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DOI 10.1034/j.1600-0714.2000.290602.x

Медицинская библиотека · Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2000

A study to assess inducible nitric oxide synthase expression in oral lichen planus.

Brennan P A, Umar T, Palacios-Callender M, Spedding A V, Mellor T K, Buckley J, Langdon J D

Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

Nitric oxide (NO) has been implicated in a variety of diseases but has not been previously studied in oral lichen planus (OLP). Since OLP has a complex immunogenesis with abundant macrophage infiltration, this study determined by immunohistochemistry whether or not the expression of the inducible form of nitric oxide synthase (iNOS) was increased in this condition relative to normal mucosa. Thirty cases of OLP and 10 normal buccal mucosa biopsies were studied utilising primary antibodies to iNOS and CD68, a myelomonocytic marker. iNOS activity was additionally assessed using a [(14-)C]-labelled arginine to citrulline assay. CD68 expression was significantly increased in the cellular infiltrate of all 30 cases of OLP compared with normal mucosa (P<0.009). Although iNOS staining was seen in a minority of cells in nine cases, this was not statistically significant when compared with the absent staining in normal oral mucosa (P=0.26). Furthermore, the minimal iNOS activity found in OLP was similar to that in normal mucosa. We conclude that expression of iNOS by macrophages is downregulated in OLP and discuss the possible reasons for this finding.

Для цитирования: Brennan P A, Umar T, Palacios-Callender M, Spedding A V, Mellor T K, Buckley J, Langdon J D. A study to assess inducible nitric oxide synthase expression in oral lichen planus.. Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology. 2000. DOI: 10.1034/j.1600-0714.2000.290602.x.

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