OPMDs Flashcards
What causes leukoplakia and erythroplakia?
Tobacco/smoking
Alcohol
Areca nut with or without tobacco
High-risk HPV infection is a rare cause of OPMDs (0.5%)
How common is leukoplakia?
Leukoplakia - 1 - 4% in Western countries
Higher prevalence in SE Asia
Global prevalence of 2 - 3%
How common is erythroplakia?
More uncommon than leukoplakia 0.02% - 0.83%
More serious with higher malignant potential than leukoplakia
What is the clinical definition of leukoplakia?
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.
What does leukoplakia typically look like?
White and somewhat variable:
Mostly well demarcated
Fissured
Can be homogenous or non-homogenous
What are the clinical features of erythroplakia?
Velvety
Granular
Red
Usually painless
Flat or indurated
What are the levels of histopathological change on the leukoplakia/erythroplakia continuum?
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
How is epithelial dysplasia graded in OPMDs?
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.
How are leukoplakia and erythroplakia diagnosed?
Diagnosis of exclusion
An incisional biopsy is indicated to establish baseline histology.
What tools can be used to aid leukoplakia and erythroplakia diagnosis?
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
How is leukoplakia and erythroplakia treated?
Discontinue deleterious social habit that is causing it.
Excisional biopsy is indicated if possible and appropriate.
Watchful monitoring is important.
What is the malignant transformation rate oral leukoplakia?
Malignant transformation rate is 1 - 20% over 1 - 30 years
What are the clinical features of palatal lesions in reverse smokers?
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
How can palatal lesions in reverse smokers be diagnosed?
Diagnosis is reached through clinical examination and history taking
How can palatal lesions in reverse smokers be treated?
Habit cessation
– Manage according to the severity of the disease
What are the histopathological features of palatal lesions in reverse smokers?
Biopsy the lesion
– May show hyperkeratosis, dysplasia or frank SCC
What causes oral sub-mucous fibrosis?
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
What are the clinical features of oral sub-mucous fibrosis?
Diffuse, pale, marble-like, and keratotic areas • Sites – Buccal mucosa – Soft palate – Tongue
• Symptoms
– Burning
– Increasing trismus
What are the histopathologic features of oral sub-mucous fibrosis?
Histopathologic features:
- Hyperkeratosis
- Epithelial atrophy
- Diffuse fibrosis
- May show evidence of dysplasia or cancer
How can oral submucous fibrosis be diagnosed?
- History and clinical presentation
- Obtain good clinical images and write comprehensive clinical notes
- Obtain a biopsy if indicated
- Watchful monitoring
- Temporomandibular disorder management
Which clinical trial drug has been indicated as potentially effective in clinical trials?
Pentoxifylline
What causes actinic cheilitis?
UV light exposure
Aetiology similar to actinic cheilitis of the skin
Who has a higher prevalence of actinic cheilitis?
Closer to the equator
Middle-aged to elderly, fair complexioned men
Outdoor occupation
Certain genetic disorders (xeroderma pigmentosum, Albinism, porphyria cutanea tarda)
What are the early clinical features of actinic cheilitis?
Atrophy (smooth blotchy pale areas)
Dryness
Fissuring
Blurring of the vermilion border
What are the late clinical features of actinic cheilitis?
Rough, scaly areas
May develop leukoplakia
What are the epithelial histolopathologic features of actinic cheilitis?
Hyperkeratosis vs atrophy
Varying degrees of epithelial dysplasia
What are the connective tissue histolopathologic features of actinic cheilitis?
Solar elastosis (Band of amorphous basophilic change)
Chronic inflammation
Dilated blood vessels
How is actinic cheilitis treated?
Many of the changes are irreversible but reducing sun exposure and wearing sunscreen can reduce progression and prevent it in the first place
How is actinic cheilitis diagnosed?
Biopsy
What are the clinical features of lichen planus?
RED WHITE AND ULCERATED.
Types:
Reticular, Papular, Erythematous, Erosive, Plaque like, Bullous
What are the histopathologic features of lichen planus?
