Abstract
tHistory of chronic periodontitis (CP) is a risk factor for oseointegration failure. The osteoclastogenesis system (RANK, RANKL and OPG) is critical for bone homeostatic control. We investigated the levels of OPG and RANKL in peri-implant tissues from volunteers with and without a history of CP and their association with mucosae inflammation. This is a single-blind case-contro study. Diagnosis of a history of CP and peri-implant examination was performed on 46 volunteers, divided into control (without history of CP, n=26) and CP group (with history of CP, n=20). Gingival biopsies were harvested during implant exposure. Quantitative PCR evaluated OPG/RANKL mRNA expressions. OPG and RANKL proteins were analyzed by western blot and immunohistochemistry assay. The chi-square test analyzed the significance of nominal variables between groups while continuous variables were analyzed by T-test or Mann-Whitney test, after Shapiro-Wilk test evaluation. The 2-ΔΔCT Livak method calculation evaluated the gene expression. Values of p<0.05 were considered statistically significant. Volunteers with CP history had 23 times higher chance of developing mucosae inflammation. High mucosae levels of RANKL (p=0.04) and RANKL/OPG (p=0.001) mRNA expressions were observed in CP group. CP volunteers showed increased RANKL protein levels in opposition to decreased OPG expression. Even without active periodontitis, volunteers with a history of CP had elevated gingival levels of RANKL/OPG and higher correlation with peri-implant mucosae inflammation and implant loss.
Highlights
The osteogenic process requires a careful chronological coordination of molecular signals to drive proliferation, migration and differentiation of mesenchymal precursor cells in osteoblasts [1]
In peri-implantitis, increased microbial activity can disrupt the balance of the host response, stimulating osteoclastic activity with consequent bone resorption and implant loss [5]
Advances in bone cell biology demonstrated that bone resorption is regulated by the interplay of a cytokine system belonging to tumor necrosis factor ligand and receptor superfamilies, which comprise the osteoclastogenesis system - the receptor activator nuclear factor kappa-B (RANK)/ RANK ligand (RANKL)/osteoprotegerin (OPG) [6]
Summary
The osteogenic process requires a careful chronological coordination of molecular signals to drive proliferation, migration and differentiation of mesenchymal precursor cells in osteoblasts [1]. Chronic periodontitis (CP) was considered a major risk factor for impaired osseointegration process [3,4]. In peri-implantitis, increased microbial activity can disrupt the balance of the host response, stimulating osteoclastic activity with consequent bone resorption and implant loss [5]. Advances in bone cell biology demonstrated that bone resorption is regulated by the interplay of a cytokine system belonging to tumor necrosis factor ligand and receptor superfamilies, which comprise the osteoclastogenesis system - the receptor activator nuclear factor kappa-B (RANK)/ RANK ligand (RANKL)/osteoprotegerin (OPG) [6]. RANKL, known as TNFSF11, is the eleventh member of the OPG ligand family, expressed by osteoblasts, stromal cells, fibroblasts, B cells and T cells when stimulated by cytokines and bacterial lipopolysaccharides [7]. Its action is conducted by connecting to RANK on the surface of preosteoclast/osteoblast cells, resulting in the enhancement of osteoclasts activity [8]
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