Chapter 16: Oral and Salivary Glands Flashcards

(127 cards)

1
Q

___________ is one of the most common diseases in the world and a major cause of tooth loss before 35YO.

A

Dental carries (tooth decay)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are dental carries?

Reversible?

A
  • Tooth decay that occurs when there is focal demineralization of a tooth – enamel and dentin—by acid metabolites of fermenting sugar that is made by bacteria.
    • Reversible up until cavitation (hole is formed)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where are rates of dental carries highest and lowest?

A
  • Dropping in countries like US where oral hygeine is improving and fluoridation of water occurs.
  • Increase rate in developing countries (eating more processed food)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are symptoms of dental carries?

A
  1. Pain to the point where it affects activities of daily living
  2. WL/nutritional problems
  3. Loss of self-esteem/confidence
  4. Potentially life threatening infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is gingivitis?

Who is it most common in?

A

a reversible inflammation of the gums due to poor oral hygeine.

Most common in adolescence.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What causes gingivitis?

A

Gingivitis is caused by dental plaques that build up under gumline, which mineralized to form calculus (tarter).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are dental plaques?

A
  • sticky, clear, biofilm that collects between and on the surface of the teeth.
  • it contains a mixture of [bacteria, salivary proteins and desquamative epithelial cells]. If plaque is not removed => mineralized => forms calculus (tarter).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What changes charcterize gingivitis?

A
  1. Redness of gums
  2. edema,
  3. bleeding,
  4. changes in countor,
  5. less of soft tissue adaptation of the teeth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

_________ is always preceeded by gingivitis, however gingivitis does not always progress into it.

A

Periodonitis (gum disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Periodontitis?

A

Chronic inflammatory process affecting the supporting structures of the teeth (peridontal lig.), alveolar bone, and cementum, that causes teeth loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Periodontitis can lead to what?

A

gums can pull away from the tooth, bone can be lost, and the teeth may loosen or fall out.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Periodontitis is caused by _______________ in the mouth that affect surrounding tissue. What bacteria is normally found in our mouth?

A
  • - Anaerobic and microaerophilic gram (-) bacteria
  • - Facultative gram (+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which systemic diseases increase the risk of Periodontitis?

A
    • AIDS
    • Leukemia
    • Chron disease
    • DM
    • Down syndrome (high risk for leukemia)
    • Sarcoidosis
    • Dz asso. w/ defect in neutrophils (Chediak-Higashi, agranulocytosis, and cyclic neutropenia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Adult periodontitis is primarily associated with which bacteria?

A
    1. Aggregatibacter (actinobaccilus) actinomycetemcomitans
    1. Prophyromonas gingivalis
    1. Prevotella intermedia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which diseases can periodontal infections be the origin for?

A

- Infective endocarditis

- Pulmonary and Brain abscesses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Common, often recurrent, painful superficial oral mucosal ulcers whose cause is not known.

A

Aphthous ulcers (canker sores)

  • D/t stress and gray/blue base surrounded by erythema.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Reactive lesions in the mouth (fibrous proliferations) include ___________ and are ALL __________.

A
  1. Traumatic fibroma/irritation fibroma
  2. Pyrogenic granuloma
    • all BENIGN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which inflammatory lesion is typically found on the gingiva of children, young adults, and pregnant woman (pregnancy tumor)?

A

Pyogenic granuloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Trauma fibroma (irritation fibroma)

A

Trauma fibroma (irritation fibroma)

Submucosal nodule of CT that formed due to trauma, most common along bite line and ginigiva.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the 3 important inflammatory/reactive lesions?

A
  • 1. Aphthous ulcers (canker sores)
    1. Fibrous proliferative lesions
      * Irritation fibroma/traumatic fibroma
      * Pyogenic granuloma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Canker sores (apthous ulcers) are most common when?

A

0-20 YO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Canker sores are commonly seen in what diseases?

A
  • 1. Celiacs disease
  • 2. IBD
  • 3. Behcets disease

CIB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is an ulcer?

A
  • Breach in the surface of a tissue or organ that is made by the shedding of inflamed necrotic tissue.
    • ONLY occurs when tissue necrosis and inflammation exist on or near a surface.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where do ulcers most commonly occur?

