplets** **Symptoms:** ‐ Fever, headache, malaise, coryza (runny nose), anorexia, pharyngitis, lymphadenopathy ▪ Rash – **maculopapular w/ desquamation** * *▪ Forchheimer sign** * *▪ Palatal petechiae** ▪ **Congenital rubella syndrome** – pandemics in past ▪ Vaccine: **MMR** – so we barely see this anymore ▪ Diagnosis**: by serology**
1095
What is the **Most common opportunistic fungal pathogen/ infection?**
**Candida Species** ● Over 200 species exist ● At least 15 distinct Candida species cause human disease
1096
Mucosal/Oral infections, which are generally non‐invasive are caused primarily by --------
**Candida albicans**
1097
\>90% of invasive disease is caused by 5 most common species, which are?
‐ C. albicans ‐ C. glabrata ‐ C. tropicalis ‐ C. parapsilosis ‐ C. krusei
1098
Candida Species have what kind of symbiosis with humans?
● **Commensalism**: ‐ “long‐term biological interaction (symbiosis) in which members of one species gain benefits while those of the other species neither benefit nor are harmed” ● \>50% of humans carry candida without harmful effects
1099
**What is Candida Species‐ Disease State**
* Becomes an “infection” called **candidiasis** when environment changes and encourages growth * ● Defect in cell‐mediated immune response * ‐ Ranges from mild superficial mucosal infection ►(can be) fatal disseminated disease (usually with people with HIV and transplants)
1100
What causes Candida Infection?
● A disrupted balance of the normal mucosal flora ● Impaired barrier functions ● Immunosuppression such as: ‐ Use of broad‐spectrum antibiotic ‐ Leukemia ‐ HIV ‐ Cancer chemotherapy ‐ Diabetes ‐ Xerostomia (what we deal with, candidiasis can persist here)
1101
Normally Candida is in the commensal state and once you reach a certain level where the fungal burden has increased, you increase the c‐FOS pathway ‐ This is when the organism forms -----; once these are formed, you see invasion into the------- cells.
Normally it is in the commensal state and once you reach a certain level where the fungal burden has increased, you increase the c‐FOS pathway ‐ This is when the organism forms **hyphae**; once these are formed, you see invasion into the **epithelial** cells.
1102
**Pathogenesis‐ Key Features**
**● Commensalism** * **Fungus is tolerated** (threshold not reached) * I**mmune cells are not activated** **● Pathogenicity** * _Fungal burden is increased_ and **hyphae** form * Immune cells are recruited by cytokines, chemokines * Neutrophils are recruited and kill fungus * Dendritic cells present antigen to T‐cells * T‐cells also decrease fungal burden (IL‐22, IL‐17) * Innate and acquired clear fungus to levels below threshold
1103
How does Candida overcome host defenses? 6
1. **Dimorphism** (can be _spore_ and a _hyphae_‐ 2 forms) 2. **Phenotypic switching** (change shape) 3. **Adhesins/Invasins** (aid in attachment) 4. **Molecular mimicry of mammalian integrins** (helps to be avoided by the immune system) 5. **Secretion of hydrolytic enzymes** (aids in invasion) 6. **Phospholipase B contributes to degradation of host tissue** (aids in degradation to gain entry)
1104
Dimorphism of Candida Two forms?
SPORES‐ when they are in this form, they do NOT invade HYPHAE‐ when they begin their invasion
1105
Crosstalk: Candida ------- play an important role in the continuous interchange that regulates the balance between saprophytism and parasitism
Crosstalk: Candida **glycans** play an important role in the continuous interchange that regulates the balance between saprophytism and parasitism
1106
TYPES OF CANDIDIASIS INFECTION
**● Superficial and localized‐more common (mild disease)** ‐ Intertrigo §Paronychia/Onychomycosis ‐ “Diaper Rash” ‐ Vulvovaginitis ‐ Esophageal Candidiasis §Oral Candidiasis (Candidosis) **● Invasive, disseminated and deep infection‐rare (moderate‐severe)** ‐ Affects blood (candidemia‐hospitalized), heart, brain, eyes, bones)
1107
What is this infectious disease?
**Onychomycosis** a type of candidiasis
1108
What is this infectious disease?
**Oral candidiasis** a type of candidiasis
1109
What is this infectious disease?
**Esophageal Candidiasis** a type of candidiasis
1110
What is this infectious disease?
**Vulvovaginitis** a type of candidiasis
1111
What is this infectious disease?
**“Diaper Rash”** a type of candidiasis
1112
What is this infectious disease?
**Intertrigo** a type of candidiasis
1117
What is this infectious disease?
**PSEUDOMEMBRANOUS CANDIDIASIS** *UNCONTROLLED DIABETIC* When you wipe away these plaques, you might see some Erythematous areas that causes some of the symptoms that the patient feels -This is **MILD DISEASE**
1118
What is this infectious disease?
* *Pseudomembranous Candidiasis‐** * Uncontrolled HIV* ● This can be mistaken with materia alba (this is just food) ‐ Should ask patient if they just ate ● This is **MODERATE DISEASE**
1119
What is this infectious disease?
**Pseudomembranous Candidiasis** *Topical Corticosteroid Use* Can be brought about from steroid use **(steroid inhaler example)** ‐ If you don’t rinse your mouth after using steroids, this can happen ■ _A proliferation of hyphae_
1120
What is this infectious disease?
PSEUDOMEMBRANOUS CANDIDIASIS **Severe dry mouth** **This is severe disease** we would want to use **systemic treatments/ intervention**
1122
What is this infectious disease
**Angular Cheilitis** ● **Erythema**, _fissuring and scaling at angles of mouth_ and _commissures of mouth_ ● ***Loss of vertical dimension*** ● ***Pooling of saliva*** ● _May be mixed bacterial/fungal infection_ ● _Differential diagnosis_ can be **Vit B Deficiency** *a subtype of Erythematous Candidiasis*
1124
What is this infectious disease
**Denture Stomatitis** ● _Chronic atrophic candidiasis_ ● **Erythema** in _denture bearing areas of maxilla_ ● **Petechiae** may be noted ● Usually, **asymptomatic** ● _Consider denture care/fit/allergy/inadequate curing of acrylic_ ● This can occur if the patient NEVER takes off their denture ● **Inflammatory papillary hyperplasia** is associated with condition ● **Treatment**‐**Nystatin** applied to intaglio surface of denture and wear denture and patient to remove denture at night *a subtype of Erythematous Candidiasis*
1125
What is this infectious disease?
**Median Rhomboid Glossitis** *a subtype of Erythematous Candidiasis* ● “**Central Papillary Atrophy”** ● _Well‐demarcated erythematous zone_ ● **Loss of papillae on midline posterior dorsal tongue** ● Usually, **asymptomatic** ● “**Kissing” palatal lesion** ‐ Because the tongue and the palate are in contact with each other ● Can have **a diamond shape**
1126
What is this infectious disease?
**ATROPHIC CANDIDIASIS** ● Erythematous on any mucosal surface **● “Bald Tongue”** ● Typically, painful ● (Chronic multifocal, looks familiar) ***a subtype of Erythematous Candidiasis***
1127
Which Candida is the most common species with what kind of Candidal Sepsis and Disseminated Candidiasis ?
**C. albicans** * **Candidal sepsis** means that you have the fungal moving around in your body * **Life‐threatening event** in individual with severely deficient cell * mediated immunity * Most commonly involves urinary tract infection (women/men 4:1) * _Very rare_
1128
What is this infectious disease?
**HYPERPLASTIC CANDIDIASIS**
1129
_Oral Candidiasis_ facts
● 30‐50% of people carry organism without infection (called candida carriage) ● Rate of carriage increases with age and risk factors ● 70‐80% of oral isolates are Candida albicans
1130
**What are the Predisposing Factors for Oral Candidiasis ?** Local and general
**Local** * denture wearing * smoking * atopic consitituion * steroid inhalation * hyperkeratosis * imblance of the oral microflora * quality and qunatity of saliva\ **General** * immunosupressive disease * impaired health status * immunosupressive drugs * endocrine disorders * hematinic deficiencies
1131
**Pseudomembranous Candidiasis** Also known as? Key feature? Symptoms? In which patients it is seen?
● “**Thrush**” ● KEY FEATURE: **Wipeable** _white plaques that resemble curdled milk_ ● Underlying mucosa is **erythematous** ● Asymptomatic usually ● Mild symptoms: burning, dysgeusia ● Seen in patients with: **HIV, broad‐spectrum antibiotics, leukemia, infants**
1132
What is this infectious disease?
**Chronic Mucocutaneous Candidiasis** Severe infection of mucosal surfaces, nails, and skin
1133
What is this infectious disease?
Mucocutaneous Candidiasis APECED Autoimmune Polyendocrinopathy Candidiasis Ectodermal Dystrophy Syndrome Biopsy of the tonuge revealed SCC
1136
What is treatment of moderate to severe Candiadisis Disease?
* **Oral fluconazole, 100–200mg daily for 7–14 days** ● For **fluconazole‐refractory disease:** ‐ **Itraconazole suspension 200 mg once daily OR posaconazole** su**spension 400 mg twice daily for 3 days then 400 mg once dail**y, for up to **28 days**, are recommended *_Alternatives for fluconazole‐refractory disease include:_* ‐ **Voriconazole, 200 mg twice daily**, OR **AmB deoxycholate oral suspension, 100 mg/mL 4 times daily**(strong recommendation; moderate‐quality evidence). ‐ **Intravenous echinocandin** (caspofungin: 70‐mg loading dose, then 50 mg daily; micafungin: 100 mg daily; or anidulafungin: 200‐mg loading dose, then 100 mg daily) (weak recommendation; moderate‐quality evidence). § **Intravenous Amphotericin B** deoxycholate, 0.3 mg/kg daily, are other alternatives for refractory disease (weak recommendation; moderate‐quality evidence).
1137
What is the treatment of mild Candiadisis Disease?
* **Clotrimazole troches**, 10 mg 5 times daily or * **miconazole mucoadhesive buccal 50 mg tablet** applied to the mucosal surface over the canine fossa once daily for 7–14 days * Alternatives for mild disease include **nystatin suspension (100 000 u/mL) 4–6 mL** swished for \>1min then swallow **4 times daily.**
1140
What are other ways to manage denture stomoatitis ?
● **Bleach‐**1 part bleach to 10 parts water (not for dentures with metallic clasps) ● **Polident** (NYU Carries Polident) ● **Microwave**? ( could be risky, careful not to ruin the denture) CLEANSERS FOR REMOVABLE PROSTHESIS- you have to use this everynight to avoid denture stomoatits **_NYU Carries Polident_** Formulation: **sodium bicarbonate, citric acid, potassium monopersulfate**, sodium carbonate, sodium carbonate peroxide, TAED, sodium benzoate, PEG‐180, sodium lauryl sulfate, VP/VA copolymer, flavor, cellulose gum, FD&C blue 2, blue 1 lake, yellow 5, yellow 5
1141
**Erythematous Candidiasis** what are its _Clinical finding?_ _Subtypes?_
● **Clinical Findings:** * Red macules or patches * Can be due to multiple things **● Subtypes:** ‐ **Atrophic Candidiasis** (acute‐feels like mouth has been scalded) ‐ **Median Rhomboid Glossitis** (asymptomatic) ‐ **Denture Stomatitis** (asymptomatic) ■ HAS THE SHAPE OF THE DENTURE ‐ **Chronic multifocal (**asymptomatic) ■ THIS HAS BEEN THERE FOR A LONG TIME
1143
What is this infectious disease?
*a subtype of Erythematous Candidiasis*
1144
How is **Histoplasmosis** Diagnosed? How about its histology?
● Histopathology (H&E and special stain‐GMS) ● Culture ● Serology as for histology ● **Epithelioid macrophages containing histoplasma capsulatum** (white arrows) ● Lymphocytes ● Plasma cells
1145
What is the infectious disease?
**Histoplasmosis** ● This can be squamous cell carcinoma, shanker, ulcers ‐ Differentials for non healing ulcerations on the lateral tongue ● The white area is called the *pseudomembrane*
1149
Which regions can **Blastomycosis** happen?
● **Eastern half of US** which extends _farther north_ ● _Seen in the wild_
1150
What is Hyperplastic Candidiasis?
● a Rare and controversial form of candidiasis ● Candidiasis superimposed on pre‐existing leukoplakic lesion ● White plaque which cannot be removed by scraping (NOT WIPEABLE) ● **Increased frequency of epithelial dysplasia** ● MUST **BIOPSY** then diagnose as hyperplastic candidiasis **if you see fungi post biopsy**
1152
What is **Chronic Mucocutaneous Candidiasis**?
● Group of rare disorders with immunologic pathogenesis ● Clinical: Severe infection of mucosal surfaces, nails and skin ● Oral‐ lesions‐thick white plaques that do not rub off but may see other forms
1153
**Chronic Mucocutaneous Candidiasis** May be associated with **endocrine abnormalities (APECED**); what does **APECED** stands with?
‐ **A**: autoimmune ‐ **PE**: polyendocrinopathy ‐ **C**: candidiasis ‐ **E**: ectodermal ‐ **D**: dystrophy **Chronic Mucocutaneous Candidiasis** is also genetic associted with **AIRE** gene
1154
What is this infectious disease?
**Blastomycosis**
1155
How to diagonse **Blastomycosis**?
● **Histopathology** (Granulomatous inflammation , Broad based budding , Double refractile cell wall) ● Cytology ● KOH ● Culture from sputum (3‐4 weeks) ● DNA probe (where you actively look for the DNA of the blastomycosis)
1156
Chronic Mucocutaneous Candidiasis is at increased risk of what?
● Increased risk of **squamous cell carcinoma**
1159
How is Oral Candidiasis Diagnosed?
● Clinical signs ● Therapeutic diagnosis ● Cytologic smear: scrape cells and look at them under the microscope and stained with PAS stain ● Periodic Acid Schiff Stain (PAS stain) ● KOH float §Biopsy (esp. hyperplastic candidiasis) ● Culture
1160
What are Antifungal Drug Classes? *3*
● **Polyene‐Nystatin, Amphotericin B** (not absorbed; used for deep fungal infections) ● **Imidazole‐Clotrimazole, Ketoconazole** (GI absorption) ● **Triazole‐Fluconazole, Itraconazole, Posaconazole, Echinocandins**
1163
What is Chronic Suppressive Therapy?
**this is when you keep the fungal infection under control for a long time** Usually **unnecessary in immunocompetent patients** ● For patients who have recurrent infections: ‐ **For HIV‐infected patients, antiretroviral therapy is strongly recommended to reduce the incidence of recurrent infections** (strong recommendation; high‐quality evidence). ‐ **Fluconazole, 100 mg 3 times weekly, is recommended** (strong recommendation; high‐quality evidence). ● **Clotrimazole 10mg troches 1 week out of every month?** (no evidence
1164
What is Denture Stomatitis Treatment?
YOU APPLY THE MEDICATION TO THE INTAGLIO PORTION antifungal medication (1) Topical Antifungal Agents ‐ Rx. Clotrimazole cream 1% vs OR ‐ Rx. Nystatin‐Triamcinolone Acetonide ointment or cream (why? To keep the inflammation down) ■ Disp: 15g tube ■ Label: apply to angles of mouth after meals and before bedtime (2) Denture adjustment, reline, remake YOU APPLY THE MEDICATION TO THE INTAGLIO PORTION
1166
What is the Most common systemic fungal infection in US?
Histoplasmosis
1167
What causes **Histoplasmosis**? what is its mode of pathogensis ?
**● Histoplasma capsulatum** ● **Dimorphic** (yeast at body temperature and mold in soil)
1168
**Histoplasmosis** is endemic where who can get infected by it? How does is spread?
● Endemic in **fertile river valleys** ‐ Seen in people who spend **a lot of time outside; near Ohio and Mississippi rivers** ● Bird and bat excrement ● Airborne spores enter lungs through inhalation ● Macrophage ingests fungusà**T‐lymphocyte immunity** ● Antibodies develop several weeks later ● **Macrophages may confine fungus** (express disease later)
1171
what is the treatment for **Histoplasmosis**? acute chronic Disseminated
● **Acute**‐Supportive (analgesics and antipyretics) ● **Chronic**‐IV lipid preparation of amphotericin B or itraconazole ● **Disseminated**‐Lipid preparation of amphotericin B (2 weeks or more) followed by daily itraconazole for 6‐18 months
1172
**Blastomycosis** _What is it?_ _What causes it?_ _What is its mode of pathogenesis?_
● _Uncommon_ **fungal infection** ● **Blastomyces dermatitidis** ● **Dimorphic**
1173
Histoplasmosis‐ Clinical Features
● **Most** cases produce **no symptoms or only mild symptoms** ● Acute‐Self‐limited lung infection (similar to influenza; the flu) ● Chronic‐Lung infection similar to tuberculosis ● Disseminated‐Extrapulmonary spread in immunocompromised (spreads from the lungs) **● Tongue, palate, buccal mucosa ● Solitary ulcer with firm rolled borders** ● **Clinically appear indistinguishable from malignancy (squamous cell carcinoma)**
1175
How does **Blastomycosis** spread? Is there any gender prediclation?
● Airborne spores enter lungs through inhalation ● **M**\>F
1176
Acute Blastomycosis resembles ----------
● **Acute**‐ Resembles pneumonia
1177
ChronicBlastomycosis resembles ----------
Chronic Resembles **tuberculosis**
1178
What are the clinical features of **Blastomycosis**?
● Skin lesions‐extrapulmonary dissemination from lungs ● Oral lesions‐extrapulmonary dissemination or local inoculation ● Skin lesions ● Granular(rough looking) erythematous plaques which may become verrucous(wart‐like) or ulcerated ● Oral lesions ‐ Erythematous or white ‐ Intact surface or ulceration with rolled borders ‐ Painful ‐ Ddx‐Squamous cell carcinoma
1181
How to treat Blastomycosis?
● Most cases **asymptomatic** ● **Itraconazole** (mild to moderate disease) ● **Systemic amphotericin B** (severe cases) ● There is a connection with people taking TNF‐alpha inhibitors
1182
Paracoccidio Mycosis What is it? What causes it?
A deep fungal infecion causes by: Paracoccidioidomycosis brasiliensis
1183
Which regions Paracoccidio Mycosis happen?
● South American blastomycosis
1184
Paracoccidio Mycosis is seen in the soil around ------- (name of an animal)
**nine‐ringed armadillos**
1185
**Paracoccidio Mycosis** what gender is more common ? which workers are more affected?
● More common in **males** ● _Agriculture workers_
1186
**Paracoccidio Mycosis** presents intially as which infection?
Pulmonary infection
1187
What is infectious disease?
**Paracoccidio Mycosis** *looks like the three tail in **Naruto** lol*
1189
what is this infection disease ?
**Paracoccidioidomycosis** looks like strawberry gingiva but it is not
1190
How is **Paracoccidioidomycosis** diagnosed?
● Histopathology (- Granulomatous inflammation, Epithelioid macrophages and multinucleated giant cells,GMS or PAS, Multiple daughter buds) ● Culture ● KOH
1191
what are the clinical presentation of **Paracoccidioidomycosis**?
●affects the Alveolar mucosa, gingiva and palate lesions with “Mulberry‐like” ulceration (little bumps around it) ● Looks like **strawberry gingivitis** (differential diagnosis)
1194
How is Paracoccidioidomycosis treated?
● **Trimethoprim/ sulfamethoxazole** (mild‐moderate) ● **IV Amphotericin B** (severe disease)
1195
What is **Coccidiomycosis**?
deep fungal infection that present as Pulmonary infection
1196
**Coccidiomycosis** is known as -------
**Valley Fever**
1197
What are the two types of Coccidiomycosis ?
* Coccidioides immitis * Coccidioides posadasii
1198
What is this infectious disease?
**Coccidioidomycosis**
1199
How is Coccidioidomycosis diagnosed?
● Histopathology ( Round spherules with numerous endospores , Granulomatous inflammation, Suppurative neutrophils infiltrate, Special Stains used: GMS, PAS) ● Culture ● In situ hybridization (ISH) ● Cytology‐ scraping ulcers then stained with GMS ● Serology‐ check for antibodies ● Skin testing (limited value)
1200
What is the mode of _pathogenesis_ of **Coccidiomycosis?**
**Dimorphic organism** (spores and hyphae)
1201
**Coccidioidomycosis** What is the Clinical Features? how does the oral and skin lesions appear?
● Oral lesions **ulcerated granulomatous nodules** ● Skin lesions: **papules**(slightly raised), **abscesses**, **verrucous**(patchy), **plaques**, **granulomatous nodules**
1202
**Coccidioidomycosis** **symptoms?** What is the Clinical Features? how does the oral and skin lesions appear?
● Most cases are **asymptomatic** ~60% ● **Flulike** ● *Fatigue, cough, chest pain, myalgia, headache* ● May see a **hypersensitivity reaction** (_valley fever)_ ‐ When you are over responding; immune system is over reacting ● **Chronic**‐_mimics tuberculosis_ ● **Disseminated**‐ \<1% of cases
1205
How is **Cryptococcus** diagnosed?
