Biomedical Engineering Reference
In-Depth Information
particularly in adults [ 39 , 47 , 60 ], and the mechanisms that link obesity to walking
disability are unclear.
Osteoarthritis (OA) is a mechanically induced disorder in which the conse-
quences of abnormal joint mechanics provoke biological effects that are mediated
biochemically, for example, through cytokines and matrix-degrading enzymes [ 6 ].
In particular, excessive impulsive forces in the knee joint have been claimed to
serve as co-factors in the initiation and progression of knee OA [ 6 ]. The finding
that increased BMI contributes to a positive effect on the susceptibility to radio-
graphic and symptomatic knee and hip OA and progression of the disease is
considered to mainly be due to increased mechanical loading [ 3 , 20 , 21 ]. However,
based on previous studies, it is difficult to draw solid conclusions about whether
obese patients with knee OA load their lower extremity more forcefully during
walking compared to healthy controls [ 28 , 30 ].
There is no cure for OA or treatment proven to slow OA progression [ 2 ]. The
main treatment goal for patients with OA is therefore considered to be the
reduction of joint pain and physical disability [ 2 , 18 ]. Weight loss has been shown
to reduce pain and improve hip and knee joint function in patients with OA [ 2 , 18 ].
Decreases in joint loading could favorably alter the mechanical and biochemical
profiles of obese adults [ 47 , 52 ]. However, few studies to date have evaluated the
effects of weight loss on joint loading in the obese [ 5 , 19 , 34 , 53 ] or assessed the
effects of sustained weight loss on the progression of OA [ 17 , 35 ]. Furthermore,
OA symptoms related to biomechanical factors remain to be demonstrated [ 1 ].
Better insight into how obesity and weight loss affect locomotion would open
new opportunities for the prevention and treatment of OA. The aims of this chapter
are as follows. First, we review the current literature pertaining to the effects of
obesity on spatio-temporal, kinematic, and kinetic gait measurements. We also
briefly present gait terminology and modern methods of gait analysis. Second, we
investigate the influence of BMI on the measured impulsive loading parameters
using data from the Kuopio Knee OA Study [ 29 ]. Third, we review the literature
regarding the effect of weight loss on gait.
2 Normal Gait Cycle
2.1 Gait Phases
The gait cycle is determined as the time period between two consecutive heel
contacts of the same foot [ 28 , 43 , 61 ]. This cycle is divided into stance (typically
60 % of the gait cycle duration) and swing (40 % of duration) phases (Fig. 1 ). The
stance phase can be further divided into a single and two double support phases.
The duration of the normal gait cycle is approximately one second. Walking speed
and gait pathologies affect these time periods [ 54 ].
Search WWH ::




Custom Search