Localization of receptor activator of NFkappaB ligand, RANKL, in periodontal tissues during experimental movement of rat molars

Abstract 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 non-invasive 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.

Download Full-text

Effects And Distribution Of The Enamel Matrix Derivative Emdogain® In the Periodontal Tissues Of Rat Molars Transplanted To The Abdominal Wall

Australian Endodontic Journal ◽

10.1111/j.1747-4477.2002.tb00400.x ◽

2002 ◽

Vol 28 (3) ◽

pp. 107-107

Keyword(s):

Abdominal Wall ◽

Enamel Matrix Derivative ◽

Enamel Matrix ◽

Periodontal Tissues ◽

Rat Molars ◽

Matrix Derivative

Download Full-text

The Possible Role of Neutrophils in the Induction of Osteoclastogenesis

Journal of Immunology Research ◽

10.1155/2019/8672604 ◽

2019 ◽

Vol 2019 ◽

pp. 1-14 ◽

Cited By ~ 1

Author(s):

Carolyn G. J. Moonen ◽

Teun J. de Vries ◽

Patrick Rijkschroeff ◽

Patrice E. Poubelle ◽

Elena A. Nicu ◽

...

Keyword(s):

Bone Resorption ◽

Polymorphonuclear Leukocytes ◽

Alveolar Bone ◽

Surface Expression ◽

Rankl Expression ◽

Experimental Conditions ◽

Periodontal Tissues ◽

Immune Mediators ◽

Receptor Activator

The ligand of the receptor activator of NF-κB (RANKL) is a key molecule in the formation of osteoclasts, the key cells that cause the disease-associated alveolar bone resorption in periodontitis. We hypothesized that polymorphonuclear leukocytes (PMNs), found as the most prominent cells of inflamed periodontal tissues, could play an important role in providing signals to trigger osteoclastogenesis and thus activating pathological bone resorption in periodontitis. RANKL expression was investigated on circulatory PMNs (cPMNs) and oral PMNs (oPMNs) taken from both controls and periodontitis patients. On average, 2.3% and 2.4% RANKL expression was detected on the cPMNs and oPMNs from periodontitis patients, which did not differ significantly from healthy controls. Since cPMNs may acquire a more osteoclastogenesis-facilitating phenotype while migrating into the inflamed periodontium, we next investigated whether stimulated (with LPS, TNF-α, or IL-6) cPMNs have the capacity to contribute to osteoclastogenesis. Enduring surface expression of RANKL for short-lived cells as cPMNs was achieved by fixating stimulated cPMNs. RANKL expression on stimulated cPMNs, as assessed by flow cytometry and immunohistochemistry, was limited (6.48±0.72%,mean expression±SEM) after 24 and 48 hours of stimulation with LPS. Likewise, stimulation with TNF-αand IL-6 resulted in limited RANKL expression levels. These limited levels of expression did not induce osteoclastogenesis when cocultured with preosteoclasts for 10 days. We report that, under the aforementioned experimental conditions, neither cPMNs nor oPMNs directly induced osteoclastogenesis. Further elucidation of the key cellular players and immune mediators that stimulate alveolar bone resorption in periodontitis will help to unravel its pathogenesis.

Download Full-text

WNT-5a and SOST Levels in Gingival Crevicular Fluid Depend on the Inflammatory and Osteoclastogenic Activities of Periodontal Tissues

Medicina ◽

10.3390/medicina57080788 ◽

2021 ◽

Vol 57 (8) ◽

pp. 788

Author(s):

Georgios S. Chatzopoulos ◽

Massimo Costalonga ◽

Kim C. Mansky ◽

Larry F. Wolff

Keyword(s):

Wnt Signaling ◽

Gingival Crevicular Fluid ◽

Diagnostic Category ◽

Cross Sectional Study ◽

Enzyme Linked Immunosorbent Assay ◽

Cross Sectional ◽

Periodontal Tissues ◽

Receptor Activator ◽

Crevicular Fluid ◽

Periodontal Tissue Remodeling

Background and Objectives: Wnt signaling leads to stimulation of osteoblasts and it reduces osteoclastogenesis and bone resorption via the regulation of the osteprotegrin and receptor activator of nuclear factor kappa-Β ligan (RANKL). Wnt signaling pathways are regulated by their physiological antagonists such as sclerostin (SOST) as well as WNT-5a. The aim of this study was to determine the total amount of Sclerostin and WNT-5a in the gingival crevicular fluid (GCF) in sites with a continuum from a healthy to diseased periodontium. Materials and Methods: In this cross-sectional study, a total of 20 patients with generalized periodontitis, 10 subjects with gingivitis as well as 14 individuals with a healthy periodontium were recruited upon clinical and radiographic periodontal examination. In patients diagnosed with periodontitis, GCF samples were collected from periodontitis, gingivitis and healthy sites, while gingivitis patients provided samples from gingivitis and healthy sites. In healthy patients, only healthy sites were sampled. Protein total amount of SOST and WNT-5a were quantified by sandwich enzyme-linked immunosorbent assay (ELISA). Results: A total of 108 GCF samples were collected from a total of 44 individuals. When all periodontitis (n = 51), gingivitis (n = 12) and healthy (n = 45) sites were analyzed regardless of the patient diagnosis, periodontitis sites demonstrated significantly elevated WNT-5a total amounts (p = 0.03) when compared to gingivitis sites. Gingivitis sites demonstrated a trend of more total SOST (p = 0.09) when compared to periodontitis and healthy sites. Within each patient diagnostic category, sites showed similar SOST and WNT-5a total amounts (p > 0.05). Conclusions: WNT-5a levels in GCF depend on the stage of periodontitis sites. SOST trended higher in the GCF of gingivitis sites but similar in chronic periodontitis and healthy sites. WNT-5a and SOST play a crucial role in periodontal tissue remodeling and depend on the inflammatory and osteoclastogenic activities.

Download Full-text