Whereas once knee osteoarthritis was considered a 'wear-and-tear' condition, it is now recognized that knee osteoarthritis exists in the highly metabolic and inflammatory environments of body fat.
Cytokines associated with adipose tissue, including leptin, adiponectin, and resistin, may influence osteoarthritis though direct joint degradation or control of local inflammatory processes. Further, pound-for-pound, not all obesity is equivalent for the development of knee osteoarthritis; development appears to be strongly related to the co-existence of disordered glucose and lipid metabolism. Additionally, obesity loads may be detected by mechanoreceptors on chondrocyte surfaces triggering intracellular signaling cascades of cytokines, growth factors, and metalloproteinases.
This review summarizes recent literature about obesity, knee osteoarthritis and joint pain. Consideration of adipocytokines, metabolic factors, and mechanical loading-metabolic factor interactions will help to broaden the thinking about targets for both prevention and intervention for knee osteoarthritis.
Before continuing with the posting, you can calculate you body mass index (BMI) here.
IntroductionOsteoarthritis is a highly prevalent joint disorder estimated to affect more than 37% of adults over the age of 60; it is a leading cause of pain and disability. Osteoarthritis is associated with considerable loss in productivity and health care expenditures, accounting for 97% of the total knee replacements and 83% of the total hip replacements in 2004. Using national data, the Healthcare Cost and Utilization Project showed that osteoarthritis accounted for US$ 10.5 billion in hospital charges in 2006, making it a more expensive condition than pneumonia, stroke, or complications from diabetes. Hospital admissions for arthritis more than doubled from 1993 to 2006.
The frequency of knee osteoarthritis continues to accelerate, likely because of the aging of the population and the increasing proliferation of the primary risk factor, obesity. There is an increasingly greater proportion of the total population, both in the United States and worldwide, over age 60, the age range typically associated with having osteoarthritis. Although the prevalence of obesity is rising in this elderly segment of the population, it is the escalating prevalence of obesity in those men and women aged 40–60 years, who are simultaneously at the leading edge of the baby boomer demographic expansion, that are the major contributors to the burgeoning osteoarthritis population.
Obesity has long been recognized as a risk factor for prevalent osteoarthritis, especially knee osteoarthritis although the obesity definition based on a BMI (body mass index) more than 30 kg/m2 was not widely adopted until the 1990s.
Data from a British study suggested that women with the highest BMI had six-fold increased odds of knee osteoarthritis (OAK) and nearly 18 times higher odds of bilateral OAK, compared with women with the lowest BMI. Similarly, a study of US African-American and Caucasian women identified higher risk of prevalent knee osteoarthritis with higher BMI levels. Researchers reported that for every standard deviation increase in BMI (3.8 kg/m2), there was a 40% increased risk for developing osteoarthritis of the knee. Studies show that increased weight precedes the presentation of osteoarthritis of the knee.
How does Obesity Increase the Likelihood of having Knee Osteoarthritis?Because of the magnitude of obesity as a risk factor for osteoarthritis, especially knee osteoarthritis, as well as the growing prevalence of obesity, including morbid obesity, there is new effort being developed to understand how obesity increases the likelihood of having knee osteoarthritis. These efforts have as their long-term goal the development of focused prevention and intervention efforts. However, not all obese persons develop knee osteoarthritis, nor are all individuals with knee osteoarthritis obese.
Osteoarthritis, Obesity, and AdipocytokinesRheumatoid arthritis has long been recognized as having a vigorous inflammatory component, and as a result, some treatments were directed at modulating the deleterious elements of that inflammatory response. In contrast, osteoarthritis was considered a 'wear-and-tear' condition with a minimal inflammatory response. However, this framework for considering osteoarthritis, especially knee osteoarthritis, is now shifting with the increasing pervasiveness of obesity and the recognition of the inflammatory reaction associated with obesity. Fat tissue, once considered a passive storage portal of energy, is now recognized as a highly metabolic endocrine organ with the capacity to secrete active agents including adipocytokines, such as leptin, resistin, and adiponectin. Over the past decade, interest in these adipocytokines has quickly become an area of intense study with respect to osteoarthritis based on evidence that they may play an important role in cartilage metabolism.