Surface epithelial findings largely depend on clinical presentation
Important criteria are:
Degeneration of the basal cell layer
Lymphocytic band of variable thickness
How is oral lichen planus diagnosed?
Paper from the american academy recommends obtaining a biopsy from everyone (this is controversial)
How is oral lichen planus treated?
Symptomatically with mainly anti-inflammatory drugs (Locally or systemically)
What causes lupus erythematosus?
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
What are the clinical features of early discoid lupus erythematosus?
Red papules/macules or small plaques and rapidly develops a hyperkeratotic surface
What are the clinical features of late discoid lupus erythematosus?
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
What are the histopathologic features of late discoid lupus erythematosus?
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
What does the lupus band test show?
Linear/granular deposition of IgG, IgM, or IgA at the basement membrane (lupus
band test)
How is discoid lupus erythematosus diagnosed?
Diagnosis based on clinical presentation and obtaining a biopsy
How is discoid lupus erythematosus treated?
– Unpredictable relapsing remitting course
– Treatment with immunosuppression
What causes oral cancer?
Smoking tobacco
Chewing tobacco
Drinking alcohol regularly
Some evidence of HPV and alcohol mouthwash use
What are the clinical features of oral cancer?
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)
What are the common sites of OSCC?
• Common sites: – Floor of the mouth – Lateral border of tongue – Retromolar areas – Lips – Palate is an unusual location for carcinoma
What are the histopathologic features of OSCC?
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
What is invasion?
Irregular extension of lesional epithelium through the basement membrane and into subepithelial connective tissue without attachment to the surface epithelium
How are OSCCs graded?
Grading*: – Well-differentiated: • Keratin pearls • Close resemblance of normal epithelium – Moderately/poorly differentiated • Less keratinisation • More nuclear and cellular pleomorphism
How are OSCCs diagnosed?
Clinical features
Histological findings
Radiographic features
How are OSCCs treated?
Surgery
Radiation therapy
Chemotherapy
How is prognosis achieved and improved for OSCC?
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
How common is oral SCC?
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.
How is OSCC treated?
Surgery
Radiation therapy
Surgery + radiation therapy
Radiation + chemo therapy
Surgery + radiation + chemo therapy
No treatment (palliation)
How much radiation is required for malignant cells?
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
What are the potential adverse effects of radiotherapy?
Radiation dermatitis
Radiation mucositis
Salivary gland dysfunction
Xerostomia and loss of taste
Dental caries
Candidosis
Trismus
Osteoradionecrosis
Pain
Dysphagia, dysarthria, and psychologicla problems
How should patients undergoing radiotherapy be managed?
Pre-radiation therapy work-up
Follow-up radiation therapy
Long term, post radiation therapy care
What should the patient know before undergoing radiation therapy?
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
What should be done prior to radiation therapy?
Medical/dental/social history
Establishing proposed radiation therapy fields
Comprehensive dental examination including radiographic examination
Dietary counselling
What should be considered in the patient’s irradiated field?
Condition of the dentition
Patient’s dental awareness
Immediacy of treatment
Prognosis for tumour control
Which teeth are recommended to be extracted prior to radiation therapy?
Non-restorable teeth
Root caries
Periodontal disease
Peri-apical disease
3rd molars
Non-functional teeth
Impacted teeth
What could complicate pre-radiation therapy?
Poor oral hygiene
Lack of dental awareness
Lack of cooperation from the patient
How should patient be managed during radiation therapy?
Manage the symptoms caused by mucositis, loss of taste, and dry mouth.
Maintenancy of good OH
What problems is a patient going to be dealing with following radiation therapy?
Dry mouth
Caries
Increased Periodontal attachment loss
Infections
Trismus
ORN
Chronic pain
How is dry mouth managed?
Stimulants of saliva secretion (Sugar free chewing gum, candies and mints)
Secretogogues (eg pilocarpine)
Electro-stimulating devices for saliva secretion
How is increased caries risk post radiation therapy managed?
OH
Daily fluoride application
Regular dental visits
How is ORN managed?
Prevention
Hyperbaric oxygen treatment (breathing 100% O2 at atm pressure (2 - 3 ATA)
Surgery
Medical treatment
