Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report a case of oral submucous fibrosis and present a review of the literature available on this subject. Oral submucous fibrosis is rare outside South-East Asia where it affects from 0.2 to 1 p. 100 of the population. A few cases have been described among Europeans. The disease seems to be specific to the oral and upper respiratory mucosae. It is characterized by the progressive development of subepithelial fibrosis and the subsequent occurrence of leukoplakia which may undergo transformation into epidermoid carcinoma. It initially presents as a non-specific stomatitis, sometimes with vesicles and ulcerations. Very gradually thereafter the buccal mucosa becomes pale in parts, as well as thicker and fibrous, while leukoplakia develops. These lesions progress slowly and may eventually result in complete and irreducible trismus. Histologically, oral submucous fibrosis is characterized by chronic subepithelial inflammatory reaction followed by hyalinization. Subsequently, the fibrosis extends to the underlying muscles. The epithelium is diversely affected: atrophy is thought to be the first lesion to appear; secondarily, and under the influence of various irritant factors, epithelial hyperplasia, ortho- or parakeratosis of the stratum corneum, or even cellular abnormalities may develop.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Oral submucous fibrosis. Review of the literature apropos of a case]. 371 61

Skin lesions are common manifestations of zinc deficiency in humans and animals, but the pathogenic mechanisms have not been fully clarified. In the present study, a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), was given to zinc-deficient (ZD) rats to see whether it prevents or delays the occurrence of skin lesions. Weanling male rats were given free access to a ZD diet (2 mg zinc/kg) for 4 wk to induce zinc deficiency. Control rats, including pair-fed (PF) and ad libitum (AL) groups, were given a diet supplemented with zinc (50.8 mg zinc/kg. L-NAME (0.3 g/L in drinking water) was given to some ZD rats for 3 wk, starting at the second week of their ZD dieting. Dermatitis of the extremities, balanitis, stomatitis, and alopecia appeared in ZD but not in AL and PF rats. Administration of L-NAME significantly reduced the frequency of cutaneous and mucocutaneous inflammatory lesions but did not prevent alopecia in the ZD rats. Reverse transcription polymerase chain reaction showed that inducible nitric oxide synthase mRNA was expressed in the paw skin of ZD but not of AL and PF rats. Evaluation of skin microvascular permeability by the Evans blue leakage technique indicated that L-NAME administration significantly attenuated extravasation of Evans blue in the paw skin of ZD rats. Furthermore, stains positive for terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling were condensed and diffusely distributed over the epidermis, dermis, and subcutaneous tissue of paws in ZD rats. ZD rats had intense cell infiltration and parakeratosis in the paw skin. L-NAME administration effectively prevented these morphologic changes. These results demonstrate that nitric oxide synthase inhibitor ameliorates inflammatory lesions of the skin in ZD rats.
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PMID:Nitric oxide synthase inhibitor attenuates inflammatory lesions in the skin of zinc-deficient rats. 1067 33