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Oral Path 100 > More diseaess > Flashcards

More diseaess Flashcards

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1
Q

What is this clinical presentation?

A

Homogeneous leukoplakia

○ Thickened leathery, White plaque
○ Well-demarcated, Deepened fissures
○ Non-wipeable white patch

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2
Q

What is this clinical presentation?

A

Homogeneous leukoplakia.

○ Non-wipeable white patch

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3
Q

What is this clinical presentation?

A

homogenous leukoplakia

Just
white color

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4
Q

What is this clinical presentation?

A

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

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5
Q

What is this clinical presentation?

A

Speckled leukoplakia.

Non-homogenous leukoplakia

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6
Q

Leukoplakia

Etiology

A

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.

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7
Q

Leukoplakia

Treatment

A
  • 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
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8
Q

What is this clinical presentation?

A

Hairy Leukoplakia

corrugated white lesion on the lateral tongue.
• It only occurs on the lateral tongue

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9
Q

What is this clinical presentation?

A

Hairy Leukoplakia

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10
Q

Hairy Leukoplakia

Etiology

A

Epstein–Barr virus seems to play an important role in the
pathogenesis.

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11
Q

Hairy Leukoplakia

Treatment

A
  • Not required
  • however, in some cases aciclovir or valaciclovir
  • can be used with success.
  • Topical retinoids or podophyllum resin for temporary remission
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12
Q

What is this clinical presentation?

A

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

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13
Q

What is this clinical presentation?

A

Proliferative Verrucous Leukoplakia

Location
○ Gingiva (Frequent)
○ Buccal Mucosa
○ Palatal Mucosa

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14
Q

What is this clinical presentation?

A

Proliferative Verrucous Leukoplakia

Multifocal

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15
Q

Proliferative Verrucous Leukoplakia

Treatment

A

complete removal: excision, electrocautery, cryosurgery, or laber ablation

Lesions rarely regress despite therapy

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16
Q

What is this clinical presentation?

A

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

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17
Q

What is this clinical presentation?

A

Oral lichen planus

on the buccal mucosa (most common site

reticular form.

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18
Q

What is this clinical presentation?

A

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

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19
Q

What is this clinical presentation?

A

Oral lichen planus

Lichen planus of the dorsum of the tongue

this is a hypertrophic form.

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20
Q

Oral lichen planus

Etiology

A

Although the cause is not well known, T cell-mediated autoimmune
phenomena are involved in the pathogenesis of lichen planus.

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21
Q

Oral lichen planus

Treatment:

A
  • Incisional biopsy on non-keratinized, non-ulcerated mucosa

○ Asymptomatic → no tx
○ Symptomatic → 0.5mg/ml Dexamethasone Elixir.

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22
Q

What is this clinical presentation?

A

Lichenoid Reactions

Contact Lesions

a sensitivity in contact with a dental amalgam
▪ When you replace these amalgams, the lichenoid reaction will typically
disappear

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23
Q

What is this clinical presentation?

A

Oral Lichenoid

Contact lesion

chenoid reaction to dental amalgam and cold: white and erythematous
lesions on the buccal mucosa.

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24
Q

What is this clinical presentation?

