A STUDY OF SERUM LEVELS OF RANKL AND OPG INPATIENTS WITH ACUTE CORONARY SYNDROME WITH AND WITHOUT PSORIATIC ARTHRITIS
Authors: Popova Velichka 
Published: August 2019

Receptor Activator of Nuclear Factor Kappa B Ligand (RANKL) is a member of the tumor necrosis factor alpha(TNFa) family.It signals by its RANK receptor on monocyte/macrophage progenitors and stimulates the formation of bone-resorbing osteoclasts [1]. In psoriatic arthritis (PsA) RANKL is produced by activated Th17 cells, synovial fibroblasts, macrophages, dendritic cells and activated lymphocytes [2,3]. These are cells involved in systemic and local inflammation and atherogenesis.Osteoprotegerin (OPG) is a glycoprotein first described in 1997 by Simonet et al. [1]who refer to it as a bone-protecting protein. OPG is a new member of theTNFa superfamily,a soluble receptor which acts as a decoy for RANKL and other ligands. It is also synthesized in many other tissues such as kidney, placenta, bones, vessels, lungs, and vascular structures. It circulates in serum and in plasma, although the concentration is much lower than locally in the bone and arterial tissue[4,5,6]. It has been found that vascular smooth muscle cellssynthesize it as a result of various stimuli. OPG also protects large blood vessels from medialcalcification[7].The biological effect of OPG is to oppose RANKL and thus prevent subsequent stimulation of the receptor, therefore the level of OPG increases and acts as a mechanism of self-defense.The role of RANKL and OPG in cardiovascular disease is still insufficiently defined and remains contradictory[8]. Also, the relationship between high serum levels of OPG in acute coronary syndrome( ACS) and their relation to inflammatory joint disease (IJD) is still discussed [9]. Evidence has been collected demonstrating the active involvement of RANKL and OPG in vascular pathology, including atherogenesis, arterial calcification and plaque instability.Epidemiological studies show that elevated OPG levels in the circulation have a prognostic function in cardiovascular mortality and morbidity and may be a serum prognostic marker for future vascular events. On the other hand, the involvement ofRANKL and OPG in the pathogenesis of local and systemic inflammation in ACS and IJD could link them to the amplification of cardiovascular risk and the severity of acute coronary syndromes, especially in patients with PsA. It is possible that the serum OPG level is increased in response to vascular wall damage and ongoing inflammation process within the atherosclerotic plaque lesion as a component of a complex compensatory mechanism in which RANKL plays a central role [11]. Serum OPG levels may be indicative of persistent damage of endothelial cells as well as the activation of VSMCs in advanced atherosclerotic plaque lesion.Together with other inflammatory mediators, RANKL and OPG can play a crucial role in the formation of the atherosclerotic plaque, its maturation and calcification[12, 13]. The present study aimed to examine and compare levels of sRANKL and sOPG in patients with ACS, divided into two groups, with and without PsA.Associations with cardiovascular mortality risk measured by the Global Registry of Acute Coronary Events (GRACE) were sought.ACS patients with and without PsA were compared in relation to sRANKL (24 and 48hrs) and sOPG (24 and 48hrs) to explore the effect of ACS.