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DMD3 > OPMDs > Flashcards

OPMDs Flashcards

1
Q

What causes leukoplakia and erythroplakia?

A

Tobacco/smoking

Alcohol

Areca nut with or without tobacco

High-risk HPV infection is a rare cause of OPMDs (0.5%)

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2
Q

How common is leukoplakia?

A

Leukoplakia - 1 - 4% in Western countries

Higher prevalence in SE Asia

Global prevalence of 2 - 3%

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3
Q

How common is erythroplakia?

A

More uncommon than leukoplakia 0.02% - 0.83%

More serious with higher malignant potential than leukoplakia

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4
Q

What is the clinical definition of leukoplakia?

A

A predominantly white lesion of questionable risk having excluded other known diseases or disorders that carry no increased risk for cancer.

It cannot have reactive, frictional, traumatic, or other causes.

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5
Q

What does leukoplakia typically look like?

A

White and somewhat variable:

Mostly well demarcated

Fissured

Can be homogenous or non-homogenous

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6
Q

What are the clinical features of erythroplakia?

A

Velvety

Granular

Red

Usually painless

Flat or indurated

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7
Q

What are the levels of histopathological change on the leukoplakia/erythroplakia continuum?

A

If it is smooth and thin it is typically consistent of hyperkeratosis, acanthosis, and lymphocytes predominantly

When it becomes more thick and fissured it exhibits hyperkeratosis, dysplasia (different degrees), lymphocytes (varaible

Verrucous or nodular leukoplakia is non-homogenous and exhibits hyperkeratosis, verrucous epithelial hyperplasia, bullous rete ridges, dysplasia, and lymphocytes.

Erythroplakia with speckled leukoplakia is also non-homogenous with variable hyperkeratosis, bulbous rete ridges, epithelial atrophy, dysplasia, lymphocytes

Erythroplakia has minimal keratosis, epithelial atrophy, bulbous rete ridges, dysplasia (can be carcinoma in situ), lymphocytes

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8
Q

How is epithelial dysplasia graded in OPMDs?

A

A. Hyperkeratosis with normal architecture and cytology

B. Mild dysplasia (lack of polarization of BL, variation in nuclear size/shape/stainability), increased mitotic figures

C. Moderate dysplasia (drop shaped rete ridges, variation in nuclear size, shape, and stainabilty) Increased N:C ratio

D. Severe dysplasia (Loss of cohesion of epithelium, loss of polarity of basal cells, variation in nuclear size and shape, variation in cell shape)

E. Severe dysplasia (Loss of basal polarity and epithelial differentiation and cellular cohesion, increased mitotic figures.

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9
Q

How are leukoplakia and erythroplakia diagnosed?

A

Diagnosis of exclusion

An incisional biopsy is indicated to establish baseline histology.

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10
Q

What tools can be used to aid leukoplakia and erythroplakia diagnosis?

A

Tolonium chloride or toluidine blue dye
– Oral CDx brush biopsy kits
– Salivary diagnostics
– Optical imaging systems
• ViziLite (Zila, Batesville, AR, USA)
• VELscope (LED Dental Inc., Vancouver, Canada)
• DIFOTI (Electro-Optical Sciences, Inc., Irvington, NY,
USA)
• Identafi 3000 (DentalEZ, Bay Minette, AL, USA

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11
Q

How is leukoplakia and erythroplakia treated?

A

Discontinue deleterious social habit that is causing it.

Excisional biopsy is indicated if possible and appropriate.

Watchful monitoring is important.

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12
Q

What is the malignant transformation rate oral leukoplakia?

A

Malignant transformation rate is 1 - 20% over 1 - 30 years

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13
Q

What are the clinical features of palatal lesions in reverse smokers?

A

Females > Males

Middle-posterior half of the palate

Palatal lesions
– Keratosis
– Excrescences
– Leukoplakia
– Ulcerations
– Frank malignancy

Hyperpigmentation
– Well-defined diffuse or focal greyish/black
pigmentation

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14
Q

How can palatal lesions in reverse smokers be diagnosed?

A

Diagnosis is reached through clinical examination and history taking

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15
Q

How can palatal lesions in reverse smokers be treated?

A

Habit cessation

– Manage according to the severity of the disease

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16
Q

What are the histopathological features of palatal lesions in reverse smokers?

A

Biopsy the lesion

– May show hyperkeratosis, dysplasia or frank SCC

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17
Q

What causes oral sub-mucous fibrosis?

A

Areca nut: Abundant copper and flavonoids. Stabilize and enhance cross-linking of collagen
– Fibrosis
– Alkaloids (arecoline)
• Stimulate collagen synthesis and reduce collagen degradation
• Can be converted to carcinogenic nitrosamines

Gutka
– Powdered tobacco, slaked lime, and spices wrapped in Piper betle leaf, also referred
to as “betel leaf”
• more rapid development of oral lesions

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18
Q

What are the clinical features of oral sub-mucous fibrosis?

