RANK-RANKL-OPG: A current trends in orthodontic tooth movement and its role in accelerated orthodontics

Abstract

RANKL is a type II membrane protein bearing close homology to TNFSF members TRAIL, FasL, and TNF-a. RANKL has been definite for its key characteristic role in bone metabolism and the immune system. It is an apoptosis regulator gene, a binding partner of osteoprotegerin OPG, a ligand for the receptor RANK, and it controls cell proliferation by modifying protein levels. Osteoblasts and stromal stem cells receptor activator of NFκ-B ligand (RANKL), binds to receptor and RANK, is apparent on the surface of osteoclasts and their predecessors. Osteoprotegerin (OPG) secreted by osteoblasts and osteogenic stromal stem cells keep the skeleton from extreme bone resorption by binding to RANKL and averting it from interacting with RANK osteocytes. The critical cause of RANKL in alveolar bone remodelling during orthodontic tooth movement. The RANKL/OPG proportion in bone marrow is thus a significant element of bone mass in normal and disease conditions. This article reviews the role of the RANKL/RANK/OPG system in bone and other tissues in Orthodontic tooth movement.

Osteocyte Mechanotransduction in Orthodontic Tooth Movement

“…The RANKL pathway defines bone mass as it discharges osteoclast progenitors into the circulation [ 105 ]. RANKL-induced osteoclast activation is vital to homeostasis over progenitor recruitment connecting bone remodelling with haematopoiesis regulation [ 105 ]. Sclerostin downregulates osteoblast activity and function [ 92 ].…”

“…During orthodontic tooth movement, RANKL expression increases in gingival crevicular fluid in juvenile patients [ 109 ]. RANKL accelerates orthodontic tooth movement by increasing the number of osteoclasts and bone resorption at the compression side [ 105 ].…”