association between selected RANKL gene polymorphisms and chronic/aggressive periodontitis in Iranian subjects

The primary aim of this study was to investigate the status of RANKL6-7 gene polymorphism in patients with chronic [mild, moderate, severe] and aggressive periodontitis as well as healthy controls. We examined 80 patients for the RANKL6-7 polymorphisms [rs1054016 and rs9567000]. Polymorphism was determined by polymerase chain reaction [PCR] followed by direct sequencing. No statistically significant association was found between the polymorphism in the RANKL 7 gene and periodontal disease [P<0.55]. There was also no polymorphic allele observed in RANKL 6 gene of the study population. We found no association between the studied RANKL polymorphisms and chronic/aggressive periodontitis

Receptor activator of nuclear factor kappa B ligand [RANKL] levels in peri-implant crevicular fluid

Receptor activator of nuclear factor kappa B ligand [RANKL] is one of the key cytokines in the induction of osteoclastogenesis both in vitro and in vivo. Several reports indicated the presence of sRANKL in gingival crevicular fluid of patients with periodontal diseases. To determine the presence of RANKL in peri-implant crevicular fluid samples of implants with peri-implantitis, peri-implant mucositis and healthy controls. In this study, 40 implants were categorized as clinically healthy, peri-implant mucositis and peri-implantitis according to the clinical and radiographic findings. Filter paper strips were used to collect peri-implant crevicular fluid for 30 seconds in the base of the crevice/pocket. Peri-implant crevicular fluid [PICF] samples were obtained from buccal and lingual aspects of implants. Plaque index, probing depth, gingival index and bleeding on probing were recorded at six sites per implant. Enzyme-linked immunosorbent assay [ELISA] was performed to determine the PICF levels of sRANKL. There were no statistically significant differences in sRANKL concentration between healthy group, peri-implant mucositis and periimplantitis [p=0.12]. There were also no statistical correlation between the concentration of sRANKL and probing pocket depth [R=0.051, p=0.65], or any of the other clinical regarding [p>0.05]. No differences between the mean sRANKL concentration in the buccal and lingual sites were found [p=0.693]. Our results may suggest that peri-implant crevicular fluid analysis of sRANKL in conjunction with some other osteoclastogenic mediators could be further investigated in further well-designed prospective longitudinal studies on a larger-scale sample size in the evaluation of dental implants