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Very interesting editorial from Annals of the Rheumatic Diseases, which can be downloaded for free:
Obesity and osteoarthritis: more complex than predicted!
...These patterns of joint involvement suggest that joint damage may be caused by systemic factors such as adipose factors, so called adipokines, which may provide a metabolic link between obesity and osteoarthritis...So, recent data strengthen the hypothesis that osteoarthritis is a systemic disorder in which dysregulation of lipid homeostasis can be one of the pathophysiological mechanisms leading to osteoarthritis...
Very interesting article worth another read later when I will have more time to take it in.
PS. One small aside. This came up in My Yahoo? Blocked by yahoo as forbidden serve and URL? Never happened before? Got here alright when I came back here though!
PPS. Has anyone ever done any work on Mechanical loading of joints caused by access weight I wonder. Engineering, steel joints friction heat increase with load? Could this happen in organic joints I wonder?
Obesity is one of the most significant, and potentially most preventable, risk factors for the development of osteoarthritis, and numerous studies have shown a strong association between body mass index and osteoarthritis of the hip, knee, foot and hand. However, the mechanism(s) by which obesity contributes to the onset and progression of osteoarthritis are not fully understood. The strong association between body mass index, altered limb alignment, and osteoarthritis of the knee - and the protective effects of weight loss - support the classic hypothesis that the effects of obesity on the joint are due to increased biomechanical loading and associated alterations in gait. However, obesity is now considered to be a low-grade systemic inflammatory disease, and recent studies suggest that metabolic factors associated with obesity alter systemic levels of pro-inflammatory cytokines that are also associated with osteoarthritis. Thus, the ultimate influence of obesity on osteoarthritis may involve a complex interaction of genetic, metabolic, and biomechanical factors. In this respect, mouse models of obesity can provide excellent systems in which to examine causal relationships among these factors. In recent years, there have been surprisingly few reports examining the effects of obesity on osteoarthritis using mouse models. In this paper, we review studies on mice and other animal models that provide both direct and indirect evidence on the role of obesity and altered diet in the development of osteoarthritis. We also examine the use of different body mass indices for characterizing "obesity" in mice by comparing these indices to typical adiposity levels observed in obese humans. Taken together, evidence from studies using mice suggest that a complex interaction of environmental and genetic factors associated with obesity contribute to the incidence and severity of osteoarthritis. The ability to control these factors, together with the development of methods to conduct more intricate measures of local biomechanical factors, make mouse models an excellent system to study obesity and osteoarthritis.
Obesity has been identified as a risk factor for osteoarthritis. For the weight-bearing joints, the combination of increased load and changed joint biomechanics could be regarded as underlying principle for this relation. This systematic review of the literature focused on the differences between obese and normal-weight subjects in biomechanics of the hip, knee and ankle joint during every day movements to summarize differences in joint load due to both higher body weight and differences in movement patterns. A systematic search, up to November 2010, was performed in the Pubmed and Embase databases. This review showed that obese individuals adjust their movement strategy of every day movements. At self-selected speed, obese individuals walked slower, with shorter and wider steps, had longer stance duration and had a greater toe-out angle compared with normal-weight individuals. Obese sit-to-stand movement was characterized by less hip flexion and greater foot displacement. Obese individuals showed altered biomechanics during every day movements. These altered biomechanics could be related to the initiation of osteoarthritis by a change in the load-bearing regions of the articular cartilage in the weight-bearing joints.
Re: Osteoarthritis and obesity: more than a mechanical link
Press Release: Weight loss may prevent, treat osteoarthritis in obese patients
Obesity may trigger biomechanical changes, pathways that contribute to osteoarthritis
ROSEMONT, Ill.—Weight loss may prevent and significantly alleviate the symptoms of osteoarthritis, a progressive disease of the joints known as "wear and tear" arthritis, according to a literature review appearing in the March 2013 issue of the Journal of the American Academy of Orthopaedic Surgeons (JAAOS).
According to the article, obesity actually may trigger the biomechanical and inflammatory changes that cause osteoarthritis, and the pain and loss of mobility associated with the condition.
"There's a clear link between obesity and osteoarthritis, and the link is both from biomechanical factors as well as systemic factors. The systemic component appears to be significant," said Ryan C. Koonce, MD, an orthopaedic surgeon at Skagit Regional Clinics in Mount Vernon, Wash., and one of the authors of the literature review.
Approximately one half of osteoarthritis cases of the knee could be avoided in the U.S. if obesity was removed as a risk factor, according to the article. Other highlights include:
Greater weight and load bearing across a particular joint leads to increased wear.
White adipose tissue (WAT), a powerful endocrine organ that can trigger inflammation, is found in abundance in obese adults.
Obesity is considered to be an underlying cause of hypertension, insulin resistance and other metabolic syndrome conditions.
Obesity is a strong independent risk factor for pain, especially in soft-tissue structures such as tendons.
Weight loss can diminish pain, and restore function and quality of life in osteoarthritis patients, and possibly avert approximately 111,206 total knee replacements each year.
"It's important that doctors are aware of the different ways that obesity causes arthritis not only for treatment but for prevention of the condition," said Jonathan T. Bravman, MD, assistant professor in the Department of Orthopaedics at the University of Colorado, an orthopaedic surgeon, and a co-author of the study. "We are underutilizing weight loss as a primary treatment option for arthritis and joint pain."
A link has been established between obesity and osteoarthritis (OA), but the precise relationship has yet to be defined. OA has a multifactorial etiology, and obesity is consistently identified as an independent and modifiable risk factor. The biomechanical relationship is intuitive: increased loads on articular cartilage cause subsequent wear and cartilage breakdown. Less intuitive, and possibly more important, are the systemic effects of obesity on OA. Promising investigations into relationships between lipid metabolism and OA have been rarely reported in the orthopaedic literature. These reports argue that, in obese patients, weight loss may not only help prevent OA but also may be an effective treatment strategy. Orthopaedic surgeons should be aware of the biomechanical and systemic implications of obesity with respect to OA so that patients may be counseled accordingly.