The influence of calcium phosphate (Ca-P) coating on the bone response of titanium implants was investigated two types of titanium implants, i.e. as -machined ,as -machined with Ca-P coating, were prepared. The Ca-P coating produced by OCT Inc technique. These implants were inserted into the left and right femur of beagle dog. After implantation periods of 3 days, 1weeks, weeks, 4weeks, 8weeks, 12weeks, 24weeks, the bone-implant interface was evaluated histologically, histomorphometrically, and removal torque. Histological evaluation revealed no new bone formation around different implant materials after 2weeks of implantation. After 4 weeks, Ca-P coated implants showed a higher amount of bone contact than either of the non coated implants. After 12weeks, bone healing was almost completed. And implant were removed by reverse torque rotation with torque-measuring device. Mean torque values for 4weeks control were 2.375Kgf.cm and experimental were 2.725Kgf.cm. And mean torque values for 8weeks control were 1.25Kgf.cm and experimental were 1.0Kgf.cm On the basis of these findings, we concluded that deposition of a Ca-P coating on an implant has a beneficial effect on the bone response to this implant during the healing phase. Besides implant surface conditions the bone response is also determined by local implant site condition.
Animals ; Calcium* ; Dogs* ; Femur ; Osseointegration* ; Osteogenesis ; Titanium ; Torque

It is well known that tumor necrosis factor (TNF-a), interleukin-1, platelet-activating factor (PAF) and arachidonic acid metabolites, such as thromboxane and leukotriens, are major mediators involved in the pathogenesis of endotoxic shock. In this study, we have investigated the effect of pentoxifylline (inhibitor of TNF-a release), BN50739 (PAF antagonist), indomethacin (cyclooxygenase inhibitor) and diethylcarbamazine (lipoxygenase inhibitor) on LPS- induced lethality as well as the relationship between major mediators in endotoxic shock. All inhibitors described above except diethylcarbamazine significantly protected mice against LPS- induced lethality. BN50739 and indomethacin were also effective in protection of TNF-a-induced lethality. The elevation of circulating TNF-a by LPS was significantly blocked by BN50739, but not affected by indomethacin. Convulsion appeared shortly after LPS injection was prevented by BN50739 but not by indomethacin, whereas diarrhea and limited movement was prevented by indomethacin but not by BN50739. These results indicate that i) TNF-a, PAF and cyclooxygenase products are important mediators involved in the pathogenesis of septic shock and ii) TNF-a directly influenced the release or production of PAF as well as cyclooxygenase products, and strongly suggest that i) TNF-a and PAF stimulate the release of each other via positive feedback network but TNF-a and cyclooxygenase products do not form the network and ii) PAF and cyclooxygenase product appear not to affect the release of each other.
Animals ; Arachidonic Acid ; Diarrhea ; Diethylcarbamazine ; Gene Expression* ; Indomethacin ; Interleukin-1 ; Mice ; Pentoxifylline ; Prostaglandin-Endoperoxide Synthases ; Seizures ; Shock, Septic ; Tumor Necrosis Factor-alpha*