Osteoarthritis year in review 2015: biology

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.

Fig. 1

Research in the past year has focused on a multitude of pro-inflammatory and pro-catabolic pathways that initiate and maintain dramatic changes in chondrocyte phenotype, cartilage homeostasis, and in the synovium. The integration of the different pathways results in complex networks that drive disease progression, affect other articular tissues such as the subchondral bone, and promote pain. These networks may be modulated by factors such as obesity, diet, age, and joint injury.