RANKL and OPG mRNA Level after Non-Surgical Periodontal Treatment (original) (raw)
Related papers
Assessment of Salivary Levels of RANKL and OPG in Aggressive versus Chronic Periodontitis
Journal of Immunology Research
RANKL (receptor activator of nuclear factor kappa-βligand) and OPG (osteoprotegerin) are two proteins involved in bone remodelling. During the active phase of periodontal disease, an imbalance between the ratios of the two elements can be noticed. While the expression of RANKL is elevated compared with that of OPG, the RANKL is available to bond with RANK (receptor activator of nuclear factor kappa-β). This study was conducted on 41 patients: 19 with generalized aggressive periodontitis, 18 with severe chronic periodontitis, and 4 periodontal healthy subjects. For each patient included, we determined the salivary levels of RANKL and OPG with the help of two Human ELISA kits. The results show that the patients affected by periodontitis, either aggressive or chronic, have significant higher values of RANKL and RANKL/OPG ratio. This values correlate with the local inflammation status.
Journal of applied oral science : revista FOB, 2018
To evaluate and correlate, in the same research, the mRNA expression and the staining of RANK, RANKL, OPG, TLR2 and MyD88 by immunohistochemistry in the apical periodontitis (AP) progression in mice. AP was induced in the lower first molars of thirty-five C57BL/6 mice. They were assigned to four groups according to their euthanasia periods (G0, G7, G21 and G42). The jaws were removed and subjected to histotechnical processing, immunohistochemistry and real-time reverse transcription-PCR (qRT-PCR). Data were analyzed with parametric and nonparametric tests (α=0.05). An increase of positive immunoreactivity for RANK, RANKL, OPG, TLR2 and MyD88 was observed over time (p<0.05). The RANKL expression was different between the groups G0 and G42, G21 and G42 (p=0.006), with G42 presenting the higher expression in both comparations. The OPG expression was statistically different between the groups G0 and G7, G7 and G21 and G7 and G42 (p<0.001), with G7 presenting higher expression in a...
Journal of Periodontal Research, 2007
Background and Objective: Receptor activator of nuclear factor-jB ligand (RANKL) is responsible for the induction of osteoclastogenesis and bone resorption, whereas its decoy receptor, osteoprotegerin, can directly block this action. Because this dyad of cytokines is crucial for regulating the bone remodelling process, imbalances in their expression may cause a switch from the physiological state to enhanced bone resorption or formation. This study investigated the mRNA expression of RANKL and osteoprotegerin, as well as their relative ratio, in the gingival tissues of patients with various forms of periodontal diseases.
Journal of Periodontal Research, 2003
Little is known about the process of alveolar bone loss that occurs in periodontitis. The inflammation and tissue destruction seen in periodontitis is associated with granulomatous tissue containing inflammatory cells, such as T and B lymphocytes, plasma cells and many cells of the monocytes/macrophage lineage. These cells are thought to produce a variety of inflammatory mediators. High levels of several inflammatory cytokines, such as inter-leukin-1a (IL-1a), IL-b, IL-6, prostaglandin E 2 (PGE 2) and tumour necrosis factor a (TNFa), have been found in the tissue and gingival crevicular fluid of patients suffering advanced periodontitis (1-4). Similar
Frontiers in Physiology, 2017
Periodontitis is based on a complex inflammatory over-response combined with possible genetic predisposition factors. The RANKL/RANK/OPG signaling pathway is implicated in bone resorption through its key function in osteoclast differentiation and activation, as well as in the inflammatory response. This central element of osteo-immunology has been suggested to be perturbed in several diseases, including periodontitis, as it is a predisposing factor for this disease. The aim of the present study was to validate this hypothesis using a transgenic mouse line, which over-expresses RANK (R Tg) and develops a periodontitis-like phenotype at 5 months of age. R Tg mice exhibited severe alveolar bone loss, an increased number of TRAP positive cells, and disorganization of periodontal ligaments. This phenotype was more pronounced in females. We also observed dental root resorption lacunas. Hyperplasia of the gingival epithelium, including Malassez epithelial rests, was visible as early as 25 days, preceding any other symptoms. These results demonstrate that perturbations of the RANKL/RANK/OPG system constitute a core element of periodontitis, and more globally, osteo-immune diseases.
Periodontitis is a destructive disease that targets tooth-supporting structures through complex and multifactorial pathogenic processes. Alveolar bone destruction, a hallmark of periodontitis progression and one of the major causes of tooth loss in human, is mediated by the host immune and inflammatory response to microbial challenge. The discovery of the receptor activator of nuclear factor-kappa B (RANK)/ RANK ligand (RANKL)/osteoprotegerin (OPG) axis has improved the knowledge of bone metabolism regulation. The RANKL/RANK interaction is needed for differentiation and maturation of osteoclast precursor cells to activate osteoclasts and for the survival of mature osteoclasts. Osteoprotegerin is the naturally occurring inhibitor of osteoclast differentiation. It binds to RANKL with high affinity and blocks RANKL from interacting with RANK. The RANKL/OPG ratio is increased in periodontitis compared to healthy individuals, suggesting that this molecular interaction may be important in modulating local bone loss.
Evolution of Periodontal Disease: Immune Response and RANK/RANKL/OPG System
Brazilian dental journal
The aim of this study was to evaluate markers of bone loss and immune response present in evolution of periodontal disease. One hundred and two Wistar rats were divided into three animals groups: PD0, without ligation and PD15 days and PD60 days, submitted to ligation placement with a sterile 3-0 silk cord in the cervical region of the upper first molar on both sides. Samples were obtained from the gingival tissue for histomorphometric analysis, immunohistochemical analysis of RANK, RANKL, OPG, characterization of the inflammatory infiltrate, quantification of nitric oxide, MCP-1, RANTES, IP10 chemokines, and expression of the TGF-b1, VEG, and bFGF. The number of inflammatory cells in gingival tissue was higher in PD60 samples. The collagen content and the area occupied by birefringent collagen fibers were lower for PD60. Differential leukocyte counting showed that there was a significantly higher polymorphonuclear influx in group PD15, while PD60 showed a greater number of lymphocy...
Periodontal diseases are chronic inflammatory disorders involving the supporting structures of the teeth. Connective tissue destruction and loss of bone support of the dentition are key features of this disease. Early studies have revealed that biofilm plaque accumulation in the dentogingival area is the primary etiological factor of periodontal diseases. Recent research has not only reinforced the bacterial etiology of periodontal disease, but has also emphasized the role of inflammation in this pathologic process. The host mounts an immune-inflammatory response to combat the bacterial attack. The host response is like a double-edged sword. It eliminates the offending pathogens, but overstimulation and amplification of the same leads to tissue destruction and bone loss. In the mid-1990s, extensive research in the field of bone biology led to the discovery of the RANKL-RANK-OPG molecular triad. This article explores the mechanisms by which inflammatory host response leads to alveolar bone loss-the role of cytokines, factors that stimulate osteoclastogenesis via the RANKL-RANK-OPG pathway and how inflammation interferes with the uncoupling of bone formation and bone resorption. In addition to the conventional therapeutic modalities aimed at eliminating the microbes, additional therapeutic strategies that interfere with the RANKL-RANK-OPG axis may have a protective effect on the bone loss. Citation: Srinivasan PC (2013) The Role of Inflammatory Cytokines and the RANKL-RANK-OPG Molecular Triad in Periodontal Bone Loss-A Review.