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EPITHELIUM
Clinical Features
Principal oral and oropharyngeal lesions which may
be precursor lesions: 1. White patches (leukoplakia) 2. Red patches (erythroplasia/erythroplakia) 3. Mixed red and white lesions.
These are considered as PREMALIGNANT LESIONS
Clinical Features
The majority of leukoplakias will not show dysplasia
and correspond to the hyperplasia category. The majority of leukoplakias may not undergo malignant change and may even regress particularly if apparent aetiologic factors are removed. Red and mixed lesions (speckled leukoplakia) show a higher frequency of dysplasia, often of higher grade.
embracing expression of the whole spectrum of epithelial changes ranging from squamous cell hyperplasia to carcinoma in situ. In their evolution, some cases of SIL are self-limiting and reversible, some persist, and some of them progress to SCC in spite of treatment.
HISTOPATHOLOGIC PICTURE
The epithelium of precursor lesions maybe thick, but
importance.
in the basal/parabasal cell layers (progenitor compartment), termed basal cell hyperplasia. The architecture shows regular stratification without cellular atypia.
cytologic atypia, the term dysplasia applies. Dysplasia is a spectrum and no criteria exist to precisely divide this spectrum into mild, moderate and severe categories.
MILD DYSPLASIA
Architectural disturbance limited to the lower third of the epithelium accompanied by cytological atypia
MODERATE DYSPLASIA
Architectural disturbance extending into
MODERATE DYSPLASIA
SEVERE DYSPLASIA
Recognition of severe dysplasia starts with
greater than two thirds of the epithelium showing architectural disturbance with associated cytologic atypia. Architectural disturbance extending into the middle third of the epithelium with sufficient cytologic atypia is upgraded from moderate to severe dysplasia.
SEVERE DYSPLASIA
Severe dysplasia into upper third of epithelium with marked cytological change
SEVERE DYSPLASIA
Severe dysplasia into upper third of epithelium with prominent cytological change including abnormal mitoses.
SIGNIFICANCE/RELEVANCE OF DYSPLASIA
It is reasonable to assume that the changes described
in dysplasia are due to genetic changes in the epithelium It is unlikely that the mutations involved are the same ones as are associated with development of malignancy More severe dysplasia has been traditionally believed to be associated with a greater likelihood of progression to malignancy
RELEVANCE OF DYSPLASIA
This might indicate that the greater the
accumulation of mutations in tissue, the greater the chance that the critical mutations for malignancy will be present. The corollary is also true in that malignancy can arise from non-dysplastic epithelium presumably because these critical mutations can be present in the absence of the mutations causing dysplasia.
orthokeratin layer or stratum corneum in a particular location Moderate amount of orthokeratin present on the surface of normal epithelium, vary slightly in amount from area to area depending upon frictional irritation
not usually found, or particularly , a thickening of the parakeratin layer But this can be a normal process in other certain areas of the oral cavity And it is also not unusual in the oral cavity to see alternating areas of orthokeratin and parakeratin
persistence of nuclei or nuclear remnants in the keratin layer The presence of a granular layer or stratum granulosum is obvious only in orthokeratinized oral epithelium The granular layer is often thickened and extremely prominent in cases of hyperkerorthokeratosis, but is seldom seen in severe cases of hyperparakeratosis
for a particular location Can be severe with elongation, thickening, blunting, and confluence of rete ridges, or may consists only of their elongation
GENETICS STUDY
There are no individual markers that
promise as predictors of development of SCC are large scale genomic status (DNA ploidy) and loss of heterozygosity (LOH) at defined loci
CARCINOMA-IN-SITU
Full or almost full thickness of the epithelium shows
architectural disturbance, accompanied by pronounced cytological atypia. Atypical mitotic figures and abnormal superficial mitoses are present. Malignant transformation has occurred but invasion is not present. It is not possible to recognize this morphologically.
CARCINOMA-IN-SITU
Three distinct morphologic characteristics are
usually present: a) Loss of stratification or maturation of the epithelium as a whole; however, the surface of the epithelium may be covered by one or at most a few layers of compressed, horizontally stratified, and sometimes keratinised cells. b) Epithelial cells may show all the cytologic characteristics of invasive squamous cell carcinoma
CARCINOMA-IN-SITU
c) Mitotic figures are usually markedly increased
throughout the whole epithelium, often more than five per high power field. Abnormal mitoses are frequently seen. Hyaline bodies and dyskeratotic cells are present, often in high numbers
CARCINOMA-IN-SITU
Carcinoma in-situ. Abnormal cells seen throughout the full thickness of the epithelium
CARCINOMA-IN-SITU
Carcinoma in situ. The lesion shows loss of stratification, malignant cells with increased mitotic activity replace the entire epithelial thickness
CLINICAL MANIFESTATIONS
Etiology
which seems to be the major carcinogen Smoking 20 or more cigarettes per day, particularly non-filtered Drinking alcohol, particularly fortified wines and spirits Chewing habits, including betel quid, strongly correlate with oral precancer and cancer development
As For ETIOLOGY.
