Synovium and the Innate Inflammatory Network in Osteoarthritis Progression

OSTEOARTHRITIS (MB GOLDRING, SECTION EDITOR)

DOI: 10.1007/s11926-013-0323-5

Cite this article as:
Liu-Bryan, R. Curr Rheumatol Rep (2013) 15: 323. doi:10.1007/s11926-013-0323-5
Part of the following topical collections:
  1. Topical Collection on Osteoarthritis

Abstract

This review focuses on the recent advancements in the understanding of innate immunity in the pathogenesis of osteoarthritis, particularly with attention to the roles of damage-associated molecular patterns (DAMPs), pattern recognition receptors (PPRs), and complement in synovitis development and cartilage degradation. Endogenous molecular products derived from cellular stress and extracellular matrix disruption can function as DAMPs to induce inflammatory responses and pro-catabolic events in vitro and promote synovitis and cartilage degradation in vivo via PRRs. Some of the DAMPs and PRRs display various capacities in driving synovitis and/or cartilage degradation in different models of animal studies. New findings reveal that the inflammatory complement cascade plays a key in the pathogenesis of OA. Crosstalk between joint tissues such as synovium and cartilage communicated at the cellular level within the innate immune inflammatory network is implicated to play an important role in OA progression. Further studies on how the innate immune inflammatory network impacts the OA disease process at different stages of progression will lead to the development of new therapeutic strategies.

Keywords

Osteoarthritis Synovium Cartilage Innate immunity Innate inflammatory network PRR DAMPs Crosstalk Toll-like receptors 

Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  1. 1.Veterans Affairs Medical Center and University of California San DiegoSan DiegoUSA