Recent investigations into the pattern of progression of lower extremity osteoarthritis (OA) have demonstrated that the evolution of end-stage OA among the large joints of the lower extremities is nonrandom. In particular, individuals with unilateral end-stage hip OA requiring total hip replacement (THR) whose OA then progresses in the knee (the noncognate joint) to require total knee replacement (TKR) have a significantly greater probability that the end-stage knee will be the contralateral, rather than the ipsilateral, joint (1). Similarly, individuals undergoing unilateral TKR for end-stage knee OA more frequently progress to a subsequent contralateral THR (noncognate joint) than an ipsilateral THR (1). This preferential evolution of advanced OA to the contralateral noncognate joint is not replicated in the pattern of progression of the systemic inflammatory arthropathy rheumatoid arthritis (1). Better understanding of the mechanism of this nonrandom evolution may yield significant insights into the pathogenesis of OA.
Biomechanical factors, such as abnormal dynamic joint loading, have been proposed to be important in the development and progression of lower extremity OA (2, 3). Dynamic loading refers to loading during physiologic activity, as opposed to static loading, which occurs when standing. The force across the knee during normal ambulation, the most common form of dynamic lower extremity loading, is approximately 3 times higher than the force during static standing (4). Thus, the “wear-and-tear” process in OA may occur during normal ambulation. An important, noninvasive technique by which to measure dynamic loading is gait analysis, which uses surface skin markers, a camera system, and a force plate on the floor to calculate biomechanical parameters such as the torque, or moment, imposed on the weight-bearing joints (5).
A number of studies have evaluated the relationship between dynamic knee loading and OA in the knees (6–11). The peak external knee adduction moment during gait is a measure of varus torque and, hence, of loading on the medial compartment of the knee. A high external knee adduction moment has been correlated with the radiographic severity of OA in a cross-sectional study of subjects with established OA (6) and imparts a poor surgical prognosis in subjects with a high tibial osteotomy (11). Moreover, there is now evidence that a high adduction moment may predict the subsequent radiographic deterioration of symptomatic knee OA (9, 10).
Normal ambulation and other physiologic activities that occur daily require intimate coordination among the joints of the lower extremities. Although it is likely that deformity and alterations of loading at one lower extremity joint have a significant effect on loading of the other joints of the lower extremities, there have been few studies to evaluate such effects systematically in OA-predisposed joints. Based on the fact that subjects with end-stage hip OA are significantly more likely to undergo contralateral TKR than ipsilateral TKR (1), the current study tested the hypotheses that during ambulation, subjects with unilateral end-stage hip OA place relatively greater loads on their contralateral knee than on their ipsilateral knee and that asymmetric loading is not alleviated by unilateral THR. Support for the hypotheses would suggest that asymmetric dynamic loading contributes to the nonrandom evolution of multiarticular OA of the lower extremities.
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- SUBJECTS AND METHODS
This is the first study to identify asymmetric dynamic loading of the knee joints in subjects with unilateral end-stage hip OA. These asymmetries in knee loading persist even after the hip pain is resolved by a THR, suggesting that subjects with advanced hip OA may undergo prolonged gait adaptations that could affect disease progression in the other joints of the lower extremities. Specifically, the external knee adduction moment (6–11) and the peak force on the medial compartment were significantly higher in the contralateral knee relative to the ipsilateral knee of subjects preoperative for a unilateral THR, and these values remained significantly elevated up to 23 months after successful THR that rendered the subjects pain-free at the hip. These results can account for the previously observed nonrandom evolution of knee OA seen in a similar population of patients with end-stage hip OA, in which the contralateral knee was almost 2.5 times more likely to develop end-stage OA than was the ipsilateral knee (1).
Results of small studies have indicated that a disruption in lower extremity coordination may lead to subsequent pathologic changes in the joints of the lower extremities. For example, a group of athletes with unilateral lower leg amputation was shown to have a higher incidence of radiographic OA of the “normal” (nonamputated) knee compared with age-matched healthy controls (22). Furthermore, results of gait evaluation in patients who had undergone lower leg amputation suggested that the patients place relatively higher loads on the nonamputated extremity compared with a normal control population (23). This was assumed to be a result of increased magnitude and duration of functional loading of the nonamputated extremity during day-to-day activities. Similarly, Loizeau et al (24) examined 4 postoperative patients who had undergone unilateral THR for end-stage OA and noted the presence of “mechanical dysfunction” based on altered energy absorbed or generated in the large joints of the nonoperated limb (24).
