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IMMUNOLABELLING OF LUMBAR FACET JOINTS IN DEGENERATIVE INSTABILITY



Abstract

Hypertrophy of lumbar articular facets and dorsal joint capsule are well documented in degenerative instability, the molecular changes occurring in the extracellular matrix (ECM) are however unknown.

The L4/L5 posterior articular complex was removed from seven individuals undergoing fusion for degenerative instability. After methanol fixation and decalcification in EDTA, specimens were cryosectioned at 12 μm and immunolabelled with monoclonal antibodies for collagen types I, II, III, V and VI; chondroitin-4 and 6 sulphates; dermatan and keratan sulphate; versican, tenascin, aggrecan and link-protein. Antibody binding was detected using the Vectastain ABC ‘Elite’ kit. Labelling patterns were compared to corresponding healthy specimens examined previously.

In comparison, the degenerative capsule was more dense and hypertrophied and the enthesis more fibrocartilaginous, with immunolabelling extensive for collagen type II, chondroitin–6-sulfate, chondroitin-4-sulfate, aggrecan and link-protein. The articular surface showed extensive evidence of degeneration, while the thickened capsular entheses encircled the articular facets dorsally. Bony spurs capped with regions of cartilaginous metaplasia were prominent in this region, the ECM labelling strongly for type II collagen and chondroitin-6-sulfate.

The hypertrophy of lumbar facet joints subject to instability of the functional spinal unit therefore appears to be due to proliferation of the capsular enthesis rather than the actual articular facet. In view of the physiological function of the dorsal joint capsule as a wrap-around ligament in assisting the limitation of axial rotation, the molecular changes found in degenerative instability suggest rotational instability, such as results from degenerative disc disease, to be a decisive factor in the development of spondylarthropathy. It is furthermore probable, that the pronounced sagittal joint orientation in degenerative instability is the result of reactive joint changes rather than a predisposing factor of instability.