Indentation assessment of biphasic mechanical property deficits in size-dependent osteochondral defect repair.
The apparent biphasic material properties of 10-month osteochondral defect repair tissue were determined for a series of full thickness defects of 1, 3, or 5 mm diameter, created in weight-bearing regions of 48 canine femoral condyles. Load cell recordings from indentation tests were compared with resultant contact forces computed using a corresponding linear biphasic finite element model. The spread of cartilage engagement by a spherical ended indentor was modeled by successively imposing an impenetrability kinematic boundary condition at cartilage surface nodes for which incipient indentor surface penetration was detected. For each indentation test, a least-squares-error curve fitting procedure was used to identify a set of biphasic coefficients (aggregate modulus, permeability, Poisson ratio) that closely modeled experimental behavior. In the near neighborhood of best-fit, the finite element solutions were found to be much more sensitive to aggregate modulus perturbations than to permeability permutations, suggesting that perceived permeability increase may be of lesser value as a discriminant of repair tissue inadequacy. Compared to surrounding cartilage, the repair tissue for all defect sizes had statistically significant decreases in aggregate modulus and in Poisson ratio (much more so for 3 and 5 mm defects than for 1 mm defects). The two larger defect diameters had significant increases in permeability, whereas the 1 mm defects did not. While the material property deficits were consistent, substantial and comparable to those in other recent animal models of osteochondral defect repair, the size-dependence per se of the observed constitutive differences was only modest.
Hale
J E
JE
Department of Orthopaedic Surgery, University of Iowa, Iowa City 52242.
Rudert
M J
MJ
Brown
T D
TD
D000465:Algorithms; D000818:Animals; D001696:Biomechanical Phenomena; D002358:Cartilage, Articular / Q000293:injuries / Q000503:physiopathology*; D004285:Dogs; D008954:Models, Biological; D013312:Stress, Physiological / Q000503:physiopathology*