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Dr. Rima Safadi Modified from Dr. Huda Hammad lectures Reference: Oral pathology book by Soams and Southam
Wide range in histological appearances reflects varying degrees of: keratosis, keratosis, epithelial thickness, thickness, epithelial dysplasia, dysplasia, chronic inflammation in the lamina propria. propria.
It is important to remember that: Leukoplakia is a clinical diagnosis arrived at after exclusion of other diseases and is not based on any specific histopathological features, i.e. the term leukoplakia has no histological connotation.
Epithelium may be hyperplastic or atrophic. Areas of erythroplakia are often associated with epithelial atrophy.
The junction between normal and abnormal epithelium may be abrupt or there may be gradual transition.
2. increased melanin production in basal keratinocytes and leakage of melanin into the underlying connective tissue (melanin incontinence).
In some leukoplakias, keratosis and change in thickness are the only abnormal features. Other cases show features of epithelial dysplasia. When dysplasia is present, not all dysplastic features are necessarily seen in any one case.
The degree of dysplasia is subjectively assessed using terms such as mild, moderate and severe based on the thickness of epithelium involved. Mild (grade I) dysplasia demonstrates proliferation of atypical or immature basal cells above the parabasal region but not extending beyond the lower third of the epithelium. Moderate (grade II) dysplasia demonstrates a similar proliferation into the middle oneonethird of the epithelial crosscrosssection.
The term severe (grade III) dysplasia is reserved for abnormal proliferation from the basal layer into the upper third of the epithelium.
Although it is not possible to predict the presence and severity of dysplasia from clinical appearance lesion, erythroplakias and nonnonhomogeneous leukoplakias are more likely to be dysplastic (or even malignant) than homogeneous leukoplakias. leukoplakias. Several studies showed only about 10% of homogeneous leukoplakias to be dysplastic, as opposed to 50% or more of nonnonhomogeneous types. types. Speckled leukoplakias show a very high incidence of dysplasia, which approaches 100% as speckling increases and as the clinical features more closely resemble erythroplakia. erythroplakia.
The individual cellular changes (cellular atypia) atypia) seen in dysplastic epithelium reflect abnormalities in proliferation, proliferation, maturation, maturation, and differentiation of epithelial cells.
Epithelial Dysplasia
Cellular atypia of minor degree may be seen in reaction to inflammation in conditions such as lichen planus and candidosis (reactive cellular atypia) atypia)
Leukoplakia: Prognosis
Unpredictable tendency to undergo malignant transformation. Marked variation in reported rates from different countries. Differences in diagnostic criteria and etiological factors. Transformation times vary from one to several years. Combining results from several studies, a rate of ~14% over a period of up to 20 years has been reported.
Potential for malignant transformation is greater in high risk sites (ventral tongue, FOM, lingual aspect of lower alveolar mucosa). Lesions in these areas are designated as sublingual keratosis to draw attention to these sites.
Leukoplakia: Prognosis
Dysplastic lesions carry an increased risk of malignant transformation (<10%->30%). (<10%The more severe the dysplastic features, the greater the risk, but no clear correlation. The majority of dysplastic lesions remain unchanged during observation period. A proportion of these will improve or regress.
Leukoplakia: Prognosis
Speckled and other nonnonhomogeneous types have an increased rate of malignant malignant transformation. Erythroplakia alone or as part of speckled leukoplakia shows invasive carcinoma or carcinoma in situ on ~ 50% of in of initial biopsies, and most of the remaining show severe dysplasia.
Epithelial dysplasia
Dysplastic leukoplakia- higher rate to leukoplakiaprogress than non neoplastic (10-30%) (10More severe dysplasia higher risk Majority of dysplasia remain unchanged
Malignant transformation likely to be due to progressive accumulation of genetic changes over time. Recent studies show that leukoplakias with abnormal DNA content of epithelial cells are more likely to undergo malignant transformation. This may become an important prognostic indicator in the future.
