Fluid film lubricating ability of a total hip prosthesis depends on the profile accuracies including surface-roughness or the sphericity of a head or a cup. Therefore, surface polishing is important. It was, however, difficult to polish the central portion of a cup or head using the conventional rotating machine. In the present study, we developed a polishing method combining a pendulum machine and a robotic arm. The effect of the accuracy improvement by this method was evaluated by the friction measurements on some test specimens.

Nine balls and a cup of Co-Cr-Mo alloy that were polished by a conventional process using a rotating machine were prepared for the prototype. The average diameter of the balls was 31.9648 mm with the sphericity of 0.0028 μm. The inside diameter of the cup was 31.9850 mm with the sphericity of 0.0044 μm. We combined a robotic arm and a pendulum apparatus to enable the further polishing. The ability of both automatic centering and change in the sliding direction was accomplished by this system. The sliding direction has been changed 180 times every ten degrees. The total distance of polishing was 120 m under vertical load of 100 N in a bath of saline solution containing abrasive grains of silicate of the diameter of 2μm. The surface roughness of the central portion of the cup, which is important area for the fluid film lubrication decreased from Ra 20.2 μm before the polishing to Ra 18.7 μm after the polishing.

A pendulum type friction tester was used for the assessment of the improvement of the lubricating ability by the polishing. The measurement was run over at 10 times under the conditions of the load of 600 N in a bath of saline solution. As the result, the frictional coefficients decreased from 0.1456–0.1720 before polishing to 0.1250–0.1300 after polishing. The polishing effect was, however, observed only at the specimens that radial clearances did not exceed the value of 50 μm.

The present results indicated that the surface polishing of the central portion of hip prostheses must improve the lubrication ability and the radial clearance before the finishing process should be chinked as possible.

We have investigated in vitro the release kinetics and bioactivity of fibroblast growth factor-2 (FGF-2) released from a carrier of fibrin sealant. In order to evaluate the effects of the FGF-2 delivery mechanism on the repair of articular cartilage, full-thickness cylindrical defects, 5 mm in diameter and 4 mm in depth, which were too large to undergo spontaneous repair, were created in the femoral trochlea of rabbit knees. These defects were then filled with the sealant.

Approximately 50% of the FGF-2 was released from the sealant within 24 hours while its original bioactivity was maintained. The implantation of the fibrin sealant incorporating FGF-2 successfully induced healing of the surface with hyaline cartilage and concomitant repair of the subchondral bone at eight weeks after the creation of the defect.

Our findings suggest that this delivery method for FGF-2 may be useful for promoting regenerative repair of full-thickness defects of articular cartilage in humans.

Chondromodulin-I (ChM-I) is a bifunctional autocrine regulator of cartilage, initially isolated from fetal bovine epiphyseal cartilage¹. ChM-I stimulates matrix synthesis of chondrocytes, but inhibits the growth of endothelial cells^1,2 thus ChM-I may be one of the anti-angiogenic molecules present in cartilage. In fetal bovine bone, ChM-I was expressed by all epiphyseal and growth plate chondrocytes except hypertrophic chondrocytes and was present in the matrix throughout the epiphysis and the growth plate, except the hypertrophic zone ^2,3, consistent with its proposed role as anti-angiogenic factor. To examine the possible role of chondromodulin-I in relation to angiogenesis at the vascular front, we studied the immunolocalisation in femoral growth plates from young and mature rats (2–16 weeks) as well as aged rats (62–80 weeks), using a rabbit polyclonal antibody raised against the entire region of mature human recombinant ChM-I.

In 2-week old rats, ChM-I was synthesised by all epiphyseal chondrocytes and strong immunostaining was found in the matrix. In the growth plates, ChM-I staining was present in chondrocytes and matrix of the reserve, proliferating and maturing zones with loss of staining in the hypertrophic zone. However, ChM-I was also present where cartilage canals had penetrated into the chondroepiphysis. In 4–16 week old rats, there was a progressive change in the localisation of ChM-I. Hypertrophic chondrocytes also became positive for ChM-I, while cellular staining gradually disappeared from the other zones. By 12–16 weeks, very strong immunostaining was present almost exclusively on the inner perimeter of the lacunae of hypertrophic chondrocytes. As lacunae were opened at the vascular front, ChM-I initially remained on the cartilage-side of the lacunae, and then disappeared completely. In aged rats, very little ChM-I was present in the cells and matrix of the growth plates, except where remodelling had occurred or chondrocytes had become re-activated.

The rate of longitudinal growth in rats is high between 1–5 weeks, then declines until skeletal maturity at approximately 12 weeks, after which a very slow rate of growth continues until 26 weeks. In young rats, the loss of ChM-I in the hypertrophic zone was as expected for an anti-angiogenic factor, i.e. loss was required before vascular invasion could take place. However, the same did not apply to cartilage canal formation, since there was no loss of ChM-I around cartilage canals. The change in the localisation of ChM-I in mature rats, in particular the very intense immunolocalisation around hypertrophic chondrocytes, might be related to the reduced rate of growth. It is possible that rapid vascular invasion must be slowed down in these growth plates and that ChM-I prevented vascular invasion until degraded by proteases, such as MMP-9.

The relative absence of ChM-I in the stationary growth plates of aged rats suggests that other anti-angiogenic factors prevent vascular invasion in these growth plates.