pts takes Thiazide Diuretic

A

Oral Lichenoid Drug
Reaction

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25
What is this clinical presentation? pts takes *allopurinol*
Oral Lichenoid Drug Reaction
26
**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
27
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
28
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.
29
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
30
What is this clinical presentation?
**Nicotinic Stomatitis** These papules represent _inflamed minor salivary glands_ and their ductal orifices.
31
What is this clinical presentation
Nicotine Stomatitis.
32
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.
33
Nicotine Stomatitis. Etiology
The elevated temperature, rather than the tobacco chemicals, is responsible for this lesion.
34
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)
35
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
36
What is this clinical presentation?
Geographic tongue/ areata migrans
37
What is this clinical presentation?
Geographic tongue/ areata migrans
38
What is this clinical presentation?
Geographic tongue/ areata migrans
39
What is this clinical presentation?
Geographic tongue, localized lesion.
40
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
41
Geographic tongue/ areata migrans _Etiology_
The exact etiology remains unknown. It may be genetic.
42
What is this clinical presentation?
**Fordyce’s granules** on the buccal mucosa. a normal anatomical variation. ectopic sebaceous glands of the oral mucosa.
43
What is this clinical presentation?
Leukoedema of the buccal mucosa. Laskaris,
44
Leukoedema Etiology Treatment
Etiology It is due to increased thickness of the epitheliumand intracellular edema of the prickle-cell layer. Treatment No treatment required
45
What is this clinical presentation?
White Sponge Nevus Diffuse, thickened white plaques of the buccal mucosa
46
What is this clinical presentation?
White Sponge Nevus | (Canon disease)
47
**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.
48
What is this clinical presentation?
**Verrucous Carcinoma** Early verrucous carcinoma of the buccal mucosa.
49
What is this clinical presentation?
**Verrucous Carcinoma** Large, exophytic, papillary mass of the maxillary alveolar ridge.
50
What is this clinical presentation?
**Verrucous Carcinoma** Large, exophytic, papillary mass of the maxillary alveolar ridge.
51
What is this clinical presentation?
Verrucous Carcinoma Extensive papillary, white lesion of the maxillary vestibule
52
**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
53
**Verrucous Carcinoma** Treatment
○ Surgical Excision ○ Radiotherapy
54
Traumatic Erythema /Traumatic Hematoma on the lower lip.
55
What is this clinical presentation?
Geographic tongue: well-demarcated red patch on the tongue.
56
What is this clinical presentation?
Median rhomboid glossitis. a Chronic hyperplastic, erythematous candidiasis
57
Median Rhomboid Glossitis Treatment
No treatment is required.
58
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**
59
what is this clinical presentation?
Denture stomatitis.
60
**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
61
What is this clinical presentation?
**Erythroplakia** of the buccal mucosa Well-demarcated erythematous patch or plaque with soft velvety texture
62
What is this clinical presentation?
Erythroplakia of the buccal mucosa.
63
What is this clinical presentation?
**Erythroplakia** of the lateral margin of the tongue. Well-demarcated erythematous patch or plaque with soft velvety texture
64
What is this clinical presentation?
Erythroplakia Firey red Well-demarcated patch or plaque with soft velvety texture transformed into SCC
65
**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
66
What is this clinical presentation?
Erythroplakia. Well-circumscribed red patch on the posterior lateral hard and soft palate
67
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.
68
What is this clinical presentation?
Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS Smokeless Tobacco–related Gingival Recession. Extensive recession of the anterior mandibular facial gingiv
69
What is this clinical presentation?
Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS Tobacco Pouch Keratosis, Severe
70
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.
71
Smokeless tobacco keratosis Treatment:
typically resolves weeks after cessation ○ if persists 6+weeks -\> biopsy to rule out dysplasia + SCC
72
What is this clinical presentation?
**Pemphigus Vulgaris.** . Multiple erosions affecting the marginal gingiva.
73
What is this clinical presentation?
**Pemphigus Vulgaris.** Multiple erosions of the left buccal mucosa and soft palate.
74
What is this clinical presentation?
**Pemphigus Vulgaris.** Large, irregularly shaped ulcerations involving the floor of the mouth and ventral tongue.
75
What is this clinical presentation?
**Pemphigus Vulgaris.**
76
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
77
What is this clinical presentation?
**Pemphigus vulgaris** PV Lesions can affect virtually any mucosal surface (oral, nasal, ocular, pharyngeal, esophageal, genital)
78
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
79
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
80
**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.
81
**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)**
82
**What is this clinical presentation?**
Mucous membrane pemphigoid
83
**What is this clinical presentation?**
Mucous membrane pemphigoid SEVERE/HIGH RISK FORMS OF MMP ▪ Ocular ▪ Esophageal can result in functional blindness
84
**What is this clinical presentation?**
Mucous membrane pemphigoid Oral Hygiene: Plaque related gingival inflammation contributing to continued VB desquamative gingivitis
85
**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
86
**Mucous membrane pemphigoid** **Etiology**
Mucocutaneous autoimmune disease characterized by sub‐epithelial blisters (bullae) which ruptures to form large, non‐healing ulcerations
87
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**
88
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

Oral Path 100 (23 decks)

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