Volume 60 (2010) Issue: 2010 No#5-6

The effect of chlorhexidine on the receptor activator of NF-êB ligand (RANKL) and osteoprotegerin (OPG) expression in chronic periodontitis in humans and companion animals

Author(s): Janković S, Aleksić Z, Nikolić Jakoba Nataša, Stanimirović D, Stojić Ž, Pucar Ana, Hadži- Mihailović M

Keywords:chlorhexidine, chronic periodontitis, ELISA, OPG, RANKL

Periodontal disease is a chronic, multi-factorial disease of the tissues supporting the teeth. Periodontitis in companion animals is an almost identical disease to that in humans in terms of disease course and clinical presentation. Receptor activator of NF-B ligand (RANKL) and osteoprotegerin (OPG) are bioactive molecules that control bone resorption. This study aims to evaluate the effect of Chlorhexidine (CXD) on the RANKL and OPG expressions in gingival crevicular fluid (GCF) collected from subjects with chronic periodontitis. GCF was obtained from subjects with chronic periodontitis.10 subjects (CXD1) rinsed the mouth with 0.12% CXD, 10 subjects (CXD2) utilized 0.20% CXD and the last 10 (PL) used Placebo solution for 7 days. RANKL and OPG concentrations in GCF were measured by enzyme-linked immunosorbent assays ELISA at baseline and after 7 days. Periodontal clinical variables: clinical attachment loss (CAL), probing pocket depth (PPD), papilla-bleeding index (PBI) were evaluated in all groups. After 7 days in CXD1 and CXD2 group RANKL/OPG ratio exhibited a significant decrease (p<0.05) in contrast to the PL group where results showed similar values of RANKL/OPG ratio at baseline and after the observation period. RANKL/OPG ratio was positively correlated with PPD, CAL and PBI before and after the observation period in both Chlorhexidine (CXD1, CXD2) groups. In an existing inflammatory response, chlorhexidine reduced the level of periodontal inflammation, which leads to reduction of RANKL/OPG relative ratio. Decrease of RANKL/OPG ratio will apparently induce maintenance of alveolar bone and slow down periodontal tissue breakdown.


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ISSN: 0567-8315

eISSN: 1820-7448

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