Levels of osteoprotegerin (OPG) and receptor activator for nuclear factor kappa B ligand (RANKL) in serum: Are they of any help?

Abstract

The coupling of bone formation and resorption is mediated through the OPG/RANK/RANKL system. OPG and RANKL are mainly produced by osteoblasts but also a variety of other tissues. The binding of RANKL to RANK, its natural receptor which is expressed by osteoclasts, accelerates bone resorption. OPG acts as decoy receptor and prevents the interaction of RANKL with RANK and therefore leads to a decrease in activity, survival and proliferation of osteoclasts. Since assays for measurements of serum OPG and RANKL have become commercially available, intense research focused on serum OPG/RANKL levels in context with underlying disease, age, co-morbidities, bone density, and fractures has derived. This review aims to provide an overview if and to which extent serum OPG and RANKL levels may reflect bone metabolism in patients with osteoporosis and metabolic bone disease.

Receptor Activator of Nuclear Transcription Factor Nf-b (Rank), Its Ligand (Rankl) and Natural Inhibitor Osteoprotegerin (Opg) in Blood Serum of Primary Bone Tumor Patients: Association With Clinicopathological Features and Inflammatory Cytokines Levels

“…These disorders might be imposed predominantly by the changes occurring directly in tumor tissue, but we cannot ignore the fact that serum levels of RANK/RANKL/OPG components, as well as the level of any other serological marker, cannot be completely determined by the secretion of corresponding protein from tumor cells. It depends on various physiological factors, on probable production of proteins studied by other tissues, and on the presence of concomitant diseases, in particular, osteoporosis and inflammatory processes [14,15].…”

Wybrane cytokiny prozapalne, metabolizm kostny, osteoprotegeryna i ligand receptora aktywatora czynnika jądrowego-kB u dziewcząt z jadłowstrętem psychicznym

“…It has been demonstrated that pro-inflammatory cytokines influence the bone tissue directly and/or indirectly, via the RANKL/RANK/OPG system [27][28][29][30][31][32][33][34][35][36][37][38][39]. Since it has been documented that IL-1β, IL-6, and TNF-α stimulate bone resorption both in vitro and in vivo [27][28][29][30], it seems reasonable to presume that any potential disturbances in the production of these cytokines in patients with AN might play a role in the development of osteoporosis.…”

“…The above data suggest that cytokines may regulate osteoclastogenesis not only directly, but also indirectly via the RANKL/ /RANK/OPG system [27][28][29][30][31][32][33][34][35][36][37][38][39]. Through an increase in the expression of RANKL and/or a decrease in OPG expression, IL-1β, IL-6, or TNF-α may suppress the OPG/RANKL ratio resulting in enhanced bone resorption [27][28][29][30][31][32][33][34][35][36][37][38][39].…”

“…In vitro studies revealed that pro-inflammatory cytokines such as IL-1, IL-6, and TNF-α are important regulatory determinants of bone remodelling [27][28][29][30]. It has been found that osteoblasts express IL-1 receptors.…”

Expression of OPG, RANKL, and RUNX2 in rabbit periodontium under orthodontic force

“…Studies demonstrated that cementoblasts that were stimulated by mechanical signals affected cementoblast functions (Brezniak and Wasserstein, 2002). Osteoprotegerin (OPG) and receptor activator of nuclear factor-κB ligand (RANKL) were thought to be widely involved in the growth of bone cells (Rody et al, 2001;Wagner and Fahrleitner-Pammer, 2010). However, whether mechanical stimulation affected the expression of OPG, RANKL, and runt-related transcription factor-2 (RUNX2) remained unclear.…”