Oral Premalignant Lesions Flashcards
(47 cards)
1
Q
What is Erythroplakia
A
A predominantly red lesion of the oral mucosa that cannot be characterised clinically or pathologically as any other definable lesion
2
Q
What is leukoplakia
A
- A white patch/plaque of questionable risk having excluded other diseases or disorders that carry no increased risk of cancer
- Biopsy mandatory
- Clinical term but no specific histology
3
Q
What is a precursor lesion
A
Any identifiable or altered mucosa with a risk of transformation
Relatively non-specific term
4
Q
What coloured lesion carries the lowest and the highest cancer risk
A
- Oral white lesions have the lower risk of malignant transformation
- Red and speckled lesions have the highest risk
- But there are completely benign white and red lesions
5
Q
Which oral cancers are classified into lesions and which are classified into conditions
A
- In reality these overlap
- Lesions: leukoplakia, erythroplakia, palatal changes in reverse smoker
- Conditions: oral sub mucous fibrosis, lichen planus, discoid lupus eruthematosus, dyskeratosis congenita, syphilis
6
Q
What are potentially malignant disorders thought to be a result from
A
- Field change or field cancerisation
- Process whereby a wide area of tissue undergoes genetic alterations or chromosomal changes, making it prone to developing cancer anywhere within the field (often never undergoes malignant transformation and is not known how many OPMDs develop into oral cancers)
- The changes may be visible or often not visible
7
Q
Why do different parts of the field change have different risks of developing into cancer
A
There are overlapping areas of slightly different changes making up the field
Each patchy is a clone of cells that has a survival advantage over normal cells
Clinical and histological visibility depends on which genes are affected
Therefore different parts have different risks for developing into cancer
8
Q
What are the implications of the extent and size of field change? And is the patient at risk of more than one type of cancer?
A
- The extent of the field may or may not be visible clinically or histologically, meaning the size of the field at risk cannot easily be determined
- The size of the field affects the success of surgical treatment because excision could only be effective for a small field
- Pts are at risk of multiple potentially malignant lesions and cancers in different sites in the field
9
Q
What is dysplasia a feature of and is it seen in a field change?
A
- Histological feature of pre-malignancy = best predictor of risk and indicator of future transformation
(but non-dysplastic lesions can transform too) - May or may not be seen in all field change
10
Q
What are the aetiological factors of OPMDs?
A
- Tobacco, alcohol, betal quid, other habits
- Genertic, idiopathic/autoimmune, candidal infection, HPV?, nutrition?
11
Q
What are the risk factors for OPMDs?
A
- More men than women
- Aged over 40
- Smokers and heavy drinkers
12
Q
What is the definition and what are the clinical features of erythroplakia?
A
- Fiery red patch of the oral mucosa that cannot be characterised clinically or pathologically as any other definable disease
- Common sites: FOM, lateral and ventral tongue and soft palate
- Features: Surface is velvety and ranges from dull matte red to bright scarlet. Lesion often flat or slightly depressed. Epithelium is atrophic and non-keratinised
- Affects: smokers and elderly
13
Q
What is the malignant transformation risk for erythroplakia?
A
- Highest risk of malignant transformation
- Annual transformation rate of ~1%
- ~50% of lesions turn out to be malignant on first biopsy, and the remainder show some degree of dysplasia, often severe
14
Q
What is the differential diagnosis for Erythroplakia?
A
Desquamative gingivitis, erythematous lichen planus, discoid lupus erythematous, pemphigoid, hypersensitivity reactions, Reiter’s disease, erythematous candidiasis, histoplasmosis, haemangioma, Kaposi’s sarcoma
15
Q
What are the steps for diagnosis of red patch
A
- Exclude other known conditions, disorders, diseases based on history and examination
- Provisional clinical diagnosis of erythroplakia
- Biopsy: gives diagnosis of erythroplakia without dysplasia or erythroplakia with dysplasia. Or confirms other known disorder
16
Q
What is the definition and how common is leukoplakia?
