In the present study, the severe KOA group showed more severe varus deformity, larger KAM, and smaller KFM. The relative contribution converted from %KFM dominance into %KAM dominance in patients with severe KOA at TJM1. In addition, knee flexion contracture and trunk flexion were observed in group G-4. We evaluated knee alignment, ROM, and trunk flexion, and clarified the pathogenesis and mechanism of OA progression from a biomechanical perspective with regard to kinematics and kinetics characteristics in each group. This is the first study to identify differences in kinematics and kinetics, including the relative contributions of each moment component according to OA severity.
Regarding the relationship between varus deformity and KAM, significant varus deformity and increases in KAM occurred in groups G-3 and G-4. This may be the result of increases in the lever arm of KAM as well as severity of varus deformity. However, there was a significant increase and decrease in the relative contributions of KAM and KFM, respectively, in grade 2 knees, with little difference between grades 2 and 3 KOA. This suggests that the conversion of relative contribution of each moment from KAM to KFM had already occurred in grade 2 KOA prior to varus deformity appearance.
Group G-4 was found to have a significantly higher %KAM and lower %KFM compared with groups G-2 and G-3, showing further drastic kinetic changes in severe KOA. Additionally, significant flexion contractures and trunk flexion were observed, indicating that grade 4 differed from grade 3 KOA. In addition to varus deformity, severe KOA was reported to have pathology of apparent sagittal imbalance [23–25]. Ohkoshi et al reported that trunk flexion, which leads to elongation of the moment arm of the trunk toward the center of gravity, reduced quadriceps muscle activity in the squat movement [26]. The same effect of reducing KFM may occur during gait. Our results suggest that grade 4 KOA has the potential to increase not only the risk of quadriceps muscle weakness [27] and patellofemoral arthropathy exacerbation [28] due to knee flexion contracture, but also the risk of erector spinae muscles weakness [29, 30] and vertebral fractures. Our data support and provide an explanation of the mechanism of the previous biomechanical study of vertebral fractures associated with KOA [31].
The results of this study showed that a change in the relative moment contribution occurred in grade 2 KOA, with significant constructive varus deformity in grade 3. The KOA progression leads to a conversion of the knee flexion moment (KFM) to the knee adduction moment (KAM). This change in moment balance subsequently exacerbates knee flexion contracture during gait, resulting in trunk flexion (Fig. 4). These outcomes suggest clinical relevance that conservative treatment, such as orthotic treatment [32] and muscle strength training [33] may particularly be effective in grade 2 KOA before constructive changes occur. This is consistent with the results of previous studies of therapeutic interventions with rehabilitation [34, 35]. It has been reported that quadriceps strength weakens with age and pain even in mild cases of KOA [35]. On the other hand, in patients with grade 3, prevention of flexion contracture and maintenance of quadriceps muscle strength are important to prevent progression to grade 4. This may indicate the need for surgical intervention (alignment surgery) to correct constructive varus deformity. In addition, patients with grade 4 KOA had trunk flexion, which also affected sagittal imbalance. Therefore, more aggressive surgical treatment of grade 4 KOA should be considered to improve overall function and prevent frailty.
The KOA progression leads to a conversion of the knee flexion moment (KFM) to the knee adduction moment (KAM). This alteration in moment balance subsequently exacerbates knee flexion contracture during gait, eventually leading to trunk flexion.
The present study has several limitations. First, this study has a relatively small number of patients. The purpose of this study was to clarify the pathophysiology of KOA by subdividing patients with KOA, including healthy participants, into grades. Thus, the number of cases in each group of grades was small. However, new findings were obtained based on this grouping, and this study is considered meaningful and relevant. Furthermore, considering the pathophysiology of KOA, the findings of the present study might be significant depending on the viewpoint that it is a comparative study of grades of KOA and healthy participants were included as controls. Second, our data are cross-sectional, and whether the result is primary or secondary to disease status is unknown. The course of the disease is also unclear. However, it is feasible to compare the characteristics of each grade at the same time. Variations in the disease status among grades may be the result of another study, but our study mainly targeted differences among grades and had an advantage at this point. This new concept comparing the changes in kinetics, including the relative contribution of moments, and kinematics data simultaneously among different severity groups, provides new insights into OA knee pathogenesis. Third, gait speed was not adjusted among groups. Generally, it is well known that it is preferable to match gait speed for comparison. However, in order to assess the natural history of KOA pathology, we have chosen to use self-selected normal walking speeds as previous studies have performed [36, 37]. Additionally, there was no difference in body weight which may have influence on biomechanics among groups.
In conclusion, the present study assessed the kinematics and kinetics according to severity of medial KOA and its relationship with trunk flexion. The relative contribution of each moment component changed from KFM to KAM dominance, and flexion contracture and trunk flexion was observed in patients with severe KOA.