A
  1. Mucosa of mouth, stomach, intestines, GU tract
  2. Skin or subQ tissue of LE in older people who have circulation problems that predispose to ischemic necrosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Describe the **bacterial infiltrates** in canker sores.
* At first, **largely mononuclear.** * Secondary bacterial infection may be d/t **neutrophilic infiltrate.**
26
Describe the features of **pyogenic granuloma** and its course.
* **Red/purple lesion** that is ulcerated. * Highly vascular proliferation of organzing granulation tissue. Course: * Regress into dense fibrous mass. * Develop into a peripheral ossifying fibroma.
27
What **infections** can occur in the **oral cavity**?
1. **HSV 1 \*\* and oral HSV 2 (genital herpes)** 2. **Candida** 3. **Deep fungal infections**
28
What are other **viral infections** that can involve the oral cavity?
* 1. **Herpes zoster** * 2. **EBV** (mononucleosis, nasopharyngeal carcinoma, lymphoma) * 3. **CMV** * 4. **Enterovirus** (herpangina, hand-foot-mouth disease, acutre lymphonodular pharyngitis) * 5. **Rubeola** (meales)
29
**HSV** occurs most commonly in _________ and are often...
* **2-4 YO** * **Asymptomatic** (& do not cause significant morbidity)
30
10-20% of primary infections of HSV can present as \_\_\_\_\_\_\_\_\_\_\_\_\_, with *abrupt onset* of vesicles and ulcers in the mouth, particularly the *gums*. These lesions are also accompanied by what symptoms?
**acute herpetic gingivostomatitis** Symptoms: * lymphadenopathy * fever * anorexia * irritability
31
Which test is diagnostic for **Acute Herpetic Gingivostomatitis**? What are you looking for?
- **Tzanck test (**microscopic examination of the vesicle fluid) 1. Multinucleate polykaryons (giant cells) 2. Eosinophilic intranuclear viral inclusions
32
What is the course of vesicles and ulcers seen in **Acute Herpetic Gingivostomatitis?**
* ***First:** vesicles* filled with a clear, serous fluid * ***Rupture quickly*** and create painful, red-rimmed shallow ulcers. - Spontaneously go away in 3-4 weeks, but the virus then travels along regional nerves and becomes latent in local ganglion (**trigeminal/semilunar ganglion)** - Reactivated during stress or sunlight, leading to vesicles (cold sores) on the lips
33
With HSV, infection is most common and most adults have \_\_\_\_\_\_\_\_.
**latent HSV-1**
34
Viral reactivation of HSV (**recurrent herpectic stomatitis**) occurs where?
* Site of primary inoculation or adjacent mucosa assx with the same ganglion & go away in 7-10 days. * Groups of small vesicles on the lips, nasal orifices, buccal mucosa, gum and hard palate.
35
What is the most common **fungal** infection of the oral cavity and a *NL part* of the oral flora in 50% of the population?
**Candidiasis (thrush)**
36
Which form of **Oral Candidiasis** is the most common? How does it appear in the oral cavity?
- **Pseudomembranous (thrush)** - Superficial, gray to white inflammatory membrane, that can be readily scraped off, revealing red inflammation.
37
**Oral candidiasis** remains \_\_\_\_\_\_\_\_, except in people with immunosupression.
**superficial**
38
Which infection produces a characteristic **dirty white, fibrinosuppurative**, **tough, inflammatory membrane** over the **tonsils** & **retropharynx**?
**Diptheria**
39
What oral findings do we see in patients with **measles?**
**1. Spotty enanthema (ulcers or eruptions in the buccal mucosa)** that occur before a skin rash 2. =\> Koplik spots via Stenson Ducts (small red lesions with blue/white centers)
40
Pt presenting w/ a fiery red tongue w/ prominent papillae (**raspberry tongue)**; white-coated tongue through which hyperemic papillae project (strawberry tongue) should raise suspicion of which infection and organism?
- **Scarlet Fever** - **Strep pyogenes --\> Gram (+)**
41
What oral findings do you see in a patient with **infectious** **mono (EBV= a dsDNA virus)?**
1. **Acute pharyngitis** and **tonsilitis** with a **grey/white exudutaive membrane** 2. **Petechiae** on the **palate** 3. **Large LN in neck**
42
