Loss of Aβ-nerve endings associated with the Merkel cell-neurite complex in the lesional oral mucosa

来源 :International Journal of Oral Science | 被引量 : 0次 | 上传用户:wzsyxz
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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. The Merkel cell-neurite complex initiates the perception of touch and mediates Ab slowly adapting type I responses. Linehen 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 fiber marker) antibodies. NF200- immunoreactive (ir) nerve fibers in healthy tissues and in the lesional oral mucosa epithelium of lichen planus and hyperkeratosis were counted and statistically analyzed. the healthy oral mucosa, K20-positive Merkel cells with and witho ut close association to the intraepithelial NF200-ir nerve fibers were detected. In the lesional oral mucosa of lichen planus and hyperkeratosis patients, extremely rare NF200-ir nerve fibers were detected in the lamina propria. Compared with healthy tissues, lichen planus and hyperkeratosis tissues had significantly decreased numbers of NF200-ir nerve fibers in the oral mucosal epithelium. Linehen 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.
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