● Biopsy ● Culture ● Serology Note: Histopathologically they appear as Granulomatous inflammation (epithelioid histiocytes trying to confide the infection) ● Yeast are surrounded by a clear halo (capsule)
1206
How is Coccidioidomycosis treated?
● **Mild symptoms**‐ no treatment usually ● **Amphotericin B** (‐ Immunosuppressed ‐ Severe pulmonary infection ‐ Disseminated disease ‐ Pregnant patients ‐ Life‐threatening situation ) ● **Itraconazole** or **fluconazole** (fewer side effects and complications)
1207
Cryptococcus How common is it? What causes it?
●Uncommon ● Cryptococcus neoformans ● Incidence increased due to AIDS epidemic in 1990s ● Pulmonary infection ● Meningitis
1208
Cryptococcus is seen in --------------
pigeon excrement (poo)
1209
Cryptococcus can cause what kind of infections?
● Pulmonary infection ● Meningitis ( after it spreads from the lungs to the brain. )
1210
What is this infectious disease?
Mucormycosis‐ arrow refers to **ESCHAR**‐ always look for this and extreme-Black and necrotic ulcer ( we can see massive tissues destruction
1211
What is this infectious disease?
Mucormycosis‐ CT Sinus opacificatio ● First thing to do is to find out more about this lesion, how did this patient get this lesion?
1212
Mucormycosis‐ Histopathology has a sepcial shape?
● Non‐septate hyphae with **90degrees branching** ● You see necrosis of tissue in the area because this attacks the blood vessels
1213
What are the Clinical Features of **Cryptococcus**?
**Lung infection often asymptomatic** ● Flulike illness ● Dissemination *‐ Meninges ‐ Skin ‐ Bone ‐ Prostate ‐ Oral‐papillary/granular erythematous plaques*
1215
How is **Cryptococcus** treated?
● Mild case: ***Fluconazole or Itraconazole*** ● Cryptococcal meningitis: ***amphotericin B + other antifungals***
1216
**Mucormycosis** is caused by what?
* **Infections** caused by **molds** belonging to the order **Mucorales** * _Grow in natural state on_ **decaying organic materials** (saprobic‐ recycling) * **Spores** may be _liberated into air and inhaled by humans_
1217
Mucormycosis can affect people with what underlying conditions?
‐ Insulin dependent diabetics ‐ Bone marrow transplant recipients ‐ AIDS ‐ Patients receiving systemic corticosteroids ‐ Neutropenic patients (no white blood cells)
1218
Which infectious disease has fruting body in its histopathology?
**Aspergillosis** Histopathology includes: ●Branching septate hyphae ● Acute angle branching **● “Fruiting body**
1219
What are the Clinical Features of Mucormycosis?
● Rhinocerebral form ● Nasal obstruction ● Bloody nasal discharge ● Facial pain ● Facial paralysis ● Facial swelling/cellulitis ● Visual disturbances ● Into cranial vault‐blindness, lethargy, seizures ● Oral swelling/ulceration of the maxillary alveolar process/palate as a result of sinus involvement ● Black and necrotic ulcer (eschar) ● Massive tissue destruction
1220
what is this infectious disease?
***Aspergillosis*** arrow points toward a violaceous‐ purple colour
1224
How is **Mucormycosis** diagnosed?
● Histopathology ● Culture
1225
How is **Mucormycosis** treated?
● Surgical debridement (massive tissue destruction) ● High doses of lipid formation of amphotericin B ● Control underlying disease (main one) ● Prosthetic obturation of palatal defects
1226
What is **Aspergillosis** *and* what causes it?
* Saprobic (in an environment rich of oxygen) * it caused by Aspergillus flavus and Aspergillus fumigatus
1227
Where is **Aspergillosis** typically seen? how it is spread?
● Seen in **hospitals** and **construction sights** ●caused by _Aspergillus flavus_ and _Aspergillus fumigatus_ **● Spores** *are* **inhaled**
1228
What is this infectious disease?
**Necrotizing Gingivitis (NG)** o No periodontitis features o SIMILAR APPEARANCE to *_gonorrhea_* ▪ Distinguishing characteristic of NG **– Fetid Odor**
1229
What is this infectious disease?
**Necrotizing Periodontitis (NP)** o Bone loss of the periodontium seen
1230
Aspergillosis‐ Clinical Features Two types noninvasive and invasive
● **Noninvasive** ‐ Allergic fungal sinusitis ‐ Aspergilloma (fungus ball, mycetoma [‐oma: like a tumour made of aspergillus]) ● **Invasive** ‐ Localized (possibly after tissue damage in oral cavity) ‐ Disseminated ‐immunocompromised
1232
How is Aspergillosis diagnosed?
● Histopathology ● Culture
1234
How is Aspergillosis treated?
● Aspergilloma‐**debridement** ● Allergic fungal sinusitis‐**debridement and corticosteroid drugs** ● Localized invasive‐**debridement & voriconazole and amphotericin B** ● Disseminated invasive‐**consider poor prognosis even with treatment**
1235
What are Oral Manifestations of Bacterial Infections?
Caries (streptococcus mutans) ‐ Gingivitis/Periodontitis ‐ Necrotizing Periodontal Diseases ‐ Noma (Cancrum Oris) Impetigo ‐ Erysipelas ‐ Streptococcal Tonsillitis and Pharyngitis Scarlet Fever ‐ Diphtheria ‐ Syphilis ‐ Gonorrhea ‐ Tuberculosis Leprosy Actinomycosis ‐ Cat Scratch Disease ‐ Bacillary Angioma
1236
What is **Necrotizing Periodontal Diseases?**
Bacterial infection which presents with a spectrum of lesions ‐ Vary depending upon the localization of lesion and predisposing factors
1237
Necrotizing Periodontal Diseases include 4 types,what are they? What do they mean?
‐ Includes: **o Necrotizing gingivitis (NG):**rapidly destructive, non-communicable microbial disease of the gingiva **o Necrotizing periodontitis (NP)**:apidly progressing disease process that results in the destruction of the periodontium o **Necrotizing stomatitis (NS):**When the bacterial infection extends further to OTHER parts of the mouth o **NOMA** (extension to skin of face) ▪ Extreme disfigurement due to bacterial infection extending onto the skin of the face
1238
Necrotizing Periodontal Diseases name has changed how?
‐ The term "**acute**" has not been included since 1999 (ANUG=old name) o As the infections are ALWAYS acute ‐ The term "**ulcerative**" removed in 2017 World Workshop proposed classification "Necrotizing Periodontal Disease (NPD)" is term proposed in 2017 World Workshop for NG, NP and NS o There is ALWAYS ulceration as a result of necrosis
1239
what are the Clinical Features of Necrotizing Periodontal Diseases?
‐ **Ulceration with necrosis of interdental papillae** o Results in a **"punched out" crater‐like appearance of the papilla** **‐ Gray pseudomembrane** o Dead tissue **‐ EXTREMELY Painful** **‐ Fetid odor** _‐ Spontaneous hemorrhage Fever, lymphadenopathy, malaise_
1240
Which population affected by Necrotizing Periodontal Diseases?
**Young and middle‐aged adults** Prevalence \<0.1%
1243
What are the risk factors of Necrotizing Periodontal Diseases?
Many related factors (Multifactorial etiology): o Psychological stress o Immunosuppression o Smoking o Local trauma o Poor nutritional status o Poor oral hygiene o Inadequate sleep
1244
Which infectious diseases was known by Trench mouth?
**Necrotizing Periodontal Diseases** o During WW1, soldiers that were fighting in the trenches were under extreme stress o they commonly developed necrotizing periodontal diseases
1245
What are the Constant bacterial species found in Necrotizing Periodontal Diseases? Will we be able to use microbiological testing to form a diagnosis?
**o Treponema spp.** **o Selenomonas spp.** **o Fusobacterium spp.** **o Prevotella intermedia** o \*Also always present in healthy gingiva ▪ so, No, Microbiological testing is NOT used to form a diagnosis
1246
What is the Treatment of Necrotizing Periodontal Diseases?
**o Removal of bacteria (scaling)** **o Chlorhexidine rinse** **o Antibiotics (fever or signs of systemic illness)** ▪ Metronidazole ▪ Penicillin **o Oral hygiene instruction** **o Supportive therapy** ▪ Rest ▪ Fluids ▪ Soft nutritious diet **o Predisposing (Immunosuppressive)factors** ▪ Smoking ▪ HIV?
1247
NOMA is also called as ------------
**cancrum oris**
1248
What is NOMA? Where it is seen?
‐ **Rapidly progressive opportunistic infection caused by many bacteria** o More commonly seen in other parts of the world o Seen in the US in immunocompromised patients ▪ HIV ‐ WHO estimates the global yearly incidence = 140,000
1249
Which bacteria involved in **NOMA**?
**‐ Polymicrobial etiology** ‐ Normal flora become pathogenic during immunocompromised states ***‐ Key bacteria:*** o **Fusobacterium necrophorum** **o Prevotella intermedium** ‐ Other common bacteria: **o Actinomyces pyogenes** o Bacillus cereus o Bacteroides fragilis o Fusobacterium nucleatum o Prevotella melaninogenica
1250
What are the Predisposing Factors of NOMA?
‐ Previous necrotizing periodontal disease Poverty ‐ Malnutrition or dehydration ‐ Poor oral hygiene ‐ Poor sanitation ‐ Unsafe drinking water ‐ Proximity to unkempt livestock ‐ Recent illness Malignancy ‐ Immunodeficiency disorder, including AIDS
1251
What is this infectious disease?
**NOMA** This is an aid patient Figure 2: Extension of infection onto the face ‐ Figure 3: Lost bone and gingiva ‐ Figure 4 & 5 Bone destruction
1252
What is this infectious disease?
**NOMA** This is an aid patient Figure 2: Extension of infection onto the face ‐ Figure 3: Lost bone and gingiva ‐ Figure 4 & 5 Bone destruction
1253
Which bacteria involved in **NOMA**?
**‐ Polymicrobial etiology** ‐ Normal flora become pathogenic during immunocompromised states ***‐ Key bacteria:*** o **Fusobacterium necrophorum** **o Prevotella intermedium** ‐ Other common bacteria: **o Actinomyces pyogenes** o Bacillus cereus o Bacteroides fragilis o Fusobacterium nucleatum o Prevotella melaninogenica
1254
What is this infectious disease?
NOMA Development of NOMA from day 1 to day 15
1255
NOMA can affect who?
Children Adults with debilitating disease
1256
What is this infectious disease?
**Impetigo** ‐ “Cornflakes glued to Surface" Appearance o Little papules that can form little vesicles around the mouth o Vesicles burst open and dry up around the skin of the mouth ‐ Bilateral
1257
What is this infectious disease?
NOMA Development of NOMA from day 1 to day 15
1258
What are the clinical features of NOMA?
Gingiva (NG) ► Adjacent tissue (necrotizing stomatitis) + Non‐ contiguous tissue (trauma) ► Blue black discoloration of skin ‐ Spreads through muscle, bone (osteomyelitis) **‐ Other features:** _o Fetid odor_ ▪ Due to tissue necrosis _o Pain o Fever o Malaise_ o Tachycardia o Increased respiratory rate o Anemia o Leukocytosis o Regional lymphadenopat
1259
What is this infectious disease?
**Impetigo** ‐ “Cornflakes glued to Surface" Appearance o Little papules that can form little vesicles around the mouth o Vesicles burst open and dry up around the skin of the mouth ‐ Bilateral
1260
What is this infectious disease?
**Erysipelas** Superficial skin infection in immunosuppressed adults ‐ Group A beta‐hemolytic streptococci ‐ Painful ‐ Bright‐red, well‐circumscribed, swollen, indurated (firm) ‐ Warm to touch ‐ Systemic manifestations: o High fever o Swollen lymph nodes Diagnosis: Cultures not useful ‐ Treatment: **o Penicillin ‐ Complications without treatment**
1261
What are the Predisposing Factors of NOMA?
‐ Previous necrotizing periodontal disease Poverty ‐ Malnutrition or dehydration ‐ Poor oral hygiene ‐ Poor sanitation ‐ Unsafe drinking water ‐ Proximity to unkempt livestock ‐ Recent illness Malignancy ‐ Immunodeficiency disorder, including AIDS
1262
What is the treatment of Noma?
o **Antibiotics** ▪ Penicillin ▪ Metronidazole **o Local wound care** _▪ Conservative debridement_ to avoid iatrogenic tissue damage **o Consider nutrition, hydration and electrolyte imbalances** **o May cause significant morbidity**
1263
What is this infectious disease?
**Erysipelas** Superficial skin infection in immunosuppressed adults ‐ Group A beta‐hemolytic streptococci ‐ Painful ‐ Bright‐red, well‐circumscribed, swollen, indurated (firm) ‐ Warm to touch ‐ Systemic manifestations: o High fever o Swollen lymph nodes Diagnosis: Cultures not useful ‐ Treatment: **o Penicillin ‐ Complications without treatment**
1264
What is this infectious disease?
_Primary Syphilis_ **Chancre** at site of inoculation (3 – 90 days later) ‐ Papule ► Ulceration ‐ Most chancres occur in genital area (4% oral
1265
What is this infectious disease?
**Primary Syphilis** _Chancre_ at site of inoculation (3 – 90 days later) ‐ Papule ► Ulceration ‐ Most chancres occur in genital area (4% oral
1266
What are the clinical features of NOMA?
Gingiva (NG) ► Adjacent tissue (necrotizing stomatitis) + Non‐ contiguous tissue (trauma) ► Blue black discoloration of skin ‐ Spreads through muscle, bone (osteomyelitis) **‐ Other features:** _o Fetid odor_ ▪ Due to tissue necrosis _o Pain o Fever o Malaise_ o Tachycardia o Increased respiratory rate o Anemia o Leukocytosis o Regional lymphadenopat
1267
What is this infectious disease?
Secondary Syphilis ‐ Disseminated lesions are discovered 4 ‐ 10 weeks after initial infection ‐ Resolve in 3‐12 weeks **‐ Diffuse maculopapular (flat, raised) rash** o May involve oral cavity ‐ **Mucous patches** **o Most common on tongue and lip** _‐ Condylomata lata_ o **Resembles viral papillomas** ‐ Systemic symptoms
1268
What is this infectious disease?
Secondary Syphilis ( Rash) here we see **muscus patches** (right) and **Condylomata lata** (left) ‐ Disseminated lesions are discovered 4 ‐ 10 weeks after initial infection ‐ Resolve in 3‐12 weeks ‐ Diffuse maculopapular (flat, raised) rash **o May involve oral cavity ‐ Mucous patches** **o Most common on tongue and lip** **‐ Condylomata lata** **o Resembles viral papillomas** ‐ Systemic symptoms
1269
What is this infectious disease?
**Tertiary Syphilis** **Gumma** ‐ **Latent** period for **1 ‐ 30 years** **‐ 30% of patients develop tertiary syphilis** ‐ Serious complications develop: * Vascular system * Central nervous system * Ocular lesions What is "Gumma"? * o Granulomatous inflammation with tissue destruction * o Common on palate and tongue * o Causes a hole in the palate
1270
What causes Impetigo?
‐ Caused by: o Staphylococcus aureus o Streptococcal pyogenes _Damaged skin allows infection to enter_ **Usually affects kids**
1271
What is this infectious disease?
**Primary Syphilis** _Chancre_ at site of inoculation (3 – 90 days later) ‐ Papule ► Ulceration ‐ Most chancres occur in genital area (4% oral
1272
What is this infectious disease?
**Congenital Syphilis** ‐ Hutchinson Incisors (left image) ‐ Mulberry molars (right image) - not part of the triad
1273
**Syphilis** Histopathology stage 1 and 2
Not specific ‐ Stage 1 and 2 similar o Ulceration o Hyperplasia (Stage 2) o Exocytosis of neutrophils into epithelium Intense Iymphoplasmacytic inflammatory infiltrate in superficial stroma and around deeper vascular channels (blood vessels)
1274
Syphilis Histopathology Stage 3
Stage 3 o Granulomatous inflammation o Ulceration may be present ‐ Special stain "**Warthin Starry"**, highlights _**corkscrew spirochetes** ‐_ **Immunohistochemical stain**
1275
How is Syphilis diagnosed?
**o Biopsy with histopathology** **o Dark field examination of a smear of active lesion** o Serologic screening lab tests * ▪ Venereal Disease Research Lab (VDRL), RPR (non‐ specific and not highly sensitive) * ▪ Fluorescent Treponemal Antibody Absorption (FTA‐ ABS), TPHA, TPPA, MHA‐TP (specific and sensitive)
1276
What is this infectious disease?
**Tertiary Syphilis** **Gumma** ‐ **Latent** period for **1 ‐ 30 years** **‐ 30% of patients develop tertiary syphilis** ‐ Serious complications develop: * Vascular system * Central nervous system * Ocular lesions What is "Gumma"? * o Granulomatous inflammation with tissue destruction * o Common on palate and tongue * o Causes a hole in the palate
1277
What is this infectious disease?
**Secondary Syphilis** Mucous Patch
1278
What is this infectious disease?
Secondary Syphilis ( Rash) here we see **muscus patches** (right) and **Condylomata lata** (left) ‐ Disseminated lesions are discovered 4 ‐ 10 weeks after initial infection ‐ Resolve in 3‐12 weeks ‐ Diffuse maculopapular (flat, raised) rash **o May involve oral cavity ‐ Mucous patches** **o Most common on tongue and lip** **‐ Condylomata lata** **o Resembles viral papillomas** ‐ Systemic symptoms
1279
Syphilis Histopathology Stage 3
Stage 3 o Granulomatous inflammation o Ulceration may be present ‐ Special stain "**Warthin Starry"**, highlights _**corkscrew spirochetes** ‐_ **Immunohistochemical stain**
1280
How is Syphilis diagnosed?
**o Biopsy with histopathology** **o Dark field examination of a smear of active lesion** o Serologic screening lab tests * ▪ Venereal Disease Research Lab (VDRL), RPR (non‐ specific and not highly sensitive) * ▪ Fluorescent Treponemal Antibody Absorption (FTA‐ ABS), TPHA, TPPA, MHA‐TP (specific and sensitive)
1281
What is this **infectious disease**?
**Gonorrhea** looks like necrotizing gingivitis (NG) but fetor oris not present
1282
**Syphilis** Histopathology stage 1 and 2
Not specific ‐ Stage 1 and 2 similar o Ulceration o Hyperplasia (Stage 2) o Exocytosis of neutrophils into epithelium Intense Iymphoplasmacytic inflammatory infiltrate in superficial stroma and around deeper vascular channels (blood vessels)
1283
What is this infectious disease?
**Secondary Syphilis** Mucous Patch
1284
What is this infectious disease?
**Congenital Syphilis** ‐ Hutchinson Incisors (left image) ‐ Mulberry molars (right image) - not part of the triad
1285
What is this infectious disease?
Secondary Syphilis ‐ Disseminated lesions are discovered 4 ‐ 10 weeks after initial infection ‐ Resolve in 3‐12 weeks **‐ Diffuse maculopapular (flat, raised) rash** o May involve oral cavity ‐ **Mucous patches** **o Most common on tongue and lip** _‐ Condylomata lata_ o **Resembles viral papillomas** ‐ Systemic symptoms
1286
What is this **infectious disease**?
**Gonorrhea** looks like necrotizing gingivitis (NG) but fetor oris not present
1287
What is this infectious disease?
_Primary Syphilis_ **Chancre** at site of inoculation (3 – 90 days later) ‐ Papule ► Ulceration ‐ Most chancres occur in genital area (4% oral
1288
What is **Impetigo** Differential Diagnosis
**o Recurrent Herpes Labialis** ▪ Resemblance to initial impetigo stages when still unilateral **o Perioral Dermatitis** ▪ Triggered by cosmetics and other substances on the skin **o Exfoliative Cheilitis (chapped lips)**
1289
How is Impetigo diagnosed and treated?
Diagnosis: o Presumptive from clinical features _‐ Treatment:_ **o Topical mupirocin** **o Systemic antibiotics**
1290
What is this infectious disease?
‐ Tuberculosis
1291
What is this infectious disease?
‐ Tuberculosis
1292
What is the treatment of Noma?
o **Antibiotics** ▪ Penicillin ▪ Metronidazole **o Local wound care** _▪ Conservative debridement_ to avoid iatrogenic tissue damage **o Consider nutrition, hydration and electrolyte imbalances** **o May cause significant morbidity**
1293
What is differential diagnosis for _Erysipelas_?
**o Systemic Lupus Erythematosus (SLE)** ▪ Due to sparing of nasolabial folds ▪ Butterfly rash in SLE resembles erysipelas **o Cellulitis (dental infection induced):** ▪ Tooth infection burrowing through the tissues rather than forming an abscess **o Actinomycosis**
1294
What is Syphilis? What causes it/
* Chronic infection * caused by *_spirochete_* **Treponema pallidum**
1295
What are the three stages of Syphillis?
Three stages 1. o Primary (**chancre**) 2. o Secondary (**rash**) 3. o Tertiary (**gumma**)
1296
What is this infectious disease?
TB Ulceration (tongue ulceration most common)
1297
What is this infectious disease?
