Bone metabolism and RANKL/RANK/OPG trail in periodontal disease
Curr Issues Pharm Med Sci., Vol. 29, No. 4, 171-175
Lukasz Czupkallo1, Mansur Rahnama1, Dominik Kielbowicz1,
Michal Lobacz1, Maryla Kozicka-Czupkallo2
2 ‘DentArtis’ Dental Office, Lublin, Poland
Periodontal disease is an inflammatory disease of multifactorial etiology. In order for it to appear there must come to an imbalance between the effects of pathogens and host defense mechanisms. As a result of its course the destruction of structures supporting the teeth appears (periodontium, cement, bone), and consequently leads to teeth loosening and loss. In recent years, the participation of RANKL/RANK/OPG in bone remodeling process was highligted.
At the molecular level the bone resorption is regulated through the interaction of the ligand receptor activator of nuclear NF-kappa B (RANKL) and osteoprotegerin (OPG), which is a system of two proteins belonging to the protein tumor necrosis factor (TNF).
Recent findings about the RANKL protein and OPG have shed new light on the previously unexplained phenomenon of the basis of bone resorption.
Research has shown that both protein OPG and RANKL can be detected in gingival crevicular fluid, which has become a window of opportunity in the analysis of noninvasive markers of periodontal tissues, confirming elevated levels of RANKL protein in periodontal disease, and decreased levels of OPG protein. Bone resorption is initiated by the binding of the RANKL protein to receptors RANK present on the surface of mature osteoclasts, and their precursors, which leads to the differentiation and activation of osteoclasts. OPG, being RANKL’s inhibitor, has, in turn, opposite characteristics to RANKL, resulting in the reduction of osteoclastogenesis process. Despite all this, the exact mechanism of bone resorption has not yet been elucidated.
bone metabolism, periodontitis, RANKL/RANK/OPG, cytokins.