Tobacco is a stronger independent risk factor for
oral SILs than alcohol Its synergistic effect with tobacco is particularly evident !!!!. The risk of the development of oral dysplasia is increased six to 15 times in smokers and heavy drinkers compared with non-smokers and nondrinkers
TOBACCO
MANY of the chemical constituents of tobacco and
its combustion end products (tobacco tar and resin) => irritating to the oral mucosa => capable of producing or leukoplakic alterations in the oral mucosa Materials which leach out of the tobacco when chewed and are allowed to rest against the moist mucosa => irritating to the oral mucosa
TOBACCO SMOKING
PIPE SMOKING IS MOST HARMFUL!!!
among heavy pipesmokers => redness and inflammation of the palate, then palate develops diffuse, grayish white, thickened, multinodular or papular appearance, fissures and cracks may appear, producing a wrinkled and irregular surface
ALCOHOL
The risk of the development of oral dysplasia is
increased six to 15 times in smokers and heavy drinkers compared with non-smokers and nondrinkers Persons who habitually consume considerable quantities of alcohol are ALSO USUALLY inveterate smokers! ALCOHOL is also irritating to the mucosa
vitamin deficiency (Vit A and B complex), and hormonal/endocrine disturbances, galvanism, actinic radiation Infections ( syphilis and fungal e.g. Candidiasis)
factor e.g. mal occlusions and ill fitting dentures which can produce chronic cheek-biting habits, and also sharp, broken-down teeth SYPHILIS it has been found out that there is higher incidence of leukoplakia among patients who have had syphilitic glossitis VITAMIN Deficiency deficiency of VIT A has been suggested with devt of leukoplakia => induction of metaplasia and increased keratinization of some epithelial structures
has been suggested as a predisposing factor => related to alteration in the oxidation patterns of the epithelium, making it more susceptible to irritation => treatment with brewers yeast is recommended CANDIDIASIS/CANDIDOSIS fungal invasion has been associated with speckled type of leukoplakia => invading Candida hyphae may be responsible for a disorderly maturation of the epithelium
years of age Only about 5% of px are under 30 yrs of age Males (69%) more predisposed than women (31%) Slight trend for earlier occurrence of leukoplakia in FEMALES
DISTRIBUTION AS TO LOCATION
Renstrup report:
lip, hard and soft palates, floor of the mouth and gingiva Hobaek report: top locations: tongue and floor of the mouth in descending order: lower lip, buccal mucosa, palate, and gingiva *** In this study of Hobaek, multiple areas of involvement were common
DISTRIBUTION AS TO LOCATION
Waldron and Shafer report:
gingiva or mucobuccal folds in descending order: buccal mucosa, lower lip (low frequency), and tongue ***In this study of Shafer, tongue is the least frequent site for males and females *** Also in this study of Shafer, no lesions in the upper lip was found
LEUKOPLAKIA
LEUKOPLAKIA
The white appearance of OL (oral leukoplakia) is
most often related to an increase in the surface keratin layer. The most common sites of lesions are the buccal and alveolar mucosa and the lower lip. Lesions in the floor of the mouth, lateral tongue and lower lip more often show epithelial atypia or even malignant growth TWO TYPES: homogenous and nonhomogenous
LEUKOPLAKIA
HOMOGENOUS TYPE Characterized as a uniform, flat, thin lesion with a
smooth or wrinkled surface showing shallow cracks, but a constant texture throughout
LEUKOPLAKIA
NONHOMOGENOUS TYPE (a.k.a
ERYTHROLEUKOPLAKIA)
be irregularly flat, nodular or exophytic. Nodular lesions have slightly raised rounded, red and/or whitish excrescences. Exophytic lesions have irregular blunt or sharp projections . The term non-homogenous is applicable to the aspect of both colour (a mixed white and red lesion) and texture (exophytic, papillary or verrucous) of the lesions.
Erythroleukoplakia of the buccal mucosa. The microscopic diagnosis was atypical hyperplasia.
Same case as shown above, two years later showing more florid verrucous hyperplasia illustrating the progressive nature of the condition.
ERYTHROLEUKOPLAKIA (OE)
Oral intraepithelial lesions that are intermixed with
white areas Also called speckled mucosa and are believed to behave similarly to pure leukoplakia. The red appearance of OE may be related to an increase in subepithelial blood vessels, a lack of surface keratin and thinness of the epithelium Although OE is a rare lesion, it is much more likely to show dysplasia or carcinoma.
Take note.
In all red lesions of the oral
mucosa that do not regress within 2 weeks of the removal of possible aetiological factors, biopsy is, therefore, Mandatory!!!!!