B K Bloor1, F K Malik, E W Odell, P R Morgan. 1. Department of Oral Medicine and Pathology, Medical and Dental School, The Guy's King's College and St Thomas' Hospitals, London, United Kingdom.
Abstract
OBJECTIVE: The aims of this study were to examine the frequency of apoptoses in oral lichen planus by in situ end labeling, to ascertain whether this technique is as sensitive as conventional histologic analysis, and to examine the effect of lymphocytic infiltration. STUDY DESIGN: Numbers of apoptoses in hematoxylin-eosin stained sections were compared with numbers of apoptotic nuclei identified by in situ end labeling in oral lichen planus (n = 26) and normal buccal epithelium (n = 8). Immunohistochemical staining with MIB-1 and for Bcl-2 and Bax enabled possible regulatory pathways to be investigated. RESULTS: In oral lichen planus, approximately 1 apoptotic cell was detected per millimeter of basal layer, cell death increasing with lymphocytic infiltration. Epithelial cell proliferation did not correlate with apoptosis. Bcl-2 expression was weak or absent in basal cells, and Bax was localized to upper prickle cells. CONCLUSIONS: Increased numbers of apoptoses were detected in oral lichen planus, especially in association with lymphocytic infiltration, higher numbers being seen with hematoxylin-eosin staining than with in situ end labeling.
OBJECTIVE: The aims of this study were to examine the frequency of apoptoses in oral lichen planus by in situ end labeling, to ascertain whether this technique is as sensitive as conventional histologic analysis, and to examine the effect of lymphocytic infiltration. STUDY DESIGN: Numbers of apoptoses in hematoxylin-eosin stained sections were compared with numbers of apoptotic nuclei identified by in situ end labeling in oral lichen planus (n = 26) and normal buccal epithelium (n = 8). Immunohistochemical staining with MIB-1 and for Bcl-2 and Bax enabled possible regulatory pathways to be investigated. RESULTS: In oral lichen planus, approximately 1 apoptotic cell was detected per millimeter of basal layer, cell death increasing with lymphocytic infiltration. Epithelial cell proliferation did not correlate with apoptosis. Bcl-2 expression was weak or absent in basal cells, and Bax was localized to upper prickle cells. CONCLUSIONS: Increased numbers of apoptoses were detected in oral lichen planus, especially in association with lymphocytic infiltration, higher numbers being seen with hematoxylin-eosin staining than with in situ end labeling.