Functional Kinematics During Walking And Osteoarthritis

As previously discussed, functional joint loading can influence the health of articular cartilage and is ultimately associated with the progression of degenerative changes to cartilage. In addition, joint motion (kinematics) can influence the initiation of osteoarthritis (Andriacchi et al., 2004). For example, the anterior cruciate ligament (ACL) of the knee, one of the four major ligaments of the knee, provides translational and rotational stability to the joint. The ACL frequently is injured during sporting activity and is the most frequently reconstructed soft-tissue structure at the knee. The ACL-deficient knee provides a basis for examining the influence of abnormal kinematics on the initiation of knee osteoarthritis. There are numerous clinical studies (Buckland-Wright et al., 2000; Daniel et al., 1994; Lohmander and Roos, 1994; Roos et al., 1995) that report premature knee osteo-arthritis in chronic ACL-deficient knees and even in knees following reconstruction. Even though ACL reconstruction does restore anterior-posterior stability (Daniel et al., 1994), it has not been documented that ACL reconstruction restores normal rotational alignment and motion to the knee, suggesting the possibility that rotational changes following ACL injury could be a factor in the initiation of knee osteoarthritis following ACL injury (Kanamori et al., 2002; Ma et al., 2000).

Studies of patient function (Andriacchi and Dyrby, 2005; Georgoulis et al., 2003; Vergis and Gillquist, 1998) following ACL injury support the observation that rotational changes following ACL injury are a major factor in the progression of knee osteoarthritis. In particular, a recent study (Andriacchi and Dyrby, 2005) demonstrated that ACL-deficient patients did not have an increased range of AP motion relative to the contralateral side. However, there was an offset in internal-external (IE) rotation position relative to the contralateral limb. The offset was determined from the temporal average of all IE values over the entire walking cycle. The tibia was more internally rotated throughout stance phase than in healthy control subjects. The fact that the rotational offset was also present at the end of swing phase where the tibia normally externally rotates with knee extension (screw-home movement) suggests that the loss of the ACL causes a reduction of the internal rotation of the tibia at the end of swing phase. This rotational offset is maintained through the stance phase of the walking cycle.

A positional offset shifts the load bearing contact areas of the knee away from normal locations. The change in the rotational characteristics at the knee could cause specific regions of the cartilage to be loaded that were not loaded prior to the ACL injury. It has been suggested (Bullough et al., 1992; Yao and Seedhom, 1993) that the altered contact mechanics in the newly loaded regions could produce local degenerative changes to the articular cartilage. As previously reported (Bullough et al., 1992; Wong et al., 1999), cartilage in highly loaded areas has mechanically adapted relative to underused areas where signs of fibrillation can be observed in healthy knees in relatively young subjects. It has been suggested (Andriacchi et al., 2004) that a spatial shift in the contact region could place loads on a region of cartilage that may not adapt to the rapidly increased load initiating degenerative changes (Wu et al., 2000). It is important to note that other studies (Kvist and Gillquist, 2001) have demonstrated a shift in the anterior-posterior position of the tibial femoral contact during walking after loss of the ACL. Thus, it is likely that ACL injury causes a shift in the load bearing location through a combination of rotational and translational changes in the normal kinematics of the joint.

Clinical and laboratory studies (Cicuttini et al., 2002; Wu et al., 2000) have suggested that changes in contact position could be a factor in the degenerative changes, even in knees with an intact ACL. In particular, rotational malalignment has been related to an increased incidence of knee osteoarthritis (Nagao et al., 1998; Yagi, 1994). A shift in the load bearing area to an infrequently loaded region would cause articular surface damage and increase fibrillation of the collagen network and lead to the degenerative changes that have been associated with increased clinical laxity.

The preceding observation for the ACL-deficient knee can be related to the changes to the musculoskeletal system that occur with aging. In particular, ligament stiffness (Noyes and Grood, 1976; Woo et al., 1991), muscle strength (Jubrias et al., 1997), and muscle activation (Stackhouse et al., 2001) decline with aging. The decline in passive joint stability derived from ligament restraint and dynamic stability derived from muscle forces can cause abnormal kinematics that increase with age. These kinematic changes will lead to a shift in the normal load bearing regions in a manner similar to the kinematic changes following ACL injury. Hormonal changes that occur with menopause produce similar changes (Phillips et al., 1993; Rasanen and Messner, 1999; Richette et al., 2003) to those described for aging and could explain the increased incidence of knee osteoarthritis reported in women over the age of 50 (Oliveria et al., 1995). In addition, aging (Buckwalter et al., 1994) and hormonal (Rasanen and Messner, 1999) changes can limit the ability of cartilage to adapt and repair (Martin and Buckwalter, 2000) cartilage damage associated with changes in load bearing regions. Chronic kinematic changes with aging and menopause can cause degenerative changes to cartilage, since older cartilage might not have the capacity to adapt to load bearing changes in contrast to younger cartilage.

Conclusion

The progression of osteoarthritis with aging is best understood by considering the interrelated biological, morphological, and neuromuscular pathways associated with the disease. The interrelationship or coupling of these pathways converges at an in vivo systems level in humans. Each of these pathways changes with aging in ways that increase the risk of osteoarthritis.

The material presented in this chapter provides an integrated in vivo framework for understanding the various factors that influence the initiation and progression of osteoarthritis that is consistent with theoretical, laboratory, and clinical observations of the pathomecha-nics of osteoarthritis. This framework provides a basis for explaining the role of kinematics and load on the progression of knee osteoarthritis. Although this framework was developed from an analysis of in vivo patho-mechanics, it also explains how the convergence of biological, morphological, and neuromuscular changes to the musculoskeletal system during aging or during menopause leads to the increased rate of idiopathic osteoarthritis with aging.

The in vivo framework presented should be helpful for the interpretation of laboratory experiments, the identification of risk factors for knee osteoarthritis, and the development of methods for the evaluation of osteoarthritis at the knee.

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