Published: Jan 1996
| ||Format||Pages||Price|| |
|PDF (144K)||11||$25||  ADD TO CART|
|Complete Source PDF (9.2M)||415||$87||  ADD TO CART|
Studies were undertaken to determine the distribution, elimination and storage of titanium and vanadium in organs and in cells. Animals (hamsters) received injections of salts of titanium and vanadium and the distribution in blood, urine, and organs was determined. At the highest doses used (600 ug total of each element) titanium could be detected just above control levels in liver, spleen, kidney, and plasma. Vanadium was rapidly excreted but could be detected just above control levels in liver, spleen, urine, and plasma. Both elements were detected in bone (femur). Studies using fretting corrosion in hamsters indicated that most of the titanium remained at the site of deposition. There was some transport to the urine and plasma and also to bone. Most of the vanadium administered can be accounted for in rapid excretion in the urine. Most of the titanium remained at the site of deposition and little was transported from the site. The in vitro studies in cell culture confirmed the cell association (and thus retention) of titanium and the lack of cell association (and thus elimination) of vanadium. The highest dose of 600–750 ug of the element administered to the hamster is below the level of body burden of titanium found in tissues from patients with revision of total joints, and thus it can be expected that transport and organ deposition of titanium would occur in the humans at low levels. However, in general, the wear debris remains at the local site without evoking much of a biological response.
Titanium, Vanadium, Cell Culture, Transport, Organs, Bone, in vivo, in vitro
Assoc. Professor, Biomedical Engineering, Case Western Reserve Univ.FDA/CDRH/OST/DLS, ClevelandRockville, OHMD
Assoc. Prof., Biomedical Engineering, Case Western Reserve Univ.FDA/CDRH/OST/DMMS, ClevelandRockville, OHMD