Which infection * **HIV** predisposes ppl to oral infections \_\_\_\_\_\_\_\_, _______ and \_\_\_\_\_\_\_\_ * OR is a common diagnosis in people with ___________ and \_\_\_\_\_\_\_\_\_
1. **Herpes** 2. **Candida** 3. **Other fungi** **Karposi sarcoma** and **hairy luekoplakia**
43
In addition to superficial funal infections, which occur at sites of infection, certain **deep fungal infections** have a predilection for the oral cavity, head and neck. What are they?
1. **Aspergillosis** 2. **Cryptococcosis** 3. **Murcomycosis** Other: * Histoplasmosis, Blastomycosis, Coccidiodomycosis, Zygmocosis
44
What is the key predisposing factor for **deep fungal infections** (infections that have a predilection for oral cavity/head and neck?
**Immunosupression**
45
46
* **Hairy leukoplakia** is caused by what virus? * Found where in oral cavity? * Oral manifestation of what systemic diseases?
- **EBV =\> squamous cell hyperplasia (**NOT pre-malignant and no dysplasia occurs) - white, fluffy (hairy), hyperkeratotic patches on l**ateral border of the tongue** **- Immunosupression (AIDS);**
47
It is __________ for oral lesions to be the 1st sign of some underlying systemic condition.
**common**
48
**Hairy leukoplakia** is characterized by what 2 distinct microscopic features?
* 1. **Hyperparakeratosis** * 2. **Acanthosis (diffuse epidermal hyperplasia)** with "balloon cells" in the upper spinous layer
49
How is oral hairy leukoplakia different than candida in how it looks?
Oral hairy leukoplakia **CANNOT** be scraped off.
50
\_\_\_\_\_\_\_\_\_\_\_\_\_ are oral mucosa lesions that can undergo **malignant transformation (dyplasia)** to **squamous cell carcinoma**
**Leukoplakias** and **erythroplakias** both precursor lesions
51
\_\_\_\_\_\_\_\_ is a **white patch** or **plaque** with **SHARP borders** that cannot be scraped off and cannot be characterized clinically or pathologically as another other disease.
**Leukoplakia** Plakia = plate or flat plane
52
Until proven otherwise, **all** **leukoplakias** must be considered \_\_\_\_\_\_\_\_\_\_.
**Precancerous** (up to 25% are precancerous)
53
What is a **erythroplakia?** How is it different from leukoplakia?
* **Red, velvety eroded patch** in the oral cavity that is at **level** or a **little depressed** with surrounding mucosa. * Different from leukoplakia: * **less common** * **epithelium** is **VERY atypical** * **malignant transformation is HIGHER.**
54
What are the histological changes of the epithelium seen in virtually all (90%) of **erythroplakia**?
1. Severe dysplasia 2. Carcinoma in situ 3. Minimally invasive carcinoma
55
What are the histological changes of the epithelium in **leukoplakias**?
**Hyperkeratosis** over a **thick, orderly acanthotic mucosal epithelium**, but can undergo severe dysplasia and become CIS.
56
Around **95% of the cancers** of the head and neck are of which type? Remainder largely consists of which type?
* - **Squamous Cell Carcinoma (SCC)** = majority (95%) * - **Adenocarcinomas of salivary gland** = remainder
57
The pathogenesis of **squamous cell carcinoma** is \_\_\_\_\_\_\_\_\_\_\_\_.
**_Multifactorial_** 1. **Smoked tobacco** & **alcohol** 2. **HPV (in oropharynx)** 3. **Betel quid** & **paan** (in **India** & **Asia**)
58
What are predisposing risk factors of **squamous cell carcinoma** of the **lower lip?**
1. **Actinic radiation (sunlight)** 2. **Pipe smoking**
59
The incidence of **oral cavity SCC** (particulary the tongue) is on the rise in whom?
**Ppl \< 40 YO** with **no known risk factors**
60
In the oropharynx, as many as **70% of SCCs,** particularly those involving the [**tonsils**, **base of the tongue**, and the **pharynx**] harbor what?
- Oncogenic variants of **HPV** - Particularly **HPV-16**
61
Unlike the \_\_\_\_\_\_\_\_, **HPV-associated SCC** of the oral cavity is \_\_\_\_\_\_\_\_.
**oropharynx** **uncommon**
62
_Survival of SCC is dependent on a number of factors including the etiology of SCC._ ## Footnote What is the prognosis (5-year survival rate) of the "classic" (smoking and alcohol related) early-stage SCC? Late stage?
- **Good (80%)** ## Footnote **- 20%**
63
Patients with **HPV (+) SCC** have _______ long-term survival than those with **HPV (-) tumors?**