A 
Diffuse, pale, marble-like, and keratotic areas
• Sites
– Buccal mucosa
– Soft palate
– Tongue

• Symptoms
– Burning
– Increasing trismus

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19
Q

What are the histopathologic features of oral sub-mucous fibrosis?

A

Histopathologic features:

  • Hyperkeratosis
  • Epithelial atrophy
  • Diffuse fibrosis
  • May show evidence of dysplasia or cancer
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20
Q

How can oral submucous fibrosis be diagnosed?

A
  • History and clinical presentation
  • Obtain good clinical images and write comprehensive clinical notes
  • Obtain a biopsy if indicated
  • Watchful monitoring
  • Temporomandibular disorder management
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21
Q

Which clinical trial drug has been indicated as potentially effective in clinical trials?

A

Pentoxifylline

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22
Q

What causes actinic cheilitis?

A

UV light exposure

Aetiology similar to actinic cheilitis of the skin

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23
Q

Who has a higher prevalence of actinic cheilitis?

A

Closer to the equator

Middle-aged to elderly, fair complexioned men

Outdoor occupation

Certain genetic disorders (xeroderma pigmentosum, Albinism, porphyria cutanea tarda)

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24
Q

What are the early clinical features of actinic cheilitis?

A

Atrophy (smooth blotchy pale areas)

Dryness

Fissuring

Blurring of the vermilion border

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25
Q

What are the late clinical features of actinic cheilitis?

A

Rough, scaly areas

May develop leukoplakia

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26
Q

What are the epithelial histolopathologic features of actinic cheilitis?

A

Hyperkeratosis vs atrophy

Varying degrees of epithelial dysplasia

27
Q

What are the connective tissue histolopathologic features of actinic cheilitis?

A

Solar elastosis (Band of amorphous basophilic change)

Chronic inflammation

Dilated blood vessels

28
Q

How is actinic cheilitis treated?

A

Many of the changes are irreversible but reducing sun exposure and wearing sunscreen can reduce progression and prevent it in the first place

29
Q

How is actinic cheilitis diagnosed?

A

Biopsy

30
Q

What are the clinical features of lichen planus?

A

RED WHITE AND ULCERATED.

Types:

Reticular, Papular, Erythematous, Erosive, Plaque like, Bullous

31
Q

What are the histopathologic features of lichen planus?

A

Surface epithelial findings largely depend on clinical presentation

Important criteria are:

Degeneration of the basal cell layer

Lymphocytic band of variable thickness

32
Q

How is oral lichen planus diagnosed?

A

Paper from the american academy recommends obtaining a biopsy from everyone (this is controversial)

33
Q

How is oral lichen planus treated?

A

Symptomatically with mainly anti-inflammatory drugs (Locally or systemically)

34
Q

What causes lupus erythematosus?

A

Contribution of genetics + environment

B and T cell signalling abnormalities

Dysregulated apoptosis and defective clearance of cellular debris

Antibody formation and perpetuation

Autoantibodies and organ damage

35
Q

What are the clinical features of early discoid lupus erythematosus?

A

Red papules/macules or small plaques and rapidly develops a hyperkeratotic surface

36
Q

What are the clinical features of late discoid lupus erythematosus?

A

Sharply demarcated discoid plaques covered by an adherent scale that extends into the orifices of dilated hair follicles

Oral lesions:

Have sharp margins

Irregular scalloped white borders with radiating striae and telandectasia

Honeycomb appearance on the palatal lesion

Painful ulceration is common

37
Q

What are the histopathologic features of late discoid lupus erythematosus?

A

Acanthosis and atrophy of the epithelium

Vacuolar degeneration of basal cells

Bandlike lymph (deep perivascular and paravascular lymphocytic infiltratesocytic infiltrate at the interface)

Positive lupus band test

38
Q

What does the lupus band test show?

A

Linear/granular deposition of IgG, IgM, or IgA at the basement membrane (lupus
band test)

39
Q

How is discoid lupus erythematosus diagnosed?

A

Diagnosis based on clinical presentation and obtaining a biopsy

40
Q

How is discoid lupus erythematosus treated?

A

– Unpredictable relapsing remitting course

– Treatment with immunosuppression

41
Q

What causes oral cancer?

A

Smoking tobacco

Chewing tobacco

Drinking alcohol regularly

Some evidence of HPV and alcohol mouthwash use

42
Q

What are the clinical features of oral cancer?