**Miliary TB** compared to miliary seeds
1298
What is this infectious disease?
‐ Tuberculosis
1299
What is this infectious disease?
‐ Tuberculosis
1300
How is Impetigo diagnosed and treated?
Diagnosis: o Presumptive from clinical features _‐ Treatment:_ **o Topical mupirocin** **o Systemic antibiotics**
1301
What are the three stages of Syphillis?
Three stages 1. o Primary (**chancre**) 2. o Secondary (**rash**) 3. o Tertiary (**gumma**)
1302
What is this infectious disease?
**Miliary TB** compared to miliary seeds
1303
What is this infectious disease?
TB Ulceration (tongue ulceration most common)
1304
What is Differential Diagnosis for Primary Syphilis (Chancre)? 3
1. **SCC** 2. **Fungal Ulcer** 3. **Trumatic Ulcer**
1305
What is Syphilis? What causes it/
* Chronic infection * caused by *_spirochete_* **Treponema pallidum**
1306
What is Differential Diagnosis for Primary Syphilis (Chancre)? 3
1. **SCC** 2. **Fungal Ulcer** 3. **Trumatic Ulcer**
1307
What is differential diagnosis for _Erysipelas_?
**o Systemic Lupus Erythematosus (SLE)** ▪ Due to sparing of nasolabial folds ▪ Butterfly rash in SLE resembles erysipelas **o Cellulitis (dental infection induced):** ▪ Tooth infection burrowing through the tissues rather than forming an abscess **o Actinomycosis**
1308
Differential Diagnosis for teritiary syphillis "Gumma"
Differential Diagnosis: 1. ▪ T‐cell Lymphoma 2. ▪ Cocaine abuse 3. ▪ Granulomatosis 4. ▪ Polyangiitis 5. ▪ Mucor
1309
**Congenital Syphilis** is associated with what Triad?
‐ Pathognomonic features in **Hutchinson triad**: **o 1. Hutchinson teeth** **o 2. Ocular interstitial keratitis** **o 3. Eighth nerve deafness** ‐ Other Features: o High arched palate o Saddle nose o Frontal bossing **Clinical changes secondary to fetal infection**
1310
What is **Impetigo** Differential Diagnosis
**o Recurrent Herpes Labialis** ▪ Resemblance to initial impetigo stages when still unilateral **o Perioral Dermatitis** ▪ Triggered by cosmetics and other substances on the skin **o Exfoliative Cheilitis (chapped lips)**
1311
**Congenital Syphilis** is associated with what Triad?
‐ Pathognomonic features in **Hutchinson triad**: **o 1. Hutchinson teeth** **o 2. Ocular interstitial keratitis** **o 3. Eighth nerve deafness** ‐ Other Features: o High arched palate o Saddle nose o Frontal bossing **Clinical changes secondary to fetal infection**
1312
Differential Diagnosis for teritiary syphillis "Gumma"
Differential Diagnosis: 1. ▪ T‐cell Lymphoma 2. ▪ Cocaine abuse 3. ▪ Granulomatosis 4. ▪ Polyangiitis 5. ▪ Mucor
1313
What causes Impetigo?
‐ Caused by: o Staphylococcus aureus o Streptococcal pyogenes _Damaged skin allows infection to enter_ **Usually affects kids**
1314
How is **Syphilis** Treated?
_o Single dose of parenteral long_‐ acting **benzathine penicillin G** (primary, secondary, early latent) o **Intramuscular penicillin** weekly for three weeks (late latent and tertiary
1315
NOMA can affect who?
Children Adults with debilitating disease
1316
What is **Gonorrhea**? What causes it?
‐ a Sexually transmitted (F\>M) caused by **‐ Neisseria gonorrhoeae**
1317
How **Gonorrhea** affects the body? what complications can arrise?
‐ Genital area usually‐**purulent discharge** ‐ **Systemic bacteremia** (myalgia, arthralgia, polyarthritis, dermatitis) ‐ **Pelvic inflammatory disease** in women (affects pregnancies) ‐ **Gonococcal ophthalmia neonatorum** (infection of infant's eyes)
1318
What are the Clinical Features of **Gonorrhea?**
‐ Oral lesions ‐ **similar to aphthous** o Very rare _‐ Tonsils edematous and erythematous_ ‐ May **simulate necrotizing gingivitis (NG)** but _fetor oris not present_
1320
How is **Gonorrhea** diagnosed?
**‐ Gram stain** **‐ Culture of** _endocervical swab_ ‐ **Nucleic acid amplification tests** (NAATs)‐_detect DNA, RNA_
1321
How is **Gonorrhea** treated?
Many cases of resistance with antibiotics §Cephalosporins *Adults with gonorrhea are treated with antibiotics. Due to emerging strains of drug-resistant Neisseria gonorrhoeae, the Centers for Disease Control and Prevention recommends that uncomplicated gonorrhea be treated with the antibiotic ceftriaxone* — given as an injection — with oral azithromycin (Zithromax)
1322
**Gonorrhea** can have coinfection with what other infectious bacteria?
**Chlamydia trachomatis**
1323
**Chlamydia trachomatis** can trigger which autoimmune disease
**Reactive arthritis (reiter)** _o Can’t see, Can’t Pee, Can’t Climb a Tree_ ▪ _Causes_: **● Conjunctivitis ● Urethritis ● Arthritis** Remember: **Chlamydia trachomatis** coininfect with **Neisseria gonorrhoeae**
1324
What is **Tuberculosis**? What causes it? How does it spread?
- _Chronic granulomatous infectious disease_ - Caused by **Mycobacterium tuberculosis** §Direct person-to-person spread through **airborne droplets**
1325
**Primary TB**
_affects previously unexposed, lungs - They breathe in the organisms that someone is coughing out_ 1st: C_hronic inflammatory reaction_ ► Next, **a fibrocalcific nodule** (_Ghon focus)_ forms at initial site of infection
1326
What are the chance active disease if you get infected with Primary TB
Only **5%-10%** infections lead to active disease i
1327
**“Secondary TB” reactivation**
* Leads to **disseminated TB** (miliary TB) * True, active TB
1328
How is **Syphilis** Treated?
_o Single dose of parenteral long_‐ acting **benzathine penicillin G** (primary, secondary, early latent) o **Intramuscular penicillin** weekly for three weeks (late latent and tertiary
1329
What are the Clinical Features of **Gonorrhea?**
‐ Oral lesions ‐ **similar to aphthous** o Very rare _‐ Tonsils edematous and erythematous_ ‐ May **simulate necrotizing gingivitis (NG)** but _fetor oris not present_
1330
What are the causes of **secondary** **Tuberculosis**?
* Immunosuppressive medications * Diabetes * Old age * Crowded living conditions * AIDS
1331
Tuberculosis Clinical Features **Extrapulmonary TB**
* Lymphatics * Skin * Skeletal system * CNS * Kidney * GI tract * **Oral cavity (uncommon)**
1332
Tuberculosis Clinical Features **Primary TB**
Usually asymptomatic
1333
Tuberculosis Clinical Features **SecondaryTB**
o Typically see lung lesions (productive cough) o _Fever, malaise, anorexia, night sweats_
1334
**Tuberculosis** CLINICAL FEATURES OF ORAL LESIONS
§Ulceration (tongue ulceration most common) §Mucosal granularity §Diffuse inflammation §Non-healing extraction socket
1335
**“Secondary TB” reactivation**
* Leads to **disseminated TB** (miliary TB) * True, active TB
1336
What are the chance active disease if you get infected with Primary TB
Only **5%-10%** infections lead to active disease i
1337
Tuberculosis Clinical Features **Primary TB**
Usually asymptomatic
1338
Tuberculosis Clinical Features **SecondaryTB**
o Typically see lung lesions (productive cough) o _Fever, malaise, anorexia, night sweats_
1339
**Tuberculosis** CLINICAL FEATURES OF ORAL LESIONS
§Ulceration (tongue ulceration most common) §Mucosal granularity §Diffuse inflammation §Non-healing extraction socket
1340
Tuberculosis Clinical Features **Extrapulmonary TB**
* Lymphatics * Skin * Skeletal system * CNS * Kidney * GI tract * **Oral cavity (uncommon)**
1341
What are the causes of **secondary** **Tuberculosis**?
* Immunosuppressive medications * Diabetes * Old age * Crowded living conditions * AIDS
1342
**Primary TB**
_affects previously unexposed, lungs - They breathe in the organisms that someone is coughing out_ 1st: C_hronic inflammatory reaction_ ► Next, **a fibrocalcific nodule** (_Ghon focus)_ forms at initial site of infection
1343
What is **Tuberculosis**? What causes it? How does it spread?
- _Chronic granulomatous infectious disease_ - Caused by **Mycobacterium tuberculosis** §Direct person-to-person spread through **airborne droplets**
1344
**Gonorrhea** can trigger which autoimmune disease
**Reactive arthritis (reiter)** _o Can’t see, Can’t Pee, Can’t Climb a Tree_ ▪ _Causes_: **● Conjunctivitis ● Urethritis ● Arthritis**
1345
**Gonorrhea** can have coinfection with what other infectious bacteria?
**Chlamydia trachomatis**
1346
How is **Gonorrhea** treated?
Many cases of resistance with antibiotics §Cephalosporins *Adults with gonorrhea are treated with antibiotics. Due to emerging strains of drug-resistant Neisseria gonorrhoeae, the Centers for Disease Control and Prevention recommends that uncomplicated gonorrhea be treated with the antibiotic ceftriaxone* — given as an injection — with oral azithromycin (Zithromax)
1347
How is **Gonorrhea** diagnosed?
**‐ Gram stain** **‐ Culture of** _endocervical swab_ ‐ **Nucleic acid amplification tests** (NAATs)‐_detect DNA, RNA_
1348
How **Gonorrhea** affects the body? what complications can arrise?
‐ Genital area usually‐**purulent discharge** ‐ **Systemic bacteremia** (myalgia, arthralgia, polyarthritis, dermatitis) ‐ **Pelvic inflammatory disease** in women (affects pregnancies) ‐ **Gonococcal ophthalmia neonatorum** (infection of infant's eyes)
1349
What is **Gonorrhea**? What causes it?
‐ a Sexually transmitted (F\>M) caused by **‐ Neisseria gonorrhoeae**
1350
What is the histological features of Tuberculosis
**Granulomas** * o Epithelioid histiocytes * o Multinucleated giant cells * ▪ \* Langhans giant cells * ● Nuclei along the periphery * o Central caseous necrosis
1352
What is this infectious disease?
Primary Oral TB Oral Primary TB clinical manifestation is very rare TB is directly in the **_epithelial cells._** Person coughs ⇒ organism enters broken skin somewhere in the oral mucosa ⇒directly causing TB in the mouth -this person would NOT have any issues in their lungs **-**primary TB = infection went directly into their mucosa from another person
1353
What is this infectious disease?
**Primary Oral TB** tongue ulceration
1354
TB staining
Special stain Epithelioid o Ziehl‐Neelson or AFB o Consider scarcity of organisms **o MAY NOT VISUALIZE ORGANISMS WITH STAIN** **_▪ NEGATIVE RESULT DOES NOT RULE OUT TB INFECTION_**
1355
What is the Differential Diagnosis of **_non‐healing ulcer?_**
**o TB o Deep fungal infections o Traumatic ulcer o SCC o Major Aphthous ulcer**
1356
How is Tuberculosis diagnosed ?
o TB‐Test **§Delayed type hypersensitivity (Type 4)** §Checks if developed an immune response to TB §**PPD (purified protein derivative)** *(what they inject under the skin)* §**T cells** are attracted by immune system to the skin site §**Lymphokines** induce _hard raised area with clear margins_ §Need to check 48-72 hours later (measure area)
1360
What is this infectious disease?
**Scrofula**
1361
How is Tuberculosis treated?
**§Multiagent therapy for active infection to prevent mutation and resistance** §8 week course §Pyrazinamide §Isoniazid §Rifampin §Ethambutol **§Followed by 16 week course** §Isoniazid §Rifampin **‐ Chemoprophylaxis** ‐ For positive PPD but no active infection **‐ BCG vaccine** o Not used in US due to controversy regarding effectiveness
1363
What is Non‐Tuberculosis Mycobacterial Infection
Scrofula
1364
What causes scrofula?
**Mycobacterium bovis** **Infected milk** leads to **scrofula** **RARE** today _as milk is pasteurized_
1365
What are the clinical features of scrofula?
o Enlargement of oropharyngeal lymphoid tissues and cervical nodes o Significant caseous necrosis may occur and cause sinus tracts to skin
1366
What is this infectious disease?
Leprosy
1367
What is this infectious disease?
**LEPROSY** _Clinical features_ * *§Bone destruction** ( hole in the palate) * *§Nodular** will become **nectortic** and then **destruction** will follow
1368
**LEPROSY** How is it diagnosed?
**Diagnosis:** o Clinical presentation o Acid fast stain Histopahology No well‐formed granulomas o Lepromatous leprosy diffuse presentation
1370
**Leprosy** is also known as ---------
**Hansen disease**
1371
What causes **Leprosy**?
**Mycobacterium leprae**
1372
What are the two types of **Leprosy**?
**1. Tuberculoid leprosy** ▪ High immune reaction ▪ Oral manifestations are **RARE** **2. Lepromatous leprosy** ▪ Reduced cell‐mediated response
1373
Leporsy prevelance & in which regions it is usually found?
**EXTREMELY RARE** o 80% of cases occur in: ▪ Brazil ▪ India ▪ Indonesia ▪ Madagascar ▪ Myanmar ▪ Nepal ▪ Nigeria
1374
What is this infectious disease?
**Actinomycoses** it's an external Sinus
1375
What are the clinical features of Leporsy ?
Clinical features: **o Leonine facies** ▪ Appearance of a lion **● Loss of eyebrows** ● **Scarring (fibrosis)** from infection prevents hair growth o **\* Oral Manifestations seen in areas of mouth with lower** temperatures: ▪ Hard/soft palate ▪ Maxillary gingiva ▪ Tongue ## Footnote **Oral‐enlarging papules ► ulcer ► necrosis**
1379
what is the histology of Actinomycoses and stain used?
‐ Colony of actinomycotic organisms surrounded by neutrophils ‐ Grocott‐Gomori methenamine silver stain (GMS) In this histo slide, we see: \* Sulfur Granule o 1. Collection of actinomycoses israelii organisms o 2. MANY neutrophils surround the periphery o BOTH are requirements for a TRUE diagnosis of actinomycoses
1380
‐ Actinomycoses o Diagnosis
* **Culture** * o \< 50% of cases are positive * ▪ Due to various types of bacteria in the culture * **Presumptive diagnosis from biopsy** **in this histology: GMS stain was used** o Correlates with top H&E histopathology o Filamentous branches are the actinomycotic organisms
1381
How is Leprosy treated?
§Rifampicin, clofazimine, dapsone
1382
What is **Actinomycoses**?
‐ Infection caused by filamentous branching gram positive anaerobic bacteria ‐ Normal component of oral flora
1383
What causes **Actinomycoses**?
‐ Associated Bacteria: **o Actinomyces israelii o Actinomyces viscosus** ‐ Normal component of oral flora -gram positive anaerobic bacteria
1384
What are the clinical features of **Actinomycoses**?
can be Acute or chronic ‐ **Hard indurated swelling** o Result of injury / trauma ▪ Tooth extraction o Erythematous o Formation of **external sinus** ▪ Drains into the skin **‐ "Sulfur granules"** o May be present in suppuration o Indurated area of fibrosis
1385
Which locations **Actinomycoses** affect?
**‐ 55% in cervicofacial area** ‐ Hard indurated swelling o Result of injury / trauma/tooth extraction o Erythematous **‐ Area overlying angle of mandible** o Formation of external sinus ▪ Drains into the skin ‐ Other locations include: **o Abdomen o Pelvis o Lungs**
1387
How does Actinomycoses infection spread?
‐ **Enters tissue through an area of prior trauma** o Soft tissue injury o Periodontal pocket o Non‐vital tooth o Extraction socket o Infected tonsil ‐ **Direct extension through soft tissue to the surface**
1388
How is Cat‐Scratch Disease diagnosed ?
‐ **Clinical features:** o Presence of a cat ▪ Presumptive diagnosis can be made ‐ Serology (antibody detection) ‐ Histopathology (biopsy) (Stellate suppurative necrosis surrounded by a band of histiocytes and neutrophils) and the use of Immunohistochemistry and Warthin‐Starry silver stain to identify the organism Left o Histiocytes on the periphery o Stellate necrosis in the center ‐ Middle Immunohistochemistry o Antibodies allow for visualization of Bartonella henselae (red little dots) ‐ Right : Warthin‐Starry silver stain o Silver stain allows for visualization of Bartonella henselae (black areas)
1389
What is "Sulfur granules" Where it is found? In which infection? color?
colonies of bacteria (o Actinomyces israelii o Actinomyces viscosus) found in suppuration (pus) which means Suppuration (pus) is dead tissue, bacteria, dead white blood cells, and other products of tissue breakdown.. Sulfur granules found in Actinomycoses yellow in color
1390
What is this infectious disease?
Cat‐Scratch Disease
1391
Differential Diagnosis to Actinomycoses
o Erysipelas
1392
What are other presentations of Actinomycoses?
‐ Tongue ‐ Tonsillar crypts ‐ Salivary gland involvement ‐ Osteomyelitis ‐ Periapical inflammatory lesions
1395
How is Actinomycoses treated?
* \* **Prolonged high dose antibiotics for _cervicofacial actinomycosis_** * Due to the fibrosis that occurs * Early cases 5‐6 weeks * Deep‐seated infections up to 12 months * **Abscess drainage** * **Sinus tract excision** * **Penicillin**
1396
What is Cat‐Scratch Disease?
‐ Infectious disease which is seen in _lymph nodes_
1397
What causes Cat‐Scratch Disease ?
‐ Causative organism: o Bartonella henselae ‐ Previous contact with a cat (scratch or saliva)
1398
What are the age of the patients that usually get Cat‐Scratch Disease ?
‐ 80% in patients **_younger than 21_**
1399
----- is the most COMMON cause of regional lymphadenopathy in children | (22,000 cases annually)
Cat Scratch Disease
1400
What are the Differential Diagnoses: of Cat Scratch Disease ?
**‐ o Swellings in the lymph node** **o Unilateral swellings of the neck**
1401
What are the clinical features of Cat Scratch Disease ?
‐ Initial **scratch** ‐ **Papule** at _inoculation site_ (3‐14 days later) **‐ Papule ► erythematous ► vesicular ►crusted** ‐ **Healing** (1‐3 weeks) ‐ **Lymph node enlargement** with _fever and malaise_
1403
How is Cat‐Scratch Disease treated?
o **Self‐limiting (resolves within 4 months)** o Local heat o Analgesics o Mechanical removal of suppuration (aspiration) o May use antibiotics for severe cases ▪ Azithromycin
1404
What are the 3 types of Benign Fibro‐Osseous Lesions?
1. Fibrous Dysplasia 2. Cemento-osseous Oysplasia 3. Ossifying Fibroma
1405
Fibrous Dysplasia Cemento‐osseous Dysplasia are both type of
Type of Bone Dysplasia
1406
Ossifying Fibroma is a ---------
Benign neoplasm
1407
What are the types of Fibrous Dysplasia?
** Monostotic  Polystotic  McCune‐Albright Syndrome  Craniofacial  Mazabraud Syndrome**
1408
What is the most common type of Fibrous dysplasia?
Monostotic
1409
What is Monostotic Fibrous dysplasia?
a Fibrous dysplasia involving **one bone** o Ex: when only the mandible involved or only the maxillae (Most common type (70%)
1410
What is Polystotic Fibrous dysplasia?
a Fibrous dysplasia involving **more than one bone**
1411
What is the Second most common type of Fibrous dysplasia?
Polystotic Fibrous dysplasia
1412
What are the two types of Polystotic Fibrous dysplasia?
** Jaffe Type  McCune‐Albright Syndrome** (involving multiple bones with endocrine abnormalities)
1413
What is **Craniofacial Fibrous dysplasia?**
-a Fibrous dysplasia limited to **Skull and Facial Bones.**..
1414
What is Mazabraud Syndrome
-Fibrous dysplasia with **intramuscular myxomas**
1415
What happens in Fibrous Dysplasia?
an aberrations in osteoblastic/osteoclastic function ► normal bone turn over affected ► normal bone structure will be affected!
1416
What is fibrous dysplasia ?
Developmental lesion characterized by substitution of normal bone by poorly organized woven bone and fibrous tissue.
1417
What is the etiology of fibrous dysplasia?
**_GNAS1 gene mutation_** in fibrous dysplasia is a potential diagnostic adjuvant, as it is not found in normal bone tissue (etiolog
1418
What gender and age affected by Fibrous Dysplasia?
* No gender predilection * commonly seen in pediatric patients and young adults
1419
What are the clinical charcterstics of **fibrous dysplasia?**
* Clinically, it causes **bone expansio**n and **asymmetry** * most typical presentation of monostotic fibrous dysplasia is **a slow growing painless enlargement in the affected area.** * so the patient may notice a slight asymmetry that won’t bother them intially, but over time~months to years ►they’ll notice that this area is slowly and steadily growing more and more ( slow and painless)
1420
What are the most common sites of **Fibrous Dysplasia**?
