Osteochondral resurfacing implantation angle is more important than implant material stiffness.

Osteochondral resurfacing implants are a promising treatment for focal cartilage defects. Several implant-factors may affect the clinical outcome of this treatment, such as the implant material stiffness and the accuracy of implant placement, known to be challenging. In general, softer implants are expected to be more accommodating for implant misalignment than stiffer implants, and motion is expected to increase effects from implant misalignment and stiffness. 3D finite element models of cartilage/cartilage contact were employed in which implantation angle (0°, 5°, 10°) and implant material stiffness (E = 5 MPa, 100 MPa, 2 GPa) were varied. A creep loading (0.6 MPa) was simulated, followed by a sliding motion. Creep loading resulted in low maximum collagen strains of 2.5% in the intact case compared to 11.7% with an empty defect. Implants mostly positively affected collagen strains, deviatoric strains, and hydrostatic pressures in the adjacent cartilage, but these effects were superior for correct alignment (0°). The main effect of implant misalignment was bulging of opposing cartilage tissue into the gap caused by the misalignment. This increased collagen strains and hydrostatic pressures. Deviatoric strains were increased adjacent to the gap. Subsequent sliding initially increased strains for a stiff, misaligned implant, but generally sliding decreased strains. In conclusion, implants can decrease the detrimental effect of defects, but correct implant alignment is crucial, more than implant material stiffness. Implant misalignment causes a gap, causing potentially damaging cartilage deformation during prolonged loading, for example, standing, even for soft implants. Mild motion may positively affect the cartilage. © 2018 The Authors. Journal of Orthopaedic Research® published by Wiley Periodicals, Inc. on behalf of Orthopaedic Research Society. J Orthop Res 36:2911-2922, 2018.

Comparison between in vitro and in vivo cartilage overloading studies based on a systematic literature review.

Methodological differences between in vitro and in vivo studies on cartilage overloading complicate the comparison of outcomes. The rationale of the current review was to (i) identify consistencies and inconsistencies between in vitro and in vivo studies on mechanically-induced structural damage in articular cartilage, such that variables worth interesting to further explore using either one of these approaches can be identified; and (ii) suggest how the methodologies of both approaches may be adjusted to facilitate easier comparison and therewith stimulate translation of results between in vivo and in vitro studies. This study is anticipated to enhance our understanding of the development of osteoarthritis, and to reduce the number of in vivo studies. Generally, results of in vitro and in vivo studies are not contradicting. Both show subchondral bone damage and intact cartilage above a threshold value of impact energy. At lower loading rates, excessive loads may cause cartilage fissuring, decreased cell viability, collagen network de-structuring, decreased GAG content, an overall damage increase over time, and low ability to recover. This encourages further improvement of in vitro systems, to replace, reduce, and/or refine in vivo studies. However, differences in experimental set up and analyses complicate comparison of results. Ways to bridge the gap include (i) bringing in vitro set-ups closer to in vivo, for example, by aligning loading protocols and overlapping experimental timeframes; (ii) synchronizing analytical methods; and (iii) using computational models to translate conclusions from in vitro results to the in vivo environment and vice versa. © 2018 The Authors. Journal of Orthopaedic Research® Published by Wiley Periodicals, Inc. J Orthop Res 9999:1-11, 2018.

A fibre-reinforced poroviscoelastic model accurately describes the biomechanical behaviour of the rat Achilles tendon.

BACKGROUND: Computational models of Achilles tendons can help understanding how healthy tendons are affected by repetitive loading and how the different tissue constituents contribute to the tendon's biomechanical response. However, available models of Achilles tendon are limited in their description of the hierarchical multi-structural composition of the tissue. This study hypothesised that a poroviscoelastic fibre-reinforced model, previously successful in capturing cartilage biomechanical behaviour, can depict the biomechanical behaviour of the rat Achilles tendon found experimentally. MATERIALS AND METHODS: We developed a new material model of the Achilles tendon, which considers the tendon's main constituents namely: water, proteoglycan matrix and collagen fibres. A hyperelastic formulation of the proteoglycan matrix enabled computations of large deformations of the tendon, and collagen fibres were modelled as viscoelastic. Specimen-specific finite element models were created of 9 rat Achilles tendons from an animal experiment and simulations were carried out following a repetitive tensile loading protocol. The material model parameters were calibrated against data from the rats by minimising the root mean squared error (RMS) between experimental force data and model output. RESULTS AND CONCLUSIONS: All specimen models were successfully fitted to experimental data with high accuracy (RMS 0.42-1.02). Additional simulations predicted more compliant and soft tendon behaviour at reduced strain-rates compared to higher strain-rates that produce a stiff and brittle tendon response. Stress-relaxation simulations exhibited strain-dependent stress-relaxation behaviour where larger strains produced slower relaxation rates compared to smaller strain levels. Our simulations showed that the collagen fibres in the Achilles tendon are the main load-bearing component during tensile loading, where the orientation of the collagen fibres plays an important role for the tendon's viscoelastic response. In conclusion, this model can capture the repetitive loading and unloading behaviour of intact and healthy Achilles tendons, which is a critical first step towards understanding tendon homeostasis and function as this biomechanical response changes in diseased tendons.