**BETTER** prognosis if p16+ - HPV (-) = worse prognosis
64
What is the basis of **"Field Cancerization"**?
* After repeated carcinogenic exposure, the entire superficial epithelium of the upper aerodigestive tract has a ↑ risk of developing pre-malignant lesions as a result of multiple genetic abnormalities * Development of tumors **decreases survival.**
65
The 5-year survival rate of the first primary tumor is \_\_\_\_\_\_\_, but in the same people, second primary tumors are \_\_\_\_\_\_\_\_\_\_\_.
* better than 50% * most common cause of death
66
Which genetic mutations are commonly associated with the **"classic - tobacco/alcohol" SCC subset**?
1. **p53 pathway** 2. Proteins that regulate squamous cell differentiation **(p63 and NOTCH1)**
67
What is typically overexpressed in **HPV-associated SCC's**? Other common genetic alterations?
**Have fewer and different genetic alterations.** 1. **p16** (cyclin dependent kinase inhibitor) **overexpression** 2. **p53 inactivation** --\> E6 expression 3. **RB inactivation** --\> E7 expression
68
What is the molecular progression of **oral** **SqCC**? Does it always progress in this manner?
**NL** =\> hyperplasia/hyperkeratosis =\> mild/moderate dysplasia =\> severe dysplasia/CIS =\> **SCC** No, not always linear over a uniform period or time.
69
What is the most common genetic alteration associated with 1. **NL** =\> hyperplasia/hyperkeratosis and mild/mooderate dysplasia? 2. **Mild/moderate dysplasia** =\> severe dysplasia/CIS? 3. **Severe dysplasia/CIS** =\> SCC?
1. 9p21 (**p16)**, **3p** 2. **TP53** 3. **Cyclin D (11q13);** 4q, 6p, 8p, 13q, 14q
70
What is the typical age of onset and sex most affected by leukoplakia and erythroplakia?
**- Age 40-70** **- M 2x** more than **F**
71
What are the 5 favored locations in the oral cavity for the development of **classic SCC**?
1. Ventral surface tongue 2. Floor of mouth 3. Lower lip (associated w/ sun exposure and pipe smoking) 4. Soft palate 5. Gum
72
What is the morphology of **oral SCC** in the early stage?
* _1. Raised, firm, pearly plaques_ * _2. Irregular, roughened or verrucous areas of mucosal thickening_ _(_may look like leukoplacia) that are superimposed on obvi leukoplakia or erythroplakia
73
As early stages of **SCC carcinoma** enlarge, what do they look like?
**Ulcerated**, **protruding** mass that have **irregular and indurated (rolled) borders.**
74
What is the difference in progression of oral SCC and cervical cancer?
* **Oral SCC:** dysplastic lesions **MAY OR MAY NOT** progress into full-thickness dysplasia (CIS) before invading underlying CT. * **Cervical cancer:** [full thickness dysplasia =\> invasion].
75
Is the degree of keratinization in **oral SCC** correlated with behavior?
**No.**
76
What are the favored sites for local metastasis of **oral SCC**? Favored sites for distal metastasis?
- **Local** ---\> cervical LN's - **Distal** ---\> mediastinal LN's, lungs, liver, and bones * Often, when primary lesion is found distant metaseses has occured.
77
Overwhelming majority of **odontogenic cysts** are derived from what?
Remant of odontogenic epithelium within jaws.
78
Which type of **cyst** occurs when fluid accumulates between developing tooth and dental follicle, forming a cyst originating around the crown of an unerupted tooth?
**Detingerous cyst**
79
Radiographically, **dentigerous cysts** are seen as what type of lesions and most often associated with which teeth? Treatment?
* **- Unilocular lesion** * **- Impacted third molar (wisdom) teeth** * - **Complete removal = curative**
80
What is the significance of **Keratocystic Odontogenic Tumors (OKC's)**?
Must be differentiated from other cysts due to its **aggressive behavior**
81
**Keratocystic Odontogenic Tumors (OKC's)** are most often diagnosed between what ages and which sex is more commonly affected? Form where in the oral cavity?
- **Ages 10-40 yo;** most often in **males** - **Posterior mandible**
82
How do you ID **OKC's** radiographically and histologically?
* Radiographically * Well-defined unilocular or multilocular * Histologically * Cyst is lined by thin layer of keratinized stratified squamous epthilium with a prominant basal layer and corrugated epithelial surface
