Immunohistochemical analysis of the extracellular matrix in the posterior capsule of the zygapophysial joints in patients with degenerative L4–5 motion segment instability

Object. Although the hypertrophied shape of the zygapophysial joints in degenerative instability of the lumbar spine is well known, its underlying pathophysiological mechanism is unclear. The authors sought to provide evidence that there is increased fibrocartilaginous metaplasia in the posterior joint capsule resulting from greater mechanical loading;. the authors suggest that these capsular changes are central to understanding the altered joint shape. Methods. The L4-5 posterior articular complex was removed in 14 patients undergoing fusion for degenerative instability. After methanol-assisted fixation, cryosections were immunolabeled for a wide range of extracellular matrix molecules. These were collagens (Types 1, 11, 111, V, and VI), glycosaminoglycans (chondroitin 4 and 6 sulfates; dermatan- and keratan-sulfate), and proteoglycans (versican, tenascin, aggrecan, and its associated link protein). The grade of degeneration of the articular complexes was assessed radiologically and histologically. Conclusions. The results of this study provide molecular evidence for an altered loading history on the joint capsule. The pronounced loss of intervertebral disc height that occurred in all patients with severe degeneration of the lumbar motion segment promotes an increased range of axial rotation that places the posterior capsule under greater mechanical load. Compared with normal joints studied previously, the posterior capsules involved in these degenerative joint complexes were hypertrophied and fibrocartilaginous throughout. Cartilaginous metaplasia was especially pronounced at the attachment sites (entheses) where the fibrocartilage now extended beyond the original level of the joint space, and capped the osseous spurs arising from these attachment sites.