Early bone growth on the surface of titanium implants in rat femur is enhanced by an amorphous diamond coating.

BACKGROUND AND PURPOSE: Amorphous diamond (AD) is a durable and compatible biomaterial for joint prostheses. Knowledge regarding bone growth on AD-coated implants and their early-stage osseointegration is poor. We investigated bone growth on AD-coated cementless intramedullary implants implanted in rats. Titanium was chosen as a reference due to its well-known performance. MATERIALS AND METHODS: We placed AD-coated and non-coated titanium implants (R(a) ≈ 0.2 µm) into the femoral bone marrow of 25 rats. The animals were divided in 2 groups according to implant coating and they were killed after 4 or 12 weeks. The osseointegration of the implants was examined from hard tissue specimens by measuring the new bone formation on their surface. RESULTS: 4 weeks after the operation, the thickness of new bone in the AD-coated group was greater than that in the non-coated group (15.3 (SD 7.1) µm vs. 7.6 (SD 6.0) µm). 12 weeks after the operation, the thickness of new bone was similar in the non-coated group and in the AD-coated group. INTERPRETATION: We conclude that AD coating of femoral implants can enhance bone ongrowth in rats in the acute, early stage after the operation and might be an improvement over earlier coatings.

Effect of locally administered zoledronic acid on injury-induced intramembranous bone regeneration and osseointegration of a titanium implant in rats.

BACKGROUND: Intramedullary implantation causes injury-induced stimulation of intramembranous bone regeneration. Intramedullary bone injury along with stress shielding may induce periimplant bone loss and cause early aseptic loosening of an implant. The aim of this study was to determine the effect of locally administered zoledronic acid on periimplant bone and injury-induced stimulation of intramembranous bone regeneration in a rat model. METHODS: A total of 28 male rats had a titanium implant inserted into their right femur. During the operation, the medullary canal was lavaged using 20 muM zoledronic acid (Zometa 4 mg/5 ml) or sodium chloride. Follow-up times were 4 and 12 weeks, with each follow-up group consisting of seven rats. The femurs with the titanium implants in situ were harvested, and three microscope sections were cut from each femur. The sections were photographed and analyzed with the Analysis computer program. RESULTS: Between 4 and 12 weeks, the length of fluorescence bone contact increased significantly in both groups (control 15.7% SD and zoledronic acid 18.8% SD), although the difference between the groups was not significant. Periimplant bone volume (thickness) was increased in the 4-week zoledronic acid group compared to the controls (+/-13.4%, P = 0.002) but at 12 weeks the groups no longer differed from each other. CONCLUSIONS: Our results suggest that zoledronic acid may prevent injury-induced bone loss near an intramedullary implant by inhibiting bone resorption shortly after implantation. This may provide better periimplant bone stock during the early postoperative period.

Collagenase-induced changes in articular cartilage as detected by electron-microscopic stereology, quantitative polarized light microscopy and biochemical assays.

The purpose of this study was to compare the ability of electron-microscopic (EM) stereology with quantitative polarized light microscopy (PLM) and biochemical collagen (hydroxyproline) and crosslink (pyridinoline) analyses to detect changes in the superficial collagen network of bovine articular cartilage after digestion in vitro with purified bacterial (Clostridium histolyticum) collagenase (30 U/ml) for 24 and 48 h. Collagen volume (V(V)) and surface (S(V)) densities of the uppermost third of the superficial zone were estimated indirectly from zonal isotropic uniform random sections using collagen length density (L(V)) and average collagen fibril diameter, or its average second power. Collagenase digestion caused a significant decrease in fibril diameter (64 to 62%), V(V) (89 to 95%) and S(V) (64 to 86%) after incubation for 24 and 48 h. Collagen L(V) remained unchanged after 24 h incubation but decreased 63% after 48 h. Collagen concentration per dry weight, assayed biochemically from the whole superficial zone, decreased also significantly (29 to 60%) after 24 and 48 h digestions, respectively. The pyridinoline concentration per dry weight of the superficial zone decreased (31 to 57%) whereas the pyridinoline concentration per collagen remained unchanged. PLM revealed that the birefringence of the uppermost third of the superficial zone was decreased by 36% after digestion for 24 h though the total birefringence of the whole zone was not reduced. However, after 48 h, the birefringence of the whole superficial zone was significantly reduced (76%). All of the techniques compared in this study could detect collagen network degradation in bovine articular cartilage but the EM stereological technique was more sensitive at detecting the changes than PLM or biochemical assays.