Analysis of Calcific Deposits in Calcifying Tendinitis

Background:Fibrin(ogen) maintains inflammation in various disorders but has never been linked to cartilage damage in rheumatoid arthritis (RA) or other forms of inflammatory arthritis.Objectives:To investigate the role of fibrin deposition on cartilage integrity in arthritis.Methods:Fibrin deposition on knee cartilage was analyzed by immunohistochemistry in RA patients and in murine adjuvant-induced arthritis (AIA). In chondrocytes, fibrinogen expression (Fgα, Fgβ, Fgγ) and procoagulant activity were evaluated by qRT-PCR and turbidimetry respectively. Fibrin-induced catabolic genes were assessed by qRT-PCR in chondrocytes. Fibrin-mediated chondro-synovial adhesion (CSA) with subsequent cartilage tears was studied in co-cultures of human RA cartilage with autologous synoviocytes, in the AIA model, and by MRI. The link between fibrin and calcification was examined in human RA cartilage stained for calcific deposits and in vitro in fibrinogen-stimulated chondrocytes.Results:Fibrin deposition on cartilage correlated with the severity of cartilage damage in human RA explants and in AIA wildtype (WT) mice, while fibrinogen deficient (Fg-/-) mice were protected. Accordingly, fibrin upregulated catabolic enzymes (Adamts5 and Mmp13) in chondrocytes. Secondly, CSA was present in fibrin-rich and damaged cartilage in AIA WT but not in Fg-/- mice. In line, autologous human synoviocytes, cultured on RA cartilage explants, adhered exclusively to fibrin-positive degraded areas. Gadolinium-enhanced MRI of human joints showed contrast-enhancement along cartilage surface in RA patients but not in controls. Finally, fibrin co-localized with calcification in human RA cartilage and triggered chondrocyte mineralization inducing pro-calcification genes (Anx5, Pit1, Pc1) and cytokine (IL-6). Although at a much lesser extent, we observed similar fibrin-mediated mechanisms in osteoarthritis (OA).Conclusion:Fibrin deposition directly impacts on cartilage integrity via induction of catabolism, mechanical stress, and calcification. Potentially, fibrin is a key factor of cartilage damage occurring in RA as a secondary consequence of inflammation.Disclosure of Interests:None declared

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Efficacy of Adjuvant Application of Platelet-Rich Plasma After Needle Aspiration of Calcific Deposits for the Treatment of Rotator Cuff Calcific Tendinitis: A Double-Blinded, Randomized Controlled Trial With 2-Year Follow-up

The American Journal of Sports Medicine ◽

10.1177/0363546520987579 ◽

2021 ◽

Vol 49 (4) ◽

pp. 873-882

Author(s):

Bart W. Oudelaar ◽

Rianne Huis In ‘t Veld ◽

Edwin M. Ooms ◽

Relinde Schepers-Bok ◽

Rob G.H.H. Nelissen ◽

...

Keyword(s):

