Reuven Mader1, Nicola Pappone2, Xenofon Baraliakos3, Iris Eshed4, Piercarlo Sarzi-Puttini5, Fabiola Atzeni6, Amir Bieber7, Irina Novofastovski7, David Kiefer3, Jorrit-Jan Verlaan8, Pasquale Ambrosino2, Dan Buskila9, Jacome Bruges Armas10, Muhammad Asim Khan11. 1. Rheumatic Diseases Unit, Ha'Emek MC, Afula, Israel. reuven.mader@gmail.com. 2. Istituti Clinici Scientifici Maugeri IRCCS, Pavia, Italy. 3. Rheumazentrum Ruhrgebiet, Ruhr-Universität Bochum, Bochum, Germany. 4. Department of Radiology, Musculoskeletal imaging Unit, Sheba Medical Center, Tel Aviv University, Tel Aviv, Israel. 5. Rheumatology Unit, L. Sacco University Hospital of Milan, Milan, Italy. 6. Rheumatology Unit, University of Messina, Messina, Italy. 7. Rheumatic Diseases Unit, Ha'Emek MC, Afula, Israel. 8. Department of Orthopedics, University Medical Center Utrecht, Utrecht, The Netherlands. 9. Ben Gurion University of the Negev, Beer-Sheva, Israel. 10. Medicine, Rheumatology, SEEBMO, Hospital de Santo Espirito da ilha Terceira, Universidade do Porto, Angra do Heroismo, Portugal. 11. Case Western Reserve University, Cleveland, OH, USA.
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. 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.
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. 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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