Biomedical Engineering Reference
In-Depth Information
between (1) systemic and local joint inflammation, and (2) the interaction of
inflammatory and biomechanical signaling pathways. In this chapter, we review
how changes in biomechanical stimulation associated with obesity and aging may
increase OA risk by modifying cartilage susceptibility to inflammation and oxi-
dative stress-mediated catabolic pathways.
1 Introduction
Osteoarthritis (OA) is the most prevalent form of arthritis and can affect any
synovial joint in the body [ 1 ]. The joints most commonly affected are the hands,
hips, knees, and spine. The disease is characterized by failed and often aberrant
repair of damaged joint tissue. A central feature of OA is damage to the articular
cartilage on load-bearing surfaces. The damage usually begins in focal areas and
expands over time. OA involves additional joint tissue pathologies to varying
degrees, including abnormal bone remodeling along the joint margins and in the
subchondral region, meniscal tears, mild synovitis, and changes in ligament,
periarticular muscle, and peripheral nerve function [ 2 ]. OA may be localized to
one joint or occur in a more generalized fashion throughout the body. Because
multiple factors can initiate the development of OA, differences in the location,
number of joints affected, and age of onset are usually attributed to different
causes. Aging is the primary risk factor for OA; most people older than 70 show
some signs of disease in at least one joint. However, many risk factors have been
identified that promote the development of OA at younger ages. For example, joint
malformations and genetic polymorphisms affecting the integrity of joint con-
nective tissues accelerate the development of OA by altering the mechanical stress
environment and impairing the structural properties of the joint [ 3 ]. Environmental
exposures and traumatic joint injury also increase OA risk through various path-
ways involving mechanical, inflammatory, and metabolic stress triggers that
up-regulate joint tissue catabolic pathways [ 4 ].
One of the most clinically significant and preventable risk factors for devel-
oping OA is obesity [ 5 , 6 ]. Obesity increases OA risk in both knee and hand joints,
although the greatest impact is on knee OA where risk is increased 1.3-6.0 fold
[ 7 - 9 ]. The effect of obesity on knee OA is highest in women, especially after about
50 years of age (Fig. 1 ). The cause of this sex-specific bias is not well understood,
although hormonal, reproductive, genetic, and metabolic factors are thought to be
involved. One important consequence of the increased incidence of knee OA with
obesity is that the onset of disease occurs at a substantially younger age in obese
individuals [ 10 ]. From a population level perspective, the equivalent prevalence of
knee OA in a population of non-obese 70-year-old men and women is reach-
ed C 20 years earlier in obese individuals (Fig. 1 ).
The accelerated onset of OA that occurs with obesity has major health and
financial consequences for individuals and society [ 11 , 12 ]. Furthermore, OA
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