Elevated Interleukin-17A expression in amlodipine-induced gingival overgrowth.

BACKGROUND AND OBJECTIVES: Amlodipine, a calcium channel blocker derivative, is frequently used by patients with high blood pressure. Studies reported that it can induce gingival overgrowth. However, the underlying mechanism is not fully described yet. Interleukin-17A (IL-17A) is known as a proinflammatory cytokine, but current studies indicate that it has a role in fibrotic disorders and epithelial-mesenchymal transition (EMT). The aim of this study was to figure out the possible role of IL-17A in amlodipine-induced gingival overgrowth. MATERIALS AND METHODS: Twenty-nine (29) individuals participated in the study, and they were assigned into 3 groups based on medical status and clinical periodontal examination; 9 patients with amlodipine-induced gingival overgrowth, 11 patients with inflammatory gingival overgrowth, and 9 healthy individuals as a control group. Clinical periodontal parameters including plaque index (PI), gingival index (GI), and gingival overgrowth index (GOI) were recorded. Blood and gingival crevicular fluid (GCF) samples were obtained. Gingival tissues were taken by appropriate periodontal surgery following initial periodontal therapy. To detect IL-17A on tissue samples, immunohistochemistry (IHC) was performed. Quantitative analysis was done, and the expression level of IL-17A was given as the percent positively stained cells. Enzyme-linked immunosorbent assay (ELISA) kits were used to analyze IL-17A in serum and GCF samples. RESULTS: All recorded clinical parameters were significantly higher in gingival overgrowth groups compared with control. Evaluation of inflammation on tissue sections did not show any significant change within the groups. Immunohistochemistry findings showed that IL-17A expression was increased in amlodipine samples (81.90%) compared with control samples (42.35%) (P < .001). There was an increase in the inflammatory group (66.08%) which is significantly less than the amlodipine group (P < .05). IL-17A levels in serum and GCF samples were not different within the study groups. CONCLUSION: In this study, elevated IL-17A expression regardless of inflammation shows that amlodipine might cause an increase of IL-17A in gingival tissues. This increase might induce fibrotic changes and EMT in gingival overgrowth tissues. The association of IL-17A with fibrosis and EMT in gingival tissues requires further investigation.

Oral mucosal lesions: a retrospective review of one institution's 13-year experience.

BACKGROUND/AIM: To investigate the relative frequency of biopsied nonneoplastic oral mucosal lesions in Ankara, Turkey. MATERIALS AND METHODS: Biopsy records of a single center from 2000-2012 were retrospectively collected. Diagnosis was recorded and evaluated with respect to patient demographics (age, sex) and location of the lesion. RESULTS: Of 11,980 biopsies, 1732 (14.5%) were mucosal nonneoplastic lesions. Hyperplastic lesions (n= 1000, 57.7%) with fibroepithelial hyperplasia in 30.9% of patients were the most common type of oral nonneoplastic lesions. The mean age of patients differed with respect to type of mucosal lesion, tending to be lower in patients with reactive lesions. Dermatoses showed a female predominance. CONCLUSION: Our ,findings revealed that hyperplastic lesions were the most common among nonneoplastic oral mucosa lesions. Geographic and ethnic.differences of patients with various types of oral mucosal lesions require further investigation.

Analysis of TNF-α (-308) polymorphism and gingival crevicular fluid TNF-α levels in aggressive and chronic periodontitis: A preliminary report.

OBJECTIVES: The purpose of this study was to determine the differences in the distribution of TNF-α (-308) gene polymorphism among aggressive periodontitis, chronic periodontitis and periodontally healthy individuals and also to investigate whether this polymorphism is associated with gingival crevicular fluid TNF-α levels and periodontal disease severity. MATERIAL AND METHODS: A total of 93 individuals were enrolled in the study including 38 aggressive periodontitis, 29 chronic periodontitis patients, and 26 healthy controls. Single nucleotide polymorphism at TNF-α (-308) is analyzed by PCR-RFLP method. Gingival crevicular fluid samples were analyzed for TNF-α, using ELISA. RESULTS: The distribution of genotypes and allele frequencies for TNF-α (-308) were similar among the groups. After stratification of patients with respect to attachment level, aggressive periodontitis patients with clinical attachment level ⩾4mm was observed to have a higher frequency of TNF-α (-308) allele 2 compared to the chronic periodontitis patients with clinical attachment level ⩾4mm. No significant differences were found between the TNF-α levels of the different genotypes in spite of an insignificant increase in patient groups carrying TNF-α (-308) allele 2. CONCLUSION: The results of this study revealed an association between TNF-α (-308) allele 2 frequency and aggressive periodontitis patients with clinical attachment level ⩾4mm in the population studied.