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Elafin Expression in Oral Lichen Planus
Korean Journal of Pathology ; : 15-22, 2004.
Article in Korean | WPRIM | ID: wpr-125103
ABSTRACT

BACKGROUND:

Elafin is a potent anti-elastase in human saliva, and is supposed to play a role in preventing oral ulceration. The expression of elafin was observed in the oral lichen planus (OLP), one of the most common noninfectious oral mucosal diseases, which frequently manifests as extensive ulceration on the involved oral mucosa.

METHODS:

50 OLP, 10 oral leuko-plakia, 3 inflammatory oral ulcers, and 3 normal oral mucosa cases were fixed with 10% buffered formalin, and immunohistochemically stained with monoclonal elafin antibody. Representative specimens were fixed with 4% paraformaldehyde, and RNA in situ hybridization, with an elafin RNA probe, was performed.

RESULTS:

With both the immunohistochemistry and RNA in situ hybridization the expression of elafin was more decreased in the OLP compared to the normal mucosa, while in the hyperplastic epithelium of the leukoplakia and inflammatory ulcers the expressions of elafin was more intense. In the thin epithelia of the reticular and atrophic OLPs the expressions of elafin were reduced compared to the normal mucosa, and became almost negative in the epithelium of the erosive OLP.

CONCLUSIONS:

These data suggested that the extensive ulceration of the OLP was closely relevant to the reduced expression of elafin in the involved epithelium
Subject(s)

Full text: Available Index: WPRIM (Western Pacific) Main subject: Saliva / Ulcer / RNA / Immunohistochemistry / In Situ Hybridization / Lichen Planus, Oral / Oral Ulcer / Epithelium / Elafin / Formaldehyde Limits: Humans Language: Korean Journal: Korean Journal of Pathology Year: 2004 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Saliva / Ulcer / RNA / Immunohistochemistry / In Situ Hybridization / Lichen Planus, Oral / Oral Ulcer / Epithelium / Elafin / Formaldehyde Limits: Humans Language: Korean Journal: Korean Journal of Pathology Year: 2004 Type: Article