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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.
Re: Osteoarthritis and obesity: more than a mechanical link
Press Release: Scientists Find Obesity Alone Does Not Cause Arthritis in Animals
The link between obesity and osteoarthritis may be more than just the wear and tear on the skeleton caused by added weight.
A Duke University study has found that the absence of the appetite hormone leptin can determine whether obese mice experience arthritis, no matter how heavy they are.
"We were completely surprised to find that mice that became extremely obese had no arthritis if their bodies didn't have leptin," said Farshid Guilak, PhD, director of orthopaedic research in the Duke Department of Surgery.
"Although there was some earlier evidence that leptin might be involved in the arthritis disease process, we didn't think that there would be no arthritis at all."
In fact, the joints from the obese mice in the study appearing in the journal Arthritis & Rheumatism looked better than those of the normal control mice, Guilak said. "However, in another study, we found that mice that gained half as much weight on a high-fat diet but processed leptin normally showed significant knee osteoarthritis."
Leptin influences many of the factors involved in osteoarthritis -- body weight, inflammation, sex hormone levels, and bone metabolism, said lead author Tim Griffin, PhD, who was at Duke Orthopaedic Department and now is an assistant member of the Free Radical Biology and Aging Program at the Oklahoma Medical Research Foundation.
"That also makes leptin challenging to study, however, because it's difficult to isolate which pathway is being altered to prevent the development of osteoarthritis."
Leptin is a well-known regulator of appetite, but this is the first time scientists have reported a role for leptin as a metabolic link between obesity and altered cartilage metabolism in joints.
The role of obesity as a risk factor for arthritis is well characterized, but it was thought to be merely a case of overloading joints with extra weight.
"It hadn't been studied beyond that," Guilak said. "We knew from other studies that obese people got arthritis in their hands, too, which don't bear weight. This indicated that something besides just body-weight level affected their joints."
The Duke team set out to learn whether the increased body fat of obesity causes an inflammatory response in joints -- an imbalance of the immune system signaling proteins called cytokines and other chemicals in osteoarthritis.
They studied mice that were leptin-deficient or deficient in leptin receptors -- mice that didn't have any effective leptin in their bodies. Both types of mice overate and gained weight.
Then they compared the study mice with normal mice to document knee osteoarthritis. The measurements included pro- and anti-inflammatory cytokines present in arthritis, and several tests to assess bone changes in the knees of the mice.
The knee bones of the leptin-free, obese mice did change, but without forming osteoarthritis. The levels of inflammatory cytokines, which correlate with arthritis, were largely unchanged in these mice. The results suggested that leptin may have a dual role in the development of osteoarthritis by regulating both the skeletal and immune systems.
What does this mean for people? "Obesity is still the number one preventable risk factor of osteoarthritis, but now it seems body fat by itself is not what is causing it," Guilak said.
"If you are obese, there are benefits to losing weight in terms of arthritis. For example, if you are obese and lose just 10 pounds, pain decreases significantly. Pain modulation is another clue it might be a chemical or systemic metabolic effect, rather than just a mechanical effect of less weight on the joints."
As with many studies that yield unanticipated findings, "we have a lot of additional questions and experiments that need to be done to further understand how leptin mediates the development of osteoarthritis," Griffin said.
"With obesity and osteoarthritis, there are good similarities between humans and mice," Guilak said. "If we can find a pathway that links a high-fat diet with arthritis, then we can try to identify and block the inflammatory mediators that are linked with the dietary fat."
The study was sponsored by the National Institute for Arthritis, Musculoskeletal and Skin Diseases and the Arthritis Foundation. Lead author Timothy M. Griffin, formerly of the Duke Department of Surgery, is now with the Oklahoma Medical Research Foundation. Co-authors Janet L. Huebner and Virginia B. Kraus are with the Duke Department of Medicine.
Re: Osteoarthritis and obesity: more than a mechanical link
Individuals with primary osteoarthritis have different phenotypes depending on the affected joint - a case control study from southern sweden including 514 participants.
Karlsson MK, Karlsson C, Magnusson H, Cöster M, von Schewelov T, Nilsson JÅ, Brudin L, Rosengren BE Open Orthop J. 2014 Dec 29;8:450-6.
The aim of this study was to evaluate whether primary osteoarthritis (OA), independent of affected joint, is associated with a phenotype that is different from the phenotype in a normative cohort. Material and.
We included 274 patients with primary OA, 30 women and 32 men (mean age 66 years, range 42-84) with primary hip OA, 38 women and 74 men (mean age 61 years; range 34-85) with primary knee OA, 42 women and 19 men (men age 64 years, range 42-87) with primary ankle or foot OA and 20 women and 19 men (mean age 66 years, range 47-88) with primary hand or finger OA. Of all patients included with OA, 23% had hip OA, 41% knee OA, 22% ankle or foot OA and 14% hand or finger OA. Serving as references were 122 women and 118 men of the same ages who were population-based, included as a control cohort. We measured total body BMD (g/cm2) and proportion of fat and lean mass (%) with dual energy X-ray absorptiometry. Height, weight and BMI (kg/m2) were also assessed. We then calculated Z-scores (number of standard deviations difference from the mean value of the control cohort) in the OA patients and compared these between the groups.
Individuals with hand OA and controls had similar phenotype. Individuals with lower extremity OA, irrespective of the affected joint, had similar weight, BMI and BMD, but higher than in individuals with hand OA and controls (all p<0.05). Individuals with lower extremity OA had higher fat and lower lean mass than individuals with hand OA and controls (all p<0.001).
Individuals with primary OA in the lower extremity have a phenotype with higher BMD, higher BMI, proportionally higher fat content and lower lean body mass content. The different skeletal phenotypes in our patients with OA in the lower extremity and patients with hand OA indicate that separate pathophysiologic pathways may be responsible for primary OA in different joints.