Abstract
In this microanatomical and biomechanical study we investigated OA lesion sites and the adjacent intact tissue in an attempt to uncover clues of a pre-OA tissue state and its progression to OA.
Bovine patellae (n=30) showing various degrees of degeneration, where lesions were located in the distal-lateral quarter, were used for the microanatomical study. Cartilage-on-bone samples were cut to include one with the lesion site and the other with the adjacent intact site. These blocks were formalin fixed. For the mechanical testing tissue samples (n=20) ranging from intact to mildly through to severely degenerate were statically compressed (7MPa) to near-equilibrium using a cylindrical indenter, and then formalin-fixed to capture this deformed state. Following mild decalcification of both sets of tissues, full-depth cartilage-bone cryo-sections incorporating the intact-lesion transition and the deformation profile were obtained and studied in their fully hydrated state using differential interference contrast optical microscopy (DIC).
There were three mechanically-significant microstructural features of the cartilage-bone system that varied with tissue degeneration:
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the integrity of the strain limiting surface layer,
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the degree of transverse interfibrillar connectivity, and
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the degree of calcification at the osteochondral junction (zone of calcified cartilage).
Importantly, our mechanical analysis showed how disruption of the cartilage continuum by surface disruption and matrix fibrillar de-structuring, had wider mechanical consequences at the biologically-active osteochondral junction of the adjacent healthy cartilage. The structural changes in the osteochondral junction beneath the still-intact articular cartilage adjacent to the lesion site included the ‘sprouting’ of bone spicules or cones that were morphologically similar to those associated with primary bone formation.
The microanatomical and micromechanical data suggests that there is a mechanobiological link between the altered microstructural response of degenerate cartilage to load and the way in which structural changes develop in the normal adjacent tissue. We propose that while the progression of OA involves first the processes of new bone formation in tissue adjacent to lesion sites, its initiation is due to a disrupted cartilage matrix that alters a regional mechanical environment that includes adjacent healthy tissue.
Correspondence should be addressed to: Associate Professor N. Susan Stott, Orthopaedic Department, Starship Children’s Hospital, Private Bag 92024, Auckland, New Zealand.
