Loose bodies of bilateral atlantoaxial joints: A rare occurrence
Correspondence Address: Source of Support: None, Conflict of Interest: None DOI: 10.4103/0028-3886.263187
Source of Support: None, Conflict of Interest: None
The formation of loose bodies (LBs) has been commonly described in various large synovial joints, and are most commonly seen in the knee., Smaller joints can be infrequently involved. Rare reports have documented the existence of such LBs in spine, the source of which is likely from the adjacent synovial facet joints.,,,, We herein present a patient with atlantoaxial dislocation (AAD), who harboured LBs in the bilateral C1-C2 joints.
A 53-year old woman presented with neck pain and spastic quadriparesis for 2-years. The computed tomography (CT) revealed AAD associated with segmentation anomalies such as assimilated-C1 and fused C2-3 vertebrae. In addition, the C1-C2 joints showed degenerative changes such as sclerosis, narrowing of joint space and formation of bridging osteophytes [Figure 1]. The magnetic resonance imaging (MRI) disclosed cervico-medullary compression. Posterior C1-C2 fusion was performed., During the exposure of facets, we observed smooth-walled, glistening white, hard masses lying adjacent to the bilateral C1-C2 joints [Figure 2]. These were suggestive of LB which was confirmed on histopathology. A retrospective review of the radiology identified the LB [Figure 1]. Postoperatively, the patient had symptomatically improved and was doing well at a 1-year follow-up visit.
The LBs are well-known entities in human joints and can be a cause of joint pain, swelling and limited joint movements., At times, they are an incidental finding during surgery for other joint pathologies.
The origin of intra-articular LBs is ascribed to conditions such as 1) synovial osteochondromatosis, 2) osteochondral fractures, and 3) degenerative joint disruption. Synovial osteochondromatosis is characterized by metaplasia of the synovial membrane of a joint to form cartilaginous/osteocartilaginous nodules; the nodules then separate to form LBs. The synovial chrondromatosis is termed primary when the phenomenon is denovo in a normal joint, and secondary when it occurs in association with an underlying joint pathology such as osteoarthritis, osteochondritis dessicans, Charcot's arthropathy and osteonecrosis. There are three stages described by Milgram in this process. Initially, the synovial lining undergoes metaplasia, followed by a transitional phase with both synovial nodules and free LBs, and the last stage of multiple LBs with no active synovial disease.
Osteochondral fractures involve the articular surfaces of joints, and during trauma, a small fragment can detach to give rise to a free lying LB. Concerning the formation of a LB secondary to degenerative arthritis, mechanisms such as fragmentation of the joint surface, fractured osteophytes and osteochondral nodule proliferation have been proposed.
The natural history of LBs has been studied., Once they detach from the synovial lining and are free within the joint, they become devoid of any blood supply. They form new surface layers due to proliferation of the chondroblasts and osteoblasts which derive their nutrition from the synovial fluid. Resorption cavities and remodelling also occurs secondary to the osteoclastic activity. Slowly, degenerative changes with secondary calcification develop in the nidus of LBs. Over a period of time, the LB reattaches to the synovial surface of the joint and becomes revascularized., The calcified cartilage is then resorbed by the synovium, and osteogenesis occurs as a body's reactive mechanism to contain the LB.
The radiologic appearance of LB depends on their bony and cartilaginous content. CT scan can identify calcific lesions which are spherical and periarticular in location. In the absence of calcification, the LB may be easily overlooked. In T1-weighted images, they appear hypointense. In T2-weighted sequences, they show a high-signal intensity due to the high water content of cartilage. The calcified areas display low-signals in both T1 and T2 sequences.
LBs in the spine (2, cervical and 3, lumbar) have been described; however, none have been reported in the C1-C2 joints.,,,, One of the patients with a cervical LB presented with cord compression due to progressive enlargement in the size of the LB. Though the LB was lying within the spinal canal in the other case, it did not cause any symptom. Its asymptomatic nature was attributed to the slowly growing nature with simultaneous adaptability of the cord tissue to chronic compression. The lumbar LB manifested with canal stenosis and neurogenic claudication; one patient among them had multiple LBs, that was associated with spondylolisthesis.,, When causing compression, the removal of the offending fragment relieves symptoms. The LB in our patient was possibly due to the degenerative arthritis of bilateral C1-2 facet joints. The long-standing instability and osseous-segmentation anomalies could have probably accelerated the degenerative phenomenon. Apart from an aging spine, the repeated micro-trauma and stress secondary to C1-C2 instability and congenital fusion of vertebrae could have contribute to such an extensive degeneration seen on imaging.
To summarize, we present the first case of occurrence of LBs in the atlantoaxial joints. The superimposed degenerative process in congenital AAD appears to be the inciting event in our patient.
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[Figure 1], [Figure 2]