Abstract
Purpose of Review
Diffuse Idiopathic Skeletal Hyperostosis (DISH) is considered a metabolic condition, characterized by new bone formation affecting mainly at entheseal sites. Enthesitis and enthesopathies occur not only in the axial skeleton but also at some peripheral sites, and they resemble to some extent the enthesitis that is a cardinal feature in spondyloarthritis (SpA), which is an inflammatory disease.
Recent Findings
We review the possible non-metabolic mechanism such as inflammation that may also be involved at some stage and help promote new bone formation in DISH. We discuss supporting pathogenic mechanisms for a local inflammation at sites typically affected by this disease, and that is also supported by imaging studies that report some similarities between DISH and SpA.
Summary
Local inflammation, either primary or secondary to metabolic derangements, may contribute to new bone formation in DISH. This new hypothesis is expected to stimulate further research in both the metabolic and inflammatory pathways in order to better understand the mechanisms that lead to new bone formation. This may lead to development of measures that will help in earlier detection and effective management before damage occurs.
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Keypoints
• DISH is characterized by new bone formation considered to be a non-inflammatory in nature.
• There is data to support that a local inflammatory condition might also promote new bone formation in DISH.
• Research should also focus on inflammatory basis in DISH due to its possible implications on future treatments.
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Mader, R., Pappone, N., Baraliakos, X. et al. Diffuse Idiopathic Skeletal Hyperostosis (DISH) and a Possible Inflammatory Component. Curr Rheumatol Rep 23, 6 (2021). https://doi.org/10.1007/s11926-020-00972-x
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DOI: https://doi.org/10.1007/s11926-020-00972-x