A
- White patch of questionable risk having excluded other known disease or disorders that carry no increased risk for cancer (a clinical term and has no specific histology)
- Common: accounts for over 3/4 of all potentially malignant disorders and is found in 1-5% of the population
17
Q
What are the clinical types of leukoplakia and what are the clinical features of each?
A
- Homogenous - lesions are uniformly flat, thin and exhibit shallow cracks of the surface keratin
- Non-homogenous - speckled, nodular, verrucous, proliferative verrucous
18
Q
What are the general clinical features of leukoplakia? what is the transformation rate?
A
- Common sites: posterior buccal mucosa, retromolar region, FOM, tongue
- Features: No specific clinical appearance but are tough and adherent white patches
- Relatively low transformation rate (but greater risk than oral LP)
- Risk of transformation:
1. severe dysplasia
2. nodular/verrucous surface greater risk than flat
3. Large patches
4. Lesions on lateral/ventral tongue and FOM
5. Lesions in older pts
19
Q
What is the differential diagnosis for leukoplakia?
A
White sponge naves, frictional keratosis, lip-cheek biting, chemical injury, acute pseudomembranous candidosis, leukoedema, lichen planus, lichenoid reaction, discoid lupus erythematous, skin graft, hairy leukoplakia, leukokeratosis nicotine palati
20
Q
What is the histopathology of leukoplakia
A
- Variable histopathology, but always keratinisiation giving lesion white appearance
- 85% of leukoplakia show no dysplasia
- Small and innocent looking white patches are as likely to show epithelial dysplasia as large and irregular ones
- However, red, nodular or verrucous areas should be regarded with particular suspicion
21
Q
What are the steps for diagnosis of a white patch?
A
- Exclude other known conditions/disorders/diseases based on history and examination
- Provisional diagnosis of leukoplakia
- Biopsy: gives diagnosis of leukoplakia with or without dysplasia, or confirms other known disorder
22
Q
What is the definition, clinical features and risk of developing carcinoma for sublingual keratosis. What is the histology and treatment similar to?
A
- Term is sometimes applied to leukoplakia on the FOM and ventral tongue
- Sublingual keratosis is not a specific entity, but white patches at this site do show some unusual features: they are often an extensive soft plaque with a finely wrinkled surface
- show low-grade dysplasia despite having significant risk of developing carcinoma
- Histology and treatment are as for leukoplakia
23
Q
What is the definition, clinical features and risk of developing carcinoma for Speckled leukoplakia. What is the histology and treatment similar to?
A
- They can be regarded as a combination of leukoplakia and erythroplakia
- Applies to lesions with red and white areas; usually white flecks or nodules on an an atrophic erythematous base
- Clinical features: resemble erythroplakia
- Similar risk of finding carcinoma in a first biopsy as erythoplakia
- Histological characteristics are intermediate between leukoplakia and erythroplasia
(- Some cases of chronic candidosis have a similar appearance but without the high risk of developing carcinoma )
24
Q
What are the clinical features of proliferative verrucous leukoplakia (PVL)?
A
- Common sites: buccal mucosa, gingiva and tongue
- Features: Distinctive presentation
1. Multiple white lesions each possibly at different stage in its evolution
2. Flat leukoplakia that over a period of decades develop a nodular or verrucous surface and progress inevitably to verrucous or squamous carcinoma - Affects 55+y, mostly female and most are non-smokers
25
what is the transformation risk of PVL and how this this 'distinctive subtype' of leukoplakia classified?
- Very high risk of malignant transformation
1. good long-term prognosis, well differentiated lesion
2. Pts can suffer several separate carcinomas over many years. Lesions are difficult or impossible to eradicate surgically. Recur or develop in new sites
- Not all verrucous leukoplakia are PVL regardless of how verrucous or how big they become - the ultimate diagnostic criterion is that all cases develop carcinoma
26
What are the clinical features of Stomatitis nicotina? What does it respond well to and what is the transformation risk?
- Affects palatal mucosa exposed to smoke and heat
- Areas protected by denture unaffected
- Palate is white from keratosis
- Umbilicated swellings with red centres are inflamed salivary ducts
- Responds rapidly to abstinence from pipe smoking
- Benign despite being tobacco induced
27
What causes Smokeless tobacco-induced keratosis (Snuff-dipper's keratosis), what are the clinical features and the character of malignant change?
