A biomechanical assessment of modular and monoblock revision hip implants using FE analysis and strain gage measurements

<p>Abstract</p> <p>Background</p> <p>The bone loss associated with revision surgery or pathology has been the impetus for developing modular revision total hip prostheses. Few studies have assessed these modular implants quantitatively from a mechanical standpoint.</p> <p>Methods</p> <p>Three-dimensional finite element (FE) models were developed to mimic a hip implant alone (Construct A) and a hip implant-femur configuration (Construct B). Bonded contact was assumed for all interfaces to simulate long-term bony ongrowth and stability. The hip implants modeled were a Modular stem having two interlocking parts (Zimmer Modular Revision Hip System, Zimmer, Warsaw, IN, USA) and a Monoblock stem made from a single piece of material (Stryker Restoration HA Hip System, Stryker, Mahwah, NJ, USA). Axial loads of 700 and 2000 N were applied to Construct A and 2000 N to Construct B models. Stiffness, strain, and stress were computed. Mechanical tests using axial loads were used for Construct A to validate the FE model. Strain gages were placed along the medial and lateral side of the hip implants at 8 locations to measure axial strain distribution.</p> <p>Results</p> <p>There was approximately a 3% average difference between FE and experimental strains for Construct A at all locations for the Modular implant and in the proximal region for the Monoblock implant. FE results for Construct B showed that both implants carried the majority (Modular, 76%; Monoblock, 66%) of the 2000 N load relative to the femur. FE analysis and experiments demonstrated that the Modular implant was 3 to 4.5 times mechanically stiffer than the Monoblock due primarily to geometric differences.</p> <p>Conclusions</p> <p>This study provides mechanical characteristics of revision hip implants at sub-clinical axial loads as an initial predictor of potential failure.</p

Biomechanical Measurement Error Can Be Caused by Fujifilm Thickness: A Theoretical, Experimental, and Computational Analysis

© 2017 Ahmed Sarwar et al. This is the first study to quantify the measurement error due to the physical thickness of Fujifilm for several material combinations relevant to orthopaedics. Theoretical and experimental analyses were conducted for cylinder-on-flat indentation over a series of forces (750 and 3000 N), cylinder diameters (0 to 80 mm), and material combinations (metal-on-metal, MOM; metal-on-polymer, MOP; metal-on-bone, MOB). For the scenario without Fujifilm, classic Hertzian theory predicted the true line-type contact width as WO={(8FDcyl)/(πLcyl)[(1-cyl2)/Ecyl+(1-flat2)/Eflat]}1/2, where F is compressive force, Dcyl is cylinder diameter, Lcyl is cylinder length, cyl and flat are cylinder and flat Poisson\u27s ratios, and Ecyl and Eflat are cylinder and flat elastic moduli. For the scenario with Fujifilm, experimental measurements resulted in contact widths of WF=0.1778×F0.2273×D0.2936 for MOM tests, WF=0.0449×F0.4664×D0.4201 for MOP tests, and WF=0.1647×F0.2397×D0.3394 for MOB tests, where F is compressive force and D is cylinder diameter. Fujifilm thickness error ratio WF/WO showed a nonlinear decrease versus cylinder diameter, whilst error graphs shifted down as force increased. Computational finite element analysis for several test cases agreed with theoretical and experimental data, respectively, to within 3.3% and 1.4%. Despite its wide use, Fujifilm\u27s measurement errors must be kept in mind when employed in orthopaedic biomechanics research

Biomechanical analysis using FEA and experiments of metal plate and bone strut repair of a femur midshaft segmental defect

© 2018 Jason Coquim et al. This investigation assessed the biomechanical performance of the metal plate and bone strut technique for fixing recalcitrant nonunions of femur midshaft segmental defects, which has not been systematically done before. A finite element (FE) model was developed and then validated by experiments with the femur in 15 deg of adduction at a subclinical hip force of 1 kN. Then, FE analysis was done with the femur in 15 deg of adduction at a hip force of 3 kN representing about 4 x body weight for a 75 kg person to examine clinically relevant cases, such as an intact femur plus 8 different combinations of a lateral metal plate of fixed length, a medial bone strut of varying length, and varying numbers and locations of screws to secure the plate and strut around a midshaft defect. Using the traditional “high stiffness” femur-implant construct criterion, the repair technique using both a lateral plate and a medial strut fixed with the maximum possible number of screws would be the most desirable since it had the highest stiffness (1948 N/mm); moreover, this produced a peak femur cortical Von Mises stress (92 MPa) which was below the ultimate tensile strength of cortical bone. Conversely, using the more modern “low stiffness” femur-implant construct criterion, the repair technique using only a lateral plate but no medial strut provided the lowest stiffness (606 N/mm), which could potentially permit more in-line interfragmentary motion (i.e., perpendicular to the fracture gap, but in the direction of the femur shaft long axis) to enhance callus formation for secondary-type fracture healing; however, this also generated a peak femur cortical Von Mises stress (171 MPa) which was above the ultimate tensile strength of cortical bone

Mutation D816V Alters the Internal Structure and Dynamics of c-KIT Receptor Cytoplasmic Region: Implications for Dimerization and Activation Mechanisms

The type III receptor tyrosine kinase (RTK) KIT plays a crucial role in the transmission of cellular signals through phosphorylation events that are associated with a switching of the protein conformation between inactive and active states. D816V KIT mutation is associated with various pathologies including mastocytosis and cancers. D816V-mutated KIT is constitutively active, and resistant to treatment with the anti-cancer drug Imatinib. To elucidate the activating molecular mechanism of this mutation, we applied a multi-approach procedure combining molecular dynamics (MD) simulations, normal modes analysis (NMA) and binding site prediction. Multiple 50-ns MD simulations of wild-type KIT and its mutant D816V were recorded using the inactive auto-inhibited structure of the protein, characteristic of type III RTKs. Computed free energy differences enabled us to quantify the impact of D816V on protein stability in the inactive state. We evidenced a local structural alteration of the activation loop (A-loop) upon mutation, and a long-range structural re-organization of the juxta-membrane region (JMR) followed by a weakening of the interaction network with the kinase domain. A thorough normal mode analysis of several MD conformations led to a plausible molecular rationale to propose that JMR is able to depart its auto-inhibitory position more easily in the mutant than in wild-type KIT and is thus able to promote kinase mutant dimerization without the need for extra-cellular ligand binding. Pocket detection at the surface of NMA-displaced conformations finally revealed that detachment of JMR from the kinase domain in the mutant was sufficient to open an access to the catalytic and substrate binding sites