Osteoarthritis year in review 2015: biology

Osteoarthritis Cartilage. 2016 Jan;24(1):21-6. doi: 10.1016/j.joca.2015.09.010.

Abstract

This review highlights a selection of recently published literature in the area of osteoarthritis biology. Major themes transpiring from a PubMed search covering the year between the 2014 and the 2015 Osteoarthritis Research Society International (OARSI) World Congress are explored. Inflammation emerged as a significant theme, revealing complex pathways that drive dramatic changes in cartilage homeostasis and in the synovium. Highlights include a homeostatic role for CXC chemokines in cartilage, identification of the zinc-ZIP8-MTF1 axis as an essential regulator of cartilage catabolism, and the discovery that a small aggrecan fragment can have catabolic and pro-inflammatory effects through Toll-like receptor 2. Synovitis can promote joint damage, partly through alarmins such as S100A8. Synovitis and synovial expression of the pro-algesic neurotrophin, Nerve Growth Factor, are associated with pain. Increasingly, researchers are considering specific pathogenic pathways that may operate in distinct subsets of osteoarthritis associated with distinct risk factors, including obesity, age, and joint injury. In obesity, the contribution of metabolic factors and diet is under intense investigation. The role of autophagy and oxidative stress in age-related osteoarthritis has been further explored. This approach may open avenues for targeted treatment of distinct phenotypes of osteoarthritis. Finally, a small selection of novel analgesic targets in the periphery is briefly discussed, including calcitonin gene-related peptide and the neuronal sodium voltage-gated channels, Nav1.7 and Nav1.8.

Keywords: Cartilage; Chondrocytes; Inflammation; Osteoarthritis; Pain; Synovium.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Autophagy
  • Calcitonin Gene-Related Peptide / metabolism
  • Calgranulin A / metabolism
  • Cartilage, Articular / metabolism*
  • Cation Transport Proteins / metabolism
  • Chemokines, CXC / metabolism
  • DNA-Binding Proteins / metabolism
  • Humans
  • Inflammation
  • NAV1.7 Voltage-Gated Sodium Channel / metabolism
  • NAV1.8 Voltage-Gated Sodium Channel / metabolism
  • Nerve Growth Factor / metabolism
  • Obesity / metabolism*
  • Osteoarthritis / metabolism*
  • Oxidative Stress
  • Synovial Membrane / metabolism*
  • Synovitis / metabolism*
  • Toll-Like Receptor 2 / metabolism
  • Transcription Factor MTF-1
  • Transcription Factors / metabolism
  • Zinc / metabolism

Substances

  • Calgranulin A
  • Cation Transport Proteins
  • Chemokines, CXC
  • DNA-Binding Proteins
  • NAV1.7 Voltage-Gated Sodium Channel
  • NAV1.8 Voltage-Gated Sodium Channel
  • SCN10A protein, human
  • SCN9A protein, human
  • SLC39A8 protein, human
  • TLR2 protein, human
  • Toll-Like Receptor 2
  • Transcription Factors
  • Nerve Growth Factor
  • Zinc
  • Calcitonin Gene-Related Peptide