• Most common sites of FD include the **ribs, femur, tibia, maxillae and mandible**  the **Maxillae** is affected more than the mandible
1421
What is this disease? Patient CC: painless mass that is growing on one side
**FD** Radiographically: you have altered trabecular pattern Clinically: Painless mass slowly growing over time is is typical presntation of Fibrous Dysplasia
1422
What is this disease?
**Fibrous Dysplasia** * ill‐defined radiolucent/radiopaque/mixed radiolucent‐radiopaque entities that blend with normal bone. * The left side is affected. Left body of the mandible and the ramus. * The cortical outlines have been expanded near the inferior border of the mandible.
1423
What is the **radiographic features** of Fibrous dysplasia (FD)
**• Maxillae affected more than mandible** • **Ill‐defined borders, blends in with the surrounding bone (not necessary to be corticated)** • **Variable density and orientation of the trabecular pattern** (radiolucent, radiopaque or a combination) * *• Ground‐glass appearance** (common) * *• Peau d'orange (surface of an orange)** (common) * *• Cotton wool appearance** (common) * *• Fingerprint pattern** ( uncommon pattern) • Typically the lesionss in the **maxillae are more homogenous and radiopaque,** whereas they may appear **more heterogenous and mixed in the mandible.** *\*typically you’ll see the ground glass appearnce and Peau d’orange on the maxilla as they are homogenous the cotton wool appearance more commonly found in the mandible since it is heterogenous.*
1425
What is this trabecular pattern of the FD?
**Fingerprint pattern** The arrow indicating the inter‐radicular area of this molar. You can see the trabecular bone has been altered into a fingerprint pattern. This is a case of localized fibrous dysplasia. Very uncommon.
1426
What is this trabecular pattern of the FD?
**Cotton wool appearance** Irregullary shaped and outlined radiopacities blending in with adjacent bone
1427
What is this trabecular pattern of the FD?
**Peau d'orange** surface of an orange – the bone shows a “pitting” appearance.
1428
What is this trabecular pattern of the FD?
**Ground Glass Pattern** it appears granular in nature. (Grainy)
1429
What is this Radigraphical finding?
**Fibrous dysplasia on the right mandible.** Note the superior displacement of the IAN Canal This is not odontogenic ( as they are usually above the canal) **Anything below th canal ►think of it as originiating from the bone itself**
1430
What is this Radigraphical finding?
Fibrous Dysplasia in the left of the maxillae. Always compare both side left and right * We see granular/glass appearance of the bone ( blue arrow) and compare it to the contralateral maxillae. The trabucular pattern has changed signficantly. * Also compare the maxillary sinus space. The left maxillary sinus appears radiopaque. * That is because the maxillae has been enlarged to the point where it is pushing the floor of the maxillary sinus superiorly and reducing the total volume of the sinus. * The purple arrows indcate the displaced floor of the maxillary sinus.
1431
what is this radiographic finding?
**FD** Note the normal left maxillary sinus and the obliterated space of the right maxillary sinus ( blue arrows). **A ground glass appearing entity** (humogenous radiopaque lesion) has obliterated the space secondary to expansion of the right maxilla. These findings are consistent and quiet common in **advanced cases Firbous dysplasia**
1434
How does **Fibrous dysplasia** affects the Surrounding structures?
* **May have no effect** ( especially if it hasn’t reached the cortical outlines) * **Expansion and thinning of cortical walls** * **Displacement of teeth** ( espically in advanced cases) * One of the few entities that cause **SUPERIOR displacement** of the mandibular canal
1440
What is this radiologic finding
Periapical COD green arrow Simple bone cysts may develop in regions of COD ( periapical or florid type) So look for areas void of trabucular bone and has scalopping of the lesion. Red arrow
1441
What is this radiologic finding
mature Periapical COD Coronal cross section of the posterior mandible in the region of the premolar ~ mixed radiolucent/radiopaque entity, the center is radiopaque and the periphery is radiolucent.
1442
What is this radiologic finding
mature Periapical COD You can have these lesions in endentulous areas as well. So this is is an endeulous area, but if there was a tooth here, this would be in the periapicel region or near it with mixed radiolucent/radiopaque entity  the differential diagonsis of this area could include Periapical COD.
1443
What is this radiologic finding?
mature Periapical COD You see a nice radiolucent rim and radiopaque center  so mixed radiolucent/radiopaque entity in the periapical region of tooth #31  most likely diagonsis would be Periapical COD.
1444
What is this radiologic finding
A very mature Periapical COD ( purple arrow) Well‐defined radiopacity in the periapical region. Sometimes you may or may not be able to differentiate a very thin radiolucent line as in this case. you might include ddx of other lesions which might present with radiopacity in the preapical region There are certain tests you can do clinically to differentiate too. or do clinical tests
1445
What is this radiologic finding
Periapical COD Sagital cross section of the anterior Mandible. Mixed radiolucent/radiopaque area (green circle)
1446
What is this radiologic finding
Early & mature Periapical COD **Preapical radiographs of the anterior mandible of the same patient at different times.** Note the differnece in density between the two radiolecency: Note the internal structure of the radiopacity is quite radiolucent ( purple arrow) The Preapical radiographs of the same region taken at a later time shows a more radiopaque internal structure (pink arrow). This reflect the maturing of the COD lesion. The lesion with Pink arrow can be described as well‐defined mixed radiolucent/radiopaque entity. ( because you have radioleucent part and radipaque part)
1447
What is this radiologic finding
Early Periapical COD well defined radiolucency surrounding the apeces of these two central When looking at such cases, it is also imporant to: 1. look at the crowns to look for carious lesions. If there is no restorations or no evidence of caries, it is likely that these lesions are arising from the bone and not secondary to pulpal involvement. 2. It also important to look at the PDL and Lamina dura, typically in COD lesions they should be visisulized and intact ( but because this is a 2D image and this area may superimpose on this region and obsecure the visulizing of the lamina dura and the PDL) **what’s the difference between COD and Inflammatory lesion?** COD won’t have effect on the PDL space itself, because it orginates from the bone! Vitality testing can help us differntiate between inflmmatory lesion and something that happeing inside of the bone.
1450
What is this radiologic finding
Florid COD Axial section of the mandible. * Notice **mixed radiolucent/radiopaque entity on the patient right side**. And **on the left the area is more radiopaque centrally and has a thin radioluceny around it.** * The arrows indicate **well‐defined radiopacities immedietly surrounded by radiolucent rims.** * Note that **the radiolucent rim on the left side is thin when compared to the lesion on the right. This likely means that the lesion on the left is more mature** ( more time has passed for the entity to produce more woven bone).
1451
What is this radiologic finding
Florid COD ## Footnote Two periapical radiographs of the left and right posterior mandible of the same patient.  In this case, note **the areas of radiolucency and radiopacity are rather ill defined but widepsread** to affect most of the teeth. Most of the teeth noted here are restored.  So even if the radiographs suggest a cemento‐osseous process, it is important to keep an eye for these teeth in term of vitality and prevent a periapical infections which would otherwise **secondarily infect** the altered bone of COD.
1452
What is this radiologic finding
Florid COD Multiple regions of COD. Notice the wide areas of scelortic/radiopaque areas on mandible and also on maxillae
1453
What is Differential Diagonsis for Firbous Dysplasia (FB) ?
**Generalized FD** * Metabolic bone diseases (hyperparathyroidism) (any disease that incrase trabacular bone density) * Paget's disease **Localized FD** * Osteomyelitis * Osteosarcoma
1454
What is the management of Fibrous Displysia?
* Consultation with an OMFR is advisable. Monitoring of the area is also advised. * Typically treatment is not needed unless there are clinical symptoms or patients present with cosmetic concerns if clinical symptoms are severe * Implants and surgical intervention should be avoided when possible as these areas are void of blood supply
1455
**Cemento‐ossifying Fibroma** _Types_ and _Location_
There are two types: **classic and juvenile form** -**juvenile** seen in younger patients and tend to be more aggressive in nature ( both radiographically and clinically aggressive features) • Young adults and females affected mostly • Bony expansion and displacement of teeth can be seen in many cases ( not suprising since it acts like a neoplasm) • _More commonly_ seen i**n the mandible and in posterior regions**
1456
what is this radiographic finding?
**Cemento‐ossifying Fibroma** ## Footnote Note **the internal granular appearance of the trabucular bone** ( black arrows) The purple arrows shows the wall of the expanded buccal/facial and lingual cortical plates caused by the neoplastic entity. This was a confirmed cased of **ossifying fibroma\*** mainly because of two things: **1. siginficant cortical expansion on buccal and lignual side 2. altered trabacular pattern.** **ddx of fibrous dysplasia b**ut you should look for a radiolucent rim if you can and if not, they maybe considered under the same differential diagosnsis. Note that may help you in differentiating : **** The **maxilla** is affected more in **_Fibrous dysplasia_** **** The **mandible** is affected more in **_Ossifying fibroma_**
1457
What is this radiographic finding?
Cemento‐ossifying Fibroma Axial section of the mandible * The granular radiopacity immediately surrounded by a radiolucent rim ( purple arrow) * **Also note the extent of the expansion of the buccal and lingual cortical plates, a feature which is common of ossifying fibroma.** * This is more clear radiographically where we see a radiolucent rim surrouding a mixed radiolucent/radiopaque center and there is a siginficant expansion of the buccal and lingual plates. ► **very common in ossifying fibroma**
1458
**Cemento‐ossifying Fibroma** is classifed as ----------- and why?
Classified as **a benign neoplasm** ## Footnote Because _it acts like a benign neoplasm_. Once you examine it under microscope, you’ll see features _resmeble_ **benign fibrous osseous lesions.** You’ll see: ** Fibrous connective tissues  cementum like material  even altered bone material (woven bone)**
1459
Cemento‐ossifying Fibroma Radiographic features
* **Well‐defined, round or oval lesion** * **Periphery of the lesion is corticated** and may **exhibit a radiolucent periphery** (sometimes referred to as **a soft tissue capsule**) * Internally, the lesion is typically **granular or radiopaque** but may show variations (**mixed radiolucent/radiopaque**) * _Strong tendency to_ **displace teeth and cortical outlines**
1460
what is this radiographic finding?
Cropped Panaromic showing **a case of** Cemento‐ossifying Fibroma * Appreciate the **radiolucent rim** indicated by the black arrows. * Also note the internal structure of the trabucular bone and compare it to adjacent unaffected areas. It is **more granular and radopaque** compared to adjacent areas. * Another important feature to appreciate is **the displacement of the anterior teeth** **(diverging roots)** * These features are usually seen **in lesions with benign neoplastic characterstics.**
1461
What is CEMENTO‐OSSEOUS DYSPLASlA (COD)?
Dysplastic lesions that are confined to the jaws.
1462
What is this disease?
**Cleido-Cranial Dysplasia** **Treatment:** For children, facial reconstructive surgery on the bones of the face to reshape the forehead or cheekbones. Spinal fusion procedures to support the spinal column. Lower leg surgery to correct knock knees (knees that bend inward toward the center of the body)
1463
What is this disease?
Gardner's Syndrome Synonym: Familial Multiple Polyposis. Remember this:  GarDENse Bone Island.  GARDEN-FOREST:  F- Familial adenomatous polyposis.  O- Osteomas.  RE- Retinal epithelial hypertropy.  ST- Supernumerary teeth. Treatment: Because people with Gardner’s syndrome have a higher risk of developing colon cancer, treatment is usually aimed at preventing this. Medications such as an NSAID (sulindac) or a COX2 inhibitor (celecoxib) may be used to help limit the growth of colon polyps. Treatment also involves close monitoring of the polyps with lower GI tract endoscopy to make sure they do not become malignant (cancerous). Once 20 or more polyps and/or multiple higher risk polyps are found, removal of the colon is recommended in order to prevent colon cancer. If dental abnormalities are present, treatment may be recommended to correct problems.
1464
What is this disease?
**Osteopetrosis** **Osteomyelitis** is a complication in patients with **osteopetrosis** as can be seen in pan image! Treatment: Bone marrow transplant (to stimulate osteoclast formation).
1465
What is this disease?
Paget's disease stages ## Footnote Early Linear lines: The bone is being resorbed in a very distinct pattern \> linear patterns of trabeculation Middle -MAY see the "cotton wool" appearance (but this is more pronounced in the third stage) -the trabecular pattern may or may not be slightly affected Late - There is MORE bone deposition -the "cotton wool" appearance is very very clear in this stage! Also-hypercementosis and spacing of teeth.
1466
What is this disease?
Paget's Disease Also Known As: **Osteitis Deformans.** **Skeletal disorder involving osteoclasts** **_Treatment:_** Osteoporosis drugs (bisphosphonates) are the most common treatment for Paget's disease of bone
1467
What is this disease?
Cherubism **Treatment**: Usually not needed as the cyst-like lesions fill in with granular bone during adolescence- conservative surgical procedures may follow for cosmetic reasons.
1468
What is this radiographic finding??
Idiopathic Osteosclerosis AKA: Dense Bone Island  Not associated with any dysplastic, neoplastic, inflammatory or systemic disorder.  **Common incidental finding.**  Slow growing, typically stops growing by the time of skeletal maturity.  Peak prevalence in the third decade of life. ** No treatment required; monitoring is suggested.**
1469
Idiopathic Osteosclerosis vs -----------
**PCOD** ## Footnote **Differentiating factor:** Radiolucent zone surrounding the radiopacities of COD lesions. No such radiolucent areas for idiopathic osteosclerosis.  Important: The root of the tooth #28 appears to be resorbed but is likely not. Look at the root of #29. These teeth are still undergoing development in a young patient.  Left is showing dense bone island.  Right is showing Periapical COD- this is intermediate stage, not fully mature. You should see a radiolucent rim.  Another more obvious radiographic feature: you see radiolucent areas surrounding in both images, the common feature is: because PCOD and dense bone island do not affect the PDL spaces – you should be able to see the PDL spaces.  Sometimes it’s not the case. Look for the PDL, look for radiolucent area surrounding possible central radiopacity, idiopathic osteosclerosis can cause resorption; PCOD hasn’t been associated with root resorption.
1470
Idiopathic Osteosclerosis vs -----------
**_Hypercementosis_** ## Footnote  **Differentiating Factor:** A well-defined radiolucent border that is continuous with the PDL of the tooth, in the case of hypercementosis. This means that whatever is happening is within the confines of the tooth-bearing region. In this case, the cementum.  Hypercementosis- Cementum is overraeacting, so there’s enlargement of cementum.  If cementum is larger, it should be pushing the PDL out (black arrow). So the PDL is enlarged meaning you should be able to see a radiolucent rim around the area. And the radiolucent rim should be continuous with the PDL of the remaining root structure.
1471
Idiopathic Osteosclerosis vs -----------
**Cementoblastoma** ## Footnote ** Differentiating Factor:** A well-defined radiolucent border that is continuous with the PDL of the tooth, similarly seen in the previous case of hypercementosis. (sometimes it is difficult to differentiate hypercementosis and cementoblastoma, in this case, the beige arrow indicates the resorbed root surface, which normally occurs in benign neoplastic cases, such as cementoblastoma.  Cementoblastoma is more of a heterogenous radiopacity- meaning you may see gaps, like radiolucent voids, in between the areas.  See radiolucent rim.  But more common feature include root resorption because it’s a neoplastic condition. It should act like a neoplasms in which it’s destroying some of the root structure.
1472
Idiopathic Osteosclerosis vs -----------
 For condensing osteitis, look for heavily restored or carious teeth. Condensing osteitis typically surrounds the initial rarefying osteitis lesion. The teeth in these cases are non-vital as they represent a condition that is secondary to pulpal necrosis.  Open necrosis, eventual PDL space widening and then once the infection reaches the bone, you have bone loss.  Now you have an overreaction or inflammatory reaction surrounding the initial inflammation.
1473
What is this disease?
**Focal Osteoporotic Marrow Defect** A large marrow defect that may mimic a cystic/neoplastic radiolucency in the jaw. common incidental finding a variation of normal anatomy within trabecular bone.
1474
What is this disease?
Simple Bone Cyst Also known as  1.) Solitary Bone Cyst.  2.) Traumatic Bone Cyst.  3.) Idiopathic Bone Cyst.  4.) Hemorhhagic Bone Cyst. Remember radiographic feature tend to Scalop between teeth  Treatment includes surgical curettage- spontaneous healing has been reported.
1475
What are these two disease?
Sometimes, simple bone cysts should be differentiated from odontogenic keratocysts (OKCs)
1476
 CGCG should be differentiated from -------------
brown tumor.
1477
What is this disease?
central giant cell granuloma CGCG
1478
What is this disease?
Aneurysmal Bone Cyst
1479
COD can be divided in to:
1) Periapical COD 2) Focal COD ( not covered) 3) Florid COD Two types of COD instead of three Perapical COD & Florid COD
1480
Cemento‐Osseous Dysplasia is Similar to Fibrous dysplasia where
cancellous bone is replaced with fibrous tissues & cementum‐like material.
1481
CEMENTO‐OSSEOUS DYSPLASlA COD is it symptomatic? is there bony expansion?
* Typically **asymptomatic**, almost always captured as incidental finding * Generally, no bony expansion but is not uncommon in the florid type
1482
Cemento‐osseous dysplasia COD Gender? Age? Ethincity?
• Commonly seen in middle‐aged patients female predilection * more commonly seen in the **Black population** * also frequently seen in **Asian population**
1483
What are the Radiographic features of **Cemento‐osseous dysplasia COD**?
* Usually **well‐defined borders** in perapical type (may be ill‐defined in florid type). * **Early lesions show radiolucent features** in the periapical area of the teeth _As times progresses, the lesion matures =_t**he entity may become radiopaque.** ‐ as a result there is also **an intermideate mixed phase** **• The lesions mature from the center outwards** ‐ as a result, **_a radiolucent rim surrounding the lesion is commonly noted._** • Typically **the periodontal ligament space** of affected areas are intact but my not be _visualized_ because _they are superimposed over the region._
1492
What is Florid COD?
Widespread form of periapical COD ## Footnote There is some discreppency on how to consider a lesion a florid COD Some people say the radiopacity entities have to be on at least 2 qudarants And other says if you have the radiopacity entities crossing the midline of the bone. If it is in 3 quadrant ► then you can defentitly say it’s the Florid type, but even if you see itone bone and it has crossed the midline ► you may consider it Florid COD
1493
What is differential diagnosis for Periapical COD? PCOD
Florid COD ## Footnote  **Rarefying osteitis** (radiolucent lesions) ( it would differentiate in the more early stages of the COD ( the radiolucent stage)  **Condensing osteitis** (considered in the differential when the lesion is more mature and more radiopaque lesions)  **Cementoblastoma** ( benign neoplasm of the cementum so we should be able to see certain features that reflect benign neoplastic lesions )  **Dense bone islands** ( a common differential when considering COD)
1497
What is differential diagnosis for florid COD? FCOD
* **Paget's disease** ( t generalized areas) * **Osteomyelitis** ( localized area because we have mixed radioluecent/radiopaque areas)
1498
What is the **Management of COD**?
* Typically, no treatment is required **unless these regions show clinical/radiographic** * Ex if patient complain of some pain of that area –\> we want to follow up that region
1505
Treatment of Cemento‐ossifying Fibroma
* Surgical excision ( need to send to **biopsy** in order to confirm the diagosnsis of that) * Wider resection with bone maybe necessary in soma larger or more clincally aggressive cases.
1506
What is this clinical presentation?
**Leukemia** o Dilantin hyperplasia (drug induced gingival hyperplasia) – fibrotic looking o Has to an addition of thromocytopenia
1507
What is this clinical presentation?
**Leukomia** ## Footnote o Leukemic infiltrate – have areas of erthema o Looks like gingival hyperplasia, but in gingivail hyperplasia you don’t have the same amount of redness. Leukemia has significant hyprotophy of gingivial papilla and areas that look like they have ptechia in them. With gingival hyperplasia drug induced they are very fibrotic
1508
What is this clinical presentation?
**Leukemia** ## Footnote ▪ Oral findings include **gingival hyperplasia, spontaneous bleeding of gingiva, mucosal ulcerations, candidiasis, recurrent herpetic lesions, etc**. ▪ Leukemic infiltrate in soft tissues (ex. gingiva) produces a diffuse, boggy, nontender swelling that may or may not ulcerate **o most common with myelo‐monocytic types** ▪ May create a tumor‐like mass in soft tissue o granulocytic sarcoma/chloroma (clinically looks green) ▪ mass infiltrate into soft tissue If you see children and notice they have prominent areas of redness or red/purple and know the child has decent oral hygiene, leukemia should be in your differential. Need to be aware of that cause patients need to be treated in a fairly quick fashion.
1509
What is this clinical presentation?
1510
What is this clinical presentation?
**Leukemia** Acute and chronic myelo‐monocytic leukemia are the most likely types of leukemia to exhibit oral manifestations o Generalized gingival hypertrophy May create a tumor‐like mass in soft tissue o granulocytic sarcoma/chloroma (clinically looks green) ▪ mass infiltrate into soft tissue
1512
What is this clinical presentation?
