Review Articles On Pemphigus Vulgaris
Pemphigus vulgaris (PV) is an autoimmune disease, normally associated with oral lesions which generally affect patients aged 40 to 60 years. PV manifests as extremely painful and persistent mouth sores. Here, we present a series of cases of PV (a man and two women aged 35 to 50). It is an attempt to emphasize its importance in diagnosis with a review of the literature on its molecular aspect.
Oral tissue biopsies were performed at the periphery of the lesions. The tissue was fixed in formalin and embedded in paraffin. The sections were stained with H and E and examined under an optical microscope. Histopathologically, the lesions presented with intraepidermal blisters, loss of intercellular attachments leading to acantholysis and an inflammatory skin infiltrate. Suprabasal epithelial clefts have been detected. Inside the slit, partially and completely detached keratinocytes (acantholytic cells) from the basal and lower layers of the prick cells were identified as single cells or clusters. In addition, lymphocytes and neutrophils were the main inflammatory cells inside the slit. In all tissue sections, the superficial parts of the connective tissue were characterized by edema, small blood vessels, a loose arrangement of collagen fibers, and inflammatory interstitial and perivascular infiltrates were evident.
Pemphigus is defined as a group of disorders the autoimmune etiology of which can be fatal and the clinical manifestations are mainly epithelial blisters affecting the skin and / or mucous surfaces, in particular the mucous membrane of the mouth, nose, conjunctiva , genitals, esophagus, pharynx and larynx. [4], [5] Although some pathogens of pemphigus are not fully understood, the high frequency of pemphigus in certain races, in particular Ashkenazi Jews and Mediterranean and South Asian origins, has been shown to be in fact linked HLA-II genes [6]. , [7] Any location of the oral mucosa can be affected; however, trauma sites such as the oral mucosa, gum and palate are particularly affected. (Dsg) 3, a protein component of desmosomes. Most PV patients have circulating IgG autoantibodies to Dsg3. These antibodies bind to Dsg3 on the membrane of epithelial cells and can cause acantholysis. [11], [12] Another desmoglein is Dsg; it is the target of the formation of autoantibodies in the leafy pemphigus. Most patients with oral lesions may be initially misdiagnosed, usually as foot and mouth disease, gingivostomatitis, erythema multiforme, erosive lichen planus, or oral thrush, and may be treated poorly for months or years. . [13] The diagram shows the mode of action of how pemphigus affects the skin and oral mucosa
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