The maintenance of bone homeostasis is dependent on a balance between osteoclasts—cells that resorb bone—and osteoblasts—cells that form bone [1
]. The past decade of research has yielded critical insights into mechanisms that underlie joint damage, but the most recent studies have unveiled an array of fascinating molecules that modulate signaling pathways of bone formation. With respect to psoriatic arthritis (PsA), long-term consequences of joint inflammation are development of bone erosions alongside new bone formation in the form of syndesmophytes, enthesophytes, and ankylosis (peripheral bony fusion) [2
]. Data from Schett and others have further validated differences in the bone pathologies of PsA and rheumatoid arthritis (RA) using new imaging modalities such as micro-CT and have lent credence to the concept of divergent mechanisms of bone repair in these two arthropathies [4
]. New insights into cytokine pathways that involve interleukin (IL)-17 and IL-33 may further differentiate mechanisms of bone resorption and repair in PsA and RA and likely will uncover additional therapeutic targets.
Recognition of bone as an active organ that interacts with its environment is a relatively new development [1
]. Indeed, the number of molecules with dual roles in bone and immune function is ever-increasing and shows the complexity of the field of osteoimmunology; it may also explain clinical findings such as the notable fragility of bone in patients with chronic autoimmune conditions. Prior hypotheses have suggested use of medications such as steroids to potentially explain increased bone demineralization, but work in osteoimmunology points to specific inflammatory mediators that can target signaling pathways and exert negative effects on bone homeostasis [6
Another central question focuses on pathways of bone formation and includes the view that endochondral bone formation, in which a cartilage template is replaced by bone via the differentiation of chondrocytes into osteoblasts, may be critical in arthritic diseases and is influenced by inflammatory signals that promote osteoblastogenesis [9
In this paper, we discuss the evolving field of osteoimmunology and how inflammation in PsA and other inflammatory arthritides is leading to new insights into bone remodeling, in particular with regard to new bone formation. We also present recent information gained from novel instruments that image joint and bone inflammation and discuss how current therapies for the treatment of inflammatory arthritis may also affect bone homeostasis.