Defining Osteoarthritis: What It Is, and What It Is Not: Page 3 of 7

Defining Osteoarthritis: What It Is, and What It Is Not: Page 3 of 7

Under these conditions, numerous trabecular microfractures occurred, with stiffening of the underlying subchondral bone. This was followed by progressive damage to the articular cartilage, with deep fibrillation and horizontal splitting. Importantly, when loads of the same or greater magnitude were applied gradually (eg, 500 milliseconds, onset to peak), they had no effect.

Because the quadriceps muscle is the major antigravity muscle of the lower extremity and serves as a brake on the pendular action of the lower limb during ambulation, minimizing the forces generated with heel strike, it plays a major role in protecting against mechanical damage to the knee. During gait, healthy subjects decelerate their leg before heel strike can create an impulsive load. Among healthy subjects who had no force-transient profile during gait, the load rate increased more than 2-fold (to about 150 × body weight/s) after a femoral nerve block to temporarily paralyze the quadriceps muscle.9

This suggests that a heel strike transient may be caused by the failure of quadriceps contraction to decelerate the lower extremity in the swing phase of gait. In healthy subjects, minor incoordination in muscle recruitment that results in failure to decelerate the leg may generate impulsive forces as high as 65 × body weight/s at heel strike.9

A comparison of young adult subjects whose knee x-ray film results were normal but who had intermittent activity-related knee pain with age-matched, asymptomatic, radiographically normal controls showed that the 2 groups were similar with respect to gait patterns, walking speeds, terminal stance phase knee flexion, maximum (peak) swing phase angular velocity, and overall shape of the ground reaction.10 However, the groups differed markedly over the few milliseconds surrounding heel strike.

The downward velocity of the ankle just before heel strike and the impact at heel strike were greater in the group that had knee pain than in the controls. Immediately after heel strike, the follow-through of the leg was more violent in the subjects who had knee pain, with larger peak axial and angular accelerations of the leg that were reflected in a more rapid increase of the ground reaction force. The mean rate of loading of the knee (velocity at heel strike adjusted for body weight) among those who loaded their knee impulsively was significantly higher than that of those who did not.

These changes, which were not visible to the naked eye, replicated those seen in experimental animals that were subjected to RIL8 and consistently resulted in OA. About one-third of the subjects exhibited microincoordination during gait and impulsively loaded their knees repetitively while they walked on a level surface. Radin and associates10 referred to these subjects as “microklutzes.” In young adults, microklutziness is associated with knee pain. A limp and reduced walking speed decrease RIL.

Peak adduction moment (PAM)
The PAM reflects the magnitude of the intrinsic compressive load on the medial tibiofemoral compartment in stance. A considerable body of work related to the PAM adds to the evidence that biomechanical abnormalities drive the etiopathogenesis of common, garden-variety knee OA.11

Varus-valgus alignment is a key determinant of the PAM. Varus malalignment further increases the medial compartment load during gait; valgus malalignment increases stress in the lateral compartment. Malalignment may be a consequence of knee OA but also may result from genetic or developmental factors or previous trauma. The PAM predicts radiographic progression in persons with medial compartment OA12 and development of knee pain in asymptomatic older persons.13

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