83
Multiple Keratocystic Odontogenic Tumors (OKC's) occuring in a patient should prompt evaluation for what?
Nevoid basal cell carcinoma **(Gorlin syndrome);** mutation in tumor suppressor PTCH on Chr 9q22
84
Tx of **OKC**
**Surgical removal,** because they are locally agressive and recurr
85
What is **xerostomia**?
**↓ production of saliva,** causing dry mouth and/or atrophy of papillae on the tongue with fissures and ulcers.
86
**Xerostomia** is a major feature of?
**Sjorgren Syndrome**
87
Complications of **Xerstomia** include increased rates of?
1. **Dental carries** 2. **Candidiasis** 3. **Difficulty swallowing** and **speaking**
88
**Xerostomia** is most frequently a side-effect of what?
**_Meds_** 1. Anti-cholinergic 2. Anti-depressant 3. Ant-psychotic 4. Diuretic 5. Anti-HTN 6. Sedative, muscle rexant, analgesic 7. Anti-histamine
89
\_\_\_\_\_\_\_\_\_\_ is an inflammation of the salivary glands, caused by what?
**Sialadenitis,** caused by trauma, infection or AI reaction
90
What is the most common type of **inflammatory** salivary gland lesion?
**Mucoceles**
91
* **Mucoceles** are caused by what? * Most commonly found where in oral cavity and due to what?
* **Trauma** or **blockage** of a salivary gland duct, causing saliva to leak into the surrounding CT stroma. * Most often _LOWER LIP_ due to TRAUMA
92
How do **mucoceles** present clinically (i.e., how do they look on examination)? Patients often report what in regards to the size of the lesion?
- Fluctuant swellings of lower lip that have a blue translucent hue - Often report hx of changes in size in assoc. w/ meals
93
What is the histological characteristics of **Mucoceles**? Most common inflammatory cell present?
- Pseudocysts w/ cyst-like spaces, filled with mucin, lined by granulation tissue or fibrous CT - **MACROPHAGES**
94
What is the Tx for **Mucoceles**?
Complete excision of the **cyst** and its accompanying minor salivary gland
95
What is a **Ranula**?
Epithelial-lined cysts that arise when duct of **sublingual gland** has been damaged
96
a 45 YO F presents with dry mouth followed by pain. Pain increases when eating. PMH dx Sjrogens sundrome. Which duct is asspocated with the involved gland? ## Footnote ***Secretion of which of the following is most likely affected?***
**Stensen's**
97
1. **Parotid gland** secretes what? 2. **Submucosa layer** of the tongue secretes what?
1. **Salivary amylase** 2. **Lingual lipase**
98
The prescence of **xerostomia** in **BMS** (**burning mouth syndrome**) suggests what?
The disease may involve **hypofunctioning of the parasympathetic NS**, a target of OMT to normalize activity.
99
**Bacterial sialadenitis**, most often involves the __________ glands and is a common condition secondary to \_\_\_\_\_\_\_\_\_\_\_
Bacterial sialadenitis, most often involves the **submandibular gland**s and is a common condition **secondary to sialolithiasis (ductal obstruction by stones)**
100
What are the 2 most common organisms responsible for **sialolithiasis** leading to sialadentitis? Unilateral or bilateral process?
**1) S. aureus** **2) S. viridans** - UNILATERAL -
101
A patient presenting with **unilateral**, sialadentitis with **overt suppurative necrosis and abscess formation** should raise suspicion of?
**Sialolithiasis** causing sialadentitis, likely due to S. aureus or S. viridans.
102
Overall, **salivary gland neoplasms** are _______________ and occur in whom? What is the difference between when benign and malignant tumors appear?
**- Relatively uncommon** **- Adults (F)** **- Benign (50-70s); malignant (later)**
103
The likelihood of a salivary gland tumor being malignant is more or less ___________ proportional to the size of the gland
* **Inversely** * **\*Smaller the gland = higher risk of malignancy**
104
Majority of salivary gland tumors arise where?
**Parotid gland**
105
What is the most common tumor of the salivary gland and is it benign or malignant?
**Pleomorphic adenoma** -- 50% of benign tumors, but 60% of tumors in parotid.
106
