The primary structural components of articular cartilage are the zonally differentiated interconnected network of collagen fibrils and proteoglycans, the latter having the potential to bind large amounts of water. Both components exist in a coupled relationship that gives rise to its remarkable mechanical properties. The response of cartilage to compression is governed both by the degree to which the hydrated proteoglycans are constrained within this fibrillar network and the ease with which the matrix fluid can be displaced. The functional properties of cartilage are therefore closely linked to the integrity of the fibrillar network. Our current understanding of this network has been derived via studies conducted at the macro, micro, and ultrastructural levels. Of particular interest to joint researchers and clinicians are issues relating to how the network structure varies both directionally and with zonal depth, how its integrity is maintained via mechanisms of fibril interconnectivity, and how it is modified by ageing, degeneration, and trauma. Physical models have been developed to explore modes of interconnectivity. Combined micromechanical and structural studies confirm the critical role that this interconnectivity must play but detailed descriptions at the molecular level remain elusive. Current computationally based models of cartilage have in some cases implemented the fibrillar component, albeit simplistically, as a separate structure. Considering how important a role fibril network interconnectivity plays in actual tissue structure and mechanical behavior, and especially how it changes with degeneration, a major challenge facing joint tissue modellers is how to incorporate such a feature in their models.
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. on behalf of the Orthopaedic Research Society. J Orthop Res 36:2076–2086, 2018.
Background: Non-degradable resurfacing implants are being developed for treatment of focal cartilage defects. Performance of these implants has been investigated opposing intact cartilage. This study investigates whether implants would perform equally well when the opposing cartilage is fibrillated. Methods: Human osteochondral strips (~2x1x1 cm) with a smooth (n = 9) or fibrillated (n = 17) cartilage surface were obtained from human tibial plateaus excised during total knee arthroscopy. A custom-made pin-onplate sliding indenter was used to apply simultaneous compression (0.75-3 MPa) and movement (4 mm/s over 6 mm). Either metal implants, polycarbonate-urethane or healthy porcine osteochondral plugs with a diameter of 6 mm were used as indenter. Findings: Cartilage roughness of the osteochondral strips was significantly higher for the fibrillated than the smooth group prior to sliding-indentation. Roughness of the indenters was not significantly altered by sliding indentation using either smooth or fibrillated cartilage. For all but one sample, sliding of smooth cartilage against any of the indenter surfaces did not cause damage. However, samples with fibrillated cartilage showed varied responses from seemingly unaffected to severe tissue wear as quantified by analysis of Indian ink staining and histology. Interpretation: This study demonstrates that the opposing cartilage quality is relevant for the clinical success of implanting an artificial implant in a focal cartilage defect. Therefore it is essential to test the efficacy of newly developed implants against arthritic joint surfaces, and care should be taken when interpreting in vivo studies in which implants are inserted in healthy joints.
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