Chemerin may be a novel biomarker in saliva to determine the severity of periodontal disease.

Aim. The aim of this study was to examine the changes in the levels of interleukine-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), malondialdehyde (MDA), nitric oxide (NO), and 8-hydroxydeoxyguanosine (8-OHdG) in saliva and IL-1β, TNF-α, and NO in gingival crevicular fluid (GCF) samples of patients with fixed orthodontic appliances. Material and Method. The subject population consisted of 50 volunteers who were in need of orthodontic treatment with fixed orthodontic appliances. GCF and saliva samples were obtained from all individuals before treatment, at 1st month of treatment and at 6th month of treatment. Periodontal clinical parameters were measured. Samples were investigated to detect IL-1β, TNF-α, and 8-OHdG levels using ELISA method and NO and MDA levels using spectrophotometric method. Results. Since IL-1β level detected in GCF at the 6th month of orthodontic treatment is statistically significant according to baseline (P < 0.05), all other biochemical parameters detected both in saliva and in GCF did not show any significant change at any measurement periods. Conclusion. Orthodontic tooth movement and orthodontic materials used in orthodontic treatment do not lead to a change above the physiological limits that is suggestive of oxidative damage in both GCF and saliva.

Understanding the role of visfatin in periodontitis will enable the development of new treatment methods for inflammation.

Adipokines may contribute to the breakdown of periodontal tissue in periodontitis by stimulating the expression of proinflammatory cytokines and MMPs.

Chemerin is a chemoattractant protein that directs inflammatory cells that express its receptor chemokine receptor-like 1 (ChemR23) towards sites of inflammation. C-C chemokine receptor-like 2 (CCRL2), is the other receptor of chemerin, improves the interaction between chemerin and ChemR23. The aim of this study was to evaluate the expression of chemerin and its receptors in gingival tissues with healthy and periodontitis. Tissue biopsy samples were obtained from 20 patients with chronic periodontitis and from the gingiva of 20 healthy individuals undergoing a crown lengthening process. Quantitative real-time PCR (qPCR) was used to examine the mRNA expression of chemerin, ChemR23 and CCRL2. Additionally, protein expression was measured by immunohistochemistry. Both qPCR and immunohistochemistry results revealed that the expression of chemerin and ChemR23 was significantly higher in tissues with periodontitis than in healthy tissues (P = 0.001 and, P = 0.015, respectively). There were no significant differences between healthy tissues and those with periodontitis in terms of mRNA expression of CCRL2, whereas a more intense staining was observed in tissues with periodontitis. The mRNA expression levels of chemerin showed a positive correlation with plaque index, gingival index, probing pocket depth and clinical attachment level (r = 0.448, r = 0.460, r = 0.439 and, r = 0.459, respectively, P< 0.01). To the best of our knowledge, this study is the first to examine the expression of chemerin, ChemR23 and CCRL2 in gingival tissues. Our study suggests that chemerin may play a role in the pathogenesis of periodontitis by causing chemoattraction of immune cells that direct ChemR23 receptors to the site of inflammation.