**Agranulocytosis** Oral findings: * include multiple ragged ulcerations of the oral mucosa * can mimic recurrent aphthous (but often no erythematous halo) * Gingiva is a common site due -can resemble NUG)
1513
What is this clinical presentation?
**Agranulocytosis** **Oral findings:** * include multiple ragged ulcerations of the oral mucosa * o can mimic recurrent aphthous depending on sites involved * (but often no erythematous halo) – more like neutropenic ulcer * **Gingiva is a common site** due to the minor trauma caused bymastication (can resemble NUG)
1515
What is this clinical presentation?
**Cyclic Neutropenia** **_o Teeth floating in air_**
1516
What is this clinical presentation?
**Cyclic Neutropenia** ▪ Gingiva is most severely affected with periodontal bone loss and tooth mobility
1517
What is this clinical presentation?
**Cyclic Neutropenia** ▪ Depending on surface involved, can mimic recurrent aphthous ulcerations o Usually do not see erythematous halo that is so typical of aphthous
1518
What is this clinical presentation?
**Cyclic Neutropenia** ## Footnote **▪ Oral ulcerations on any mucosal surface exposed to minor trauma (L,T, BM and oropharynx) last 5‐7 days** ▪ Depending on surface involved, **can mimic recurrent aphthous ulcerations** o Usually do not see erythematous halo that is so typical of aphthous ▪ **Gingiva is most severely affected with periodontal bone loss and tooth mobility**
1519
What is this clinical presentation?
**Cyclic Neutropenia** ## Footnote Oral ulcerations on any mucosal surface exposed to minor trauma & can mimic recurrent aphthous ulcerations without the erythematous halo that is so typical of aphthous ▪ Gingiva is most severely affected with periodontal bone loss and tooth mobility
1520
What is this clinical presentation?
**Hematoma** because of THROMBOCYTOPENIA or Trauma
1521
What is this clinical presentation?
Hematoma because of THROMBOCYTOPENIA orTrauma
1522
What is this clinical presentation?
o hematoma because of THROMBOCYTOPENIA orTrauma THROMBOCYTOPENIA:▪ Markedly decreased numbers of circulating blood platelets (severe cases \< 10,000/mm³) Etiology: Can be from: o Decreased production (malignancy, drugs) o Increased destruction (immunologic, drugs) o Sequestration in the spleen (splenomegaly) ▪ Clinically see spontaneous gingival bleeding, petechiae, ecchymosis and hematomas o Clinically see some type of bleeding ▪ Treatment is usually platelet transfusion
1523
What is this clinical presentation?
o hematoma because of THROMBOCYTOPENIA or Trauma
1525
What is this clinical presentation?
**Aplastic Anemia** ## Footnote ▪ Failure of the **hematopoietic precursor cells to produce adequate numbers of all types of blood components** ▪ Rare, but life threatening ▪ **_Associated with_** **environmental toxins (benzene), certain drugs (antibiotic chloramphenicol), or infection with certain viruses (non‐A, non‐B, non‐C, non‐G hepatitis)** ▪ **Fanconi’s anemia and dyskeratosis congenita patients** _have an increased risk of developing this_ **Oral signs:** are associated with the **thrombocytopenia** and include **spontaneous gingival hemorrhage, mucosal petechiae, purpura,** *and* **ecchymoses** ▪ **Nonspecific oral ulcerations** **(neutropenic ulceration)** may also be seen on any mucosal surface, but especially in areas of trauma (even minor trauma, ex. gingiva) **o Neutropenic = low neutrophils**
1526
What is this clinical presentation?
**Sickle Cell Anemia** Can see prominent trabeculae left, looks like steps on a ladder
1527
What is this radiographic presentation?
**Sickle Cell Anemia** Radiographic findings include: o decreased trabecular pattern in the mandible (due to increased extramedullary hematopoiesis) o laddering of inter‐radicular trabeculae o “hair‐on‐end” appearance of skull films (less prominent than with thalassemia) Can see spontaneous pulpal necrosis in the absence of trauma or caries
1529
What is this clinical presentation?
**Beta‐thalassemia** ▪ Two defective genes – **thalassemia major (Cooley’s anemia, Mediterranean fever)** o Disease detected when fetal hemoglobin ceases to be made (~3‐4 months old) o Extramedullary hematopoiesis cause hepatosplenomegaly, bone marrow hyperplasia, and lymphadenopathy o In jaws, painless enlargement of maxilla and mandible (“chipmunk” facies) o Skull films show “hair‐on‐end” appearance o Untreated, patient dies by about one year of age o Treatment is repeated blood transfusions or bone marrow transplant this pt was treated with
1530
What is this clinical presentation?
**Macrocytic (megaloblastic) Anemias:** **▪ Folic acid and B12 deficiencies** * _Glossitis_ * Denuded dorsal surface * Burning, stinging pain Seen in older patients and seen in patients with poor nutrition **_Etiology:_** alcoholism, malabsorption, medications (trimethoprim, oral contraceptives, anticonvulsants
1531
What is this clinical presentation?
Iron deficiency anemias Microcytic hypochromic ▪ **Atrophic glossitis** – tongue has been a little denuded of papilla ▪ **Angular cheilitis** – white and redness at angle of mouth/ commissure **▪ Plummer‐Vinson Syndrome**: type of iron deficiency anemia o Chronic iron def, dysphagia (esophageal webs), atrophic glossitis. * **Significantly increased risk of esophageal cancer (SCC)** * More commonly seen in European women * Have difficulty swallowing
1532
What is this clinical presentation?
**microcytic, hypochromic anemias (iron deficiency):** Pallor ▪ **Anemia**: reduction in O2 carrying capacity ▪ **Diagnosis**: RBC counts, Hg, HCT, red cell indices for dx of type of anemia ▪ Normal upper labial mucosa ▪ Pale lower labial mucosa
1533
What is this clinical presentation?
**Aplastic Anemia** * One of the main differences between and neutropenic ulcer and an empthis ulcer? Is the red halo, the mucosa surroundingneutropenic ulcer Is pale and not red. * The center of a neutropenic ulcer has granulation tissue with a little bit of white
1534
**Aplastic Anemia** **treatment**
``` supportive care initially, attempts to stimulate bone marrow (androgenic steroids), and bone marrow transplants for severe cases (prognosis is guarded at best) ```
1536
What is this clinical presentation?
Multiple Myeloma Elevated M spike in serum ‐ abnormal increase in immunoglobulin (**hyperglobulinemi**a), most commonly IgG ▪ Reversal of normal albumin/globulin ratio
1537
**Agranulocytosis** Symptoms Treatment
**Symptoms** * ▪ Initial symptoms include non‐specific symptoms of infection **malaise, sore throat, swelling, fever, chills, etc.** * Oral findings include multiple ragged ulcerations of the oral mucosa, o can mimic recurrent aphthous but no erythematous halo, Gingiva is a common site & can resemble NUG **Treatment** * Remove offending drug, numbers should replenish in 10‐14 days * Agranulocytosis secondary to cancer therapy ‐ meticulous oral hygiene, chlorhexidine rinse (non alcohol type) , etc.
1538
What is this clinical presentation?
Non‐Hodgkins Lymphoma (NHL) o Typically presents with painless lymphadenopathy (often unilateral) ▪ up to 40% are extranodal ▪ 5‐10% arise in Waldeyer’s ring ▪ _Inflamatory or reactive enlarged lymph nodes_ tend to be * *soft, tender, and movable** * *▪** _Lymph nodes associated with malignancy_ tend to be * *hard/firm, fixed, and non‐tender**
1539
What is this clinical presentation?
Non‐Hodgkins Lymphoma (NHL) o The most common of the lymphoproliferative diseases o Uncontrolled proliferation of B or T cell origin derived from a single cell (or clone) o Typically presents with painless lymphadenopathy (often unilateral) ▪ up to 40% are extranodal ▪ 5‐10% arise in Waldeyer’s ring
1540
What is this clinical presentation?
**Non‐Hodgkins Lymphoma (NHL)** ## Footnote o The most common of the lymphoproliferative diseases o Uncontrolled proliferation of B or T cell origin derived from a single cell (or clone) o Typically presents with painless lymphadenopathy (often unilateral) ▪ up to 40% are extranodal ▪ 5‐10% arise in Waldeyer’s ring
1541
What is this clinical presentation?
Adult acute myeloid leukemia (AML) is a type of cancer in which the bone marrow makes a large number of abnormal blood cells. We see in these images: o Hemorrhagic ulcer right vestibule o Ulcers are deep and can go down to bone o Ulcers resolved after treatment
1542
What is this clinical presentation?
leukomia o Multifocal bony destruction o Widened PDL with leukemic infiltrate ▪ Symmetric widening of PDL space in a patient that doesn’t have that normal vertical bone loss that you associate with periodontal disease. ▪ If see symmetrical bone loss in PDL space think malignancy, neoplastic **● Lymphomas, leukemias, osteocarcoma, chondro scaroma can do this**
1543
What is this clinical presentation?
leukomia Cause of infiltrate they has bone loss
1544
What is this clinical presentation?
**Leukemia** This is **Chloroma**, inflitrate gets so dense they look green. On buccal or lingual mucosa chloroma are more of a solitary mass, gingival it more diffuses
1546
What is this clinical presentation?
**Hodgkins lymphoma**
1547
What is this clinical presentation?
**Hodgkin Lymphoma** **o Begins in lymph nodes o 70‐75% cervical/supraclavicular o Painless but unresolving,** **o Night fevers/sweats**
1548
What is this clinical presentation?
**Hodgkin Lymphoma** ## Footnote **▪ Cell of origin is unknown** ▪ Often begins as a unifocal disease above diaphragm and then spreads to other sites ▪ Present with painless cervical lymphadenopathy in 60‐80% of cases ▪ **Bimodal ‐ late twenties and after 50 years old** ▪ In North America and Europe, **EBV positivity has been noted in over 50 percent of mixed cellularity cases and 10 to 50 percent of nodular sclerosis cases**
1549
What is this clinical presentation?
**T cell Lymphoma** _Less common than B cell lymphomas_ ▪ One variant associated with **palatal perforation** o Old name **midline lethal granuloma**
1550
What is this clinical presentation?
**Burkitt’s Lymphoma** Scattered throughout the lymphocytes are macrophages containing nuclear debris (tingible body macrophages) o Creates **a “starry sky”** appearance
1551
What is this clinical/radiographic presentation?
Burkitt’s Lymphoma * **North American type (sporadic)** * Typically older children (mean of 11 years) * Involves abdomen as a mass * uncommon in the jaws * No association with EBV * More localized disease * **HIV type** * Adults * 25% associated with EBV * GI, marrow and CNS **Teeth floating** as shown in the image
1552
What are the Lymphoma Classifications?\
* **Low grade B cell** (disseminated but slow growing) * Small lymphocytic, Mantle cell, Marginal zone * Follicular center (35‐40 % of all B cell lymphomas) * **Moderate** (aggressive) * Diffuse B‐cell, Peripheral T‐cell * **High Grade B cell** (disseminated and rapidly progressive) * Anaplastic large cell, lymphoblastic * Large cell (25‐30 % of all B cell lymphomas) * Burkitt’s * Immunoblastic (increasingly seen in AIDS) * As AIDS patients live longer we see this more * **T cell lymphoma** (less common than B cell, associated with **palatal perforation** [midline lethal granuloma]) (in differntial with deep fungal infections/candidiasis, TB, use of cocaine * Precursor T‐lymphoblastic, T cell chronic lymphocytic, * **Hodgkin’s** (bimodal ‐ late twenties and after 50 years old)
1553
What is this clinical presentation?
**Burkitt’s Lymphoma** **African type (endemic**) * More common * Peak incidence 3‐8 years of age * _Twice as common in males_ * **~95% associated with the Epstein‐Barr virus** * North american or non edemic type is not associated * with EBV * ~88% under 3 yrs of age have jaw lesions * Only 25% of those older than 15 do * Typically involves: * MD, MX, (often affects all 4 quadrants) * Mandible or maxilla * Abdomen * grow quickly
1555
What is this clinical presentation?
Multiple Myeloma **Pathological fracture**
1556
What is this clinical presentation?
Multiple myeloma
1557
What is this clinical presentation?
Multiple Myloma ## Footnote **Punched out translucency in crest**
1558
What is this clinical presentation?
**Multiple Myeloma** Monoclonal expansion of malignant plasma cell ▪ Most common in 40‐70 year old (mean 63 yo.) ▪ Present with bone pain (\> 70%) and pathologic fractures Punched out radilucency
1559
What is this histological presentation?
**Plasma Cell Disorders** Clock face nucleaus
1560
What is this clinical presentation?
**Plasma cell gingivitis** ▪ Allergen causes mass infiltrate into gingival ▪ Benign ▪ Diet log to identify allergen, allergy testing
1561
**Plasma cell gingivitis Treatment**
**▪ Diet log** to **identify allergen,** allergy testing ▪ Ideally **eliminate offending substance** ▪ **Can manage with topical steroids**
1562
What is this clinical presentation?
**Plasma cell gingivitis** ▪ Allergen causes mass infiltrate into gingival ▪ Benign
1563
What is this clinical finding?
**Multiple Myeloma** Deposition of amyloid in soft tissues o Can cause macroglossia if tongue is involved
1564
What is this radiographical presentation?
**Plasmacytoma** **▪ Unifocal, monoclonal neoplastic ▪ proliferation of plasma cells** **▪ 30% develop into MM over 10 yrs ▪ 50% disseminate w/in 2‐3 yrs ▪ Central Bone lesion o Unilocular radiolucency o Swelling or bone pain o Non‐tender soft tissue mass** **▪ 90% occur in Head and neck**
1565
What is this clinical presentation?
Multiple Myeloma
1566
o Differential diagnosis when you see this “floating in air teeth” in children
* **Cyclic** **neutropenia** * **aggressive periodontitist** * **pamiona fav** * **burkitts lymphoma** * **langerhan cell histocytosis** **o All these things can occur in children and lead bone destructions and look like teeth are floating**
1568
How is Multiple Myeloma treated? Prognosis?
* **Chemotherapy** with or without RT * **Bone marrow transplant,** interferon, antibodies made * against tumor cells, thalidomide, bisphosphonates, * corticosteroids, melphalan, etc. * Even with treatment, most patients do not survive more than * 18‐24 months * older patients – better prognosis * younger patients – more aggressive and worse prognosis * IV bisphosphonate therapy puts patients at increase risk for MRONJ
1569
What is this clinical presentation?
**microcytic, hypochromic anemias (iron deficiency):** Pallor ▪ **Anemia**: reduction in O2 carrying capacity ▪ **Diagnosis**: RBC counts, Hg, HCT, red cell indices for dx of type of anemia ▪ Normal upper labial mucosa ▪ Pale lower labial mucosa
1577
If a patient has a Burning Tongue What steps must we take
fungal (candidiasis) --\> mucosal smear/ Empirically can give antifungals (to figure out if it is candidiasis can do a smear or give antifungal) If not candidiasis order cbc ▪ Order CBC with diff ▪ Order blood levels on Fe, Folate, B12, zinc ▪ Rule out : diabetic neuropathy If not candidiasis and blood work didn’t show anything abnormal patient has **burning mouth syndrome** ▪ **TIBC tests** to see if theres too much or too little FE in the blood, measures the bloods capacity to bind fe with transferrin ▪ **B12 def can be from pernicious anemia** ( **Schilling test for Pernicious Anemia**) lack intrinsic factor to allow proper absorption, malnutrition or malabsorption from GI conditions can lead to this as well.
1578
What is **Pernicious anemia?** ## Footnote **What causes it?** **Which age and race does it most affect?**
**Pernicious – “highly injurious or deadly”** ▪ Lack of intrinsic factor protein in stomach decreases absorption of vitamin B12 **Etiology** is usually the body making antibodies against parietal cells which make intrinsic factor o Autoimmune disease effecting parietal cells leads to decreased intrinsic factor ▪ More common in **elderly** ▪ More common in patients of **Northern European and African decent** _This anemia can lead to death_
1580
**Hemophilia A & dental treatment**
▪ Partial thromboplastin time (PTT), prothrombin time (PT), bleeding time (BT) and platelet counts, as well as consultation with physician, should be done prior to any dental treatment ▪ (PT is like INR, Normal INR between 0.8 and 1.2) ▪ Clotting factor replacement therapy (synthetic) given as indicated ▪ Avoid aspirin
1583
What is this clinical presentation?
Beta‐thalassemia ▪ Two defective genes – thalassemia major (Cooley’s anemia, Mediterranean fever) Hyperplasia of maxilla, body is trying to make more rbc so bone marrow enlarges to support space of those red blood cells but rbc are abnormal so spleen keeps destroying them
1585
**Sickle Cell Anemia** Types and which is resistant to malaria?
* Sickle cell trait ‐ one allele is affected, only 40‐50% of hemoglobin will be abnormal, no significant clinical manifestations * **Sickle cell disease** ‐ both alleles affected, close to 100% of hemoglobin is abnormal**, significant clinical problems** ▪ **Abnormal gene** confers **resistance to malaria,** therefore**, sickle cell trait is seen most frequently in populations from areas endemic for malaria (Africa, the Mediterranean, and Asia)**
1586
What is Polycythemia
**▪ Increase in the number of circulating red blood cells**
1587
People with chronic Polycythemia are at increased risk of ------ or -------
* *of MI or CVA (cerebral vascular accident or stroke) **
1588
What are the types Polycythemia ?
**▪ Types** * **Primary polycythemia:** polycythemia vera * **Secondary polycythemia:** response to low O2 environment such as sleep apnea, living in high elevations, smoking * **Relative polycythemia** * Dehydration, diuretics, vomiting
1589
What is this clinical presentation?
**Secondary Polycythemia** Oral manifestation ▪ Oral mucosa appears deep red ▪ Glossitis ▪ Gingiva appears edematous and bleeds easily ▪ Consequent “crowding out” of WBCs and platelets may result in other manifestations
1593
What is **Aplastic Anemia?** What it is associated with? Who are at increased risk of developing this anemia?
▪ **Failure** of the **hematopoietic precursor cells to produce adequate numbers of all types of blood components** ▪ Rare, but life threatening ▪ **_Associated with_** **environmental toxins (benzene), certain drugs (antibiotic chloramphenicol), or infection with certain viruses (non‐A, non‐B, non‐C, non‐G hepatitis)** ▪ **Fanconi’s anemia and dyskeratosis congenita patients** _have an increased risk of developing this_
1595
What is this clinical presentation?
**o Hemophilia A** ▪ **A patient with only 25% of normal clotting factor VIII levels may function normally, but less than 5% will likely manifest as bruising and bleeding problems** ▪ Deep hemorrhage in joints is a major complication resulting in **arthritis, ankylosis and deformity** **▪ Oral findings include bleeding** (often uncontrolled) upon scaling and root planing, tooth extractions and any oral lacerations **▪ Pesudotumor of hemophilia** o Tissue hemorrhage can result in a submucosal tumor‐like mass **o Bone hemorrhage can result in intraosseous radiolucency**
1596
What is THROMBOCYTOPENIA? What causes it?
Markedly decreased numbers of circulating blood platelets (severe cases \< 10,000/mm³) Etiology: Can be from: o Decreased production (malignancy, drugs) o Increased destruction (immunologic, drugs) o Sequestration in the spleen (splenomegaly)
1597
What is the treatment of THROMBOCYTOPENIA?
▪ Treatment is usually **platelet transfusion**
1598
What is THROMBOCYTOPENIA? How it presents clinically?
▪ Clinically see spontaneous gingival bleeding, petechiae, ecchymosis and hematomas o Clinically see some type of bleeding
1600
What is Agranulocytosis? Etiology? pts at increase risk of what?
**Agranulocytosis** ## Footnote Decrease in the number of cells from the granular cell lineage (neutrophils, eosinophils, basophils, etc.) o Decreased production or increased destruction ▪ Some cases are idiopathic, most are drug induced ▪ Anticancer chemotherapeutics ‐ inhibit mitotic division and maturation of hematopoietic stem cells. ▪ In rare cases, agranulocytosis is a congenital syndrome. ▪ Increase risk of **infections**
1601
etiology of **leukemia**
* Probably caused by **a combination of environmental and genetic factors** * Some leukemias have specific genetic alterations (ex. **CML –** * **Philadelphia chromosome)** * t(9;22)(q34;q11) fusion gene BCR‐ABL1) * **Translocation of 9 and 22 and fusion gene BCRABL1** * **Environmental factors include**: * ionizing radiation * pesticides * benzene * viruses (ex. HTLV‐1)
1602
What is Leukemia?
**▪ Represents several types of malignancies derived from hematopoietic stem cells** **▪ ~ 2.5% of all cancers in US**e
1603
Types of **leukemia**
**Divided into acute and chronic, myeloid and lymphoid** o Acute myeloid, chronic myeloid, acute lymphoid, and chronic lymphoid **▪ Acute leukemia** o Typical course under 6 mos o Untreated, runs an aggressive course often causing death **▪ Chronic leukemia** o 2‐6 or more years o More indolent course, although, they too often result in death **▪ Leukemia, like lymphoma, can cause bone destruction and the radiographic appearance of “teeth floating in air” in children**
1604
AML in which age group is found and which leukemia has peak in 3rd to 5th decade?
