RBs develop as a response to chronic synovial inflammation. Although it was identified with Tb arthritis at the beginning, later many articles were published indicating that they could be detected in many inflammatory cases such as, rheumatoid arthritis, septic arthritis, juvenile rheumatoid arthritis, osteoarthritis, hypocomplementemic arthritis and subacromial bursitis 1,3-5
. In 1993 Stein et al. 6
defined MRI findings of RBs at subacromial bursa. Size of RBs can be changing. In the literature it has been stated that 55% of them is 2-7 mm, 35% of them is smaller than 2 mm and about 10% of them is bigger than 7 mm 7
. In our case, they were between 2-8 mm (mostly 4-5 mm) which varied in form and sizes. Discussion about the etiopathology still continues. According one of the theories, in the later stages of RA number of increase and hypertrophy in synovial villi occur. In these villi fibrins pile up then they stretch and break away 5
. According to Popert et al. 7,
the reason of the RBs formation is the fibronectin and fibrin sediments that formed with the effect of glycosaminoglycan which is secreted by the abraded cartilage. Changes in the histological structure of RBs are in relation with their maturation degrees.
Finally McCarty DJ and Cheung 8 argued that as a result of microcirculation failure at synovium and as a result of hypoxia related to these synovial micro infarctions the infarcted fragments fall into joint cavity and were covered with fibrin rings. In pathological examinations it was observed that some of these bodies are of completely fibrin structure and some have a collagen nucleus and covered with a fibrin coat. It was understood that this nucleus is composed of collagen type I (40%) and type V (20%). This composition is the same of the rheumatoid synovial membrane configuration. From this viewpoint, it was assumed that these bodies are formed from infarcted synovial tissue or synovial membrane origin collagen being covered with fibrin 1,4,8. Although RBs is almost always of synovial origin, its clinical meaning has almost always remained ambiguous 3. It can sometimes be seen as a reason for subacromial bursitis 1, sometimes as a reason for synovial cyst at intrapelvic region 9 and sometimes as reason for synovial hypertrophy at knee and painless effusion 4. No underlying pathology was reported with these patients. On the other hand, it was related with Tb, RA, JRA, septic arthritis, hypocomplementemic arthritis and atypical mycobacterial tenosynovitis and bursitis 2,3,10. RBs are not special to any one single disease and as in the present case it can be seen in the cases where there is no underlying pathology. Mostly RBs are confused with synovial chondromatosis at shoulder joint. Synovial chondromatosis frequently affects one joint, more often at 3-5th decants and ratio between male and female is 2 to 1. In the conventional graphic classifications are examined. It generally affects big joints such as hip and knee (5). RBs are distinguished from chondromatosis with no calcifications in the preoperative conventional graphs, a great number of free bodies in the joint cavity and bladder at MRI and histologically having cartilaginous tissue 3,4. In many centers radiologists may have difficulty in making diagnosis since they are not used to RBs. As a matter of fact, RBs at both of the shoulders of our case was diagnosed as synovial chondromatosis. Another disease which is confused with RBs is pigmented villonodular synovitis (PVNS). PVNS is also often monoarticular and affects big joints like synovial chondromatosis. At MRI T2 based imaging low signal areas with viewing hemosiderin deposits and intraoperative findings are distinguished from PVNS (5). Conventional graphs are not useful enough in diagnosing the disease, it can only give soft tissue swelling views 4,8. Especially, USG also has the property of diagnosing at bigger RB 8. However, the most effective diagnosing device in the imaging methods is MRI 3-6. At T1 and T2 weighted images hypo- and isointense nodules seen in muscular tissues lead to RB diagnosis 5,6,10. In addition to this MRI is important in the aspect of diagnosing free bodies, and distinguishing from tumoral structures and showing the size of captured joint 1. When this pathology is ascertained, the patient should be examined in terms of rheumatology, Tb and hypocomplementemic arthritis. Sedimentation rate, rheumatoid factor, complement series and antinuclear antibody should be detected. Resection of bursa or synovia, bodies being taken out reduces the complaints but never ends the real pathology. If etiology was unveiled, one or two years after the operation orthopedic examinations together with rheumatologic follow-up should be done 1,4,8. In 2-year follow-up, our patient had no complaints and had no signs of rheumatological symptoms.