- Application of pure tobacco to the mucosa induces hyperkeratosis and inflammation
- Features:
1. limited to the site where tobacco is held - usually buccal sulcus and lesions do not have sharply defined margins
2. take prolonged period to develop
3. early stages: erythema and mild whiteish thickening of the epithelium
4. later: extensive white thickening and wrinkling of the mucosa
5. Distinctive feature: unlike other habits, snus (Swedish moist snuff) induced lesion often found on anterior buccal sulcus
- Malignant change follows at the site of tobacco placement but only after many years of use
- Most habits induce squamous cell carcinoma but snuff dippers develop verrucous carcinomas much more frequently
28
What are other adverse effects of smokeless tobacco
Gingival and alveolar bone recession at the site
| increased risk of carcinoma in the oesophagus and pharyngeal area
29
What is the histopathology of Smokeless tobacco-induced keratosis
- varying degrees of dysplasia
- thickening of the epithelium with varying degrees of hyperorthokeratosis or parakeratosis
- develop a thickened basement membrane and superficial fibrosis in the area where the tobacco is held
- Atrophy of underlying salivary glands
- Later, there may be epithelial atrophy
30
How is smokeless tobacco-induced keratosis diagnosed?
- Diagnosis is based off
1. history of tobacco use, type of tobacco used and how it is prepared
2. lesion in the area where the tobacco is held
3. biopsy is required to exclude dysplasia or early malignant change
31
What is the management of smokeless tobacco-induced keratosis
- Stop tobacco habit by pt education
- Lesions that are dysplastic may resolve completely or may regress, although there is a risk of delayed progression and malignant transformation
- Non-dysplastic lesions will resolve on stopping the habit even after 25 years of use, if habit continues regular follow up needed
32
Arguments for and against swapping from smoking to smokeless tobacco
For:
1. Much lower risk of lung and laryngeal carcinoma, of CVD and other risk
2. Smokers also find this type of tobacco more acceptable than nicotine patches
Against:
1. No tobacco product is safe
2. Still addictive
33
What are the clinical features of chronic hyperplastic candidiosis and what is the malignant transformation risk
- Common site: postcommissural buccal mucsoa
- Features: florid, speckled appearance. Flat, white and nodular
1. difficulty distinguishing a 'pure' chronic candida infection from a leukoplakia with superimposed candidosis (usual to try treat infection)
2. leukoplakia infected by candida has an increased risk of transformation (although still very low). Candida can produce known chemical carcinogens
- Low risk of malignant transformation
34
When do you treat a chronic hyperplastic candidosis lesion as leukoplakia?
- If white plaque, suspected from its clinical presentation to be candida, fails to respond to tx
- Or if there is dysplasia on biopsy
35
What is oral submucous fibrosis, what is the risk of malignant transformation and what are the causes?
- An important and readily recognised condition in which the oral mucosa becomes fibrotic, immobile and contracts progressively causing limitation of opening
- High risk of malignant transformation (~4-8% of cases)
- Causes: chewing betal quid
Most cases follow years of exposure to Areca. Occasionally there is a familial incidence
36
What are the ingredients in betal quid and by how many times does it increase cancer risk?
- Primary ingredient- Areca nut (contains alkaloids). other ingredients (tobacco, spices, flavourings)
- Extremely potent carcinogen - relative risk for users is almost x100
- Quid is folded tightly and held in buccal sulcus
- Addictive
- Heavy user consume 20-30 a day and some sleep with quid in mouth
37
What are the two main adverse affects of chewing betal quid? What else is it linked to?
1. Oral cancer
2. Submucous fibrosis
- Other risks include carcinoma of pharynx and oesophagus
- Areca nut alone carries highest risk for sub mucous fibrosis but also carcinoma at a lower rate
- Linked to diabetes and exacerbation of asthma
37
What are the two main adverse affects of chewing betal quid? What else is it linked to?
