This study aimed to explore the relationship between the geometry of the tuberosity located superior to the Achilles tendon enthesis and the thickness of its fibro-cartilaginous periosteum. The tuberosity acts as a pulley for the tendon during dorsiflexion of the foot and is thus compressed by the overlying tendon. This can result in pressure-related injuries which account for a significant number of Achilles-related problems among sportsmen or women. We postulated that variations in the contact area between the tendon and the tuberosity (and consequently the pressure exerted by the tendon) affects the periosteum thickness. Here, we report four methods of portraying the two dimensional geometry of the superior tuberosity. Material was obtained from 10 elderly dissecting room cadavers donated to the Cardiff University for anatomical examination and prepared for routine histology. Serial sagittal sections were collected at 1 mm intervals, and stained with Masson’s trichrome, toluidine blue and haematoxylin & eosin. In the first method, the area of the bursal cavity was measured between the deep surface of the tendon and the tuberosity within a 9mm radius of the proximal part of the attachment site. The second technique was similar, though used the long axis of the tendon as a reference, rather than its deep surface. The third technique measured the area of the tuberosity within 20 degrees of the tendon long axis. The final technique measured the cumulative gradient of the first 5 mm of the tuberosity, with reference to the tendon long axis. The periosteum thickness was measured at 500 μm intervals from the proximal part of the enthesis and mean values calculated. A good correlation was seen between all techniques, with the tuberosities having the most localised area of contact with the tendon, showing the thickest periosteum.

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.