**Pleomorphic adenomas** contain a mixture of _________ and _________ cells
Pleomorphic adenomas contain a mixture of **ductal (epithelial)** and **myoepithelial cells** * \*MIXED tumor
107
Exposure to what increases risk for **Pleomorphic Adenomas**? Associated with what genetic mutation?
- **Radiation** - **PLAG1 overexpression** --\> ↑ cell growth
108
How do **pleiomorphic adenomas** present clinically (i.e., mass where, any pain, and rate of growth)?
* **Painless**, **slow-growing**, **mobile**, **discrete masses** in the _parotid/__submandibular gland_ or in the **buccal cavity**
109
What type of tumor is shown here and how can you tell?
* **Pleomorphic adenoma** * DOMINANT histological feature = **GREAT heterogeneity** * Well-demarcated tumor w/ epithelial cells and myoepithelial cells arranged in ducts, strands or sheets within a chondroid matrix.
110
In most cases of **pleomorphic adenoma,** is there epithelial dysplasia or mitotic activity?
**No**
111
What is the prognosis of a **malignant pleomorphic adenoma** (i.e., carcinoma ex pleomorphic adenoma)?
- Most aggressive of all salivary gland tumors - Mortality rates of 30-50% at 5 years
112
Which **benign** tumor almost always occurs in the **parotid gland**?
**Warthin Tumor** (aka papillary cystadenoma lymphomatosum): a cystic tumor with alot of lymphocytes + germinal centers that almost ALWAYS occurs in parotid gland
113
When do **Warthin tumors** usually arise? Which sex is most affected? What is a major risk factor?
- **50-70s** - **Males** - **Smokers** have 8x the risk
114
What are some of the distinct morphological characteristics of a **Warthin tumor**?
- Round to oval encapsulated mass (2-5 cm in diameter) in superficial parotid gland - Lined by double layer of cells resting on dense lymphoid stroma, sometimes w/ GERMINAL centers * Upper layer = palisading columnar cells w/ abundant, finely granular, eosinophilic cytoplasm. * Granular bc many mT (oncocytic) * Lower layer = cuboidal to polygonal cells
115
What is the reason for the granular appearance of the cytoplasm in the upper layer of cells seen in **Warthin Tumors?**
**NUMEROUS mitochondria**, feature referred to as "oncocytic"
116
What is the most common primary **malignancy** of the **oral mucosal**?
**Mucoepidermoid carcinoma** (makes up 15% of all salivary gland tumors)
117
Where do **mucoepidermoid carcinom**a occur most often?
**60-70%** occur in **parotid gland**, but also minor salivary glands
118
Which genetic mutation (i.e., translocation and gene products) is thought to play a key role in **Mucoepidermoid carcinoma?**
- **Balanced (11;19) (q21;p13) translocation,** creating **MECT1-MAML2 fusion gene.**
119
The prognosis of **mucoepidermoid carcinoma** depends on what?
**GRADE**
120
What are the histological characteristics of a **mucoepidermoid carcinoma**? How large do they grow?
- Cords, sheets, or cystic configurations of **squamous**, **mucous**, or **intermediate cells** - Grow to 8 cm in diameter and are **circumscribed**, but **lack well-defined capsules** and are **infiltrate** at margins
121
Which stain helps to visualize a **mucoepidermoid carcinoma?**
**Mucin stains**
122
What is the prognosis of both low-grade and high-grade Mucoepidermoid Carcinomas?
- **Low grade** ---\> 5-year survival of **90%** - **High grade** ---\> 5-year survival of **50%**
123
**Adenoid cystic carcinoma** is most often seen where?
- **Minor salivary glands** (particularly the *palatine glands); 50%* - May also be seen in major salivary glands (parotid and submandibular)
124
What is the morphology of **Adenoid cystic carcinomas?**
- Small, poorly encapsulated, infiltrative, gray-pink lesions that create a a cribiform pattern - Small cells w/ dark, compact nuclei and scant cytoplasm
125
**Describe the cancer seen here and its distinct morphology.**
Adenoid cystic carcinoma of the salivary gland creating a **Cribiform pattern** \*Gaps between the cancer cells within the duct, with an appearance similar to the ‘holes in swiss cheese‘ or perhaps ‘ripples‘.
126
**Adenoid cystic carcinomas** cause what distinct symptom?
**Pain**, bc invade perineural spaces and metastize to bone, liver, and brain
127