A computer model to simulate patellar biomechanics following total knee replacement: the effects of femoral component alignment.

OBJECTIVE: The objective of this study is to analyze the biomechanics of the patellar component following total knee replacement. More specifically we investigated the effect of displacing the femoral component of an Insall-Burstein II total knee replacement on the patellar tracking and patello-femoral contact pressures. DESIGN: We used a validated computer simulation of the knee joint to virtually insert the femoral component with the following four types of placements: (1) no misplacement, (2) 5 degrees of internal rotation, (3) 5 degrees of external rotation and (4) 5 degrees of flexion rotation. The patellar 3D tracking and patello-femoral contact pressures were computed for each femoral component placement as a function of knee flexion angle. BACKGROUND: Complications at the patello-femoral joint are the among most frequent following total knee replacement. RESULTS: Femoral component placement unevenly affected the associated patellar tracking: a 5 degrees internal rotation tilted and rotated the patella laterally by about 5 degrees throughout knee flexion. A 5 degrees external rotation of the femoral component had less effect on patellar tracking. A rotation of 5 degrees in flexion primarily caused patellar rotation (5-10 degrees lateral rotation). Femoral component malalignment had only minor effects on the peak pressure distributions at the patello-femoral interface. CONCLUSION: These results suggest that femoral component positioning primarily affects patellar tracking, with a possible threat for patellar subluxation under external rotation of the femoral component. RELEVANCE: Precise alignment of the prosthetic components is difficult to control during total knee replacement due to the lack of precise anatomical landmarks in the human knee joint. Consequently, the position of each prosthetic component may differ from the ideal one suggested by the manufacturer. Improper alignment of the prosthetic components during total knee replacement may lead to premature implant failure.

Simulation of initial frontside and backside wear rates in a modular acetabular component with multiple screw holes.

A sliding distance-based finite element formulation was implemented to predict initial wear rates at the front and back surfaces of a commercially available modular polyethylene component during in vitro loading conditions. We found that contact area, contact stress, and wear at the back surface were more sensitive to the liner/shell conformity than the presence of multiple screw holes. Furthermore, backside linear and volumetric wear rates were at least three orders of magnitude less than respective wear estimates at the articulating surface. This discrepancy was primarily attributed to the difference in maximum sliding distances at the articulating surfaces (measured in mm) versus the back surface (measured in microm). This is the first study in which backside wear has been quantified and explicitly compared with frontside wear using clinically relevant metrics established for the articulating surface. The results of this study suggest that with a polished metal shell, the presence of screw holes does not substantially increase abrasive backside wear when compared with the effects of backside nonconformity.

The genotoxicity profile of atorvastatin, a new drug in the treatment of hypercholesterolemia.

While HMG-CoA reductase inhibitors such as fluvastatin, lovastatin, pravastatin and simvastatin demonstrate lack of in vitro and in vivo mutagenicity and clastogenicity in bacterial and mammalian cells, long term rodent carcinogenicity studies resulted in an increased incidence in neoplasms at high doses. These effects may be attributable to an exaggeration of the desired biochemical effect of the drug and/or a tumor promoting effect. The genotoxicity of atorvastatin, a newly developed HMG-CoA reductase inhibitor, was evaluated in a variety of test systems. In bacterial mutagenicity tests, the E. coli tester strain WP2(uvrA) and S. typhimurium strains TA98, TA100, TA1535, TA1537, and TA1538 were exposed to concentrations of atorvastatin as high as 5000 micrograms/plate both in the absence (S9-) and presence (S9+) of metabolic activation. Atorvastatin was not mutagenic in either E. coli or S. typhimurium. Chinese hamster lung V79 cell cultures were exposed to atorvastatin at concentrations of 50-300 micrograms/ml (S9-) and 100-300 micrograms/ml (S9+) and structural chromosome aberrations were assessed. Mutation at the hgprt locus was assessed at concentrations of 100-300 micrograms/ml (S9-) and 150-275 micrograms/ml (S9+). Atorvastatin was neither mutagenic nor clastogenic in the absence or presence of S9. The lack of in vitro genotoxicity was corroborated in vivo in a mouse micronucleus study in which single oral doses of atorvastatin were administered to male and female CD-1 mice at 1, 2500, or 5000 mg/kg. No biologically significant increases in the frequency of micronucleated polychromatic erythrocytes in bone marrow at 24, 48, or 72 h postdosing were observed. Thus, atorvastatin, as with the other tested HMG-CoA reductase inhibitors, is not genotoxic.

Management of carcinoid syndrome.

Two patients who had severe carcinoid syndrome are presented. In one patient prednisone relieved symptoms for 20 months, and in the second patient chemotherapy appears to have precipitated fatal carcinoid crisis. Changes in mentation, increased frequency and intensity of flushing, and hypotension indicate increased risk of a chemotherapy induced carcinoid crisis. Since prednisone may produce relatively long control of carcinoid syndrome, it should be tried before chemotherapy in patients who have increased risk of carcinoid crisis. If chemotherapy is given, doses should be decreased by 50%, and patients should be followed closely.