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The Paradox of Bone Formation and Bone Loss in Ankylosing Spondylitis: Evolving New Concepts of Bone Formation and Future Trends in Management

  • Spondyloarthritis (M Khan, Section Editor)
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Abstract

Purpose of Review

The purpose of the study is to briefly review the molecular mechanisms that leads to structural damage in ankylosing spondylitis (AS), defined as new bone formation resulting in complete or incomplete ankylosis of the spine, and the impact of treatment with biologics to retard this process.

Recent Findings

The understanding of molecular mechanisms leading to new bone formation in AS has significantly improved but is still incomplete. Availability of biologics has greatly enhanced the treatment of patients with AS, but its impact on slowing the structural damage is still a matter of debate, although a few observational studies have shown that long term use of TNF-α blockers may slow radiographic progression. The availability of newer biologics targeting IL-17/1L23 has shown some promising results in slowing radiographic progression in AS.

Summary

Although the availability of TNF-inhibitors has greatly enhanced the treatment options for patients with AS, their impact on slowing the structural damage is still not clearly established. However, preliminary results using newer biologics targeting IL-17/1L23 axis are more encouraging but longer follow-up is needed.

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Acknowledgements

We would like to thank Dr. Irving Kushner, Dr. Stanley Ballou, and Dr. Maria Antonelli for reviewing the paper and making necessary edits.

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Correspondence to Marina N. Magrey.

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Dr. Magrey reports personal fees from UCB PHARMA and personal fees from Jansenn, outside the submitted work.

Dr. Khan declares no conflicts of interest.

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This article is part of the Topical Collection on Spondyloarthritis

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Magrey, M.N., Khan, M.A. The Paradox of Bone Formation and Bone Loss in Ankylosing Spondylitis: Evolving New Concepts of Bone Formation and Future Trends in Management. Curr Rheumatol Rep 19, 17 (2017). https://doi.org/10.1007/s11926-017-0644-x

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