A

Usually asymptomatic
• The most common chief complaint: discomfort (it usually occurs at late stages)
• Patient may also present with an awareness of a mass in the mouth or neck
• Dysphagia, Odynophagia, otalgia, limited movement, oral bleeding (less
frequently)

43
Q

What are the common sites of OSCC?

A 
• Common sites:
– Floor of the mouth
– Lateral border of tongue
– Retromolar areas
– Lips
– Palate is an unusual location for carcinoma
44
Q

What are the histopathologic features of OSCC?

A

Invasive islands and cords of malignant squamous epithelium

Tumour may also invade deeper structures: bone, muscle, blood vessels.

Inflammatory response to invading epithelium (often) and presence of focal
necrosis

The lesional epithelium is capable of angiogenesis and occasionally
desmoplasia

The lesional cells have eosinophilic cytoplasm and hyperchromatic nuclei (N/C
↑)

Cellular and nuclear pleomorphism

Keratin pearl

45
Q

What is invasion?

A

Irregular extension of lesional epithelium through the basement membrane and into subepithelial connective tissue without attachment to the surface epithelium

46
Q

How are OSCCs graded?

A 
Grading*:
– Well-differentiated:
• Keratin pearls
• Close resemblance of normal epithelium
– Moderately/poorly differentiated
• Less keratinisation
• More nuclear and cellular pleomorphism
47
Q

How are OSCCs diagnosed?

A

Clinical features

Histological findings

Radiographic features

48
Q

How are OSCCs treated?

A

Surgery

Radiation therapy

Chemotherapy

49
Q

How is prognosis achieved and improved for OSCC?

A

Early diagnosis is the key

Site and late onset of symptoms adversely affect early diagnosis

Prognosis decreases with increasing clinical stage

Histopathological features influence prognosis

50
Q

How common is oral SCC?

A

In Australia 3000 new cases of oral or oropharyngeal cancer are diagnosed every year.

> 90% of oral cancers and oropharyngeal cancers are SCCs

Incidence of oral SCC is increasing among young patients.

51
Q

How is OSCC treated?

A

Surgery

Radiation therapy

Surgery + radiation therapy

Radiation + chemo therapy

Surgery + radiation + chemo therapy

No treatment (palliation)

52
Q

How much radiation is required for malignant cells?

A

Doses required to kill malignant cells range
from 50-70Gy -> High dose!

Radiation is fractionated into daily doses of ~ 2Gy

Delivered Monday to Friday, usually over a 6-7 week period

53
Q

What are the potential adverse effects of radiotherapy?

A

Radiation dermatitis

Radiation mucositis

Salivary gland dysfunction

Xerostomia and loss of taste

Dental caries

Candidosis

Trismus

Osteoradionecrosis

Pain

Dysphagia, dysarthria, and psychologicla problems

54
Q

How should patients undergoing radiotherapy be managed?

A

Pre-radiation therapy work-up

Follow-up radiation therapy

Long term, post radiation therapy care

55
Q

What should the patient know before undergoing radiation therapy?

A

Ensure that a patient is
dentally fit

Ensure that a patient
understands the
implication of radiation
therapy from the dental
point of view
Ensure that a patient
understands the required
life style changes to
maintain dentition post
radiation therapy
56
Q

What should be done prior to radiation therapy?

A

Medical/dental/social history

Establishing proposed radiation therapy fields

Comprehensive dental examination including radiographic examination

Dietary counselling

57
Q

What should be considered in the patient’s irradiated field?

A

Condition of the dentition

Patient’s dental awareness

Immediacy of treatment

Prognosis for tumour control

58
Q

Which teeth are recommended to be extracted prior to radiation therapy?

A

Non-restorable teeth

Root caries

Periodontal disease

Peri-apical disease

3rd molars

Non-functional teeth

Impacted teeth

59
Q

What could complicate pre-radiation therapy?

A

Poor oral hygiene

Lack of dental awareness

Lack of cooperation from the patient

60
Q

How should patient be managed during radiation therapy?

A

Manage the symptoms caused by mucositis, loss of taste, and dry mouth.

Maintenancy of good OH

61
Q

What problems is a patient going to be dealing with following radiation therapy?

A

Dry mouth

Caries

Increased Periodontal attachment loss

Infections

Trismus

ORN

Chronic pain

62
Q

How is dry mouth managed?

A

Stimulants of saliva secretion (Sugar free chewing gum, candies and mints)

Secretogogues (eg pilocarpine)

Electro-stimulating devices for saliva secretion

63
Q

How is increased caries risk post radiation therapy managed?

A

OH

Daily fluoride application

Regular dental visits

64
Q

How is ORN managed?

A

Prevention

Hyperbaric oxygen treatment (breathing 100% O2 at atm pressure (2 - 3 ATA)

Surgery

Medical treatment

DMD3 (53 decks)

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