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      Enthesopathies and enthesitis. Part 2: Imaging studies Translated title: Entezopatie i zapalenie entez. Część II. Diagnostyka obrazowa

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          Abstract

          The pathologies of tendon and ligament attachments are called enthesopathies. Enthesitis is one of enthesopathies and it is considered a characteristic sign of rheumatic diseases from the spondyloarthritis group, including peripheral spondyloarthritis. Therefore, enthesitis has been included in a number of clinical classifications for diagnosing these diseases. Clinical diagnosis of enthesitis is based on rather non-specific clinical signs and results of laboratory tests. It is believed that imaging examinations might improve diagnosis, particularly because numerous papers prove that differentiating enthesitis from other enthesopathic processes is possible. On the other hand, a number of authors report the lack of specific signs in imaging as well as typical histological and immunological features that would enable confirmation of clinical diagnosis of enthesitis. The first part of the publication presented theories on the etiopathogenesis of enthesitis (inflammatory, mechanical, autoimmune and associated with the synovio-entheseal complex) as well as on the formation of enthesophytes (inflammatory, molecular and mechanical). This paper – the second part of the article, is a review of the state-of-the-art on the ability of imaging examinations to diagnose enthesitis. It turns out that none of the enthesitis criteria used in imaging examinations is specific for inflammation. As enthesitis may be the only symptom of early spondyloarthritis (particularly in patients with absent HLA-B27 antigen), the lack of its unambiguous picture in ultrasound and magnetic resonance imaging prompts the search for other signs characteristic of spondyloarthritis and more specific features in imaging in order to make a diagnosis as early as possible.

          Translated abstract

          Patologie przyczepów ścięgien i więzadeł są określane mianem entezopatii. Jednym z rodzajów entezopatii jest zapalenie ( enthesitis). Uznaje się je za charakterystyczny objaw chorób reumatycznych z grupy spondyloartropatii (spondyloarthritis), w tym głównie spondyloartropatii obwodowych. Z tego powodu enthesitis włączono do szeregu klasyfikacji klinicznych, służących m.in. do rozpoznawania tych chorób. Klinicyści diagnozują enthesitis na podstawie mało specyficznych objawów oraz wyników badań laboratoryjnych. Duże nadzieje na poprawę możliwości diagnostycznych są wiązane z badaniami obrazowymi. Niektóre prace naukowe dowodzą możliwości różnicowania zapalenia entez z innymi procesami entezopatycznymi. Z drugiej strony szereg doniesień wskazuje na brak specyficznych zmian w badaniach obrazowych oraz typowych cech histologicznych i immunologicznych pozwalających na potwierdzenie klinicznego rozpoznania enthesitis. W pierwszej części publikacji przedstawiono teorie etiopatogenezy entezopatii (teorię zapalną, mechaniczną, kompleksu entezy i autoimmunologiczną) oraz koncepcje powstawania entezofitów (zapalną, molekularną i mechaniczną). W niniejszej, drugiej części zaprezentowano zaś przegląd wiedzy na temat możliwości badań obrazowych w rozpoznawaniu enthesitis. Jak się okazuje, żadne z kryteriów enthesitis stosowanych w badaniach obrazowych nie jest specyficzne dla zapalenia. Zważywszy na to, że enthesitis bywa jedynym objawem spondyloartropatii w początkowym okresie (zwłaszcza u chorych z nieobecnym antygenem HLA-B27), brak jednoznacznego obrazu w badaniach ultrasonograficznych i rezonansu magnetycznego wymaga poszukiwania innych objawów charakterystycznych dla spondyloartropatii i bardziej specyficznych markerów w badaniach obrazowych w celu jak najszybszego ustalenia rozpoznania.

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          Most cited references 38

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          Where tendons and ligaments meet bone: attachment sites ('entheses') in relation to exercise and/or mechanical load.

          Entheses (insertion sites, osteotendinous junctions, osteoligamentous junctions) are sites of stress concentration at the region where tendons and ligaments attach to bone. Consequently, they are commonly subject to overuse injuries (enthesopathies) that are well documented in a number of sports. In this review, we focus on the structure-function correlations of entheses on both the hard and the soft tissue sides of the junction. Particular attention is paid to mechanical factors that influence form and function and thus to exploring the relationship between entheses and exercise. The molecular parameters indicative of adaptation to mechanical stress are evaluated, and the basis on which entheses are classified is explained. The application of the 'enthesis organ' concept (a collection of tissues adjacent to the enthesis itself, which jointly serve the common function of stress dissipation) to understanding enthesopathies is considered and novel roles of adipose tissue at entheses are reviewed. A distinction is made between different locations of fat at entheses, and possible functions include space-filling and proprioception. The basic anchorage role of entheses is considered in detail and comparisons are explored between entheses and other biological 'anchorage' sites. The ability of entheses for self-repair is emphasized and a range of enthesopathies common in sport are reviewed (e.g. tennis elbow, golfer's elbow, jumper's knee, plantar fasciitis and Achilles insertional tendinopathies). Attention is drawn to the degenerative, rather than inflammatory, nature of most enthesopathies in sport. The biomechanical factors contributing to the development of enthesopathies are reviewed and the importance of considering the muscle-tendon-bone unit as a whole is recognized. Bony spur formation is assessed in relation to other changes at entheses which parallel those in osteoarthritic synovial joints.
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            The anatomical basis for disease localisation in seronegative spondyloarthropathy at entheses and related sites.

