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In this article, the authors posit that, because osteoarthritis (OA) involves all of the tissues of the synovial joint, the emphasis on the loss of cartilage, in particular, is misguided. In contrast, the authors view OA as a process that is attempting to contain a mechanical problem in the joint. They argue that OA is best defined as failed repair of damage that has been caused by excessive mechanical stress on joint tissues. Because the body's innate mechanisms for repairing the damaged tissues cannot be effective in the face of the overwhelming mechanical abnormality, they cannot solve the problem of OA.

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The existing data are consistent with the view that reactivation of the secondary center of ossification and not the stiffening of the metaphyseal trabecular bone is a mechanism of cartilage loss in idiopathic OA. The stiffening of the subchondral calcified structures would appear to be etiologically incidental and, as the arthrotic process progresses, sometimes locally transient. It is also now clear that although the apparent density of the subchondral cortical plate increases because of thickening of the plate as the OA process progresses, the elastic modulus of the bone might be reduced locally because of increases in vascularization and in the rate of bony remodeling subjacent to the cartilage. Microcracks in the subchondral mineralized tissues might contribute to degeneration of the hyaline cartilage by initiating vascular invasion of the calcified cartilage, leading to reactivation of the tidemark and enchondral ossification with subsequent thinning of the overlying articular cartilage. The thinning would tend to increase shear stresses at the base of the articular cartilage [38], overwhelming the ability of the cartilage to repair itself, resulting in cartilage degeneration. The pathogenesis of cartilage breakdown in OA is a biological and a mechanical process. OA can be understood only if the relationship between the mechanics and the biology is fully appreciated. Failure to properly absorb impact leads to microdamage in the subchondral plate and calcified cartilage. The authors believe that this action causes the secondary center of ossification at the tidemark to advance by enchondral ossification, leading to thickening of the mineralized tissues and thinning of the overlying hyaline articular cartilage. Microcracks will cause the initiation of targeted remodeling, accounting for the increased turnover and reduced material density of the subchondral plate. The resultant thinning of the articular cartilage might lead to initiation of further microdamage in bone and cartilage through a positive feedback mechanism, which can ultimately lead to complete loss of the articular cartilage. In this view, the mechanical overload that initiates microdamage of the subchondral bone provokes a biological response that potentiates the progression of articular cartilage damage in OA.

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OBJECTIVE: To examine the hypothesis that the differences reported in incidence of osteoarthrosis in Chinese and Caucasians could be associated with differences in habitual gait. DESIGN: The effects of race and age on walking speed and heelstrike transient were examined.Background. The relatively low incidence of gonarthrosis in Chinese populations compared to Caucasians remains unexplained. Repetitive impulsive loading exhibited at heel strike in the walking process has been linked to the development of gonarthrosis, while the gait characteristics of people at different risk levels for gonarthrosis have not been compared quantitatively. METHODS: The gait of 117 healthy women, 76 Chinese and 41 Caucasians, was studied with an optometric system and two force plates in an 8-m walkway. Natural walking speed, stride length, cadence and maximum loading rate at heelstrike were collected. RESULTS: The Caucasian women over age 45 walked significantly faster with significantly higher maximal loading rate than age-matched Chinese women (P<0.005). Age effects on most gait parameters measured were found significant in the Chinese group (P<0.01) but not in the Caucasian group. CONCLUSIONS: Chinese women slow down their walking speed and reduce the cadence of their gait earlier in their life span and, thus, lower their heelstrike transients. Significant racial differences in gait might explain the lower prevalence of gonarthrosis reported in Chinese women. RELEVANCE: Significantly larger heelstrike transients and significantly faster walking speed were seen in the population at higher risk for gonarthrosis. Walking slowly with lower heelstrike transients might be an effective preventive measure against gonarthrosis.

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