Role of RANKL in bone diseases

Trends Endocrinol Metab. 2009 Mar;20(2):88-94. doi: 10.1016/j.tem.2008.10.007. Epub 2009 Jan 29.

Abstract

Bone remodeling is a tightly regulated process of osteoclast-mediated bone resorption, balanced by osteoblast-mediated bone formation. Disruption of this balance can lead to increased bone turnover, resulting in excessive bone loss or extra bone formation and consequent skeletal disease. The receptor activator of nuclear factor kappaB ligand (RANKL) (along with its receptor), the receptor activator of nuclear factor kappaB and its natural decoy receptor, osteoprotegerin, are the final effector proteins of osteoclastic bone resorption. Here, I provide an overview of recent studies that highlight the key role of RANKL in the pathophysiology of several bone diseases and discuss the novel therapeutic approaches afforded by the modulation of RANKL.

MeSH terms

  • Animals
  • Arthritis / complications
  • Arthritis / metabolism
  • Arthritis / physiopathology
  • Bone Diseases / etiology*
  • Bone Diseases / physiopathology
  • Bone Remodeling / physiology
  • Humans
  • Models, Biological
  • Neoplasms / complications
  • Neoplasms / metabolism
  • Neoplasms / physiopathology
  • RANK Ligand / metabolism
  • RANK Ligand / physiology*
  • Signal Transduction / physiology

Substances

  • RANK Ligand