A review of the literature identified four fairly recent studies that report some of the spatiotemporal, kinematic, or kinetic gait variables discussed above in patients with hip dysplasia (Table 5.1) [24–27]. Unfortunately the literature is relatively sparse and the study populations are very different so it is difficult to identify common trends. Compared to control subjects, subjects with hip dysplasia may have less hip extension during walking [25, 27]. This restriction may be compensated for with increased pelvic excursion [25]. Reduced peak hip extension moments have also been seen [25, 27]. This indicates reduced net activity of the hip flexors in terminal stance or preswing. Two studies that evaluated subjects before and after a surgical intervention found that surgery did not significantly alter spatiotemporal or kinematic measures taken [24, 26]. One study did find that the peak flexion moment, which peak during loading response and indicates net activity of hip extensors, decreased after surgery [24].

A methodological aside: Two studies [24, 26] employed an interesting technique of analyzing gait variables that was not discussed above. In both studies, the angular impulse—the time integral of the moment—was calculated. This technique takes advantage of more of the available information. In knee OA, the angular impulse of the adduction moment has been shown to be a more sensitive marker of disease than the peak adduction moment [28]. The significance of the angular impulses of moments at the hip has not been fully established but this use of this new variable is an interesting emerging trend. Similarly, two studies analyzed the temporal properties of the sagittal plane moments. Omeroglu et al. noted that the transition between having an external flexion moment and an external extension moment, which usually occurs in the middle of the stance phase of gait (see center of Fig. 5.2) was delayed in subjects with hip dysplasia [25]. We have noticed this trend in subjects with hip OA (unpublished additional finding from a previously published study [29]). Again, the significance of this is as yet unknown, but it may indicate a subtle deficit in postural control during single limb stance. Finally, the paper by Pedersen et al. offers a good example of the need to ascertain whether or not the terminology being used matches the terminology with which one is familiar. When describing the sagittal plane moments that were analyzed, Pedersen refers to “maximal extensor dominance in the first half of the stance phase (H1) and maximal flexor dominance in the second half of the stance phase (H2).” [24] The reference to the timing of these peaks tells us that the authors are referring to what we have called, respectively, the peak external flexion moment—balanced by net hip extensor activity, and the peak external extension moment—balanced by net hip flexor activity.

Gait alterations associated with FAI both before and after surgical intervention have been nicely summarized in two very recent review articles [30, 31]. Only five studies, so far, have reported results of walking gait analysis studies (Table 5.2) [32–36]. Across these studies, limitations in range of motion in all planes have been found in people with FAI compared to self-reported healthy subjects or, where available, subjects with verified radiographically normal hips. Hip kinetics have been less frequently reported, and findings have been less consistent so far. While Hunt and Brisson have found reduced hip moments either before [35] or after [36] surgery for FAI, others have not. It should be noted that so far, gait studies of FAI subjects have had small sample sizes (typically fewer than 20 subjects) and have not been heterogeneous with respect to type of FAI (cam vs. pincer vs. mixed) or surgical approach and management. Thus it is so far difficult to draw detailed conclusions about the effect of FAI on gait.

An additional methodological note: Some studies have observed a reversal of sagittal plane hip motion during walking (Fig. 5.3) [33–35]. We have also identified this kinematic pattern in patients with mild to severe hip OA [29], and others have seen it in endstage hip OA [37]. Brisson and Kennedy specifically noted that they did not observe this motion pattern [32, 36], but this could be because their studies were restricted to cam-type FAI, or because of slightly different gait methodologies. (See Michaud 2014 for a discussion of different methods of identifying relative joint motions [38].)

Today, both hip dysplasia and FAI can best be understood as heterogeneous families of hip morphologic abnormalities. It is clear that altering the shape of the femoral head and its articulation with the pelvis results in some gait changes. The fact that restoring normal morphology only partially normalizes gait (with even more residual abnormalities observed during more demanding activities like squatting and stair climbing [34, 39]), however, demonstrates that abnormal bony morphology is not solely responsible for gait changes. Weakness of the gluteus medius and other muscles, as well as alterations in the anatomy of the hip abductors has been observed in both hip dysplasia and FAI [40, 41]. These and other structural changes in the soft-tissue could certainly contribute to the gait alterations seen before surgery in both disorders. Liu in particular notes that the surgeon must be mindful of muscular abnormalities when planning treatment and postoperative physical therapy so that a fuller recovery can be achieved.

