Primary synovial chondromatosis (PSC) is a rare benign disorder characterised by development of foci of cartilage in the synovial membrane of the joint, bursa or tendon sheath that was first described by Reichel in 1900. The disorder has traditionally been considered as a metaplastic condition, but was recently assoicated with structural chromosomal abnormalities, suggesting a neoplastic origin. The aim of the present study was to evaluate the clinical, arthroscopic and histopathological aspects of PSC involving both the glenohumeral joint and tendon sheath of the biceps. An 18-year-old, right-hand dominant boy presented with right shoulder pain. There was no history of trauma. Pain began in his shoulder about 1 year prior to his clinical visit. Physical examination revealed an active range of motion of the affected side measuring 90 ° of abduction and 150° of forward flexion; internal rotation to the greater trochanter of the hip and external rotation were slightly limited. Plain radiographs revealed multiple calcific nodules in the right glenohumeral joint, the subcoracoid recess, and anterior to the humeral head. There appeared to be mild degenerative changes in the gleno-humeral joint. Magnetic resonance imaging was performed to assess the location of the loose bodies and evaluate intra-articular degenerative changes. It demonstrated multiple loose bodies within the glenohumeral joint, the proximal tendon sheath of the biceps, and also in the subscapularis bursa. There was irregularity involving the anterior aspect of the humeral head consistent with erosive changes. The patient underwent arthroscopic surgery to remove the loose bodies, arthroscopic partial synovectomy and decompression of the biceps tendon sheath, with removal of multiple loose bodies. For partial synovectomy a motorized suction-cutting device alternated between anterior and posterior portals. The biceps tendon was identified through an anterior deltopectoral incision and multiple loose bodies were removed from within the tendon sheath. Specimens for histological analyses were stained with haematoxylineosin (H&
E) and safranin-O. Polyclonal anti-type II collagen was used at 1:100 dilution for immunohistological analyses At 2–year follow-up examination the patient was asymptomatic and there was no clinical or radiographic evidence of recurrence. Lobulated areas of hyaline cartilage just below the synovial surface were easily identified. Chondrocytes were clustered together in nests and were not uniformly distributed throughout the ground substance. Safranin-O staining showed evident meta-chromasia of the cartilaginous matrix. Immunolabelling for type II collagen was observed in cartilaginous areas with marked cytoplasmic staining. We believe that arthroscopy is an easy and safe method for the management of this disorder and that the support of an experienced pathologist is necessary to avoid differential diagnostic problems with the uncommon malignant transformation.
