Passive (no muscle contraction) joint laxity is dependent on the conformity of the articular geometry, the properties of the ligaments, menisci (at the knee), and the capsule at the joint. Any changes in the mechanical properties of these structures, whether they occur with aging, disease, or following a joint injury, will have an effect on this mechanical environment. For instance, joint laxity appears to be critically important for the health of a joint (Sharma et al., 1999). Joint laxity can produce large displacements of the articular surfaces, alter congruity and contact sites, and increase local shear and compressive stresses. Joint laxity depends on several factors including the mechanical properties of ligaments and muscle strength and coordination (see Figure 77.4).
The knee, a common site of osteoarthritis, provides a good illustration of the primary components of the joint that maintain joint stability and thus influence joint laxity. The major ligaments stabilizing the knee in translation and rotation are the anterior (ACL) and posterior (PCL) cruciate ligaments. The stiffness and elastic modulus of these ligaments decrease with age (Noyes and Grood, 1976; Woo et al., 1991). The major changes in muscle with age include reduced muscle activation (Stackhouse et al., 2001; Stevens et al., 2003), cross-sectional area (Frontera et al., 2000; Jubrias et al., 1997; Kent-Braun and Alexander, 1999), force per cross-sectional area (Jubrias et al., 1997), and maximum muscle strength (Frontera et al., 2000; Jubrias et al., 1997; Lindle et al., 1997). These age-associated changes in the properties of ligaments and muscle can cause increased joint laxity with age.
Active muscle contraction plays an important role in the dynamic stability of the joint during functional activities such as walking. As illustrated in Figure 77.4, the lateral stability (resistance to lateral joint opening) is dependent on the tension in passive soft tissue (lateral collateral ligament) and active muscle force producing a moment (tendency of a force to produce a rotation) resisting the extrinsic moment tending to adduct the
Ligament 4 Force
Muscle Force il'
I ^ Producing y^JJ^ Lateral Opening
A. Muscie force + Ligament Force Do
Resist Lateral Joint Opening
B. Muscle force + Ligament Force Do Not
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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