RANKL Expression in Periodontal Disease: Where Does RANKL Come from?

Yin Xiao,Wenlei Wu,Weibin Sun,Bin Chen,Fuhua Yan,Qian Zhang

doi:10.1155/2014/731039

Abstract

Periodontitis is an inflammatory disease characterized by periodontal pocket formation and alveolar bone resorption. Periodontal bone resorption is induced by osteoclasts and receptor activator of nuclear factor-κB ligand (RANKL) which is an essential and central regulator of osteoclast development and osteoclast function. Therefore, RANKL plays a critical role in periodontal bone resorption. In this review, we have summarized the sources of RANKL in periodontal disease and explored which factors may regulate RANKL expression in this disease.

Highlights

Periodontitis is an inflammatory disease characterized by periodontal pocket formation and alveolar bone resorption, and it is one of the most common chronic inflammatory diseases in aged populations
Porphyromonas gingivalis (P. gingivalis), Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans), and Treponema denticola (T. denticola) are major periodontal pathogens involved in various forms of periodontitis; the variety and count cannot determine the type or severity of periodontitis, which indicated that immune responses against periodontal pathogens may greatly affect the course of periodontal diseases, but the mechanisms of periodontal bone resorption remain to be established [1]
We have summarized the sources of RANKL in periodontal disease and explored which factor may regulate RANKL expression in this disease

Summary

Introduction

Periodontitis is an inflammatory disease characterized by periodontal pocket formation and alveolar bone resorption, and it is one of the most common chronic inflammatory diseases in aged populations. Periodontal bone resorption is induced by osteoclasts. A balance between bone resorption by osteoclasts and bone formation by osteoblasts determines the level of bone mass. Receptor activator of nuclear factor-κB ligand (RANKL), its receptor RANK, and a decoy receptor osteoprotegerin (OPG) are key molecules in regulating osteoclast differentiation, recruitment, and function [2, 3]. RANKL is essential for the complete differentiation of osteoclast precursor cells [4] and plays a critical role in periodontal bone resorption [1]. We have summarized the sources of RANKL in periodontal disease and explored which factor may regulate RANKL expression in this disease

RANKL Expression in Periodontal Disease

Findings

Conculsions