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Nat Rev Rheumatol. 2017 Nov 21;13(12):731-741. doi: 10.1038/nrrheum.2017.188.

Enthesitis: from pathophysiology to treatment.

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Department of Internal Medicine 3, Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nuremberg and Universitätsklinikum Erlangen, Ulmenweg 18, 91054 Erlangen, Germany.
Laboratory for Tissue Homeostasis and Disease, Skeletal Biology and Engineering Research Center, Department of Development and Regeneration, Catholic University Leuven, Herestraat 49, B-3000 Leuven, Belgium.
University Paris Ouest-Versailles-Saint-Quentin-en-Yvelines and Rheumatology Department of Ambroise Paré Hospital, APHP, 92100 Boulogne-Billancourt, France.
Laboratory for Molecular Immunology and Inflammation, Department of Rheumatology, University Hospital Ghent, De Pintelaan 185, B-9000 Ghent, Belgium, and the Vlaams Instituut voor Biotechnologie (VIB) Center for Inflammation Research (IRC), Fiers-Schell-Van Montagu Building, Technologiepark 927, Ghent University, B-9052 Ghent, Belgium.
Rheumatology Department, Guy's & St Thomas' NHS Foundation Trust, Guy's Hospital, Great Maze Pond, London SE1 9RT, UK.
Rheumatology Unit, Internal Medical Service, and University Institute, Hospital Italiano de Buenos Aires, Juan D. Perón 4190 (C1181ACH), Buenos Aires, Argentina.
Section of Musculoskeletal Diseases, Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds and Chapel Allerton Hospital, Chapeltown Road, Leeds, West Yorkshire LS7 4SA, UK.


Entheses are the insertion sites of tendons and ligaments to the bone surface and are essential structures for locomotion. Inflammation of the entheses (enthesitis) is a key feature of psoriatic arthritis and spondyloarthritis. To date, our conceptual understanding of enthesitis remains limited. This Review provides an insight into the pathophysiology of enthesitis, addressing the role of biomechanics, prostaglandin E2-mediated vasodilation and the activation of innate immune cells in the initiation phase of enthesitis, as well as the role of entheseal IL-23-responsive cells that augment inflammation by producing pro-inflammatory mediators such as IL-17A, IL-22 and TNF. In addition, the molecular steps that translate inflammation into resident tissue responses, resulting in new bone formation, are discussed. The second part of the article summarizes the clinical features of enthesitis, and the role of clinical and imaging instruments in detecting enthesitis are discussed together with their challenges and limitations. Finally, the Review summarizes the current treatment possibilities for enthesitis based on the aforementioned pathophysiological concepts, focusing on the role of cytokine-blocking agents.

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