Interleukin-33 could play an important role in the pathogenesis of periodontitis

• Published in: Journal of periodontal research Vol. 50; no. 4; pp. 525 - 534
• Main Authors: Köseoğlu, S., Hatipoğlu, M., Sağlam, M., Enhoş, Ş., Esen, H. H.
• Format: Journal Article
• Language: English
• Published: United States Blackwell Publishing Ltd 01.08.2015
• Subjects: alveolar bone loss; Alveolar Bone Loss - etiology; Alveolar Bone Loss - pathology; Animals; Cell Count; Dentistry; Inflammation - pathology; interleukin-33; Interleukin-33 - physiology; Mast Cells - pathology; Osteoblasts - pathology; Osteoclasts - pathology; Osteogenesis - physiology; osteoprotegerin; Osteoprotegerin - physiology; periodontal disease; Periodontitis - etiology; Periodontitis - pathology; RANK Ligand - physiology; RANKL protein; rat; Rats; Rats, Wistar; Sutures - adverse effects; RANKL protein; alveolar bone loss; rat; interleukin-33; osteoprotegerin; periodontal disease
• ISSN: 0022-3484; 1600-0765
• DOI: 10.1111/jre.12235

Background and Objective Interleukin‐33 (IL‐33) controls T‐helper type 2 (Th2) cytokines and the development of mast cells. This study aimed to investigate the expression of IL‐33 and its association with RANKL and osteoprotegerin (OPG) in periodontal health and experimental periodontitis. Material and Methods Eighteen Wistar rats were assigned to two study groups of nine animals each: ligature only (LO) and nonligated (NL). Silk sutures were placed subgingivally, surrounding the right lower first molars. The animals were killed on day 11 after ligature placement, and the alveolar bone loss at the first molars was determined histometrically. Periodontal tissues were examined histopathologically to evaluate the differences between the groups. The expression of IL‐33, RANKL and OPG was detected immunohistochemically. Results The LO group showed significantly greater alveolar bone loss compared with the NL group (p < 0.05). The numbers of osteoclasts, osteoblasts and inflammatory cells were significantly higher in the LO group compared with the NL group (p < 0.05). Osteoblastic activity was significantly lower in the LO group than in the NL group (p < 0.05). There was significantly higher expression of IL‐33 and RANKL and a greater number of OPG‐positive cells in the LO group (p < 0.05). IL‐33 expression showed a positive correlation with RANKL expression and with the number of mast cells (p < 0.05). Conclusion The experimental periodontitis group exhibited increased expression of IL‐33 and RANKL compared with the healthy group. Additionally, there was a positive correlation between these expressions. According to these results, IL‐33 could be associated with the pathogenesis of periodontal disease.