Leptin, adiponectin and resistin levels have been detected in the joint fluid and plasma of patients with osteoarthritis. Leptin, adiponectin, and resistin are thought to influence osteoarthritis through direct joint degradation or through control of local inflammatory processes.
Leptin is generally higher in obese individuals; the extremely high amounts of circulating leptin have led investigators to suggest a leptin resistance syndrome as a parallel concept to insulin resistance. BMI and body weight are consistently associated with leptin levels among those with osteoarthritis. Leptin and its receptor have been identified in human tissue that make both bone and cartilage.
Examination of cartilage, subchondral bone, and the bone spurs associated with arthritis show evidence of increased leptin levels. Increased leptin levels have been directly associated with the degree of cartilage degeneration.
Inflammation is an important hallmark of osteoarthritis, and the adipocytokines may be important in the creation of the inflammatory processes. Leptin and resistin levels may be associated with the promotion of inflammation but adiponectin appears to reduce production of pro-inflammatory cytokines.
Osteoarthritis, Obesity, and Metabolic FactorsIn addition to the adipocytokines, obesity may generate other systemic effects related to osteoarthritis, including abnormal glucose and fat metabolism. Metabolic changes resulting from insulin resistance and increased glucose load are closely related to proinflammatory cytokine production, characteristic of a chronic inflammatory state.
A recent report considered both obesity status and cardiac risk factors. Mid-aged women who were obese (defined as BMI ≥30 kg/m2) and had two or more cardiovascular risk factors had more than six times increased odds of having prevalent knee osteoarthritis as compared with nonobese women without cardiac risk factors.
Osteoarthritis, Obesity, and Mechanical LoadingObesity has the potential for a major impact metabolically in the presentation of osteoarthritis while concurrently contributing to a major mechanical load on the joint. Studies of joint loading have provided evidence that abnormal loads can lead to changes in the composition, structure, and mechanical properties of joint cartilage. These abnormal loads have been attributed to obesity, joint instability, or trauma.
Muscle forces are a major determinant of how loads are distributed across a joint surface. Decreasing the muscle forces (as a result of inactivity or age related weakness) acting about a joint or misaligned joints will ultimately change the mechanical forces on the knee. Failure by the quadriceps (the thigh muscle) to adequately absorb forces about the knee can cause greater dynamic loads being placed on the joint cartilage, resulting in progressive degeneration. As a result, quadriceps weakness has been shown to be an important risk factor for osteoarthritis in some studies.
This makes a case for physical therapy as a potential treatment for certain types of arthritis in certain patients.
Loss of muscle strength may reduce the shock-absorbing potential of the joint, thereby causing cartilage breakdown. Changes to the cartilage structure may initiate a local immune response, resulting in systemic inflammatory responses throughout the joint. Increased loading on the knee joint may be detected by mechanoreceptors on the surface of cartilage cells; this may trigger release of cytokines, growth factors, and other chemicals which break down cartilage.
The role of body composition, however, is not unique to the compartment representing skeletal muscle mass. Some researchers have suggested that loss of muscle is the primary event for osteoarthritis onset, but this then contributes to fat gain, which then reinforces further muscle loss. The process of fat gain and muscle loss may act simultaneously within and around the joint to not only initiate joint damage, but also allow further progression through the effects of insulin and inflammation.
This is an abridged version of an article modified for increased patient understanding from Current Opinion in Rheumatology.
In my experience, patients with arthritis have a hard time exercising in order to lose weight. Studies have shown that even after a knee replacement, when their knee pain has been relieved, they remain unable to lose the weight. This can lead to continued pain despite a technically well done knee replacement.