Changes in lower limb biomechanics when following floor-projected foot placement visual cues for gait rehabilitation.

BACKGROUND: Lately, the projection of foot placement visual cues onto the floor has been considered for use in gait rehabilitation. While promising, this approach needs further basic assessment to ensure proper uses. RESEARCH QUESTION: Does following floor-projected foot placement visual cues of one's natural walking pattern induce gait mechanics changes immediately or after a practice period? METHODS: Gait mechanics data from fifteen healthy individuals (7 female, 25.4 ±â€¯5.0 years, 21.5 ±â€¯1.68 kg/m2) was collected during normal walking without visual cues, and during two testing phases (immediate and after 45-60 min of practice) of walking with floor-projected visual cues depicting their normal spatial parameters. Magnitudes and variabilities of spatial gait parameters and sagittal plane lower limb kinematics and kinetics were compared between the three testing phases using repeated measures ANOVA and post-hoc paired t-tests. RESULTS: Compared to normal walking without foot placement visual cues, there was a statistically significant (p < 0.05) increase in stride length (maximum change of 0.01 ±â€¯0.01 m), stance phase knee flexion (2.0 ±â€¯2.5°), and swing phase hip flexion (1.2 ±â€¯1.3°) in both immediate and post-practice testing phases, along with an increase in terminal stance hip (0.28 ±â€¯0.38 %BW*Ht) and knee (0.25 ±â€¯0.25 %BW*Ht) flexion moments in the immediate testing phase. All of these changes between testing phases were smaller than their corresponding normal gait smallest real differences (SRD). With the addition of visual cues, variability was statistically significantly decreased in spatial parameters and increased in knee flexion angle at heel strike and knee flexion moment in terminal stance. SIGNIFICANCE: While biomechanical changes were observed, their magnitudes were small enough to suggest that floor-projected visual cues can be used in gait retraining without introducing unintended gait changes. Furthermore, the results suggested that lengthy practice periods are not necessary. The validity of these observations will, however, need to be confirmed in cases of severe impairments.

Modeling knee osteoarthritis pathophysiology using an integrated joint system (IJS): a systematic review of relationships among cartilage thickness, gait mechanics, and subchondral bone mineral density.

OBJECTIVE: To introduce an integrated joint system (IJS) model of joint health and osteoarthritis (OA) pathophysiology through a systematic review of the cross-sectional relationships among three knee properties (cartilage thickness, gait mechanics, and subchondral bone mineral density). METHODS: Searches using keywords associated with the three knee properties of interest were performed in PubMed, Scopus, and Ovid databases. English-language articles reporting cross-sectional correlations between at least two knee properties in healthy or tibiofemoral OA human knees were included. A narrative synthesis of the data was conducted. RESULTS: Of the 5600 retrieved articles, 13 were included, eight of which reported relationships between cartilage thickness and gait mechanics. The 744 tested knees were separated into three categories based on knee health: 199 healthy, 340 at-risk/early OA, and 205 late OA knees. Correlations between knee adduction moment and medial-to-lateral cartilage thickness ratios were generally positive in healthy, inconclusive in at-risk/early OA, and negative in late OA knees. Knee adduction moment was positively correlated with medial-to-lateral tibial subchondral bone mineral density ratios in knees of all health categories. One study reported a positive correlation between lateral tibial subchondral bone mineral density and femoral cartilage thickness in at-risk/early OA knees. CONCLUSIONS: The correlations identified between knee properties in this review agreed with the proposed relationship-based IJS model of OA pathophysiology. Accordingly, the IJS model could provide insights into overcoming current barriers to developing disease-modifying treatments by considering multiple aspects of OA disease, aspects that could be assessed simultaneously at an in vivo system level.

Altered gait mechanics and elevated serum pro-inflammatory cytokines in asymptomatic patients with MRI evidence of knee cartilage loss.

OBJECTIVE: To test if sagittal plane gait mechanics parameters and serum inflammation levels differ between healthy asymptomatic subjects and asymptomatic subjects with magnetic resonance imaging (MRI) evidence of cartilage loss. DESIGN: Gait mechanics and resting serum tumor necrosis factor-α (TNFα) concentrations were measured for two groups of asymptomatic subjects recruited for a previous study: Pre-Osteoarthritis (OA) subjects had MRI evidence of partial- or full-thickness knee cartilage loss in at least one compartment (n = 52 (30 female), 1.7 ± 0.1 m, 85.3 ± 18.9 kg, 44 ± 11 years); Control subjects had no MRI features of cartilage loss, osteophytes, bone marrow lesions, nor meniscal pathology in either knee (n = 26 (13 female), 1.7 ± 0.1 m, 74.6 ± 14.9 kg, 34 ± 10 years). Discrete measures of sagittal plane gait kinematics and kinetics were compared between subject groups and adjusted for age and body mass index (BMI) using analysis of covariance (ANCOVA). Serum TNFα concentrations were compared between groups using bootstrap t-test. RESULTS: The Pre-OA group had less extended knees (P = 0.021) and decreased maximum external knee extension moment (P = 0.0062) in terminal stance during gait, as well as increased resting serum TNFα concentration (P = 0.040) as compared to Control subjects. There were no group differences in heel strike flexion angle (P = 0.14), in maximum knee flexion moment (P = 0.91), nor in first peak knee adduction moment (KAM) (post-hoc analysis, P = 0.39). CONCLUSIONS: The finding that asymptomatic subjects with cartilage loss had gait and inflammatory characteristics similar to those previously reported in symptomatic OA patients supports the idea that there are specific mechanical and biological factors that precede the onset of knee pain in the pathogenesis of OA.