Randomized Controlled Trial ◽

Rotator Cuff ◽

Mixed Model ◽

Platelet Rich Plasma ◽

Controlled Trial ◽

Needle Aspiration ◽

Randomized Controlled ◽

Clinical Scores ◽

Calcific Deposits

Background: Needle aspiration of calcific deposits (NACD) is a frequently used treatment for rotator cuff calcific tendinitis (RCCT). However, a substantial number of patients experience recurrent or persisting shoulder symptoms after NACD. Purpose: To compare the effects of adjuvant application of platelet-rich plasma (PRP) after NACD (NACP+PRP) with those of conventional NACD with corticosteroids (NACD+corticosteroids) on pain, shoulder function, and quality of life (QoL). Study Design: Randomized controlled trial; Level of evidence, 1. Methods: In a single-center, double-blinded, randomized controlled trial, 80 adults with symptomatic RCCT were randomly allocated to receive NACD+corticosteroids or NACD+PRP. Pain, shoulder function, and QoL were assessed at baseline; 6 weeks; and 3, 6, 12, and 24 months after treatment using a numeric rating scale for pain (NRS); the Constant-Murley score (CMS); the Disabilities of the Arm, Shoulder and Hand questionnaire (DASH); the Oxford Shoulder Score (OSS); and the EuroQol 5-dimension scale (EQ-5D). Additionally, resorption of calcific deposits and the integrity of rotator cuff tendons were assessed by using standard radiographs and ultrasound examination, respectively. The results were analyzed using noninferiority analysis for NRS scores and a mixed model for repeated measures. Results: Eighty patients were included (48 female; mean age, 49 ± 6 years; 41 patients in the NACD+PRP group). Both groups showed improvement of clinical scores at the 2-year follow-up ( P < .001 for all clinical scores). NACD+PRP was found to be noninferior to NACD+corticosteroids with regard to the mean decrease of NRS scores (4.34 vs 3.56; P = .003). Mixed-model analysis showed a significant difference in favor of NACD+PRP (CMS, P < .001; DASH, P = .002; OSS, P = .010; EQ-5D, P < .001). However, clinically relevant differences in favor of NACD+PRP were only seen at the 6-month follow-up for NRS and CMS scores, whereas at the 6-week follow-up a clinically relevant difference in favor of NACD+corticosteroids was found for all clinical scores except for the NRS. Full resorption of calcific deposits was present in 84% of the NACD+PRP group compared with 66% in the NACD+corticosteroids group ( P = .081). In the NACD+PRP group, 10 (24%) patients required a second NACD procedure compared with 19 (49%) patients in the NACD+corticosteroids group ( P = .036). Six complications, of which 5 were frozen shoulders, occurred in the NACD+PRP group compared with 1 complication in the NACD+corticosteroids group ( P = .11). Conclusion: NACD+PRP resulted in worse clinical scores at the 6-week follow-up but better clinical scores at the 6-month follow-up compared with NACD+corticosteroids. At the 1- and 2-year follow-ups, the results were comparable between groups. Furthermore, PRP seemed to reduce the need for additional treatments but was associated with more complications. In conclusion, NACD+corticosteroids had a favorable early effect on pain and function combined with low comorbidity. Thus, it remains the treatment of choice for patients with RCCT. Registration: NCT02173743 (ClinicalTrials.gov identifier).

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Global Hypertrophic Calcification of Shoulder Joint Capsule

Clinical Medicine Insights Case Reports ◽

10.1177/11795476211025351 ◽

2021 ◽

Vol 14 ◽

pp. 117954762110253

Author(s):

Abdulkarim Yousef Aldehaim ◽

Abdurhman Saud Alarfaj

Keyword(s):

Rheumatoid Arthritis ◽

Shoulder Joint ◽

Joint Capsule ◽

Surgical Approaches ◽

Contributing Factors ◽

Severe Arthritis ◽

History Of ◽

Excellent Control ◽

Specific Symptoms ◽

Calcific Deposits

Background: Calcification around the shoulder joint usually occur inside or around the tendons of the rotator cuff. We herein report on a case of global hypertrophic calcification of shoulder joint capsule in a patient with Rheumatoid arthritis. Case Report: An 86 years-old male with a long-standing history of seropositive Rheumatoid arthritis. The treatment for his Rheumatoid arthritis included Methotrexate and Hydroxychloroquine initially, but due lack of control, adalimumab was added with excellent control of his arthritis. He has progressively experienced an increasing pain and stiffness in his shoulders, in addition to an increasing limitation of shoulder movement. Magnetic Resonance Imaging revealed severe arthritis with remoulding deformity with extensive capsular calcification, intra-articular loose-bodies. Discussion: This phenomenon of calcification of shoulder capsule has not been reported before. The pathophysiology of calcific tendinopathy of the shoulder remains controversial. The calcific deposits consist of poorly-crystallized hydroxyapatite. Conclusion: Global hypertrophic calcification of shoulder joint capsule is unique and unreported in the literature. We can postulate that the long-standing inflammation of the synovial lining of the capsules had a major part. Moreover, Diabetes Mellitus, smoking, and repetitive manoeuvres are recognized contributing factors as well for similar conditions. Genetic predisposition seems to play a role as well. We think all those have played part in the development of this unprecedented presentation. Management should be tailored to target specific symptoms for pain, rigidity, and decreasing calcification size. Several options are available, including Kinesiotherapy, electrotherapy modalities, iontophoresis, electroshock wave therapy, and finally surgical approaches for progressive and refractory cases.

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