As was hinted at in the discussion of hip dysplasia and FAI, there is a rapidly emerging body of evidence suggesting that femoral head shape is an important contributor to hip OA etiopathogenesis [44–47]. Modeling studies reveal that cartilage stresses are sensitive to the shape of the femoral head [21]. It would not be a stretch to consider that gait differences associated with early OA may be associated with subtle alterations of hip articular structure. There is evidence of a relationship between radiographic hip OA severity, as determined by the modified Kellgren–Lawrence (KL) grading system [48], and peak external moments during gait (Fig. 5.5). KL grading is arguably a relatively crude metric of hip structure, as it is based on a visual inspection of the joint space, and does not account for the morphologic changes that have recently been associated with OA. Nevertheless, an overall unloading pattern can be seen as hip OA severity increases. We have also demonstrated that having the sagittal plane motion discontinuity described above is associated with having reduced sagittal plane range of motion and peak flexion, extension, and internal rotation moments. As discussed above, several authors have speculated that there is an association between this sagittal plane motion discontinuity and abnormal hip morphology. Together these findings provide at least circumstantial evidence for a link between abnormal hip structure and abnormal gait function in hip OA.

Endstage hip OA, which is the indication for more than 80 % of all THAs [49], is associated with markedly abnormal gait. Most of the gait anomalies seen in endstage OA can be viewed as more severe forms of the adaptations discussed above. Slower gait speeds, reduced stride lengths, reduced range of motion, and markedly reduced peak external moments have all been reported. Figure 5.5 illustrates how subjects with moderate to severe hip OA (KL Grade 3 and 4) have markedly reduced external moments compared to their counterparts with less severe disease. Sagittal plane gait mechanics have been discussed in detail above; reductions in hip range of motion, peak flexion and peak extension moments are even more dramatic in endstage hip OA. Arguably the most vulnerable muscle group in hip OA and THA, however, is the hip abductors. The frontal and transverse plane gait moments reflect the role of these muscles so they are important to consider in a bit more detail. The peak hip adduction moment in endstage hip OA is markedly reduced compared to healthy subjects [50, 51]. As we have previously discussed, an external adduction moment must be balanced by an internal hip abduction moment. The hip abductors (i.e., gluteus medius and gluteus minimus) are primarily responsible for this balance, so this gait deficit is usually interpreted as a sign of dynamic abductor dysfunction. During walking, the hip abductors are also well positioned to balance transverse plane loads [52, 53]. Thus the reduced internal rotation and external rotation moments that are also seen before surgery [50, 51] may reflect abnormal function of these muscles as well.

Spatiotemporal and sagittal plane gait deficits in endstage OA may be associated with the sagittal plane motion restrictions associated with endstage OA and apparent on clinical exam. Loss of passive hip extension and hip flexion contractures are common in people with severe hip OA. Loss of passive extension is associated with restricted dynamic range of motion in the sagittal plane in people with hip OA as well as healthy elderly [37, 54, 55]. Hip extension is needed in the second half of stance to achieve “normal” gait patterns. Restricted hip extension will necessarily reduce stride length, which will in turn reduce speed. (Recall that speed = stride length × cadence). Flexion contractures can also influence the sagittal plane moments by affecting the position of the ground reaction force with respect to the hip center. If a patient has a flexed hip for most or all of stance, as in the example shown in Fig. 5.3, even in late stance she may not be able to move the ground reaction force posterior to the hip center. This means it will not be possible to produce the large hip extension moment typically seen in late stance (refer back to Fig. 5.2c).

The frontal and transverse plane gait abnormalities could be partly explained by structural changes that happen within the abductor muscles. Hip OA is associated with atrophy and fatty infiltration of the hip abductors, as well as weakness [56–58]. While strength and external moments are not always directly correlated [59], these structural changes can still affect external moments. Maintaining a level pelvis during single limb stance is conventionally thought of as the primary role of the abductors during gait. If the abductors cannot function normally to achieve this, the body must compensate. This compensation is commonly done with exaggerated trunk lean. Even a small amount of lateral trunk lean moves the ground reaction force closer to the hip center in the frontal plane. This action thus reduces the effective moment arm and reduces the external adduction moment and thus the demand on the hip abductors. To understand the transverse plane moment deficits, consider both about a permanently flexed hip and weakened abductors. With persistent hip flexion, the anterior fibers of the gluteus medius and minimus, which contribute most to internal rotation, are being shortened and the posterior fibers, which contribute most to external rotation are being stretched. Neither position will result in an optimal fiber length for contraction, and the transverse plane moment generating capacity of the abductors will be diminished.