``` **▪ Acute myeloid leukemia** o Adult (and children) ``` **▪ Chronic myeloid leukemia** o Peak 3rd ‐ 5th decade
1605
**which leukemia always in children?**
Acute lymphoblastic leukemia (ALL) Success in treatment of a previously fatal disease Children age 1‐10 years have higher success with treatments than teenager do (10‐20yrs) o And infants (under 1yr) do the worst Chemotherapy that are given for curing ALL actaully causes problems when they are older.
1606
What are the **Clinical signs and symptoms of** Leukemia
▪ related to crowding out of normal hematopoietic stem cells in the bone marrow o ↓ in normal WBC, RBC, and platelets ▪ See **fatigue, bleeding, bruising, fevers and infections, etc.**
1607
**which leukemia in eldery and most common?**
**Chronic lymphocytic leukemia** o Elderly o Most common type o Considered incurable at this time o unchecked proliferation of B‐cells o no good treatment
1608
What is the treatment of Leukemia?
* **Treatment** depends on specific type of leukemia, but includes multi‐agent chemotherapy (often an initial high dose induction and then a lower maintenance dose) * And for lymphoma * **Bone marrow transplant** has been used with limited success
1610
**Cyclic Neutropenia** _​length of the cycle_ _Symptoms_ _Diganosis_ _Treatment_
**▪ Usually a 21 day cycle** **o Dx –** when count falls below 500/ul for 4‐5 days every 21 days **▪ Patients experience recurrent fever, mallaise, anorexia, cervical lymphadenopathy, oral ulcerations, etc.** ▪ Treatment can be just supportive in mild cases, granulocyte colony‐stimulating factor for more severe cases
1612
What are the Clinical and radiological features of **Multple Myeloma MM**
▪ **Bones** most commonly involved include **ribs, vertebrae and skull** **o 70‐90% will have jaw involvement at some point** ▪ **Anemia, thrombocytopenia and neutropenia** due to crowding out of normal cells within bone marrow by proliferating malignant cells ▪ **50‐60% have Bence‐Jones proteins in urine** (light chains, usually kappa) **o Due increased plasma cells ⇒ plasma cells make antibodies ⇒ antibodies/proteins gets excreted** **Solitary plasmacytoma can be the first sign of multiple myeloma** ▪ Radiographically, see **punched out radiolucencies** (no sclerotic margin) often with an irregular outline
1620
What are the Stages of o Hodgkins lymphoma
▪ Stage I and II – localized disease curable with RT ▪ Stage III and IV – more widespread and treated with chemo and RT, worse prognosis ▪ Stage determined by sites involved o Above diaphragm – stage 1 and 2 o Above and Below diaphragm – stage 3 and 4 having it above diaphragm is bette than having it below so stage 1 and 2 are better than stage 3 and 4
1629
o Palatal perforations differerntial diagnosis
* Midline lethal granuloma (T cell Lymphoma) * deep fungal * malignancy * TB * tertiary syphilis gumma, * cocaine abuse (necrotizing sialometaplasia‐ soft * tissue)
1641
What is the prognosis of **Plasmacytoma** and how it is treated?
▪ Tx: **radiation**, better prognosis than MM ▪ Solitary better prognosis than disseminated MM
1642
What is Neoplasias?
* Immune cell tumors primarily involving bone marrow and peripheral blood are classified as leukemias * while those of lymph nodes are classified as lymphomas, * however there is often overlap of these entities
1645
What causes **Myelodysplastic Syndrome?**
**– environmental**
1646
What causes Megaloblastic Anemias ?
**o Folic Acid def o Vit B12 def (pernicious anemia)**
1647
What causes Iron Deficiency anemia?
* *menstruation, pregnancy, malabsorption diseases (eg. Celiac)**
1648
What causes **Aplastic Anemia ?**
**– environmental, things like bensin**
1649
What causes **Thalassemia & Sickle Cell anemia ?**
**Genetic**
1650
What causes **Anemias of Chronic Disease?**
**inflammatory conditions, malignancy – organ disease**
1651
What causes **Anemias of Chronic Renal Insufficiency****?**
**low levels of erythropoietin – organ disease**
1654
What is the treatment for Deficiency Anemias ## Footnote **B12 def?**
* 1mg IM injections weekly for 1‐2 months * Monitored for lifetime
1655
What is the treatment for Deficiency Anemias Folic Acid def?
o 1mg PO, 5mg in malabsorptive disease o Pregnant women given folic acid to decrease spina bifida o Can be given IM injections if have malabsorption
1656
What is the treatment for Deficiency Anemias Iron def?
▪ Ferrous sulfate 325 mg TID between meals o can cause Constipation ▪ add on fiber to diet, green leafy vegetables o IV doses for absorptive problems ▪ 125mg in 100ml saline infused over 1 hour
1657
What is **Thalassemia**?
▪ A group of disorders of hemoglobin synthesis characterized by decreased synthesis of either the alpha‐globin or beta‐globin chains of the hemoglobin molecule Patients get a microcytic, hypochromic anemia ▪ People with the abnormal gene have a resistance to malaria ▪ People who have the trait rather than the disease are more likely to live and not die from malaria and spread that gene to their children ▪ Severity depends on the specific genetic alteration and whether it is homozygous (severe) or heterozygous (no clinical sign to mild manifestations)
1659
What type of Alpha‐thalassemia is not compatible with life
When there are **Four defective genes – Hb Bart’s hydrops fetalis** o Lethal in utero or within a few hours of birth o Not compatible with life **▪ Estimated that 5% of world population carries a variant of Alpha‐thalassemia (over 100 genetic forms)** ▪ One defective gene – o no disease detected ▪ Two defective genes – **alpha‐thalassemia trait** o Mild degree of anemia (usually not clinically significant) ▪ Three defective genes – Hb (hemoglobin) H disease **o Hemolytic anemia and splenomegaly**
1660
Which ares alpha thalassemia is common?
Areas with a lot of malaria
1665
What is Sickle Cell Anemia? Type of inheritance What causes it?
▪ Genetic disorder of hemoglobin synthesis (one of the hemoglobinopathies) **▪ Autosomal recessive pattern** ▪ **Mutation in DNA of *thymine* for adenine causes alteration of codon resulting in the substitution of the amino acid valine for glutamic acid in the beta‐globin chain of hemoglobin** ▪ This transformed hemoglobin is prone to molecular aggregation and polymerization to form a rigid and curved shape (sickle shape)
1666
**What is Sickle cell crisis** treatment and how it diagnosed?
* ▪ Transcranial Doppler scan used to evaluate blood flow in brain ▪ **Hydroxyurea** may be used as a therapy o Induces Hb F formation (doesn’t sickle) o But can be carcinogenic and teratogenic
1667
**What is Sickle cell crisis** What trigger it? What are the symptoms? effect on dental tx? consequences?
* sickling of the RBCs becomes severe * precipitated by such things as **hypoxia, infection, hypothermia, or dehydration** * Symptoms include **pain (**which may be severe) due to ischemia and infarction of affected tissues ▪ Long bones, lungs and abdomen are common sites of occurrence for “crises” ▪ Episodes last from 3‐10 days, some patients have monthly crises, some may go a year or more between ▪ May need **pre‐medication prior to dental treatment** * **infections** are the most common cause of death in sickle cell patients (in the US) ▪ Patients also have impaired kidney function and CNS involvement (strokes in 5‐8%, often prior to age of 10)
1669
What is this ## Footnote **Hemophilia ?** **What are its types**
Bleeding disorders associated with a genetic deficiency of any one of the clotting factors **o Hemophilia A (classic type, most common type )** ▪ Factor VIII deficiency ▪ X‐linked recessive ▪ Abnormal PTT **o Hemophilia B (Christmas disease)** ▪ Factor IX deficiency, ▪ X‐linked recessive, Abnormal PTT **o Von Willebrand’s disease** ▪ Abnormal von Willebrand’s factor, abnormal platelets ▪ Autosomal dominant ▪ Abnormal BT, abnormal PTT
1674
What is **Cyclic Neutropenia?** ## Footnote **What causes it** **When do symptoms begin?** **What problems patients deal with?**
**Cyclic Neutropenia** ## Footnote ▪ A rare idiopathic disorder characterized by regular periodic reductions in the neutrophil population **_Etiology:_** Underlying cause is a defect in hematopoietic stem cells in the marrow _▪ Symptoms_ usually _begin in childhood_ ▪ Most symptoms when neutrophil count is at its lowest point (nadir), usually lasts 3‐6 days (even when neutrophil counts are at their highest, it’s often lower than normal) **▪ Patients have repeated problems with infections** Oral ulcerations on any mucosal surface exposed to minor trauma & can mimic recurrent aphthous ulcerations without the erythematous halo that is so typical of aphthous ▪ Gingiva is most severely affected with periodontal bone loss and tooth mobility
1675
What is this radiographical presentation?
**Mucositis** Thickening of the mucous of the sinus - normally we don’t see mucosa because it is very thin membrane 10 to 15 times thicker. Most common incidental findings that we can see on radiographs
1676
What is this radiographical presentation?
**Sinusitis** Sinus mucosa becomes inflamed and thickened from infection or allergen, which may lead to ciliary dysfunction, retention of sinus secretions and blockage of sinus drainage ● 10% of maxillary sinusitis are related to dental infections
1677
What is this radiographical presentation?
**Sinusitis** In this cone beam CT scan, we can see opacification of the sinus + sometimes we see gaseous bubbles. It is fluid that is forming inside the sinus.
1678
What is this radiographical presentation?
**Sinusitis** Sinusitis can be secondary to oral antral communication (communication between maxillary sinus and oral cavity) this can happen due to extraction
1679
What is this radiographical presentation?
``` Antral Pseudocyst (Retention Pseudocyst) ``` Localized, submucosal accumulation of fluid forming a sessile, domeshaped swelling along a sinus border ● Common incidental radiographic finding on panoramic ● Well-defined, non-corticated and dome shape radiopacity mostly along the floor of maxillary sinus
1680
What is this radiographical presentation?
``` Antral Pseudocyst (Retention Pseudocyst) ```
1681
What is this radiographical presentation?
``` Antral Pseudocyst (Retention Pseudocyst) ```
1682
What is this radiographical presentation?
**Antrolith** ## Footnote Deposition of mineral salts (calcium phosphate/carbonate/magnesium) around an exogenous or endogenous (due to blood, pus or mucous) nidus ● Pediatric and adult population ‐ **Small antroliths** – incidental radiographic finding ‐ **Large antroliths** – sinus obstruction, sinusitis, nasal discharge, pain ● Mostly adjacent to the floor of the maxillary sinus ● We see combination of radiopacity and radiolucency due to layers of calcification.
1683
Radicular Cyst VS Antral Pseudocyst
One of the ways to differentiate antral pseudocyst from radicular cyst is by the presence of cortication. ‐ Reticulosis is a cystic lesion that happens around the apex of the nonvital tooth. ‐ They have a round and domed shaped appearance too, but they are from a different origin 􀀀 happening inside the alveolar processes
1684
What is this radiographical presentation?
**Antrolith** ## Footnote Deposition of mineral salts (calcium phosphate/carbonate/magnesium) around an exogenous or endogenous (due to blood, pus or mucous) nidus We see a presence of radiopacity which is antrolith inside the maxillary sinus
1685
What is this radiographical finding?
**Foreign Body in Maxillary Sinus**
1686
What is this radiographical finding?
Foreign Body in Maxillary Sinus
1687
What is this radiographical finding?
**Periostitis** ## Footnote **•**Lamellar, periosteal reaction **from periapical inflammatory disease** •**Exudate** from infected tooth diffuses through the cortical bone, (elevation of periosteum) lifts and stimulates the periosteal lining to produce layer(s) of new bone **•Floor of maxillary sinus** •Inferior, buccal, lingual mandibular cortices
1688
What is this clinical presentation?
**Homogeneous leukoplakia** ○ Thickened leathery, White plaque ○ Well-demarcated, Deepened fissures ○ Non-wipeable white patch
1689
What is this clinical presentation?
Homogeneous leukoplakia. *○ Non-wipeable white patch*
1690
What is this clinical presentation?
**homogenous leukoplakia** Just white color
1691
What is this clinical presentation?
**Non-homogenous leukoplakia** Nodular leukoplakia ~ Largely white Verrucous leukoplakia ~ Largely white Erythroleukoplakia ~ Red and white Speckled and verrucous leukoplakia have a greater risk for malignant transformation than the homogeneous form
1692
What is this clinical presentation?
**Speckled leukoplakia.** **Non-homogenous leukoplakia**
1695
What is this clinical presentation?
**Hairy Leukoplakia** corrugated white lesion on the lateral tongue. **• It only occurs on the lateral tongue**
1696
What is this clinical presentation?
**Hairy Leukoplakia**
1699
What is this clinical presentation?
**Proliferative Verrucous Leukoplakia** Patient with proliferative verrucous leukoplakia but manifesting more as an erythroplakia in multiple sites than a leukoplakia **Proliferative verrucous leukoplakia has very high risk (49.5% in malignant transformation)** almost 10% risk for malignant transformation every year
1700
What is this clinical presentation?
**Proliferative Verrucous Leukoplakia** **Location** ○ Gingiva (Frequent) ○ Buccal Mucosa ○ Palatal Mucosa
1701
What is this clinical presentation?
**Proliferative Verrucous Leukoplakia** Multifocal
1703
What is this clinical presentation?
**Oral lichen planus** White lacy appearance, with a network reticular appearance (Wickham’s striae) sometimes punctate or plaque‐like lesions predominate o **Wickham’s striae**→ very characteris► white wispy changes
1704
What is this clinical presentation?
**Oral lichen planus** on the buccal mucosa (most common site reticular form.
1705
What is this clinical presentation?
Oral lichen planus slightly more **red** as you move to the left of the picture ● The white lines have small sunburst effect at the periphery ○ Very very characteristic of lichen planus ○ Will never see this in a leukoplakia
1706
What is this clinical presentation?
**Oral lichen planus** Lichen planus of the dorsum of the tongue this is a hypertrophic form.
1707
**Leukoplakia** Etiology
**Etiology** The exact etiology remains unknown. Tobacco, alcohol, chronic local friction, and Candida albicans are important predisposing factors. Human papilloma virus (HPV) may also be involved in the pathogenesis of oral leukoplakia.
1708
**Leukoplakia** **Treatment**
* Biopsy to rule out malignancy * Elimination or discontinuation of predisposing factors, * systemic retinoid compounds. * Smoking cessation (leukoplakias often disappear or become smaller within first year of smoking cessation) * Complete removal with surgical excision, electrocautery, cryosurgery, or laser ablation
1709
What is this clinical presentation?
**Lichenoid Reactions** **Contact Lesions** a sensitivity in contact with a **dental amalgam** ▪ When you replace these amalgams, the lichenoid reaction will typically disappear
1710
What is this clinical presentation?
**Oral Lichenoid** **Contact lesion** chenoid reaction to dental amalgam and cold: white and erythematous lesions on the buccal mucosa.
1711
What is this clinical presentation? pts takes *Thiazide Diuretic*
Oral Lichenoid Drug Reaction
1712
What is this clinical presentation? pts takes *allopurinol*
Oral Lichenoid Drug Reaction
1714
Oral Lichenoid Drug Reaction Etiology
* Lichenoid reactions may develop after exposure to a medication for periods of \> 1 year * May develop very slowly after the problem is initiated so it can be very challenging to connect the dots **Many different medications that can lead to lichenoid reactions** * Beta blockers, ACE inhibitors, Rituxumab etc… * A number of new targeted agents “mabs” and “nibs” can cause lichenoid reactions * In cancer centers, this has become quite a problem because they are taking disease‐modifying drugs
1716
What is this clinical presentation?
**Nicotinic Stomatitis** also known as Smoker’s keratosis smoker’s palate * the palatal mucosa becomes diffusely gray or white; numerous slightly elevated papules are noted, usually with punctate red centers
1717
What is this clinical presentation?
**Nicotinic Stomatitis** These papules represent _inflamed minor salivary glands_ and their ductal orifices.
1718
What is this clinical presentation
Nicotine Stomatitis.
1719
Hairy Leukoplakia ## Footnote **Etiology**
Epstein–Barr virus seems to play an important role in the pathogenesis.
1720
Hairy Leukoplakia ## Footnote **Treatment**
* Not required * however, in some cases aciclovir or valaciclovir * can be used with success. * Topical retinoids or podophyllum resin for temporary remission
1721
What is this clinical presentation?
**Pseudomembranous candidiasis** on the palate. usually caused by Candida albicans Predisposing factors are local (poor oral hygiene, xerostomia, mucosal damage, dentures, antibiotic mouthwashes)
1722
What is this clinical presentation?
Geographic tongue/ areata migrans Multiple, well-demarcated zones of erythema (due to filiform atrophy) surrounded by slightly elevated, yellow-white, serpentine/ scalloped border annular - serpiginous - atrophic - Fissured
1723
What is this clinical presentation?
Geographic tongue/ areata migrans
1724
What is this clinical presentation?
Geographic tongue/ areata migrans
1725
What is this clinical presentation?
Geographic tongue/ areata migrans
1726
What is this clinical presentation?
Geographic tongue, localized lesion.
1729
What is this clinical presentation?
**Fordyce’s granules** on the buccal mucosa. a normal anatomical variation. ectopic sebaceous glands of the oral mucosa.
1730
What is this clinical presentation?
Leukoedema of the buccal mucosa. Laskaris,
1732
What is this clinical presentation?
White Sponge Nevus Diffuse, thickened white plaques of the buccal mucosa
1733
What is this clinical presentation?
White Sponge Nevus | (Canon disease)
1734
Proliferative Verrucous Leukoplakia ## Footnote **Treatment**
complete removal: excision, electrocautery, cryosurgery, or laber ablation ## Footnote *Lesions rarely regress despite therapy*
1735
What is this clinical presentation?
**Verrucous Carcinoma** Early verrucous carcinoma of the buccal mucosa.
1736
What is this clinical presentation?
**Verrucous Carcinoma** Large, exophytic, papillary mass of the maxillary alveolar ridge.
1737
What is this clinical presentation?
**Verrucous Carcinoma** Large, exophytic, papillary mass of the maxillary alveolar ridge.
1738
What is this clinical presentation?
Verrucous Carcinoma Extensive papillary, white lesion of the maxillary vestibule
1741
Traumatic Erythema /Traumatic Hematoma on the lower lip.
1742
What is this clinical presentation?
Geographic tongue: well-demarcated red patch on the tongue.
1743
What is this clinical presentation?
Median rhomboid glossitis. a Chronic hyperplastic, erythematous candidiasis
1746
what is this clinical presentation?
Denture stomatitis.
1747
Oral lichen planus Etiology
Although the cause is not well known, T cell-mediated autoimmune phenomena are involved in the pathogenesis of lichen planus.
1748
What is this clinical presentation?
**Erythroplakia** of the buccal mucosa Well-demarcated erythematous patch or plaque with soft velvety texture
1749
What is this clinical presentation?
Erythroplakia of the buccal mucosa.
1750
What is this clinical presentation?
**Erythroplakia** of the lateral margin of the tongue. Well-demarcated erythematous patch or plaque with soft velvety texture
1751
What is this clinical presentation?
Erythroplakia Firey red Well-demarcated patch or plaque with soft velvety texture transformed into SCC
1752
Oral lichen planus Treatment:
* Incisional biopsy on non-keratinized, non-ulcerated mucosa ○ Asymptomatic → no tx ○ Symptomatic → 0.5mg/ml Dexamethasone Elixir.
1753
What is this clinical presentation?
Erythroplakia. Well-circumscribed red patch on the posterior lateral hard and soft palate
1754
What is this clinical presentation?
Erythroplakia. Erythematous macule on the right floor of the mouth. Biopsy-- Turned out to be early invasive squamous cell carcinoma.
1755
What is this clinical presentation?
Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS Smokeless Tobacco–related Gingival Recession. Extensive recession of the anterior mandibular facial gingiv
1756
What is this clinical presentation?
Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS Tobacco Pouch Keratosis, Severe
1757
What is this clinical presentation?
Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS Tobacco Pouch Keratosis, Mild. A soft, fissured, gray-white lesion of the lower labial mucosa located in the area of chronic snuff placement.
1759
What is this clinical presentation?
**Pemphigus Vulgaris.** . Multiple erosions affecting the marginal gingiva.
1760
What is this clinical presentation?
**Pemphigus Vulgaris.** Multiple erosions of the left buccal mucosa and soft palate.
1761
What is this clinical presentation?
**Pemphigus Vulgaris.** Large, irregularly shaped ulcerations involving the floor of the mouth and ventral tongue.
1762
What is this clinical presentation?
**Pemphigus Vulgaris.**
1763
What is this clinical presentation?