1. Oral cancer
2. Submucous fibrosis
- Other risks include carcinoma of pharynx and oesophagus
- Areca nut alone carries highest risk for sub mucous fibrosis but also carcinoma at a lower rate
- Linked to diabetes and exacerbation of asthma
38
What are the clinical features of submucous fibrosis?
- Teeth are stained dark brown by dye from Areca nut
- At the site of betal quid placement: erythema, keratosis and flaking surface, and sometimes erythroplakia or leukoplakia
- Long term users have periodontitis and recession of the adjacent gingiva
- Symmetrical fibrosis develops in the buccal mucosa, soft palate or inner aspect of the lips.
In the earliest stages there may be burning sensation and scattered small vesicles.
Later, fibrosis and loss of vascularity cause extreme pallor of the affected area which appears white and marble-like
Tissue eventually becomes so hard it cannot be indented with finger MoM eventually become involved causing limited mouth opening
39
What is the histopathology of submucous fibrosis?
- May show dysplasia on bisopsy
- Subepithelial CT becomes thickened, hyaline and avascular and there may be infiltration by modest numbers of chronic inflammatory cells
- The epithelium usually becomes thinned and may show dysplasia
- Underlying muscle fibres undergo passive atrophy and replacement by dense fibrous tissue
40
What is the management of submucous fibrosis?
- Tx largely ineffective
- Pts must stop habit - usually no regression, only stabilisation of trismus, reduces risk of malignancy
- Intra-lesional injections of corticosteroids may be tried in associated with muscle stretching exercises to stretch bands of scar tissue
- Wide surgical excision of affected tissues including underlying buccinator muscle with skin graft can be done but likely to be followed by relapse
41
What is the transformation rate for lichen planus? When should LP be sent for biopsy and what is often misdiagnosed as LP?
- Low transformation rate. Unlikely to exceed 0.05% in 10y
- Apparent LP with unusual features, such as lesions in FOM or soft palate, late onset or unusual red areas should be submitted for biopsy and followed up
- Many causes of proliferative verrucous leukoplakia are initially misdiagnosed as LP
42
What is lupus erythematous, what are the clinical features and how is it diagnosed?
- Autoimmune CT disease with two main forms, systemic and cutaneous. Can both give rise to oral lesions that resemble oral LP
- Small risk of malignant change especially if found on lower lip
- Oral changes are variable patterns of white and red areas
1. they may be identical to LP
2. the most indicative presentation is patches of atrophy and keratosis on each side of hard/soft palate or a single milling palatal patch (LP usually spares palate so this distribution aids diagnosis)
3. May form discrete patch, unilateral lesions, symmetrical ulcers
- Diagnosis depends on clinical features and biopsy (autoantibodies are helpful in systemic disease)
43
What is the histopathology of lupus erythematosus
The features are as lichen planus with some subtle differences
- Thickening of BM zone and around BCs due to fibrosis and inflammation triggered by deposition of antigen/antibody complexes
44
What is the management of lupus erythematosus
Oral lesions may respond to topical corticosteroids but those in systemic diseases tend to be resistant
45
What are the clinical features of dyskeratosis congenita, what is the risk of malignant change and what is the cause of death?
- Rare disease caused by loss of chromosomal telomeres
- Features:
1. Main: dysplastic white or red lesions of the buccal mucosa, tongue and soft palate
2. Other: cutaneous pigmentation, dystrophies of the nails and haematological abnormalities
- High risk of malignant change: oral carcinoma develops in up to 1/3rd cases
- Cause of death: infections resulting from bone marrow failure (50% cases), cancers of the mouth or other sites, bleeding (GI or cerebral)
46
What is HPV-associated dysplasia? Why is the incidence going down and how is it distinguished from other leukoplakia?
- During early years of AIDS epidemic, oral white patches caused by infection with HPV were recognised, but these became rare following introduction of antiretroviral tx
- Increasing incidence of similar white patches in non-immunocompromised pts
- Indistinguishable clinically from other leukoplakia but histologically distinctive
- Almost all are infected by HPV subtypes as found in oropharyngeal carcinomas
