Introduction: apoptosis in the basal cell layers of the epithelium is a feature of lichen planus (LP). Apoptosis can be triggered by genetic damage, UV- or gamma-irradiation, chemotherapeutic drugs, direct killing by lymphocytes, some receptors and growth factor withdrawal. p75 (low-affinity nerve growth factor receptor, NGFR) is a putative death receptor in cells other than neurones including keratinocytes. Conversely, trk (high-affinity NGF receptor) induces cell proliferation in keratinocytes. The balance between p75 and trk activity might modulate susceptibility to apoptosis in LP. Objectives: the aims were to assess the expression of p75 and trk receptors in oral LP lesions. Methods: eleven oral lichen planus biopsy specimens from the buccal mucosa were snap frozen in liquid nitrogen and immunostained using a streptavidin-biotin peroxidase method for trk and p75 using monoclonal (Santa Cruz, sc-7268) and polyclonal (Santa Cruz, sc-5634) antisera respectively. Staining intensity and distribution were assessed qualitatively and compared to control tissues from fibroepithelial hyperplasia (FEH) and hyperplastic prostate gland. Results: both trk and p75 stained the basal and suprabasal epithelium. trk was detected in most of the mononuclear inflammatory cells in both LP and FEH, whereas p75 was almost undetected. Conclusions: on the basis of these immunohistochemical results, we suggest that p75 does not function as a death receptor in oral LP. Trk expression may contribute to the reactive proliferation seen in some cases.

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