Leukoplakia Prognosis
DNA content is related to number of chromosomes: Malignant cells have abonormal number of chromosomes (deletions replications etc..) Variation in number of chromosomes: aneuoploidy Duplication of chromosomes: tetraploidy Normal cells with 2 copies: diploidy
Leukoplakia: Leukoplakia: Diploid low risk Aneuploid high risk Tetraploid intermediate risk
At present, risk assessment is based on: Size Site Clinical appearance Degree of epithelial dysplasia.
Lichen Planus
Name provided by Erasmus Wilson in 1869. He probably thought the skin lesions looked like lichens growing on rocks. Lichens are primitive plants composed of symbiotic algae and fungi.
Lichen Planus
Relatively common disease (0.5-2% population). (0.5Worldwide distribution. Involves skin and mucous membranes. Peaks between ages 30-50. 3060% females. Oral lesions detected in ~50% of patients with initial skin lesions. Skin lesions in 10-50% of patients with initial oral lesions. 10Oral lesions may occur before, at the same time as, or after skin lesions.
Violaceous, itchy papules, may have white streaks on surface (Wickham s striae). Variable patterns for papules: discrete, linear, annular, bullous, or widespread rash.
Predilection to flexor surface of wrist. 10% with nail involvement in the form of vertical ridges. Lesions develop slowly and 85% resolve within 18 months, sometimes with recurrence.
In contrast to skin lesions, oral lesions pursue a much more chronic course, sometimes extending over many years. Mostly affect buccal mucosa, may also affect tongue, gingiva, palate, and lips. Bilateral and wide spectrum of presentations, alone or in combination.
Lichen planus involving the gingiva often presents as a desquamative gingivitis. More typical areas can usually be seen elsewhere on the oral mucosa.
Regezi
OrthoOrtho- or parakeratosis. Epithelial atrophy or acanthosis (sawtooth pattern of rete ridges). Dense, well-defined band of wellsubepithelial mononuclear infiltrate, mainly T-cells. T-
Liquefactive degeneration of basal cell layer associated with edema and lymphocytic infiltration. Civatte bodies: hyaline shrunken bodies representing apoptotic cells.
Basal cell degeneration may result in subepithelial bullae formation and ulceration.
Almost all cases run a benign course. Malignant transformation has been described in a very small proportion (0.5%-2.5% over 5 (0.5%years). Some studies suggest that atrophic/erosive forms are more likely for such transformation. Other studies found it more likely with plaque lesions.
Not fully understood. Widely accepted that cell-mediated immune responses to cellan external antigen, or internal antigenic changes in epithelial cells, are involved. Response resembles type IV hypersensitivity. Cytotoxic lymphocytes damage basal epithelium. In most cases the precipitating factors are unknown. May be hypersensitivity to drugs and dental materials Association with systemic conditions: Hep C Graft versus host reaction presents with LP like lesions
In some patients, lesions are triggered by hypersensitivity to drugs or dental materials. In such cases the condition resolves upon withdrawal of the offending agent. Such lesions are referred to as lichenoid reactions to distinguish them from idiopathic lichen planus. planus.
Antigen challenge
Langerhans cells
Cytokine release
Lichen planus has been associated with some systemic diseases. In many of these, a cause-and-effect relationship has not cause-andbeen established. The systemic condition may merely exacerbate a prepreexisting lesion. Strong evidence of association of chronic liver disease associated with hepatitis C virus infection. Oral and cutaneous lesions resembling lichen planus occur in graft vs. host disease
GVH
Lupus Erythematosus
1. 2.
Two main forms: Chronic discoid LE: localized. Systemic LE: disseminated.
A variety of autoantibodies are present in SLE, e.g. antinuclear antibodies (ANAs).
Sometimes facial lesions in both forms have a symmetric distribution (butterfly rash).
Oral lesions in up to 50% of cases. Buccal mucosa most frequently affected. Considerable variation in oral lesions. Most common is a discoid area of erythema or ulceration surrounded by white keratotis border sometimes with radiating striae. striae. Main D/D lichen planus. planus.
Disseminated disease almost involving every organ. Skin rashes: maculopapular, photosensitive especially on face (butterfly rash). Oral lesions variable. May be fatal.
Lupus erythematosus
Immunofluorescence studies show abundant deposits of IgG and complementcomplement- Lupus Band
Revision slides
Leukoplakia
SCC