Soluble RANKL in Crevicular Fluid of Dental Implants: A Pilot Study

ABSTRACT Background  Receptor activator of NF‐κB ligand (RANKL), a member of the tumor necrosis factor superfamily, is a key mediator of osteoclast formation, activation, and survival. Thus, it is reasonable to hypothesize that there might be a functional relationship between RANKL expression and pe...

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Veröffentlicht in:Clinical implant dentistry and related research 2006-01, Vol.8 (3), p.135-141
Hauptverfasser: Monov, Gabriel, Strbac, Georg D., Baron, Monika, Kandler, Barbara, Watzek, Georg, Gruber, Reinhard
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Sprache:eng
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Zusammenfassung:ABSTRACT Background  Receptor activator of NF‐κB ligand (RANKL), a member of the tumor necrosis factor superfamily, is a key mediator of osteoclast formation, activation, and survival. Thus, it is reasonable to hypothesize that there might be a functional relationship between RANKL expression and peri‐implantitis. Purpose  This pilot study was performed to determine the reference levels for soluble RANKL (sRANKL) in peri‐implant crevicular fluid and to correlate them with the clinical parameters associated with inflammatory reactions and bone destruction. Materials and Methods  The clinical parameters probing depth (PD), modified bleeding index (MBI), and modified plaque index (MPI) served as indicators for bone resorption and inflammation. Exclusion criteria for calculations were the detection limit of the immunoassay and the minimum acceptable crevicular volume for measurement. From the 84 collected samples of 16 patients, 30–84 years of age, with a total of 19 implants, 29 met these criteria. The absolute amount of sRANKL within crevicular fluid adsorbed to filter strips was a median of 0.18 femtomol (fmol; range, 0.08–0.53) and 0.26 nM (range, 0.09–1.21) when normalized by volume. PD was 4 mm in median and varied within a range between 2 and 12 mm. Results  Absolute amounts of sRANKL showed no correlation with the adsorbed volume and the clinical parameters PD, MBI, and MPI. When sRANKL was normalized by volume, no correlation with the clinical parameters PD, MBI, and MPI was observed either. The patients’ age was not associated with total sRANKL and the concentration of RANKL within crevicular fluid. Absolute levels of sRANKL and sRANKL concentration did not show any differences based on the sampling sites buccal and lingual, or on the patients’ gender. A significant difference in sRANKL concentration was detectable when samples from maxillary implants (0.31 nM median; range, 0.12–1.21) were compared with samples from mandibular implants (0.21 nM median; range, 0.09–0.6) (p=.03). Absolute levels of sRANKL were not different between the maxilla and the mandible. Conclusion  Given the limited sample size, our data provide a basis for future prospective longitudinal studies on the possible relevance of sRANKL as a prognostic marker in peri‐implantitis, and for an understanding of the pathophysiologic process of the disease as a prerequisite for the design of treatment strategies.
ISSN:1523-0899
1708-8208
DOI:10.1111/j.1708-8208.2006.00012.x