TY - JOUR
T1 - The shear strength and the failure mode of plasma‐sprayed hydroxyapatite coating to bone
T2 - The effect of coating thickness
AU - Wang, B. C.
AU - Lee, T. M.
AU - Chang, E.
AU - Yang, C. Y.
PY - 1993/10
Y1 - 1993/10
N2 - Plasma‐sprayed hydroxyapatite coated (HAC) 50 and 200 μm thick on Ti‐6Al‐4v cylinders was transcortically implanted in the femora of canines to to evaluate in detail the effect of coating thickness on the pushout shear strength and failure mode examined under scanning electron microscope after the periods of 4, 6, 8, and 12 weeks. The HAC coating exhibited higher shear strength at 50 μm than at 200 μm. Its failure mode was conclusively at or near the HAC–bone interface, and the slight attack of body fluid had not degraded the implant to the extent that failure occurred at the HAC‐Ti alloy interface after 12 weeks of observation. For 200 μm‐HAC, failure was found at the HAC–bone interface, inside the HAC lamellar splat layer and at the HAC‐Ti alloy substrate interface, depending on the period of implantation. It was also deduced that the variation of failure mode of 200 μm‐HAC with time could not be accounted for by the attack of body fluid alone; the degradation must be a synergetic adverse result of residual stress in the HAC and the attack of body fluid. © 1993 John Wiley & Sons, Inc.
AB - Plasma‐sprayed hydroxyapatite coated (HAC) 50 and 200 μm thick on Ti‐6Al‐4v cylinders was transcortically implanted in the femora of canines to to evaluate in detail the effect of coating thickness on the pushout shear strength and failure mode examined under scanning electron microscope after the periods of 4, 6, 8, and 12 weeks. The HAC coating exhibited higher shear strength at 50 μm than at 200 μm. Its failure mode was conclusively at or near the HAC–bone interface, and the slight attack of body fluid had not degraded the implant to the extent that failure occurred at the HAC‐Ti alloy interface after 12 weeks of observation. For 200 μm‐HAC, failure was found at the HAC–bone interface, inside the HAC lamellar splat layer and at the HAC‐Ti alloy substrate interface, depending on the period of implantation. It was also deduced that the variation of failure mode of 200 μm‐HAC with time could not be accounted for by the attack of body fluid alone; the degradation must be a synergetic adverse result of residual stress in the HAC and the attack of body fluid. © 1993 John Wiley & Sons, Inc.
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U2 - 10.1002/jbm.820271012
DO - 10.1002/jbm.820271012
M3 - Article
C2 - 8245046
AN - SCOPUS:0027686549
VL - 27
SP - 1315
EP - 1327
JO - Journal of Biomedical Materials Research
JF - Journal of Biomedical Materials Research
SN - 1552-4973
IS - 10
ER -