Rheumatoid arthritis-associated bone erosions: evolving insights and promising therapeutic strategies

Biosci Trends. 2020 Nov 4;14(5):342-348. doi: 10.5582/bst.2020.03253. Epub 2020 Sep 10.

Abstract

The human immune system has evolved to recognize and eradicate pathogens, a process that is known as "host defense". If, however, the immune system does not work properly, it can mistakenly attack the body's own tissues and induce autoimmune diseases. Rheumatoid arthritis (RA) is such an autoimmune disease in which the synovial joints are predominately attacked by the immune system. Moreover, RA is associated with bone destruction and joint deformity. Although biologic agents have propelled RA treatment forward dramatically over the past 30 years, a considerable number of patients with RA still experience progressive bone damage and joint disability. That is to be expected since current RA therapies are all intended to halt inflammation but not to alleviate bone destruction. A better understanding of bone erosions is crucial to developing a novel strategy to treat RA-associated erosions. This review provides insights into RA-associated bone destruction and perspectives for future clinical interventions.

Keywords: RANKL; bone erosions; rheumatoid arthritis; synovial fibroblasts.

Publication types

  • Review

MeSH terms

  • Arthritis, Rheumatoid / complications*
  • Arthritis, Rheumatoid / drug therapy
  • Arthritis, Rheumatoid / immunology
  • Arthritis, Rheumatoid / pathology
  • Biological Factors / pharmacology*
  • Biological Factors / therapeutic use
  • Bone Density Conservation Agents / pharmacology*
  • Bone Density Conservation Agents / therapeutic use
  • Cadherins / pharmacology
  • Cadherins / therapeutic use
  • Humans
  • Joint Capsule / drug effects
  • Joint Capsule / immunology
  • Joint Capsule / pathology
  • Osteoblasts / drug effects
  • Osteoblasts / immunology
  • Osteoclasts / drug effects
  • Osteoclasts / immunology
  • Osteogenesis / drug effects
  • Osteogenesis / immunology
  • Osteoporosis / drug therapy
  • Osteoporosis / immunology*
  • Osteoporosis / pathology
  • Proteins / antagonists & inhibitors
  • Proteins / metabolism
  • RANK Ligand / antagonists & inhibitors
  • RANK Ligand / immunology
  • RANK Ligand / metabolism
  • Recombinant Proteins / pharmacology
  • Recombinant Proteins / therapeutic use
  • Signal Transduction / drug effects
  • Signal Transduction / immunology
  • Synovial Fluid / drug effects
  • Synovial Fluid / immunology

Substances

  • Biological Factors
  • Bone Density Conservation Agents
  • Cadherins
  • Proteins
  • RANK Ligand
  • Recombinant Proteins
  • TNFSF11 protein, human
  • bromodomain and extra-terminal domain protein, human
  • osteoblast cadherin