Bone formation in axial spondyloarthritis: Is disease modification possible?
Akihiro Nakamura1, Ayantika Talukdar2, Sayaka Nakamura2
1The Arthritis Program, Toronto Western Hospital, 399 Bathurst Street, Toronto, M5T 2S8, ON, Canada; Division of Genetics and Development, Krembil Research Institute, University Health Network, 60 Leonard Avenue, Toronto, ON, M5T 0S8, Canada; Division of Rheumatology, Department of Medicine, Toronto Western Hospital, University of Toronto, 399 Bathurst Street, Toronto, Ontario, M5T 2S8, Canada; Institute of Medical Science, University of Toronto, ON, Canada.
Abstract:
Axial spondyloarthritis (SpA) is a chronic disease characterised by new bone formation (NBF) in the axial skeleton as well as at peripheral entheseal sites. NBF is thought to arise in areas of previous inflammation or osteitis visualised on MRI, with mechanical stress playing a role in disease pathogenesis. The interface between bone and immune cells is complex with the RANKL-OPG system being key to NBF. The IL-17/23 axis and other cytokines such as TNFα and MIF are thought to play a central role. The transition from inflammation to NBF is mediated via the Wnt, BMP and Hedgehog signalling pathways. An altered microbiome has been reported in SpA, which is a potential trigger of NBF in SpA. There is now data to show that treatment with TNF inhibitors prevents NBF and hence modifies disease progression. More research into identifying newer targets for disease modification is needed to alter the course of the disease.
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