The purpose of this study was to evaluate the effects of increased OA severity on dynamic joint stiffness during walking. From our results we can conclude that subjects with more advanced disease ambulate with higher dynamic joint stiffness values at the knee. We also found that increasing walking speed resulted in further increases in dynamic joint stiffness values (). Moreover, subjects with severe OA have higher dynamic knee joint stiffness values irrespective of freely chosen walking speed.
In this study, persons with more severe knee OA presented with lower functional ability compared to healthy controls and persons with moderate OA (). Since instability is related to a person's self-perceived functional ability, individuals with more severe OA may also demonstrate the highest amount of instability during walking (Fitzgerald et al., 2004
). This may result in the need for higher muscular resistance to external forces. It is known that persons with severe OA utilize a motor coordination strategy that results in higher antagonistic muscle activity at the knee (Lewek et al., 2004
, Astephen et al., 2008b
). The increase in stabilizing muscle forces may decrease the sagittal plane knee range of motion during loading response and result in the larger dynamic joint stiffness values that were found in this study when persons with severe OA were compared to healthy controls and persons with less severe OA. This result is similar to previous findings (Lark et al., 2003
) Although they compared younger individuals to healthy elderly individuals, they concluded that the increased dynamic joint stiffness in the elderly group may represent a compensatory strategy to overcome a reduced ability to generate quick ankle torques in response to changes in external forces. Because persons with OA have decreased joint stability, reduced proprioception, and reduced efferent response to changes in external forces, they may develop higher dynamic joint stiffness as a method to safely navigate through their environment (Shakoor et al., 2008
, Hortobagyi et al., 2004
, Sharma and Pai, 1997
, Fitzgerald et al., 2004
While an increase in dynamic joint stiffness and antagonistic muscle activity may act to maintain stability of the knee that has been compromised as a result of the disease process, it may have deleterious effects on the integrity of the cartilage. It has been shown in vivo and experimentally that higher amounts of muscular forces can result in higher amounts of joint compression forces (Kellis, 2001
, Taylor and Walker, 2001
). This increase in compression force may advance the disease process (Griffin and Guilak, 2005
). Coupled with the fact that the severe persons were also significantly heavier than persons without OA, this may dramatically increase the compression forces in these subjects (Messier et al., 2005
With our present subject population, we found no differences in dynamic joint stiffness between persons with moderate OA and persons without radiographic evidence of the disease. It should be noted, however, that subjects in the moderate OA group had knee excursions that were smaller than the control group and similar to that of the severe OA group (). Although the range of motion was similar, the subjects with severe OA had a larger average change in knee moment at each time step resulting in higher dynamic joint stiffness values. It is possible that higher loads over a smaller range of articular surface may initiate the disease process or expedite cartilage degeneration. Diseased cartilage has a reduced ability to repair itself in the presence of external loads (Griffin and Guilak, 2005
). If similar loads were to be placed on a smaller range of articular surface (or if these loads were to remain on the same area for longer periods of time), this may result in further deterioration of the articulating surface. Increased dynamic joint stiffness values, or higher loads over a smaller range, may play an important role in OA pathogenesis.
Unlike other gait parameters in persons with knee OA, differences in dynamic joint stiffness between healthy controls and persons with severe OA does not seem to be related to self-selected walking speed. While it has been shown that persons with knee OA may walk with reduced joint moments and excursions, many previous studies have not accounted for differences in walking speed between healthy subjects and persons with knee OA (Al-Zahrani and Bakheit, 2002
, Astephen et al., 2008a
, Gok et al., 2002
). It has been well documented that these variables are highly influenced by walking speed (Chiu and Wang, 2007
, Bejek et al., 2006
, Landry et al., 2007
, Mockel et al., 2003
, Lelas et al., 2003
, Andriacchi et al., 1977
). In this study, we found that dynamic joint stiffness significantly increased with an increase in walking speed. Intuitively we would expect that if differences between subjects were a result of differences in walking speed, the subjects that walked slower (persons with severe knee OA) would have lower stiffness values. We found the exact opposite relationship such that subjects with severe OA had the highest stiffness values at freely chosen walking speeds. This was further highlighted by the fact that differences also existed when subjects walked at a constrained speed. Additionally, when walking speed was included as a covariate in the analysis at freely chosen walking speeds, the severe group still showed statistically higher dynamic joint stiffness values. We can conclude that persons with knee OA demonstrate higher dynamic joint stiffness, irrespective of freely chosen walking speed.
Differences in temporo-spatial variables may also influence joint excursions, joint moments and subsequently dynamic joint stiffness. Despite this, it appears that inter-group alterations in these variables cannot explain all of significant differences that we found between groups for dynamic joint stiffness. At 1.0 m/s, no differences were found for stride duration, stride length and cadence between groups, although we still saw differences in dynamic joint stiffness between the severe and control and moderate groups. This further supports the thought that higher dynamic joint stiffness is used by the severe group as an intrinsic response to instability or the result of higher muscular forces at the knee joint, not merely a result of altered walking speed and temporo-spatial values.
One limitation of this study is the inability to determine the physiological cause of altered dynamic joint stiffness. While neuromuscular changes are often cited as the reason for increases in joint stiffness during dynamic activities (Rudolph et al., 2007
), it is possible that changes in intrinsic joint mechanics result in higher joint stiffness. Alterations in the joint environment have been cited in the presence of degenerative changes to the articular surface (Link et al., 2003
, Phan et al., 2006
). Although medial laxity may persist in the presence of advanced disease, a reduction in the anterior/posterior laxity of the knee joint has been found with end-stage knee OA (Wada et al., 1996
). Physical changes such as the presence of osteophytes and hardening of the joint capsule have been suggested as potential causes for the increased stiffness.
Anterior/posterior stiffness coupled with increased friction due to osteophyte formation and incongruent joint surfaces may reduce the ability of the tibiofemoral joint to translate during knee flexion. While this may increase dynamic joint stiffness, it may also increase the pain response associated with knee flexion during the loading phase of gait. Higher muscle activity aimed at reducing the knee flexion and pain with movement would also result in higher dynamic joint stiffness. Future research aimed at determining the underlying cause of joint stiffness would greatly improve our knowledge of mechanical and neuromuscular changes that occur in the presence of advanced knee OA.
In the current study, we evaluated a cross-sectional sample of persons with progressive grades of knee OA. Thus, we are unable to determine whether the differences that we see in joint stiffness arise as a result of the increase in OA severity, or whether changes in joint stiffness may be partially responsible for the progression of the disease. Future work should include a longitudinal assessment to determine if subjects that present with high dynamic joint stiffness at baseline show advanced disease progression at follow-up.
From this study, we conclude that persons with advanced stages of OA walk with greater dynamic joint stiffness. While further research into the cause of dynamic joint stiffness is warranted, subjects with severe OA may reduce knee joint excursion in an attempt to stabilize the joint against external joint moments. Similar to other gait parameters, dynamic joint stiffness values increase in the presence of increased walking speeds. Despite this, persons with severe OA develop a higher level of dynamic joint stiffness irrespective of freely chosen walking speed which may have detrimental consequences for disease progression.