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      Rotator cuff calcific tendinopathy: from diagnosis to treatment

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          Abstract

          Rotator cuff calcific tendinopathy (RCCT) is a very common condition caused by the presence of calcific deposits in the rotator cuff (RC) or in the subacromial-subdeltoid (SASD) bursa when calcification spreads around the tendons. The pathogenetic mechanism of RCCT is still unclear. It seems to be related to cell-mediated disease in which metaplastic transformation of tenocytes into chondrocytes induces calcification inside the tendon of the RC. RCCT is a frequent finding in the RC that may cause significant shoulder pain and disability. It can be easily diagnosed with imaging studies as conventional radiography (CR) or ultrasound (US). Conservative management of RCCT usually involves rest, physical therapy, and oral NSAIDs administration. Imaging-guided treatments are currently considered minimally-invasive, yet effective methods to treat RCCT with about 80% success rate. Surgery remains the most invasive treatment option in chronic cases that fail to improve with other less invasive approaches. (www.actabiomedica.it)

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          Most cited references126

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          Calcific tendinitis of the shoulder.

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            A novel Ca²⁺-mediated cross-talk between endoplasmic reticulum and acidic organelles: implications for NAADP-dependent Ca²⁺ signalling.

            Nicotinic acid adenine dinucleotide phosphate (NAADP) serves as the ideal trigger of spatio-temporally complex intracellular Ca(2+) signals. However, the identity of the intracellular Ca(2+) store(s) recruited by NAADP, which may include either the endolysosomal (EL) or the endoplasmic reticulum (ER) Ca(2+) pools, is still elusive. Here, we show that the Ca(2+) response to NAADP was suppressed by interfering with either EL or ER Ca(2+) sequestration. The measurement of EL and ER Ca(2+) levels by using selectively targeted aequorin unveiled that the preventing ER Ca(2+) storage also affected ER Ca(2+) loading and vice versa. This indicates that a functional Ca(2+)-mediated cross-talk exists at the EL-ER interface and exerts profound implications for the study of NAADP-induced Ca(2+) signals. Extreme caution is warranted when dissecting NAADP targets by pharmacologically inhibiting EL and/or the ER Ca(2+) pools. Moreover, Ca(2+) transfer between these compartments might be essential to regulate vital Ca(2+)-dependent processes in both organelles.
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              Multi-modal imaging of adhesive capsulitis of the shoulder

              Abstract Adhesive capsulitis of the shoulder is a clinical condition characterized by progressive limitation of active and passive mobility of the glenohumeral joint, generally associated with high levels of pain. Although the diagnosis of adhesive capsulitis is based mainly on clinical examination, different imaging modalities including arthrography, ultrasound, magnetic resonance, and magnetic resonance arthrography may help to confirm the diagnosis, detecting a number of findings such as capsular and coracohumeral ligament thickening, poor capsular distension, extracapsular contrast leakage, and synovial hypertrophy and scar tissue formation at the rotator interval. Ultrasound can also be used to guide intra- and periarticular procedures for treating patients with adhesive capsulitis. Key Points • Diagnosis of adhesive capsulitis is mainly based on clinical findings. • Imaging may be used to exclude articular or rotator cuff pathology. • Thickening of coracohumeral and inferior glenohumeral ligaments are common findings. • Rotator interval fat pad obliteration has 100 % specificity for adhesive capsulitis. • Ultrasound can be used to guide intra- and periarticular treatments.
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                Author and article information

                Journal
                Acta Biomed
                Acta Biomed
                Acta bio-medica : Atenei Parmensis
                Mattioli 1885 (Italy )
                0392-4203
                2018
                : 89
                : Suppl 1
                : 186-196
                Affiliations
                [1 ]Department of Advanced Biomedical Sciences, Federico II University, Napoli, Italy
                [2 ]Department of Radiology, DIBIMED, University of Palermo, Palermo, Italy
                [3 ]Scuola di Specializzazione in Radiodiagnostica, Università degli Studi di Milano, Milano, Italy
                [4 ]University of Palermo, Palermo, Italy
                [5 ]Division of Interventional Radiology, Istituto Europeo di Oncologia, Milano, Italy
                [6 ]Unit of Radiology, Istituti Clinici Zucchi, Monza, Italy
                [7 ]Unit of Diagnostic and Interventional Radiology, IRCCS Istituto Ortopedico Galeazzi, Milano, Italy
                [8 ]Unit of Diagnostic and Interventional Radiology, Università dell’Aquila, Italy
                [9 ]Department of Biomedical Sciences for Health, Università degli Studi di Milano, Milano, Italy
                Author notes
                Correspondence: Luca Maria Sconfienza Unit of Diagnostic and Interventional Radiology, IRCCS Istituto Ortopedico Galeazzi, Milano Phone +39 02 6621 4497 E-mail: io@ 123456lucasconfienza.it
                Article
                ACTA-89-186
                10.23750/abm.v89i1-S.7022
                6179075
                29350647
                b7e34045-1751-4c0e-a117-2b0d13ee7695
                Copyright: © 2018 ACTA BIO MEDICA SOCIETY OF MEDICINE AND NATURAL SCIENCES OF PARMA

                This work is licensed under a Creative Commons Attribution 4.0 International License

                History
                : 15 September 2017
                : 20 December 2017
                Categories
                Review

                calcific tendinopathy,rotator cuff,us,mri,percutaneous treatments

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