Lupus Erythematosus

Proven Lupus Treatment By Dr Gary Levin

Natural Lupus Treatment System by Dr. Gary Levin

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Lupus erythematosus is an autoimmune disease of unknown origin. The two main forms that affect the mouth are discoid lupus erythematosus (DLE; chronic cutaneous lupus erythematosus) and systemic lupus er-ythematosus (SLE). Oral lesions are present in over 20% of patients with SLE.

The clinical features of oral DLE closely resemble those of lichen planus [157]. They typically show a central area of atrophic, erythematous or granular mucosa with a surrounding radiating, striated white halo. The central area occasionally ulcerates. Lesions are most common in the centre of the palate and on the labial aspect of the upper lip, but they can be seen elsewhere in the mouth. Sometimes there are adjacent "kissing lesions" on the gingiva opposite labial lesions. The lesions of DLE lack the symmetrical distribution characteristic of oral lichen planus. Patients with SLE may have the classical photosensitive butterfly rash in the midface and show other evidence of a systematised disease. The mucosal lesions may resemble those of DLE or show evidence of more severe mucositis and non-specific ulceration. Shallow linear ulcers running parallel to the palatal gingiva are sometimes a striking feature.

Microscopy shows many similarities to lichen planus [90, 156]. There is either hyperorthokeratosis or hyperparakeratosis. The follicular plugging characteristic of cutaneous lesions has been described in oral lesions, but it is an inconsistent and frequently poorly defined feature (Fig. 3.10). The rete processes are hyperplastic and can form flame-like downgrowths into the

Discoid Lupus Erythematosus Dle
Fig. 3.10. Discoid lupus erythematosus showing irregular focal epithelial hyperplasia and follicular plugging

underlying corium. This feature is sometimes so florid that it produces a pseudoepitheliomatous appearance. The slender downgrowths can also show a tendency to fuse with each other producing an appearance simulating an embedding artefact. Dyskeratotic cells are an occasional feature. There is apoptosis and liquefaction degeneration of the basal cells, sometimes with Civatte body formation. The BMZ may become hyalin-ised and thickened and this is sometimes a notable feature. There is a band-like infiltrate of lymphohistiocyt-ic cells in the superficial corium similar to that seen in lichen planus, but the lower border tends to be less well defined and the infiltrate often extends into the deeper tissues in a perivascular distribution. Reactive follicles may form in the lymphoid infiltrate. In cases of SLE there may be evidence of fibrinoid necrosis in vessels. Direct immunofluorescence of lesional tissue for IgG, IgM or IgA shows a granular deposit in the BMZ of about 75% of cases of oral DLE and all cases of SLE. A lupus band test in clinically normal skin or mucosa is diagnostic of systemic disease. The presence of C3 or fibrinogen in the BMZ is not specific and is frequently demonstrated in lichen planus.

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