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Structural Disease Progression in Axial Spondyloarthritis: Still a Cause for Concern?

  • Spondyloarthritis (M Khan, Section Editor)
  • Published:
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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.

Summary

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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Acknowledgements

B.N obtained an “aspirant” fellowship from the Fund for Scientific Research Flanders (FWO Vlaanderen). Laboratory studies by the authors on the topic are supported by FWO grant G.0946.14.

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Correspondence to Rik J. Lories.

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Barbara Neerinckx declares that she has no conflict of interest.

Rik Lories reports grants and personal fees from Pfizer, personal fees from Abbvie, personal fees from Celgene, personal fees from Jansen, personal fees from UCB, grants from Boehringer-Ingelheim, and personal fees from Novartis during the conduct of the study.

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This article does not contain any studies with human or animal subjects performed by any of the authors.

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This article is part of the Topical Collection on Spondyloarthritis

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Neerinckx, B., Lories, R.J. Structural Disease Progression in Axial Spondyloarthritis: Still a Cause for Concern?. Curr Rheumatol Rep 19, 14 (2017). https://doi.org/10.1007/s11926-017-0639-7

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