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Oral Path 100 > More diseaess > Flashcards

More diseaess Flashcards

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
Q

What is this clinical presentation?

pts takes allopurinol

A

Oral Lichenoid Drug
Reaction

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26
Q

Oral Lichenoid
Contact Lesions

Etiology

A

Hypersensitivity

to

  • dental restorative materials, amalgam or other metal, composite resins
  • Foods, oral products
  • Especially cinnamon
  • dental plaque accumulation are the most common
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27
Q

Oral Lichenoid Drug
Reaction

Etiology

A
  • 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
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28
Q

Oral lichenoid reaction

Treatment

A

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.

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29
Q

What is this clinical presentation?

A

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
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30
Q

What is this clinical presentation?

A

Nicotinic Stomatitis

These papules represent inflamed minor salivary glands and their ductal orifices.

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31
Q

What is this clinical presentation

A

Nicotine Stomatitis.

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32
Q

Nicotine Stomatitis

Treatment

A

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.
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33
Q

Nicotine Stomatitis.

Etiology

A

The elevated temperature, rather than the tobacco chemicals,
is responsible for this lesion.

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34
Q

What is this clinical presentation?

A

Pseudomembranous candidiasis

on the palate.

usually caused by Candida albicans

Predisposing factors are local

(poor oral hygiene, xerostomia, mucosal
damage, dentures, antibiotic mouthwashes)

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35
Q

What is this clinical presentation?

A

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
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36
Q

What is this clinical presentation?

A

Geographic tongue/
areata migrans

37
Q

What is this clinical presentation?

A

Geographic tongue/
areata migrans

38
Q

What is this clinical presentation?

A

Geographic tongue/
areata migrans

39
Q

What is this clinical presentation?

A

Geographic tongue, localized lesion.

40
Q

Geographic tongue/
areata migrans

Treatment

A
  • 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
Q

Geographic tongue/
areata migrans

Etiology

A

The exact etiology remains unknown. It may be genetic.

42
Q

What is this clinical presentation?

A

Fordyce’s granules

on the buccal mucosa.

a normal anatomical variation.

ectopic sebaceous glands of the oral
mucosa.

43
Q

What is this clinical presentation?

A

Leukoedema of the buccal mucosa.
Laskaris,

44
Q

Leukoedema

Etiology

Treatment

A

Etiology

It is due to increased thickness of the epitheliumand intracellular
edema of the prickle-cell layer.

Treatment

No treatment required

45
Q

What is this clinical presentation?

A

White Sponge Nevus

Diffuse, thickened white plaques
of the buccal mucosa

46
Q

What is this clinical presentation?

A

White Sponge Nevus

(Canon disease)

47
Q

White Sponge Nevus

Etiology

A

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
Q

What is this clinical presentation?

A

Verrucous Carcinoma

Early verrucous carcinoma of the buccal mucosa.

49
Q

What is this clinical presentation?

A

Verrucous Carcinoma

Large, exophytic, papillary
mass of the maxillary alveolar ridge.

50
Q

What is this clinical presentation?

A

Verrucous Carcinoma

Large, exophytic, papillary
mass of the maxillary alveolar ridge.

51
Q

What is this clinical presentation?

A

Verrucous Carcinoma

Extensive papillary, white
lesion of the maxillary vestibule

52
Q

Verrucous Carcinoma

Etiology

A

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
Q

Verrucous Carcinoma

Treatment

A

○ Surgical Excision

○ Radiotherapy

54
Q
A

Traumatic Erythema /Traumatic Hematoma

on the lower lip.

55
Q

What is this clinical presentation?

A

Geographic tongue: well-demarcated red patch on the tongue.

56
Q

What is this clinical presentation?

A

Median rhomboid glossitis.

a Chronic hyperplastic, erythematous candidiasis

57
Q

Median Rhomboid Glossitis

Treatment

A

No treatment is required.

58
Q

Median Rhomboid Glossitis

Etiology

A

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
Q

what is this clinical presentation?

A

Denture stomatitis.

60
Q

Erythroplakia

Malignant transformation

A

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
Q

What is this clinical presentation?

A

Erythroplakia

of the buccal mucosa

Well-demarcated erythematous patch or plaque with soft velvety texture

62
Q

What is this clinical presentation?

A

Erythroplakia of the buccal mucosa.

63
Q

What is this clinical presentation?

A

Erythroplakia

of the lateral margin of the tongue.

Well-demarcated erythematous patch or plaque with soft velvety texture

64
Q

What is this clinical presentation?

A

Erythroplakia

Firey red Well-demarcated patch or plaque with soft velvety texture

transformed into SCC

65
Q

Erythroplakia

Treatment

A

○ 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
Q

What is this clinical presentation?

A

Erythroplakia.

Well-circumscribed red patch on the
posterior lateral hard and soft palate

67
Q

What is this clinical presentation?

A

Erythroplakia.

Erythematous macule on the right
floor of the mouth.

Biopsy–

Turned out to be early invasive squamous cell
carcinoma.

68
Q

What is this clinical presentation?

A

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS

Smokeless Tobacco–related Gingival Recession.
Extensive recession of the anterior mandibular facial gingiv

69
Q

What is this clinical presentation?

A

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS

Tobacco Pouch Keratosis, Severe

70
Q

What is this clinical presentation?

A

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
Q

Smokeless tobacco keratosis

Treatment:

A

typically resolves weeks after cessation

○ if persists 6+weeks -> biopsy to rule out dysplasia + SCC

72
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

. Multiple erosions affecting the
marginal gingiva.

73
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

Multiple erosions of the left
buccal mucosa and soft palate.

74
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

Large, irregularly shaped ulcerations
involving the floor of the mouth and ventral tongue.

75
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

76
Q

What is this clinical presentation?

A

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
Q

What is this clinical presentation?

A

Pemphigus vulgaris

PV Lesions can affect
virtually any mucosal
surface (oral, nasal,
ocular, pharyngeal,
esophageal, genital)

78
Q

What is this clinical presentation?

A

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
Q

What is this clinical presentation?

A

Pemphigus vulgaris

Combination of PV
inflammation and
gingival inflammation
accumulating local
factors can result in
advanced loss of
attachment and tooth
loss

80
Q

Pemphigus vulgaris

Etiology

A

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
Q

Pemphigus vulgaris

A

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
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

83
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

SEVERE/HIGH RISK FORMS OF MMP
▪ Ocular
▪ Esophageal

can
result in functional
blindness

84
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

Oral Hygiene: Plaque
related gingival
inflammation
contributing to
continued VB
desquamative
gingivitis

85
Q

What is this clinical presentation?

A

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
Q

Mucous membrane pemphigoid

Etiology

A

Mucocutaneous autoimmune disease characterized by sub‐epithelial
blisters (bullae) which ruptures to form large, non‐healing ulcerations

87
Q

Mucous membrane pemphigoid

Treatment

A

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
Q

MMP & PV BIOPSY

A

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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