Complexity of enthesitis and new bone formation in ankylosing spondylitis: current understanding of the immunopathology and therapeutic approaches

Author:

Kusuda Masaki1,Haroon Nigil1234,Nakamura Akihiro1234

Affiliation:

1. Schroeder Arthritis Institute, Krembil Research Institute, University Health Network, Toronto, ON, Canada

2. Spondylitis Program, Division of Rheumatology, Toronto Western Hospital, University Health Network, Toronto, ON, Canada

3. Division of Rheumatology, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada

4. Institute of Medical Science, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada

Abstract

ABSTRACT Despite increasing availability of treatments for spondyloarthritis (SpA) including tumour necrosis factor (TNF) and interleukin-17 (IL-17) inhibitors, there is no established treatment that abates new bone formation (NBF) in ankylosing spondylitis (AS), a subset of SpA. Recent research on TNF has revealed the increased level of transmembrane TNF in the joint tissue of SpA patients compared to that of rheumatoid arthritis patients, which appears to facilitate TNF-driven osteo-proliferative changes in AS. In addition, there is considerable interest in the central role of IL-23/IL-17 axis in type 3 immunity and the therapeutic potential of blocking this axis to ameliorate enthesitis and NBF in AS. AS immunopathology involves a variety of immune cells, including both innate and adoptive immune cells, to orchestrate the immune response driving type 3 immunity. In response to external stimuli of inflammatory cytokines, local osteo-chondral progenitor cells activate intra-cellular anabolic molecules and signals involving hedgehog, bone morphogenetic proteins, receptor activator of nuclear factor kappa-B ligand, and Wnt pathways to promote NBF in AS. Here, we provide an overview of the current immunopathology and future directions for the treatment of enthesitis and NBF associated with AS.

Funder

N.H. from the Canadian Institute of Health Research

Publisher

Oxford University Press (OUP)

Subject

Rheumatology

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