**Pemphigus vulgaris** ● Multiple, chronic, mucocutaneous ulcers ● Many patients also have ● Relatively non‐specific ● Very superficial, only in epithelium ● Occur on any mucosal surface: oral, ocular, nasal, GI, esophageal, genital
1764
What is this clinical presentation?
**Pemphigus vulgaris** PV Lesions can affect virtually any mucosal surface (oral, nasal, ocular, pharyngeal, esophageal, genital)
1765
What is this clinical presentation?
**Pemphigus vulgaris** **usually suffer from Desquamative gingivitis (DG)** More superficial erosion of the marginal gingiva, typically with an intense erythema and inflammation, and very often in the absence of local factors that would typically cause a gingivitis o Hurts to brush their teeth Immediately look for areas where there are no local factors and look for inflammation there o To check the possibility of systemic factors causing local gingivitis
1766
What is this clinical presentation?
**Pemphigus vulgaris** Combination of PV inflammation and gingival inflammation accumulating local factors can result in advanced loss of attachment and tooth loss
1769
**What is this clinical presentation?**
Mucous membrane pemphigoid
1770
**What is this clinical presentation?**
Mucous membrane pemphigoid SEVERE/HIGH RISK FORMS OF MMP ▪ Ocular ▪ Esophageal can result in functional blindness
1771
**What is this clinical presentation?**
Mucous membrane pemphigoid Oral Hygiene: Plaque related gingival inflammation contributing to continued VB desquamative gingivitis
1772
**What is this clinical presentation?**
Mucous membrane pemphigoid REMEMBER: ▪ Plaque and calculus can be the consequence of painful MMP lesions ▪ When assessing MMP lesions/desquamative gingivitis, look for areas of intense inflammation WITHOUT local factors as evidence of VB disease
1774
**Oral Lichenoid Contact Lesions** Etiology
**Hypersensitivity** to * dental restorative materials, amalgam or other metal, composite resins * Foods, oral products * Especially cinnamon * dental plaque accumulation are the most common
1775
MMP & PV BIOPSY
take two different sites ○ For H&E, still must be perilesional ○ If you get only ulcer just because the clinician thinks ○ that is the pathology → there is no epithelium! ○ The sample is useless and no diagnosis can be made
1776
What is this clinical presentation?
Actinic cheilitis (Solar cheilosis) Early presetation: Smooth, blotchy, pale, dry areas Diffuse, irregular white plaque around line of the lip Crusted, Scaly **​**
1777
What is this clinical presentation?
Actinic cheilitis (Solar cheilosis) Typical presentation of angular cheilitis with erythema, crusting and mild fissuring of the angles of the mouth bilaterally.
1779
Oral lichenoid reaction _Treatment_
**Insicional biopsy Mandated to distinguish from OLP** ○ Biopsy white areas on non-keratinized mucosa NOT ulcerated OR red areas Treatment Replacement of the restorative material, polishing and smoothing, and good oral hygiene are recommended. Topical steroid treatment for a short time is also helpful.
1781
What is this clinical presentation?
**_SCC_** arising from **Actinic Cheilitis**
1782
What is this clinical presentation?
**Oral Melanoma** Large, blue-black, irregularly bordered lesion on the upper lip of a male Japanese patient. The diagnosis is oral melanoma.
1783
What is this clinical presentation?
Amalgam tattoo This image depicts two diffusely bordered, dark gray macules in the left posterior buccal mucosa adjacent to molar teeth that have been restored. .
1784
What is this clinical presentation?
**Oral Melanoma** a highly malignant neoplasia, arising from melanocytes, the cells that produce the brownish pigment melanin.
1785
What is this clinical presentation?
**Oral Melanoma** an ulcerated, blue-black, slightly elevated lesion in the edentulous, posterior right maxilla. The lesion extends across the residual alveolar ridge onto the palate and onto the facial aspect of the ridge.
1786
What is this clinical presentation?
**Oral Melanoma** patient with extensive, black-pigmented and irregularly bordered macule in the maxillary labial mucosa and midline facial gingiva, (teeth 8 and 9). (The patient's fingers are depicted.)
1787
What is this clinica presentation?
Oral melanoacanthoma. the buccal mucosa of a middle-aged, black woman with a brown-black, irregularly bordered macule that arose suddenly. The patient was unaware of its presence.
1788
What is this clinical presentation?
**Oral melanotic macule** an irregularly shaped, tan-brown macule on the left hard palate in an edentulous patient.
1791
Nicotine Stomatitis Treatment
Smoking Cessation. * Nicotine stomatitis is completely reversible, even when it has been present for many decades. * The palate usually returns to normal within 1 to 2 weeks of smoking cessation.
1792
What is this clinical presentation
Oral Melanoma
1793
What is this clinical presentation
Oral Melanoma
1794
What is this clinical presentation?
Traumatic Granuloma (traumatic ulcertaive granuloma)
1795
What is this clinical presentation
Oral Melanoma
1796
Nicotine Stomatitis. Etiology
The elevated temperature, rather than the tobacco chemicals, is responsible for this lesion.
1797
What is this clinical presentation?
Traumatic ulcer Most often on tongue, lips, buccal mucosa Any sites that may be injured by dentition
1799
What is this clinical presentation?
Traumatic ulcer a chronic ulcer on the left posterior lateral border of the tongue caused by lingually tilted mandibular 3rd molar. Note central ulceration with peripheral keratosis
1800
What is this clinical presentation?
Traumatic ulcer caused by sharp or puncturing food stuff
1801
What is this clinical presentation?
Traumatic Granuloma
1802
What is this clinical presentation?
**Traumatic Granuloma** | ( Traumatic Ulcerative Granuloma)
1804
What is this clinical presentation?
Squamous cell carcinoma on the buccal mucosa)
1805
What is this clinical presentation?
**Erythroplakia and Squamous Cell Carcinoma** Erythroplakia is a general term for red, flat, or eroded velvety lesions that develop in the mouth. In this image, an exophytic squamous cell carcinoma on the tongue is surrounded by a margin of erythroplakia
1806
What is this clinical presentation?
Leukoplakia and Squamous Cell Carcinoma Leukoplakia is a general term for white hyperkeratotic plaques that develop in the mouth. About 80% are benign. However, in this image, squamous cell carcinoma is present in one of the leukoplakic lesions on the ventral surface of the tongue (arrow).
1809
What is this clinical presentation?
**Graphite tattoo** Gray, black, or blue-ish macule
1810
What is this clinical presentation?
**Graphite tattoo** Most common location on the palate and gingiva Gray, black, or blue-ish macule
1813
Geographic tongue/ areata migrans _Treatment_
* Generally no treatment is indicated * Reassuring the patient that the condition is completely benign is often all that is necessary. * In case of tenderness or a burning sensation that is so severe --topical corticosteroids, such as fluocinonide or betamethasone gel, may provide relief
1814
Geographic tongue/ areata migrans _Etiology_
The exact etiology remains unknown. It may be genetic.
1817
Leukoedema Etiology Treatment
Etiology It is due to increased thickness of the epitheliumand intracellular edema of the prickle-cell layer. Treatment No treatment required
1820
**White Sponge Nevus** Etiology
**Autosomal dominant skin disorder** Etiology: ● This condition is due to a defect in the normal keratinization of the oral mucosa in the 30-member family of keratin filaments, the pair of keratins known as **keratin 4 and keratin 13** is specifically expressed in the spinous cell layer of mucosal epithelium.
1825
**Verrucous Carcinoma** Etiology
a low-grade variant of squamouscell carcinoma. Etiology Leading theories include * human papillomavirus (HPV) infection * chemical carcinogenesis induced by smoking and chewing tobacco * alcohol consumption * betel nut chewing (oral lesions), * chronic inflammation
1826
**Verrucous Carcinoma** Treatment
○ Surgical Excision ○ Radiotherapy
1830
Median Rhomboid Glossitis Treatment
No treatment is required.
1831
Median Rhomboid Glossitis Etiology
**Atrophy of central filiform papillae** Presumably developmental. Candida albicans may also be involved. but smokers, people with xerostomia , who use inhalation steroids and denture wearers are **at increased risk**
1833
**Erythroplakia** Malignant transformation
Erythroplakia is a high risk for malignant transformation. So, if you encounter an erythroplakia, it's probably already a cancer or it's fast‐tracking towards a cancer
1838
**Erythroplakia** Treatment
○ Biopsy required for diagnosis ○ If a source of irritation can be identified and removed, biopsy may be delayed for 2 weeks to allow lesion to heal ○ Complete excision
1844
Smokeless tobacco keratosis Treatment:
typically resolves weeks after cessation ○ if persists 6+weeks -\> biopsy to rule out dysplasia + SCC
1853
**Pemphigus vulgaris** **Etiology**
Pemphigus vulgaris is not fully understood. Experts believe that it's triggered when a person who has a genetic tendency to get this condition comes into contact with an environmental trigger, such as a chemical or a drug. In some cases, pemphigus vulgaris will go away once the trigger is removed.
1854
**Pemphigus vulgaris**
Treatment has 3 stages: **● Stage 1: Control** ○ Suppress inflammation / lesion activity with Systemic **Corticosteroid: Remains initial / 1st‐line treatment…** ○ Then quickly add steroid‐sparing agents (mycophenolate mofetil) to minimize dose and duration of corticosteroid treatment as well as improve disease control **● Stage 2: Consolidation** ○ Reducing auto‐antibody production with the addition of Immunosuppressants ○ Assessed by the lack of development of NEW lesions **● Stage 3. Remission / Maintenance:** ○ achieving complete remission of lesion activity OFF medication is the GOAL ○ When lesion activity OFF medications cannot be achieved, principle of MINIMALLY effective therapy is the goal, typically with combination of immunosuppressant medications **○ RITUXIMAB has become the FIRST CHOICE treatment after ○ the consolidation phase to achieve DISEASE REMISSION** _● TOPICAL / INJECTABLE CORTICOSTEROID MEDICATIONS_ ○ o Can be used to help control limited number of lesions resistant to systemic therapy: it treats ONLY the disease ○ outcome (lesions) and not the systemic illness / pathologic antibody production **○ ex:clobetesol 0. 05% , halbetesol 0.05% (most potent)**
1859
**Mucous membrane pemphigoid** **Etiology**
Mucocutaneous autoimmune disease characterized by sub‐epithelial blisters (bullae) which ruptures to form large, non‐healing ulcerations
1860
Mucous membrane pemphigoid _Treatment_
o Approach is similar to PV – but generally not as aggressive unless hi‐risk areas ( ocular, esophageal ) where more intense immunosuppression indicated ▪ NON‐immunosuppressive treatments uniquely effective: * *o** **Dapsone** * *o Tetracycline + nicotinamide**
1864
**Actinic cheilitis** malignant transformation
Actinic cheilitis has **2 times** of risk for developing SCC of the lip. SCC on the lips is 11 times as likely to metastasize compared to SCC found on other parts of the body
1865
**Actinic cheilitis** Etiology
due to chronic ultraviolet light exposure.
1866
**Actinic cheilitis** Treatment
* avoid sun exposure * Laser ablation is preferred for severe actinic cheilitis * surgical excision is recommended for severe actinic cheilitis with evidence of high-grade dysplasia * Lip Shaving” (Vermilionectomy) * can also use cryotherapy, electrodesiccation It requires long term follow up and **prognosis is good if caught early**
1875
Oral Melanoma ## Footnote **Etiology**
Unknown. Ultraviolet radiation is an important causative factor for skin melanoma **Acute sun damage** can cause it more than chronic exposure
1876
Oral Melanoma Risk Factors
Fair skin A history of sunburn Excessive ultraviolet (UV) light exposure. Living closer to the equator or at a higher elevation Having many moles or unusual moles A family history of melanoma Weakened immune system.
1877
**Oral Melanoma** Treatment
* Surgical excision * Radiotherapy * Chemotherapy
1882
Traumatic ulcer/Traumatic ulcerative granluoma Etiology
**Etiology** * typically caused by trauma. In more than half the cases, the patient does not recall traumatizing the area although this may have occurred during sleep. * Chronic mucosal trauma from adjacent teeth * Some adjacent source of irritation
1884
What is this clinical presentation?
Traumatic ulcer Post-anaesthesia traumatic ulcer on lower lip.
1889
Traumatic ulcer/Traumatic ulcerative granluoma Treatment
**Remove cause of irritation** Topical anesthetic or film for pain relief If there is no obvious cause then ► **biopsy**
1893
squamous cell carcinoma Risk factors
**HPV + SCC** Area affected: ( Oropharynx cancers largely involved tonsils, . Posterior 3rd of the Tongue) Younger pts, 3:1 Males to females ratio, high socio-eco status Incidence is decreasing less aggressive → higher survival rates ( Better than HPV negative SCC) **HPV - SCC** The chief risk factors for oral squamous cell carcinoma are Smoking (especially \> 2 packs/day) Alcohol use Risk increases dramatically when alcohol use exceeds 6 oz of distilled liquor, 15 oz of wine, or 36 oz of beer/day. The combination of heavy smoking and alcohol abuse is estimated to raise the risk 100-fold in women and 38-fold in men. ( this affects these ares : the tongue, floor of mouth, buccal mucosa, or gingiva) mostly men, low socio-economic factors Incidence is decreasing Very aggressive → lower survival rates
1894
SCC treatment
Early stage: Radiation and/or Surgical removal Late stage : combination of surgery, radiation therapy, or chemotherapy
1897
Graphite tattoo Etiology
result from pencil lead that is traumatically implanted, usually during the elementary school years
1898
Graphite tattoo Treatment
If patient is concerned for cosmetic reasons ► then removal of lesion with autogenous graft
1899
What is this clinical presentation?
**Hemangioma of Infancy** a relatively common benign proliferation of blood vessels that primarily develops during childhood. display a rapid growth phase with endothelial cell proliferation, followed by gradual involution.
1900
What is this clinical finding?
Hemangioma of Infancy
1902
What is this clinical presentation?
Traumatic ulcer of the tongue.
1904
**Hemangioma of Infancy** Treatment
○ Because most hemangiomas of infancy undergo involution, management often consists of “watchful neglect.”
1906
What is this clinical finding?
**Necrotizing Sialadenometaplasia** *we see two ulcers on the palate* *Mostly ● Palatal salivary glands ○ Possible for parotid ● 75% of case on posterior palate ● Hard\>Soft palate ● 2/3rd are unilateral*
1907
What is this clinical finding?
Necrotizing Sialadenometaplasia an uncommon, usually self-limiting, benign inflammatory disorder of the salivary glands. *Here it is on the palate*
1908
What is this clinical finding?
**Xerostomia-related Caries** **Or** **Dry Mouth** . Extensive cervical caries of mandibular dentition secondary to radiation-related xerostomia.
1909
**Necrotizing Sialadenometaplasia** _Etiology_
*The cause is uncertain, although the hypothesis of ischemic necrosis after vascular infarction seems acceptable.*
1911
**Necrotizing Sialadenometaplasia** _Treatment_
No Treatment Needed but we need to biopsy to rule out other diseases
1912
**Dry mouth** Subjective vs Objective
**Xerostomia** The subjective experience of a dry mouth (ie a symptom) **Salivary Hypofunction** The objective measurement of a reduction in salivary flow (a sign)
1913
What is the normal rate for Unstimulated Saliva Production
**300 ml/day ▪ Flow rate: mean 0.3 ml/min**
1914
What is the normal rate for **Stimulated Saliva Production**
**Stimulated Saliva Production** **▪ 200+ ml/day ▪ Flow rate: mean 1-2 ml/min, maximum 7 ml/min** o “Normal” range is very wide
1915
What are Factors affecting unstimulated flow include?
* **Dehydration** * **Medical conditions** * **Body posture** * **Lighting conditions** * **Circadian/circannual rhythm (lowest during)** * **Medications** Age is an independent factor for whole saliva andsubmandibular/sublingual gland secretion (but notparotid).
1916
What is this clinical presentation?
**dry‐mouth** from radiation Note the Ropy, frothiness on the palate. - The tissues are red and irritated due to candida infection as well.
1917
What is this clinical presentation?
**dry‐mouth** patient a classic example **• Classic fissuring • depapillation of the tongue papilla • some white changes on the tongue.**
1918
What is this clinical presentation?
**dry Mouth** Cervical caries related to radiation. The patient is a smoker and coffee drinker --\> explains the staining
1919
What is this clinical presentation?
dry Mouth Incisal caries in a radiation patient: **Incisal caries is a sure sign of severe dry mouth/ significant salivary gland hypofunction**
1920
What are Factors affecting stimulated flow include:
* **Mechanical stimuli** * **Vomiting** * **Gustatory/olfactory stimuli (acid/smell)** * **Gland size** Age is an independent factor for whole saliva (but not for parotid and minor gland secretions)
1921
Severity of patients with xerostomia using objective measures
1922
What causes dry mouth?
Central inhibition as a result of connections between the primary salivary centers and the higher centers of the brain.
1923
● What causes xerostomia in absence of measurable salivary hypofunction?
* **May be a reduction in baseline sialometry which is still above “normal.”** * *If they get a decrease in the salivary flow, they still may be in the normal range, but for them the experience is that they have got dry mouth.* * **Saliva film thickness** * *Palatal mucous gland secretions?* * *Anterior dorsum of tongue?* * **Relative contributions by glands** * Mucins, proteins? * **Alterations in sensory perception?** * **Mental status/central inhibition?**
1924
What cause Salivary Hypofunction?
**● Dehydration ● Medications (Rx & OTC)** * *Direct damage to glands* * *Head and neck radiotherapy* * *As a result of radiation it’s irreversible damage to the glands* * *Chemotherapy (reversible)* * *Autoimmune diseases* * *Primary vs Secondary Sjögren’s Syndrome, GVHD* * *HIV disease* **● Decreased mastication (tooth loss, soft diet) ● Conditions affecting the CNS:** * Psychologic disorders (depression/anxiety?), Alzheimer’s, Parkinson’s, Cerebral palsy
1926
What is this clinical presentation?
**SJÖGREN’S SYNDROME** _Dry Mouth_ very severe cervical disease & very dry lips
1928
What is this clinical presentation?
a patient with a **_bacterial sialadenitis_** who has **_SJÖGREN’S SYNDROME_** When we examine such patients and ”milk” the gland ► you actually see a purulent drainage from the gland itself.
1929
What is this clinical presentation?
Depapillated & Fissured Tongue ## Footnote **SJÖGREN’S SYNDROME**
1930
What is this clinical presentation?
**Sjögren Syndrome** * bilateral enlargement of the submandibular glands * angular cheilitis, dry and cracked lips and fissured and despapilated tongue * severe ocular lesions.
1931
**SJÖGREN’S SYNDROME** **Management**
These patients **LOW USFR, no response to stimulation (aka abnormal USFR/SFR)** * Rehydrate if dehydrated * Treat underlying conditions (i.e. DM) * Salivary substitutes (glycerin) * Minimize damage to glands from radiation * Prevention of complications & palliative treatment * Optimal hygiene * Restore caries * Smooth sharp edges in oral cavity * Fluoride therapy * Antifungals * Chlorhexidine rinses w/o alcohol * Sialendoscopy * Salitron - salivary pacemaker * ALTENS (acupuncture like transcutaneous electrical nerve stimulation)
1934
To have dry mouth xerostomia what is the rate of Unstimulated and Stimulated Salivary flow **USFR** and **SFR**
**Abnormal unstimulated USFR= \<0.1–0.2ml/min** **Abnormal stiumated SFR = \<0.5ml/min**
1936
How to manage with normal USFR and SFR?
* Salivary stimulation (OTC) to stimulate their glands * Salivary lubrication ( to improve it) * Humidification ( like a humidifier in the room at night) * Hydration/prevent dehydration (ie avoid alcohol, caffeine both will act as a * diuretic and lead to dehydration). * Monitor closely to rule out emerging disease ( to see whether they are developing Sjogren’s or something else 􀀀 we want to follow them over time)
1937
How to manage with abnormal USFR and abnormal SFR? Abnormal unstimulated USFR= \<0.1–0.2ml/min Abnormal stiumated SFR = \<0.5ml/min
* If dehydrated ► rehydrate or treat underlying condition * People with uncontrolled diabetes, once you control the diabetes‐ their flow comes back. * All we can do is offering Salivary substitutes (sprays, gels, rinses ) * For patients with high dose radiation treatment ► makes sure they get the INRT * Minimizing damage to salivary glands ( there are other strategies for that) * Prevention and treatment of oral complications
1938
How to manage with abnormal USFR and normal SFR? (respond to stimulated) Abnormal unstimulated USFR= \<0.1–0.2ml/min
* Look for possible causes (major cause will be medications & can dehydration or others) * Restore chewing function (Masticatory issues) * Reduce medication‐induced salivary hypofunction * Prescribe Salivary stimulation OTC, Rx medications, others * Prescribe Salivary lubrication * Humidification ‐use humidifiers * Hydration/prevent dehydration (ie avoid alcohol, caffeine) * Treat oral consequences (such as candidiasis treated with an antifungal or caries with management of caries).