Although these previous investigations hinted at the importance of the biomechanical interrelationship between the joints of the lower extremities, this is the first systematic study to quantify asymmetries in knee joint loading in subjects with hip OA. The specific mechanisms that initiate and maintain differential limb loading are not completely clear. Asymmetric knee loading may be a consequence of gait alterations in response to chronic hip pain and structural pathology. Thus, subjects may unload the symptomatic extremity and relatively “overload” the contralateral limb. Gait analysis has previously shown that the mean peak external knee adduction moment in healthy adults is ∼3.0 %BW × height (8) and approaches 4.0 %BW × height in subjects with radiographic evidence of medial compartment knee OA (8, 25), in those who undergo radiographic deterioration after longitudinal followup (9), and in those who have a poor prognosis after high tibial osteotomy (11).
In the current investigation, although the knee contralateral to the limb with end-stage hip OA had relatively higher loads than did the knee ipsilateral to the end-stage hip, subjects had external knee adduction moments below 3.0 %BW × height in both the contralateral and ipsilateral knees and, therefore, appeared to be “underloading” both knees compared with a normal population or with a knee OA population. Although these subjects appear to be relatively more disposed to developing OA in the knee contralateral, rather than ipsilateral, to their end-stage hip, it is not clear that they are at higher risk for any knee OA compared with the general population (i.e., without hip OA). Perhaps the proportion of subjects who eventually develop end-stage knee OA has biochemical abnormalities in the cartilage that make it more susceptible to wear and tear from nominally “normal” loads (26, 27).
If preoperative pain and pathology in the diseased hip are responsible for differential knee loading in subjects with end-stage hip OA, why does that differential loading persist postoperatively after THR? Perhaps an initial gait adaptation occurs in response to hip pain and, possibly, structural disease that is subsequently maintained through more permanent neuromechanical changes that function in ambulation and are unaffected by THR (28–30). Alternatively, since the peak external knee adduction moment has been correlated with the presence of radiographic knee OA, the relatively higher external knee adduction moment in the contralateral knee may be a reflection of asymptomatic radiographic knee OA that has already developed, is present at the time of THR, and will, in some patients, eventually be manifested by clinical symptoms. Unfortunately, knee radiographs were not available for the subjects of the present study. Regardless of the underlying cause, a better understanding of the specific neuromechanical factors involved in the asymmetric loading in this population may help target future pre- and postoperative physical therapy aimed at the prevention of knee OA (31–33). Similarly, if it is the case that subjects already have established knee OA at the time of THR, then perhaps recognizing this as a potential consequence of end-stage hip OA would encourage radiographic evaluation of the knees and, perhaps, earlier consideration of THR in this population.
Several of the knee moments actually did become symmetric after THR and were no longer significantly different between the knees. The reason for this is unclear. However, it is important that differences in both the peak external knee adduction moment and the peak medial compartment load in the two knees persisted after successful THR. These knee loading parameters are regarded as physiologically the most important parameters in the development and progression of medial compartment knee OA (6–11, 25).
In conclusion, in light of what is known about the effects of loading on knee OA (6–11) and the previous observation of a nonrandom pattern in the evolution of lower extremity OA that favors progression in the contralateral knee (1), the present finding of relatively increased dynamic loading in the contralateral knee of subjects with end-stage hip OA provides further, compelling evidence that dynamic loading is an important risk factor in knee OA and may explain the nonrandom evolution of OA in multiple joints of the lower extremities. Furthermore, the persistence of asymmetric knee loading after THR indicates that fundamental changes in the neuromuscular control of gait or irreversible asymptomatic radiographic knee OA may already be present at the time of development of end-stage hip OA. Future investigations should focus on delineating the specific neuromuscular, biomechanical, and structural factors that may be involved.