Cellular and molecular mechanisms of bone damage and repair in inflammatory arthritis

•An increased RANKL:OPG ratio favours osteoclastogenesis and bone resorption.•TH17 cells (and IL-17) are crucial regulators of osteoclast activity.•IL-23 is central to the pathobiology of the spondylarthropathies.•DKK-1 and other inhibitors of the Wnt pathway impair osteoblast activity.•MicroRNAs play an important part in bone homeostasis and musculoskeletal disease. Bone remodelling relies on tightly controlled cycles of bone resorption and formation, mediated by osteoclasts and osteoblasts, respectively. The past two decades have seen a huge increase in our understanding of immune modulation and disruption of bone homeostasis in rheumatic diseases; identification of the molecular pathways responsible for accelerated bone loss in such conditions has given rise to potential novel therapeutic targets. Most recently, the role of microRNAs in inflammatory and noninflammatory bone loss raises the intriguing possibility that modification of cellular protein translation could also be a treatment strategy for bone damage.