Barbara Neerinckx1, Rik J Lories2. 1. Laboratory of Tissue Homeostasis and Disease, Skeletal Biology and Engineering Research Center, Department of Development and Regeneration, KU Leuven & Division of Rheumatology, University Hospitals Leuven, Leuven, Belgium. 2. Laboratory of Tissue Homeostasis and Disease, Skeletal Biology and Engineering Research Center, Department of Development and Regeneration, KU Leuven & Division of Rheumatology, University Hospitals Leuven, Leuven, Belgium. Rik.Lories@kuleuven.be.
Abstract
PURPOSE OF THE REVIEW: Progressive ankylosis is a feared consequence of long-standing axial spondyloarthritis. We aim to critically review current insights into the effect of therapy, the molecular pathways involved in this process, and to present a model explaining the sequence of events. RECENT FINDINGS: Long-term follow-up data suggest that successful control of inflammation may slow down radiographic progression of disease in axial spondyloarthritis. Structural effects of new therapies such as interleukin-17 targeting need to be further studied. Bone loss and architectural changes could act as driver for the tissue remodeling process trying to maintain spinal stability in the presence of inflammation. Despite some progress, the nature and mechanisms of new bone formation in axial spondyloarthritis still remain incompletely understood. However, long-term control of inflammation appears critical to avoid progressive disability due to structural damage.
PURPOSE OF THE REVIEW: Progressive ankylosis is a feared consequence of long-standing axial spondyloarthritis. We aim to critically review current insights into the effect of therapy, the molecular pathways involved in this process, and to present a model explaining the sequence of events. RECENT FINDINGS: Long-term follow-up data suggest that successful control of inflammation may slow down radiographic progression of disease in axial spondyloarthritis. Structural effects of new therapies such as interleukin-17 targeting need to be further studied. Bone loss and architectural changes could act as driver for the tissue remodeling process trying to maintain spinal stability in the presence of inflammation. Despite some progress, the nature and mechanisms of new bone formation in axial spondyloarthritis still remain incompletely understood. However, long-term control of inflammation appears critical to avoid progressive disability due to structural damage.
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