الفهرس 
COVEROnly 14 pages are availabe for public view
 |  | from | 155 |  |  |
| | | from | 155 | | |
Abstract
Periodontitis is associated with a constellation of oral microorganisms that infect the gingival crevice (Socransky and Haffajee, 1997).These polymicrobial infections cause gingival inflammation and resorption of alveolar bone. Host mediated immune responses (both innate and adaptive) to these microorganisms lead to the destruction of periodontal tissues. Recent studies have suggested that the host immune response can contribute to protective and/or destructive effects in periodontal disease. In particular, attention has been focused on receptor activator of NF-kB ligand (RANKL), a member of the tumor necrosis factor ligand family, because of the requirement of this key regulatory molecule for osteoclastogenesis (Yasuda et al., 1998 and Kong et al., 1999).
Receptor activator of NF-B ligand (RANKL), RANK, and osteoprotegerin (OPG) (Suda et al., 1999), interactions are important in coordinating osteoclastogenesis and alveolar bone resorption. RANKL is expressed by osteoblasts ⁄ stromal cells (Lacey et al., 1998 and Yasuda et al., 1998), fibroblasts (Takayanagi et al., 2000 and Quinn et al., 2000) and activated T cells (Teng et al., 2000). It binds directly to RANK on the surface of preosteoclasts and osteoclasts. RANKL stimulates both the differentiation of osteoclast progenitors and the activity of mature osteoclasts (Matsuzaki et al., 1999 and Hsu et al., 2000). This ligand can be found as a cell membrane-bound variant (mRANKL) or a primary soluble (secreted) form which has been described in activated T cells (Kong et al., 1999). OPG is the naturally occurring inhibitor of osteoclast differentiation. It is a soluble molecule that binds to RANKL with high affinity and blocks RANKL from interacting with RANK (Lacey et al., 1998).
Smokers have been reported to be more susceptible to advanced forms of periodontal disease than non- smokers (Haber et al., 1993 and Calsina et al., 2002), although smoker and non-smoker patients exhibit more or less the same periodontal pathogens (Preber et al., 1992 and Buduneli et al., 2005). Immune response plays a major role in the alveolar bone destruction observed in chronic periodontitis. Smoking has been suggested to have an influence on host cytokine levels (Buduneli et al., 2006).
The present clinical trial was designed to compare between smokers and non-Smokers, we analysed saliva and serum levels of RANKL and OPG as well as the clinical parameters of periodontal tissue destruction in thirty systemically healthy patients, with chronic periodontitis. The study compared fifteen chronic periodontitis patients who are smokers with another fifteen chronic periodontitis patients who were non smokers, and with ten patients as a control group (mild gingivitis) and to assess the effect of periodontal treatment on the level of RANKL and OPG in those patients.
The results of this study revealed that chronic periodontitis patients showed statistically significant higher RANKL levels than control group, whereas OPG was significantly lower than that in the healthy control group and Smoking seems to suppress OPG levels and might contribute towards the increased bone destruction often seen in smokers, moreover Our work proved that scaling and root planning which reduce inflammation decreased RANKL level and increased OPG level.
The current study revealed that RANKL and OPG has a potential role in chronic periodontitis.