Cartilage-on-bone samples from bovine patellae containing a defined stellar or linear initiating split in the articular surface were incrementally loaded in direct compression with intervening rehydration, until articular surface rupture occurred. All patellae were either normal or exhibited a mild level of surface fibrillation. In all cases the actual loading site was free of disruption. The average rupture stress of the healthy cartilage was significantly higher than that of the mildly degenerate cartilage, and in both tissue categories average rupture stresses were lower for the linear split morphology than for the stellar. We propose that this contrasting rupture behavior is explained by differences in both secondary lineal surface strains associated with the depth of compressive indentation and in the ability of the fibrillar network within the surface layer to re-arrange itself in the localized regions of stress concentration around the initiating split.

Bovine cartilage-on-bone samples taken from healthy mature patellae and from the intact regions of degenerate patellae were subjected to dynamic and static compressive loading. In-plane articular surface strain and rupture behavior were investigated and compared with previously published data obtained from immature bovine patellae. Both aging and proximity of the intact tested region to the fibrillated lesion increase the likelihood of articular surface rupture under both impact and static loading. Substantially higher levels of stress can be applied dynamically than statically without increasing the risk of articular surface rupture. Articular surface rupture is a result of lineal strains generated by the indentation profile, but any direct measurement of its in situ rupture strength is not possible. However, differences in both measured articular surface strains and rupture characterisitics between the three categories of tissue suggest that there is a progressive reduction in the intrinsic strength of the intact surface layer of cartilage with both aging and proximity to site of fibrillation.

This study uses a bovine patella model to compare the relative merits of on-bone compliance and thickness measurements, free-swelling behaviour, and structural imaging with differential interference contrast (DIC) light microscopy to assess the biomechanical normality of the cartilage matrix. The results demonstrate that across a spectrum of cartilage tissues from immature, mature, through to mildly degenerate, and all with intact articular surfaces, there is a consistent pattern of increased free swelling of the isolated general matrix with age and degeneration. High swelling was always associated with major structural alterations of the general matrix that were readily imaged using DIC light microscopy. Conversely, for all tissue groups, no relationship was observed between thickness vs. compliance and compliance vs. general matrix swelling. Only in the proximal aspects of the normal mature and degenerate tissues was there a correlation between thickness and general matrix swelling. Free-swelling measurements combined with fibrillar texture imaging using DIC light microscopy are therefore recommended as providing a reliable and quick method of assessing the biomechanical condition of the cartilage general matrix.

Cartilage-on-bone samples were dynamically and statically compressed at various stress levels to determine the deformation and rupture behaviour of the articular surface (AS). Instantaneous deformations were captured photographically by using a transparent indenter in combination with a ultra high speed flash. Principal strains (PS) were evaluated using large deformation theory. The tensile strains induced indirectly in the AS were a function of the rate at which the direct compressive force was applied. At the same compressive stress the tensile strains induced statically were approximately twice those induced dynamically. Rupture of the AS occurred in about 60% of those specimens tested statically at 15 MPa and followed approximately the split-line direction. By contrast, no rupture was observed dynamically even at stresses as high as 28 MPa. In terms of joint function the research demonstrates that the AS is considerably more resistant to rupture under dynamic than under static loading. The biomechanical parameter governing rupture appears to be the level of indirectly induced surface strain rather than the directly applied compressive stress. The very different mechanisms controlling the compressive deformation of articular cartilage (AC) at high vs low rates of loading clearly influence the levels of in-plane strain induced in the AS.

A biomechanical investigation of the dynamic shear failure of the osteochondral region of immature, adolescent, and mature bovine cartilage bone laminates was performed. The osteochondral junction was loaded in pure shear under impact conditions through the cartilage layer only. The results indicate the adolescent tissue fails at a nominal shear stress of 2.0 MPa, whereas the immature and the mature tissues fail at 3.8 MPa and 2.6 MPa, respectively. The adolescent tissue had a significant reduction in the fracture toughness of its osteochondral junction compared with that of the immature or mature tissues. The fracture toughness, describing the energy required to initiate and propagate a crack to failure, was 3.6 kN/m, 2.3 kN/m, and 10.2 kN/m for the immature, adolescent, and mature bovine tissues, respectively. This significant reduction associated with the adolescent osteochondral junction is explained in terms of the structural changes occurring within this important anchoring region during maturation. These findings question the wisdom of subjecting the adolescent joint to high levels and rates of loading.

This paper presents a biomechanical study of the dynamic fracture response of the osteochondral regions of both immature and mature cartilage-bone laminates induced through shear loading. An instrumented impact machine, providing both mechanical and real-time macro-photographic fracture data, was used to load the osteochondral region in shear by means of a direct compressive force applied to the cartilage layer only, and in a direction parallel to the plane of the osteochondral junction. This force was applied at a known velocity of 2500 mm/s. Our results show that under these conditions of shear loading the dynamic mode II fracture toughness of the osteochondral region of the mature tissue is approximately 1.5 times that of its immature counterpart, and that the derived dynamic shear stiffness of the immature tissue is about 4 times that of the mature. The structural studies demonstrated that the mature tissue delaminates within a well-defined tidemark region whilst the immature fractures through the subchondral bone into which fingers of articular cartilage penetrate. We suggest that this pseudo-brittleness of the immature tissue could explain why there is an increased susceptibility to osteochondral failure in the younger human joint. Finally, we note that the strength-to-toughness relationship, in which stiffer engineering materials are known to exhibit lower fracture toughness, also applies to the cartilage-bone system.

We have examined the effect of strain-rate on the mechanism of failure of the osteochondral region of immature and mature cartilage-on-bone in unconstrained shear, loaded through the cartilage layer only. Strain-rate did not effect the fracture mechanism or the fracture load levels in either tissue but only influenced the extent of cartilage deformation before fracture initiation. The exact mechanism of osteochondral failure was found to be the same as observed during impact loading where it depended on skeletal maturity only. Shear fracture of the immature tissue always occurred subchondrally and progressed in a stepwise manner by the propagation of a relatively large crack. By contrast, failure in the skeletally mature tissue occurred by the advance of a much smaller crack which propagated within the well-defined tidemark region.

The effect of strain rate on the mechanism of failure of the osteochondral region of immature and mature cartilage on bone in unconstrained shear, loaded through the cartilage layer only, is examined. Strain rate did not affect the fracture mechanism or the fracture load levels in either tissue but only influenced the extent of cartilage deformation before fracture initiation. The exact mechanism of osteochondral failure was found to be the same as observed during impact loading where it depended on skeletal maturity only. Shear fracture of the immature tissue always occurred subchondrally and progressed in a stepwise manner by the propagation of a relatively large crack. By contrast failure in the skeletally mature tissue occurred by the advance of a much smaller crack which propagated within the well-defined tidemark region. (A) For the covering abstract of the conference see IRRD 873507.

Experiments were carried out to investigate the influence of loading velocity on the stiffness of the articular cartilage matrix. Compression tests were conducted on cartilage alone and cartilage-on-bone at strain-rates ranging from 10(-5)sec-1 to 10(3)sec-1 and it was established that matrix stiffness increased progressively in the "low" and "medium" strain-rate regimens and assumes a limiting value at "high" rates of loading up to impact. Analysis of the strain field characteristics associated with the compression process, both at low and high velocities, suggests that two fundamentally different mechanisms of deformation control the development of cartilage matrix stiffness. At low strain-rates a consolidation-dependent stiffness occurs while at high strain rates the high stiffness results from a classical elastic deformation process. This bifurcation in the tissue's response to loading is likely to affect the redistribution of joint contact stresses being transmitted into the subchondral bone.