            The 2 major categories of idiopathic inflammatory arthritis are rheumatoid arthritis and the seronegative spondyloarthropathies. Whilst the synovium is the primary site of joint disease in the former, the primary site in the latter is less well defined. However, it has recently been proposed that enthesitis-associated changes in the spondyloarthropathies are primary and that all other joint manifestations are secondary. Nevertheless, some of the sites of disease localisation have not been adequately explained in terms of enthesitis. This article summarises current knowledge of the structure, function, blood supply, innervation, molecular composition and histopathology of the classic enthesis (i.e. the bony attachment of a tendon or ligament) and introduces the concept of 'functional' and articular 'fibrocartilaginous' entheses. The former are regions where tendons or ligaments wrap-around bony pulleys, but are not attached to them, and the latter are synovial joints that are lined by fibrocartilage rather than hyaline cartilage. We describe how these 3 types of entheses relate to other, and how all are prone to pathological changes in spondyloarthropathy. We propose that the inflammatory responses characteristic of spondyloarthropathies are triggered at these seemingly diverse sites, in genetically susceptible individuals, by a combination of anatomical factors which lead to higher levels of tissue microtrauma, and the deposition of microbes.
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              Ultrasonography of entheseal insertions in the lower limb in spondyloarthropathy.

              To compare ultrasonography (US) with clinical examination in the detection of entheseal abnormality of the lower limb in patients with spondyloarthropathy (SpA). 35 patients with SpA (ankylosing spondylitis 27; psoriatic arthritis 7; reactive arthritis 1) underwent independent clinical and ultrasonographic examination of both lower limbs at five entheseal sites-superior pole and inferior pole of patella, tibial tuberosity, Achilles tendon, and plantar aponeurosis. US was performed using an ATL (Advanced Technology Laboratories, Bothell, Washington, USA) high definition imaging 3000 machine with linear 7-4 MHz and compact linear 10-5 MHz probes to detect bursitis, structure thickness, bony erosion, and enthesophyte (bony spur). An enthesitis score was formulated from these US findings giving a possible maximum total score of 36. On clinical examination 75/348 (22%) entheseal sites were abnormal and on US examination 195/348 (56%) sites were abnormal. In 19 entheseal sites with bursitis on US, only five were detected by clinical examination. Compared with US, clinical examination had a low sensitivity (22.6%) and moderate specificity (79.7%) for the detection of enthesitis of the lower limbs. There was no significant correlation between the US score of enthesitis and acute phase parameters such as erythrocyte sedimentation rate (ESR) or C reactive protein (CRP). The intraobserver kappa value for analysis of all sites was 0.9. Most entheseal abnormality in SpA is not detected at clinical examination. US is better than clinical examination in the detection of entheseal abnormality of the lower limbs in SpA. A quantitative US score of lower limb enthesitis is proposed but further studies are required to validate it in SpA.
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                Author and article information

                Journal
                J Ultrason
                J Ultrason
                JoU
                Journal of Ultrasonography
                Medical Communications Sp. z o.o.
                2084-8404
                30 June 2015
                June 2015
                : 15
                : 61
                : 196-207
                Affiliations
                [1 ]Department of Radiology, Institute of Rheumatology, Warsaw, Poland
                [2 ]Department of Diagnostic Imaging, Second Faculty, Warsaw Medical University, Poland
                [3 ]Early Arthritis Clinic, Institute of Rheumatology, Warsaw, Poland
                [4 ]Department of Diagnostic Hematology, Institute of Hematology and Transfusion Medicine, Warsaw, Poland
                [5 ]Department of Pathophysiology, Immunology, and Pathological Anatomy, Institute of Rheumatology, Warsaw, Poland
                Author notes
                Correspondence: Prof. Iwona Sudoł-Szopińska, MD, PhD, Department of Radiology, Institute of Rheumatology, Spartańska 1, 02-637 Warsaw, Poland. tel./fax: +48 22 844 42 41. e-mail: sudolszopinska@ 123456gmail.com
                Article
                0017
                10.15557/JoU.2015.0017
                4579753
                2015 Polish Ultrasound Society. Published by Medical Communications Sp. z o.o. All rights reserved.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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