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To test the hypothesis that appropriate and timely neuromuscular control of limb motions plays an important role in the preservation of joint health, we kinematically and kinetically examined the behavior of the legs of young adult subjects at heel strike during natural walking. We compared a group of 18 volunteers, who, we presumed, were preosteoarthrotic because of mild, intermittent, activity-related knee joint pain, with 14 age-matched asymptomatic normal subjects. The two groups of subjects exhibited similar gait patterns with equivalent cadences, walking speeds, terminal stance phase knee flexion, maximum (peak) swing angular velocity, and overall shape of the vertical ground reaction. However, our instrumentation detected statistically significant differences between the two groups within a few milliseconds of heel strike. In the knee pain group, the heel hit the floor with a stronger impact in this brief interval. Just before heel strike, there was a faster downward velocity of the ankle with a larger angular velocity of the shank. The follow-through of the leg immediately after heel strike was more violent with larger peak axial and angular accelerations of the leg echoed by a more rapid rise of the ground reaction force. This sequence of events represents repetitive impulsive loading, which consistently provoked osteoarthrosis in animal experiments. We refer to this micro-incoordination of neuromuscular control not visible to the naked eye as "microklutziness."

We studied changes in subchondral bone and articular cartilage in an animal model of osteoarthrosis. In this model we applied repetitive impulsive loads to rabbits' knees. Their legs were held in short leg splints so the rabbits were unable to dampen the peak applied load with ankle flexion. After sacrifice, at 1 day to 6 weeks, we studied proximal tibial load-bearing cartilage histologically, biochemically, and with radioactive sulfate uptake. We also studied the subchondral bone under that cartilage histologically, histomorphometrically, with bone scan (99mTc pyrophosphate), and by tetracycline labeling. An increase in 99mTc labeling of the subchondral bone was the first reliable change observed. This was followed by an increase in tetracycline labeling, bone formation, and a decrease in porosity, which has been associated with relative stiffening of bone. Horizontal splitting and deep fibrillation of the overlying articular cartilage followed the early bone changes. All of these changes preceded changes in content and characterization of cartilage proteoglycans or increased chondrocyte activity as manifested by incorporation of radioactive sulfate. In this model the early bone changes preceded changes in the articular cartilage. The deep splitting of articular cartilage occurred prior to metabolic alteration of that tissue.

When compact bone is subjected to fatigue loading, it develops matrix microdamage, which reduces the tissue's ability to resist fracture. The relative influence of different strain modes on damage and strength in compact bone has not been characterized, to our knowledge. In this study, the nonuniform strain field produced by four-point bending was used to introduce fatigue damage into tibial bending beam specimens from men 40-49 years old. The specimens were then bulk-stained with basic fuchsin to mark damage surfaces and were examined histologically and with confocal microscopy to describe damage morphologies and position relative to tension and compression-strained regions of the specimen. Histomorphometric methods were used to quantify the amounts of different types of bone microdamage. Three major types were observed. In regions subjected to tensile strains, the bone had focal regions of diffusely increased basic fuchsin staining (i.e., diffuse microdamage). Confocal microscopy of these regions showed them to be composed of extensive networks of fine, ultrastructural-level cracks. In compressive strain regions, the tissue developed linear microcracks in interstitial areas similar to those originally described by Frost. Fine, tearing-type (wispy-appearing) cracks were observed near and in the plane of the neutral axis. The paths of these fine cracks were not influenced by microstructural boundaries. Other minor damage morphologies (sector-stained osteons, delamination of regions of lamellae, and intraosteonal cracking) were observed, but their distribution was unrelated to local strain field. Thus. in fatigue of human compact bone, the principal mechanisms of matrix failure (i.e., linear microcrack, diffuse damage foci, and tearing-type damage) are strongly dependent on local strain type.

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