ArticleOdontology2018
Evaluation of chemerin and its receptors, ChemR23 and CCRL2, in gingival tissues with healthy and periodontitis.
Article in Odontology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 21 citations in OpenAlex.
- Adipose tissue: an inflammatory organ that can not be ignored in periodontal disease related to obesity.Frontiers in immunology · 2025Review
- Transcriptomic analysis identifies diagnostic genes in polycystic ovary syndrome and periodontitis.European journal of medical research · 2024Article
- A genome-wide association analysis: m6A-SNP related to the onset of oral ulcers.Frontiers in immunology · 2022Article
- Evaluation of adipokines and inflammatory mediator expression levels in patients with periodontitis and peri-implantitis: a cross-sectional study.Clinical oral investigations · 2021Article
- Adipokines and Inflammation: Focus on Cardiovascular Diseases.International journal of molecular sciences · 2020Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
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.
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