Introduction: The literature regarding the functional outcome following C1–C2 surgeries for non-rheumatoid C1–C2 pathologies following selective arthrodesis is sparse.

Aim: To determine the long term correlation between functional outcome and radiological determinants following C1–C2 fusion for conditions other than RA.

Methods: All C1–C2 surgeris performed between 1988–2002 for non-RA etiologies were reviewed retrospectively. Selective C1–C2 fusion performed in 32 pts with a min f/u of 5 yrs formed the study group. The mean age at surgery was 57.2 yrs (r 22–84yrs). The etiologies were trauma (15), non-union (6), congenital AAD (2), C1–C2 deg. arthropathy (2), os odontoideum (2), tumours (4) and instability due to TB (1). Neurodeficit were present in 7 pts. Transarticular (TA) screws supplemented with posterior wiring was performed in 27 & posterior wiring alone in 5 pts respectively. A monocortical H-shaped autograft from iliac crest was used in all cases. There were two deaths & two pts were lost for F/U. The mean F/U was 7.8 yrs (r 5–13 yrs). Disability & pain using NDI & VAS and subjective satisfaction were recorded in all pts. We measured 1) C1/2 fixation angle, 2) Inclination of C1, 3) Anterior shift of C2 and 4) C2–7 lordosis on pre and final F/U lateral x-rays.

Results: Optimal TA screw placement was seen in 78.5% of pts. The mean improvement in NDI & VAS were from 55.4% to 19.6% and 8.4 to 1.6 respectively and was better in younger pts. Fusion was seen radiologically in 82.1% of pts at 12 mo post surgery. Segmental stability and resolution of symptoms was seen in all patients despite implant failure in 4 and incomplete fusion 5 cases respectively. Two wound dehiscences needed debridement of which one elderly pt died of MRSA sepsis 2 mo post-op. The C1–C2 segmental lordosis was significantly increased by surgery (−4.2 0 vs. −11.80; P=0.016). The subaxial cervical spine became less lordotic in initial few months post-op but eventually regained more lordosis as time progressed. The C1 inclination came into more extended position w.r.t horizontal line post-op with minimal loss of inclination subsequently. C1–C2 fixation angle and anterior shift of C2 did not have significant correlation with long term functional outcome i.e. NDI and VAS (r=0.35, p=0.17).

Conclusion: The functional outcome following C1–C2 arthrodesis is usually good despite metalwork issues and incomplete fusion in these selective group of non-rheumatoid arthritis pathologies.

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.