Loss of Ap-nerve endings associated with the Merkel cell-neurite complex in the lesional oral mucosa epithelium of lichen planus and hyperkeratosis

摘要

The Merkel cell-neurite complex initiates the perception of touch and mediates Ab slowly adapting type I responses.Lichen planus is a chronic inflammatory autoimmune disease with T-cell-mediated inflammation,whereas hyperkeratosis is characterized with or without epithelial dysplasia in the oral mucosa.To determine the effects of lichen planus and hyperkeratosis on the Merkel cell-neurite complex,healthy oral mucosal epithelium and lesional oral mucosal epithelium of lichen planus and hyperkeratosis patients were stained by immunohistochemistry(the avidin-biotin-peroxidase complex and double immunofluorescence methods)using pan cytokeratin,20(K20,a Merkel cell marker),and neurofilament 200(NF200,a myelinated Ab-and Ad-nerve fibre marker)antibodies.NF200-immunoreactive(ir)nerve fibres in healthy tissues and in the lesional oral mucosa epithelium of lichen planus and hyperkeratosis were counted and statistically analysed.In the healthy oral mucosa,K20-positive Merkel cells with and without close association to the intraepithelial NF200-ir nerve fibres were detected.In the lesional oral mucosa of lichen planus and hyperkeratosis patients,extremely rare NF200-ir nerve fibres were detected only in the lamina propria.Compared with healthy tissues,lichen planus and hyperkeratosis tissues had significantly decreased numbers of NF200-ir nerve fibres in the oral mucosal epithelium.Lichen planus and hyperkeratosis were associated with the absence of Ab-nerve endings in the oral mucosal epithelium.Thus,we conclude that mechanosensation mediated by the Merkel cell-neurite complex in the oral mucosal epithelium is impaired in lichen planus and hyperkeratosis.