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Articular cartilage degeneration in osteoarthritis has been linked to abnormal mechanical stresses that are known to cause chondrocyte apoptosis and metabolic derangement in in vitro models. Evidence implicating oxidative damage as the immediate cause of these harmful effects suggests that the anti-oxidant defenses of chondrocytes might influence their tolerance for mechanical injury. Based on evidence that anti-oxidant defenses in many cell types are stimulated by moderate oxidant exposure, we hypothesized that oxidant pre-conditioning would reduce acute chondrocyte death and proteoglycan depletion in cartilage explants after exposure to abnormal mechanical stresses. Porcine cartilage explants were treated every 48 hours with tert-butyl hydrogen peroxide (tBHP) at non-lethal concentrations (25, 100, 250, 500 µM) for a varying number of times (1, 2 or 4) prior to a bout of unconfined axial compression (5 MPa, 1 Hz, 1800 cycles). When compared with untreated controls, tBHP had significant positive effects on post-compression viability, lactate production, and proteoglycan losses. Overall, the most effective regime was 100 µM tBHP applied 4 times. RNA analysis revealed significant effects of 100 µM tBHP on gene expression. Catalase, hypoxia-inducible factor-1alpha (HIF-1α), and glyceraldehyde 6-phosphate dehydrogenase (GAPDH) were significantly increased relative to untreated controls in explants treated 4 times with 100 µM tBHP, a regime that also resulted in a significant decrease in matrix metalloproteinase-3 (MMP-3) expression. These findings demonstrate that repeated exposure of cartilage to sub-lethal concentrations of peroxide can moderate the acute effects of mechanical stress, a conclusion supported by evidence of peroxide-induced changes in gene expression that could render chondrocytes more resistant to oxidative damage.

The purpose of this study was to determine some of the morphological and biochemical effects of sodium morrhuate injections into intact rabbit patellar tendons and Achilles tendons. The effects of one, three, and five 100 microliters injections of sodium morrhuate on tendon circumference, cell content, collagen fibril diameter, collagen-proteoglycan relationships, water content, amino sugar content, and hydroxyproline content were investigated over periods of 1, 4, and 9 weeks. In general, sodium morrhuate injected tendons were larger in diameter and contained more cells, smaller collagen fibrils, increased water and amino sugar content, and reduced hydroxyproline content compared with their contralateral controls. As a sclerosing agent, sodium morrhuate appears to mimic the early stages of an injury-repair sequence when injected directly into intact tendons. Whether sodium morrhuate may hasten repair responses or improve joint laxity remains to be determined.

To investigate the adaptive responses of immature bone to increased loads, young (3-wk-old) White Leghorn roosters were subjected to moderately intense treadmill running for 5 or 9 wk. The training program induced significant increases in maximal O2 consumption and muscle fumarase activity in the 12-wk-old birds, demonstrating that growing chickens have the ability to enhance their aerobic capacity. The structural and mechanical properties of the runners' tarsometatarsus bones were compared with sedentary age-matched controls at 8 and 12 wk of age. Suppression of circumferential growth occurred with exercise at both ages, whereas exercise enhanced middiaphysial cortical thickening, especially on the bones' concave surfaces. Although cross-sectional area moments of inertia did not change with exercise, significant decreases in bending stiffness, energy to yield, and energy to fracture were observed. It was concluded that strenuous exercise may retard long-bone maturation, resulting in more compliant bones.

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