Elevated Interleukin‐17A expression in amlodipine‐induced gingival overgrowth

• Published in: Journal of periodontal research 2020-10, Vol.55 (5), p.613-621
• Main Authors: Sume, Siddika Selva, Berker, Ezel, Ilarslan, Yagmur, Ozer Yucel, Ozlem, Tan, Cagman, Goyushov, Samir, Gultekin, Sibel E., Tezcan, Ilhan
• Format: Article
• Language: English
• Subjects: Amlodipine - adverse effects; Antihypertensive Agents - adverse effects; Blood pressure; Calcium; Cytokines; Dental Plaque Index; Enzyme-linked immunosorbent assay; epithelial mesenchymal transition; Fibrosis; Gingiva; Gingival Crevicular Fluid; Gingival index; gingival overgrowth; Gingival Overgrowth - chemically induced; Gingival Overgrowth - genetics; Humans; Hypertension; Immunohistochemistry; Inflammation; Interleukin-17 - metabolism; Interleukin-17A; Mesenchyme; Patients; Plaque index; Surgery
• ISSN: 0022-3484; 1600-0765
• DOI: 10.1111/jre.12747

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