Immunohistochemical Study on Intraepithelial Distribution and Density of Langerhans Cells in Nifedipine-induced Overgrown Gingival Tissues.

In order to clarify the roles of Langerhans cells (LCs) associated with host defence mechanisms in nifedipine (NF) -induced gingival overgrowth, the intraepithelial distribution and density of LCs in tissues from the following four groups were examined. Using a rabbit anti-human S-100 protein antibody assay, gingival tissue samples from patients with NF-induced gingival overgrowth (NF-responders, R group) were compared with those from NF-nonresponders (NR group), proliferative gingivitis patients secondary to the presence of dental plaque (ND group) and systemically healthy subjects (Ctrl group). Five patients in each group were randomly selected and all gave informed consent to take part in this study. Gingival tissue samples were carefully taken during periodontal flap surgery or tooth extraction and the serial specimens were embedded in paraffin and routinely processed. The specimens were immunostained with anti-S-100 protein polyclonal antibody followed by histological analysis of the positive cells in gingival epithelium. The S-100 positive LCs were defined as the total S-100 positive cells minus those positive cells identified with Schmorl stain. Histologically, the S-100 positive cells from the specimens in all groups were scattered in both the basal and the spinous layers. The percentages of positive cells per total epithelial cells in all groups were increased in the following order, R>ND>NR>Ctrl. Statistically significant differences were seen between the groups, R and ND (p<0.05), R and NR (p<0.01), ND and NR (p<0.05), R and Ctrl (p<0.01), and ND and Ctrl (p<0.05). On the contrary, no significance was seen between the groups of NR and Ctrl. The gingival epithelium investigated in this study was divided into two groups, S-100 protein positive LC-rich area and S-100 protein positive LC-poor area in each group. CD3-positive cells appeared to be greatly infiltrated in the connective tissue beneath the epithelium accumulated by LCs. This tendency was remarkable especially in the R group. Similarly, the connective tissues examined were divided into two regions, the densely and/or sparsely infiltrated region by inflammatory cells. In comparison with the frequency of S-100 positive LCs in the connective tissues beneath each region, a significant relationship was seen only in the ND group (p<0.05). Also, the frequency of LCs in the epithelium of the R group among the sparsely infiltrated regions was significantly higher than any other groups (p<0.01). Considering that the S-100 positive LCs were significantly increased in the oral epithelium and that a large number of CD 3-positive cells was infiltrated beneath the epithelium, our findings suggest the enhancement of the pathophysiological roles of LCs and CD 3-positive cells in NF-induced gingival overgrowth.