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Moment

I ^ Producing y^JJ^ Lateral Opening

A. Muscie force + Ligament Force Do

Resist Lateral Joint Opening

B. Muscle force + Ligament Force Do Not

Resist Lateral Joint Opening

Figure 77.4 This diagram of the knee illustrates how stability of the joint is maintained by passive ligament forces and active muscle contraction. In this example, the passive ligament force in the lateral collateral ligament and the active force generated by the quadriceps muscle resist a moment tending to create lateral joint opening (A). Loss of passive stiffness of the ligament and/or a reduction in muscle force can result in a pathological condition where the joint opens laterally, transferring the entire load to a single compartment of the knee (B). Both ligament stiffness and muscle control of the joint decline with aging.

tibia. If the passive soft tissue and muscle forces do not balance the extrinsic moment tending to adduct the knee, then the lateral side of the knee will open and all the force at the knee will be transferred across the medial side of the knee. This condition will potentially overload the medial compartment of the knee and is likely one of the reasons that patients with increased laxity are at higher risk for knee osteoarthritis. As will be discussed later in this chapter, there is a large extrinsic moment that tends to adduct the knee during the stance phase of gait.

The importance of muscle force in the development of osteoarthritis during aging is illustrated by the fact that muscle function and strength decline with aging. Patients with knee osteoarthritis experience changes in their muscle strength and coordination that are independent of the aging process. For instance, activity of the vastus lateralis muscle relative to maximal vastus lateralis muscle activity is much greater in patients with knee osteoarthritis compared to age-matched controls and young adults (Hortobagyi et al, 2005). Decreased quadriceps muscle strength per muscle mass suggests that osteoarthritis patients experience muscle inhibition due to altered afferent input from the diseased joint and consequent reduction in efferent motor neuron stimulation of the quadriceps muscle (Slemenda et al., 1997). In addition, medial compartment knee osteo-arthritis is associated with a greater loss of cartilage in the medial compared to the lateral compartment of the knee, and leads to increasing varus alignment with increasing severity (Miindermann et al., 2004). These age-independent changes in muscle properties and cartilage morphology likely contribute to a further increase in joint laxity in patients with knee osteoarthritis.

Menopause may accelerate the loss of muscle mass and result in decreased muscle performance and functional capacity (Sipila, 2003). Although differences in ligament properties between men and women are unknown, ACL stiffness does correlate with estrogen and progesterone levels (Romani et al., 2003), and estrogen levels are lower in postmenopausal women. Probably resulting from these differences in ligament and muscle properties, even healthy women have greater varus-valgus laxity than healthy men (Sharma et al., 1999), potentially contributing to the higher incidence of osteoarthritis in women after menopause. Thus the increased incidence of osteoarthritis in postmenopausal women is likely related to increased passive and dynamic laxity of the joint.

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