1939
**What are the** **Prescription Medications** for people with low USFR and some oral signs, but responds to stimulation ? (abnormal USFR, Normal/improved SFR) **(include dosage and usage)**
– Muscarinic agonists: – **Pilocarpine** 5‐7.5mg tid & qhs (can go as high as 10mg qid) – **Cevimeline** 30mg tid (can go as high as 60mg tid) _Contradicated for_ : **CV disease, hepatic, renal or respiratory diseases or narrow angle glaucoma** **Pilocarpine affects M1 & M3** _side effects_ (sweating, flushing, rhinitis, increased urination, weakness and some experience the shakes. ) **Cevimeline affects M3 only** fewer side effects
1941
What is this clinical finding?
Frictional keratosis on the tongue
1942
What is this clinical finding?
**Frictional Keratosis** **the white surrounding a a traumatic ulcer** Symptomatic traumatic ulceration of the left mid-ventral tongue associated with a sharp left lower molar. The ulcer has flat edges and is surrounded by an area of frictional keratosis.
1943
**Frictional Keratosis.** Differential Diagnosis
Leukoplakia Linea alba Chronic cheek chewing (bite injury) Candidiasis Oral Lichen planus Squamous cell carcinoma
1944
What is this clinical finding?
**Frictional Keratosis.** There is a rough, hyperkeratotic change to the posterior mandibular alveolar ridge (“alveolar ridge keratosis”), because this area is now edentulous and becomes traumatized from mastication. **Such frictional keratoses should resolve when the source of irritation is eliminated and should not be mistaken for true leukoplakia.**
1945
**Frictional Keratosis** **Etiology**
* Trauma from Sharp cusp & ortho appliance * Chronic mechanical irritation (chronic biting) * Masticatory function * Normal hyperplastic response * Dentures/missing teeth
1946
**Frictional Keratosis** **Treatment**
* Remove the cauative factor that caused the trauma * observe large lesion regularly excellent prognosis
1947
What is this clinical presentation?
**SJÖGREN’S SYNDROME** Autoimmune exocrinopathy Dry mouth and eyes resulting from a chronic progressive loss of secretory function (Slowly but surely, the salivary glands and/or lacrimal glands (some cases are more lacrimal & less salivary or vice versa); slow & progressive Patients with Sjogren’s can have bilateral salivary gland enlargement (parotid) (Sometimes we may see a unilateral enlargement of the salivary glands due to retrograde infections.) **increased risk of lymphoma (MALT type)**
1952
For Smoking Cessations Prescribe Nicotinic Drugs (memorize any of them + dosage)
**Nicotine Patch Generic Name-Nicodern CQ/Habitrol** * 21 mg/24 hr\> 10 dgs/d * 14 mg/24 hr or 7 mg/24 hr \<10 mg cig/d or \<100 lbs **Nicotine Gum Generic Name -Nicorette** 2 mg \< 25 cig/d 4 mg \> 25 cig/d **Nicotine lozenge - Commit** 2 mg if smoke 1st cig more than 30 minutes after waking 4 mg 4 mg if smoke 1st cig within 30 minutes after waking ( no more than 20 a day) **Nicotine Inhaler -Nicotrol lnholer** 6-16 cartridges/ d Use 1 cartridge/hour **Nicotine Nasal Spray- Nicotrol NS** Mox 40 doses/d (1 dose = 1 spray per nostril}
1953
For Smoking Cessations Prescribe Non-Nicotinic Drugs (memorize any of them + dosage)
Sustained release buprorpion **Zyban or Wellbutrin** Can be used w/NRT Start 1-2 weeks before quit date. Option 1 : 150 mg/ day for 3 days then 150 mg BID (doses at least 8 hrs apart) Option 2: 150 mg q AM is recommende~ Fewer adverse eff eds better tolerated iin older adult) **Varenidine tartrate** **Chontix** Start 1 week before quit date 0. 5 mg/ d for 3 days then 0.5 mg BID for next 4 days (one in AM, and one in PM). After firs1 7 days 1 mg/810
1954
What are the adverse effects of Nicotine Inhaler Nicotrol lnholer
* Mouth and throat irritation * Cough • Side effem generally caused by inappropriate use
1955
What are the adverse effects of Nicotine Nasal Spray- Nicotrol NS
* Nasal irrttation * Sneezing * Cough * Teary eyes
1956
What are the adverse effects of Nicotine Patch ?
* local skin irritation * insomonia
1957
What are the adverse effects of **Nicotine Gum?**
* hiccups * Dyspepsia * mouth sorness
1958
What are the adverse effects of **Nicotine lozenge?**
* Dyspepsia * local irrttation mouth & throat * Rarely causes coughing & hiccups
1959
What are the adverse effects of **Sustained release bupropion (Zyban or Wellbutrin)?**
* Insomnia * Dry mouth * Anxiety
1960
What are the adverse effects of **Varenidine tartrate Chontix ?**
* Nausea * Insomnia * Abnormal dreams
1961
What is this clinical finding?
**Urticaria** Well defined erythematous papules/plaques which are pruritic (itchy) We’ll see them on the skin ‐ Not found intraorally
1962
What is this clinical finding?
**Urticaria** (HIVES) this person was exposed to extreme temperature developed hives ( not really red but very itchy) no skin scarring is noted it goes in about a day
1965
What is this clinical finding?
**Angioedema** ❖ **Diffuse edematous swelling** of the soft tissues that most commonly involves the subcutaneous and submucosal connective tissues ❖ Results from local vasodilatation and increased vascular permeability of DEEPER blood vessels
1966
What is this clinical finding?
**Angioedema**
1967
Urticaria Etiology
❖ Medications ► causing rash ❖ Foods ► like peanuts ❖ Airborne allergens ► pollen ❖ Physical stimuli ► ex cold weather
1968
**Urticaria** Treatment
❖Avoid known triggers avoid the penicillin, any of the triggers ❖ Antihistamines ( to prevent it from happening in the first place) Corticosteroids (prevents the inflammatory effect)
1969
What is this clinical finding?
**Cinnamon Contact Stomatitis** * It can present similar to leukoplakia * So you’d think it is pre‐malignant lesion * But after asking the patients ► you’ll realize they are chewing like 10 cinnamon gums every day.
1970
What is this clinical finding?
**Allergic Contact Stomatitis** ## Footnote ❖ Mild‐severe redness, edema, vesicles, erosions, ulcerations ❖ Burning, itching, stinging, tingling *●We can't know what is this right away.* *Patients may say it burns, tingles, there could be peeling (desquamation). We might think it’s a **vesiculobullous diseases.** ● So these cases require more consulative‐investigative work.*
1971
What is this clinical finding?
**Allergic Contact Stomatitis‐Clinical** * slight vesicales and diffused erythemya * we wouldn’t always know this is Allergic contact stomatitis * This occured due to allumnium chloride on gingival retraction cord.
1973
What is this clinical finding?
**Exfoliative cheilitis** Allergic Contact Reactions‐ Non‐ Mucosal dry, scaly, fissured, cracking lips This is a mild case that affect the non‐mucosal around the the skin
1974
What is this clinical finding?
**Exfoliative Cheilitis** *caused by titanium implants and some mercury in amalgam.*
1975
What is this clinical finding?
**Perioral Dermatitis** Allergic Contact Reactions‐ Non‐ Mucosal erythematous papules/vesicles – papules ( raised) & vesicles (actual blisters)
1976
What is this clinical finding?
**Erythema Multiforme** Rapidly rupturing vesicles/bullae forming erosions/ulcerations and hemorrhagic encrusted lip lesions, with greyish pseudomembrane Fast expansion, ► the skin is just peeling off. Type 4 hypersensitivity. Has prodrome phasesudden *Rapid onset, crusted hemorrhagic swollen lips, and desquamative gingivitis.*
1977
What is this histological finding?
**Granuloma** This is a granuloma. It’s composed of histeocytes that looks epithelioid. This is a collection of epithelioid histeocytes **Found in:** * TB (**They’ll be holding TB inside. But in TB you have caseous necrosis of granuloma.** * Deep fungal infections (**they holding? fungal organisms)** * GRANULOMATOUS DISEASES **( if with Asteroid bodies & Schaumann Bodies)** **In these granulomas we don’t know why they are forming.**
1978
What is this clinical finding?
Orofacial Granulomatosis **Cheilitis granulomatosa=Involvement of lips alone** Non‐tender, persistent swelling NEED To BIOPSY to RULE OUT angioedema
1979
What is this clinical finding?
**Orofacial Granulomatosis** Papules, slightly raised areas, fissures, cobblestone appearance **DDx** We could suspect a traumatic injury early signs of Crohn’s
1980
What is this clinical finding?
Orofacial Granulomatosis
1981
**Orofacial Granulomatosis** Treatment
❖ Discover cause ( we need to find out the cause.) ❖ Topical or intralesional corticosteroids (maybe try steroids) ❖ Other (topical tacrolimus, sulfazalazine, methotrexate, etc) ❖ Some cases resolve spontaneously *(This photo shows a person has puffiness because of granulomas. Sometimes it goes away on its own. We can use injection steroids on the lips too.)*
1983
What is this clinical finding?
**Sarcoidosis‐Organ Systems** ❖ Lungs ❖ Lymph Nodes (bilateral hilar lymphadenopathy) ❖ Skin (25% of time) ❖ Eyes ❖ Salivary Glands ❖ Other (endocrine, gastrointestinal, heart, kidney, liver, nervous system, spleen, skeletal
1984
What is this radiological finding?
Sarcoidosis‐Hilar Lymph Node Enlargement popcorn‐like calcifications in the hilar lymph nodes. granulomas from sarcoidosis being inside .
1985
What is this clinical finding?
**Sarcoidosis**‐Skin Lesions **Lupus pernio** (nose, ears, lips and face) ‐ when we have these erythematous indurated, hard on face.
1986
What is this clinical finding?
**Sarcoidosis** **DDX** in the oral cavity. It could be one of the three P’s: ❖ pyogenic granuloma ❖ peripheral ossifying fibroma ❖ peripheral giant cell granuloma.
1987
What is this clinical finding?
**❖ This is Strawberry gingivitis** Granulomatosis with Polyangiitis "Wegener’s” Orally ❖ Ulceration, ❖ Mucosal nodules ❖ Facial paralysis ❖ Enlarged major gland from granulomas * we need to biopsy, as this also looks like a deep fungal infection. *
1988
What is this clinical finding?
**Granulomatosis with Polyangiitis** Orally We want to biopsy to confirm because it Could be contact mucositis.
1989
What is this clinical finding?
**‐ Cinnamon contact mucositis** This could be oral hairy leukoplakia. It could be hyperplastic candidiasis it could be tongue chewing it could be a leukoplakia. We’ll know what it is by biopsy and investigate
1990
What is this clinical finding?
Urticaria.
1991
What is this clinical finding?
Erythema multiforme
1992
What is this clinical finding?
\* Erythema multiforme
1993
What is this clinical finding?
**‐ Orofacial granulomatosis.** We make sure there’s no tb, no fungal, no foreign material in the granulomas
1994
What is this clinical finding?
Sarcoidosis \*Erythemous papules (grey circle) Asteroid bodies ( blue arrow) Hilar lymph nodes (green circle)
1995
What is this clinical finding?
1996
What is this clinical finding?
**orofacial granulomatosis.** What is the common way to describe this? **Cobblestone**. This is the classic cobblestone. Cobblestone and fissuring DDx: people with Crohn’s with oral manifestations it looks like this too.
1997
What is this clinical finding?
**Sarcoidosis**
1998
What is this clinical finding?
angioedema
1999
What is this clinical finding?
**Fixed Drug Eruption** –This case has both the skin and oral appearance. This happened every time this person took NSAIDs that’s not used in the USA. A person gets a reaction to a medication they take. It occurs at the same place each time because there’s s**ome memory T cell at these sites.**
2000
Angioedema Etiology
Causes include: ❖ **IgE mediated** ( most common types are allergy related) * Hypersensitivity reaction * drugs, foods, plants, dust * Contact allergic reactions * foods, cosmetics, topical medications, rubber dam * Physical stimuli * heat, cold, exercise, emotional stress, solar exposure, vibration ❖ Drug reaction to **ACE inhibitors** * Does not respond well to **antihistamines** ❖ Hereditary or acquired activation of the complement pathway ❖ Other (high levels of antigen‐antibody complexes and in elevated blood eosinophil counts) * Complexes in lupus, viral and bacterial infections * Patients with grossly elevated blood eosinophilia
2001
Angioedema Treatment
❖ **Antihistamine/IM epinephrine/IV corticosteroids** ( typical treatment for allergy) ❖ **Intubation and tracheostomy** ( if the patient can’t breathe, so we can get air in) ❖ **Avoid medications in ACE Inhibitor class of drugs** ( for people who has Ace inhibitor induced angieodema) ❖ **C1 esterase inhibitor** concentrate and esterase inhibiting drugs
2002
What is this clinical finding?
**Granulomatosis with Polyangiitis** extra-oral Joint pain, weakness, tiredness ❖ Known as **Saddle nose deformity** ❖ First signs may be recurrent respiratory infection, cough or runny nose ❖ Oral lesions initial presentation in 2% of patients
2003
**Granulomatosis with Polyangiitis** Treatment
**First line: oral prednisone** ❖ After remission immunosuppressive drugs: ❖ Methotrexate ❖ Cyclosporine ❖ Rituximab ❖ Treatment induces prolonged remission ❖ May have relapses
2007
White wipeable plaque in the mouth DDx
● pseudomembranous candidiasis ● Mucosal sloughing‐ Allergic Contact Stomatitis ● Food particles
2008
What is this clinical finding?
**Mucosal sloughing** **Allergic Contact Stomatitis** caused by tooth paste (Colagate Total) white area‐like a film peeling out slowly **Wipeable** *could be confused with candidasis*
2010
**Exfoliative cheilitis** causes
Medications, lipsticks, sunscreens, toothpaste floss, cosmetics
2011
What is this clinical finding?
**Erythema Multiforme** Acute, vesiculobullous, ulcerative mucocutaneous disorder Immunologically mediated **_Target lesions on skin_** (typical board question) Healthy young adults in 20‐40’s
2013
**Erythema Multiforme** Triggers
❖ 50% of cases precipitating cause is identified * Infectious Agents: Herpes simplex virus, Mycoplasma pneumonia, Adenovirus, Enterovirus, Coccidiomycosis * **Most of the time, erythema multiforme is related to a previous infection with herpes simplex virus.** * Drugs: Penicillin, Cephalosporins, Sulphonamides, NSAID’s, Phenytoin * Other: Foods (Benzoates, Nitrobenzene), Chemicals (Perfumes) ❖ it’s not an infection, it’s our body reacting to the infectious organism or pieces of it in a wrong way
2014
What is this histological finding?
**Sarcoidosis** discrete clear granulomas. 2nd schaumann body in a giant cell (3rd to the right) Asteroid bodies ( right)
2015
What is this clinical finding?
**Erythema Multiforme** Focal hemorrhagic crusting of the lips is seen in conjunction with diffuse shallow ulcerations and erosions involving this patient’s mandibular labial mucosa
2016
What is this clinical finding?
**Erythema multiforme** The concentric erythematous pattern of the cutaneous lesions on the fingers resembles a target or bull’s-eye.
2017
What is this clinical finding?
**Sarcoidosis** large red nodule on the lower lip.
2018
What is this clinical finding?
**Urticaria** developed after bites from an imported fire ant.
2019
What is this clinical finding?
**Erythema multiforme** multiple erosions on the lips and tongue.
2020
What is this clinical finding?
(Granulomatosis with polyangiitis) *formerly Wegener Granulomatosis.* Hyperplastic and hemorrhagic mucosa of the facial mandibular gingiva on the left side. ((strawberry gingivitis).
2028
Orofacial Granulomatosis Etiology
**❖ Idiopathic** **❖ Abnormal immune reaction** ❖ in orofacial granulomatosis, people form granulomas and it’s idiopathic ❖ we don’t know why they’re forming them so that’s an abnormal immune reaction.
2046
**Sarcoidosis** Treatment
Depends on the case! ❖ 60% of cases resolve within 2 years ❖ Initial diagnosis 3‐12 mo. observationàactive intervention as needed ❖ First line tx: corticosteroids ❖ Refractory dx: * Cytotoxic drugs (methotrexate, azithioprne) * TNF blockers * Hydroxychloroquine ❖ 4‐10% die of pulmonary, cardiac or CNS complications
2047
**Sarcoidosis** Etiology
❖ **Granulomatous disorder** ❖ Multisystem ❖ Unknown cause
2050
**Granulomatosis with Polyangiitis** Etiology
First line: oral prednisone ❖ After remission immunosuppressive drugs: ❖ Methotrexate ❖ Cyclosporine ❖ Rituximab ❖ Treatment induces prolonged remission ❖ May have relapses
2051
**Urticaria** DDX
* erythema multiforme * morbilliform drug eruption
2052
Cinnamon Contact Stomatitis DDx
* Oral hairy leukoplakia * hyperplastic candidiasis
2053
**What are List of Agents that causes Allergic Contact Stomatitis**
❖ Foods ❖ Food additives ❖ Chewing gums ❖ Candies ❖ Dentifrices ❖ Mouthwashes ❖ Gloves ❖ Rubber dam material ❖ Topical anaesthetics ❖ Restorative metals ❖ Acrylic denture materials ❖ Dental impression materials ❖ Denture adhesive preparations ❖ Cinnamon (mainly artificial flavoring)
2055
**Allergic Contact Stomatitis** _Treatment_
* *❖ Remove the suspected antigen** * *❖** **Severe cases‐Antihistamine** (combined with a topical anaesthetic) ( because it’s an allergy) * *❖** **Chronic cases‐Apply topical corticosteroid** **❖ Recommendations to AVOID:** * ❖ Mouthwash * ❖ Gum/mints * ❖ Cinnamon * ❖ Excessive salty, spicy, acidic ❖ **Patch testing** (we send them to allergist )
2058
**Erythema Multiforme** Treatment
❖Self‐limiting, resolves in a few weeks (It will go away on its own, you just have to manage symptomatically.) ❖Symptomatic management, IV rehydration, corticosteroids (topical and oral), antivirals in recurrent cases (We may use antivirals if they tell us they get cold sores every now and then this means they do have a history of herpes simplex.) ❖ Avoid causative drug (If drug‐related) ❖ Other second‐line systemic therapies (like cyclosporin, azathioprine and other serious drugs) ❖ Usually not life threatening unless in major form.
2059
Nicotine inhaler Precautions/Contraindications
Reactive Airway Disease
2060
Nictotine Nasal Spray Precautions
Reactive Ariway diseases Not recomended for pts with Chronic Nasal diseases ( nasal polyps & sinusitis)
2061
**Sustrained Release Buprooion** Contraindications
* Seizure disorders * Current use of bullrin or MAO inhibitor * Eating disorder (bulimia, anorexia) * Alcohol * Head trauma ## Footnote *Moniter Blood presssure*
2062
**Varenicline Tartlrate** Precaustions
* women breasfeeding should avoid * pt with kidney problems -adjust dose
2063
Nictoine Patch Precutions
* Caution with 6 months of MI
2064
Nictotine Gum Precuations
* poor dentition * maybe inappropriate for use for pts with compelete or partial denture (hard for them to chew)
2065
Nictotine Lozenge Precautions
* Xerostomia
2066
Is Treating Tobacco is within the Scope of Practice of dentists?
Yes ## Footnote •New York State Education Department has deemed that treating tobacco use is part of the scope of practice for dentistry, this includes prescribing smoking cessation products.
2067
First Line Pharmacotherapy in combatting smoking?
* Combination long- and-short acting **Nicotine Replacement Therapy (NRT) (e.g., patch and gum, patch and inhaler)** * **Varenicline alone** * **Bupropion SR** with **NRT** (long- or short-acting)
2068
* What is NRT at the POC? * Rationale for NRT at the POC * Who will hand the patient NRT? * What kind of NRT will be on stock? * How to distribute NRT at POC?
**•What is NRT at the POC?** –Distribution of a free starter pack of NRT to all smokers by clinic staff during the clinic visit **•Rationale for NRT at the POC** –NRT doubles the success rate of patients’ quit attempts –Inconvenience of purchasing RNT or filling a prescription creates barriers –The clinic is an opportune time to intervene **•Who will hand the patient NRT?** –Dental Students **•What kind of NRT will be on stock?** •Nicotine Patch, Gum, and Lozenge **•How to distribute NRT at POC?** –Take faculty-approved NRT request form to dispensary, where NRT is stored.
2069
What is the The most effective treatment for smoking cessation
**a combination of pharmacotherapy and counseling**
2070
TREATING TOBACCO DEPENDENCE: A 2-PART PROBLEM
2071
Why is it so hard to quit: Nicotine addiction?
2072
What are the symptoms of Nicotine Withdrawal?
■Irritability/frustration/anger ■Anxiety ■Difficulty concentrating ■Restlessness/impatience ■Depressed mood/depression ■Insomnia ■Impaired performance ■Increased appetite/weight gain ■Cravings
2073
WHAT WORKS (5A’s)
* **Ask** about tobacco use and secondhand smoke exposure * **Advise** to quit * **Assess** interest in quitting * **Assist** in quit attempt (referral and or pharmacotherapy) * **Arrange** for a follow-up
2074
Assist-Prescribe FDA-Approved Medications