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.
Articular surface fibrillation and the loss of both transverse interconnectivity and zonal differentiation are indicators of articular cartilage (AC) degeneration. However, exactly how these structural features affect the load-redistributing properties of cartilage is still poorly understood. This study investigated how a single radial incision made to varying depths with respect to the primary zones of AC influenced its deformation response to compression. Three depths of incision were applied to cartilage-on-bone tissue blocks: one not exceeding the transition zone; one into the mid-radial zone; and one down to the calcified cartilage. Also included were non-incised controls. All samples were compressed to a near-equilibrium strain using a flat-faced indenter that incorporated a central relief channel within which the incision could be positioned lengthwise along the channel axis. Employing fixation under load followed by decalcification, the structural responses of the cartilage-on-bone samples were investigated. The study provides an analysis of the micro-morphological response that is characteristic of a completely normal cartilage-on-bone system but which contains a defined degree of disruption induced by the focal radial incision. The resulting loss of transverse continuity of the cartilage with respect to its zonally differentiated structure is shown to lead to an altered pattern of internal matrix shear whose intensity varies with incision depth.
Results: ACLRs and controls had similar participant characteristics (height, age, gender and tested limb-side). Controls had significant positive relationships between maximum walking medial contact forces and both medial cartilage volume ( Fig 1A) (R2¼0.33, b¼0.9, 95% CI 0.32e1.5, p¼0.003) and thickness (R2¼0.17, b¼0.0001, 95% CI 0.000004e0.0003, p¼0.04). ACLRs had no significant relationships in the medial compartment, and the group differences between the relationship slopes were significant (p¼0.02). Neither group had significant relationships in the lateral compartment. Adjusting for the size of the joint did change relationships slightly ( Fig 1B), but controls still had significant positive relationships between contact pressure and cartilage thickness in the medial compartment (R2¼0.22, b¼0.38, 95% CI 0.07e0.70, p¼0.02), while ACLRs had no significant relationships in any compartment. Both ACLRs and controls had significant positive relationships between maximum walking medial tibiofemoral contact forces and medial tibial subchondral bone area ( Fig 1C)(ACLRs R2¼0.11, b¼0.27, 95% CI 0.09e0.45, p¼0.003, controls R2¼0.42, b¼0.63, 95% CI 0.31e0.96, p<0.001), and the slopes of these relationships were significantly different between the two groups (p¼0.025). Conclusions: Compared with healthy controls, ACLRs at 2e3 years post-reconstruction had significantly different relationships between their walking tibiofemoral contact forces and articular tissue morphology. Healthy controls showed significant positive relationships between contact loading and articular cartilage volume, confirming previous in vitro studies, but ACLRs had no such significant relationships. These group differences in the relationships between loading and morphology persisted when adjusting for participant joint size. It is concerning that the normal adaptive response of cartilage may not be occurring in ACLRs as little as 2e3 years post-operation. While the subchondral bone had significant positive relationships with contact loading in both groups, the relationship was statistically weaker in ACLRs. We are currently conducting follow-up studies to explore the relationship between contact forces at 2e3 years post-operation and the change in articular tissue morphology at 4e5 years post-operation.
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