Osteoarthritis (OA) is a chronic, heterogeneous disease affecting the entire joint, including the articular cartilage, subchondral bone, synovium, ligaments, menisci, joint capsule, and surrounding muscles. It should therefore not be regarded simply as passive “wear and tear.” Mechanical loading, metabolic dysfunction, low-grade inflammation, ageing, previous joint injury, genetic factors, and impaired neuromuscular function all contribute to its development and progression. Obesity is one of the most important modifiable risk factors, particularly for knee osteoarthritis. (Nature)
In a large population-based cohort study involving approximately 1.76 million adults aged 40 years or older, the incidence rates of clinically diagnosed knee, hip, and hand osteoarthritis among individuals of normal weight were 3.7, 1.7, and 2.6 cases per 1,000 person-years, respectively. Among individuals with class II obesity, generally defined as a body mass index of 35.0–39.9 kg/m², the corresponding incidence rates were 19.5, 3.8, and 4.0 cases per 1,000 person-years. Compared with individuals of normal weight, those with class II obesity had an approximately 4.7-fold higher risk of knee osteoarthritis. The association was less pronounced but still present for hip and hand osteoarthritis. These figures originate from one large regional cohort and should not be interpreted as universally applicable incidence rates for all populations. (PubMed)
The relationship between body mass index and osteoarthritis risk is dose dependent: the risk generally increases as BMI rises. The association is strongest for the knee, where both excess mechanical loading and obesity-related metabolic processes are relevant. The association between obesity and osteoarthritis of non-weight-bearing joints, particularly the hands, indicates that mechanical loading alone cannot explain the relationship. (ePrints Soton)
Excess body mass increases the forces transmitted through weight-bearing joints during standing, walking, climbing stairs, and other daily activities. The increase in dynamic joint loading during movement may be substantially greater than the additional static body weight alone. Repeated excessive loading can disturb the homeostasis of cartilage, subchondral bone, menisci, and other joint structures, thereby contributing to structural damage and pain.
The knee is particularly vulnerable because it is exposed to high repetitive forces and depends on normal alignment, muscle control, and ligament stability. Although obesity is also associated with hip osteoarthritis, the relationship is generally weaker than that observed for the knee. (PubMed)
Obesity may alter walking speed, step width, joint alignment, balance, and the distribution of forces across the lower extremities. Changes in gait can increase loading in specific compartments of the knee or hip. Varus or valgus malalignment, reduced mobility, and compensatory movement patterns may further concentrate mechanical stress on already vulnerable joint structures.
Pain can subsequently reduce physical activity, leading to further loss of mobility and physical fitness. This may create a cycle in which pain causes inactivity, inactivity promotes weight gain and muscle weakness, and these changes further increase symptoms and functional limitations.
Adipose tissue is a metabolically active endocrine organ rather than merely an energy store. In obesity, adipose tissue releases adipokines, cytokines, and other inflammatory mediators that may affect cartilage, synovium, subchondral bone, and pain-processing pathways.
Obesity-associated low-grade systemic inflammation may promote synovial inflammation, cartilage-matrix degradation, and abnormal bone remodelling. Adipokines such as leptin, resistin, visfatin, and adiponectin have been investigated as possible mediators, although their individual roles are complex and have not yet been fully established. (PMC)
Insulin resistance, dyslipidaemia, hyperglycaemia, and other components of metabolic syndrome may adversely affect joint tissues independently of mechanical loading. Oxidative stress, altered lipid metabolism, vascular dysfunction, and chronic inflammation may impair cartilage homeostasis and tissue repair.
These metabolic mechanisms may help explain why obesity is also associated with osteoarthritis in the hands and why individuals with similar levels of mechanical loading do not necessarily have the same risk of developing the disease. (Nature)
Obesity does not inevitably cause a loss of muscle mass. However, it may coexist with reduced muscle quality, fatty infiltration of skeletal muscle, impaired physical performance, or sarcopenia. This combination is often described as sarcopenic obesity.
Weakness of the quadriceps, hip abductors, and other stabilising muscles may reduce joint stability and shock absorption. It can also impair balance and movement control, thereby increasing abnormal loading of the knee and hip. A longitudinal cohort study found that low muscle strength and sarcopenic obesity were associated with an increased risk of symptomatic knee osteoarthritis, although further interventional research is required to establish whether improving muscle strength directly prevents the disease. (PLOS)
Osteoarthritis may cause activity-related joint pain, short-lasting stiffness after rest, restricted movement, reduced walking capacity, sleep disturbance, and limitations in work and everyday activities. The severity of symptoms does not always correspond closely to the degree of structural change visible on radiographs.
Not every person with obesity develops osteoarthritis, and many people with osteoarthritis do not have obesity. Other important risk factors include increasing age, previous joint injury, occupational or sporting overload, joint malalignment, muscle weakness, genetic predisposition, and female sex, particularly after menopause. Obesity should therefore be understood as one influential and potentially modifiable component of a multifactorial disease.
Education, therapeutic exercise, and weight management are the core non-pharmacological treatments for hip and knee osteoarthritis. Exercise programmes should be tailored to the individual’s symptoms, physical capacity, comorbidities, preferences, and treatment goals. Appropriate options include muscle-strengthening exercises, aerobic activity, flexibility training, balance exercises, and neuromuscular training. Supervised exercise may be particularly helpful when a person is initially inactive, has marked functional limitations, or is uncertain about exercising safely. (EULAR)
Patients should be informed that discomfort may temporarily increase when an exercise programme is started. Regular and appropriately progressed exercise is nevertheless safe and can reduce pain and improve physical function and quality of life over time. Exercise should not be withheld solely because radiographs demonstrate advanced osteoarthritis. (NCBI)
For individuals with overweight or obesity, weight reduction can decrease mechanical joint loading and improve pain, mobility, physical function, and general health. Any sustained weight loss may be beneficial, but current guidance indicates that losing approximately 10% of initial body weight is likely to produce greater clinical benefits than losing 5%. Weight-loss goals should nevertheless be realistic, individualised, and developed jointly with the patient. (NICE)
Weight management should ideally combine an appropriate nutritional intervention with regular aerobic and resistance exercise. The aim is not only to reduce body weight but also to preserve or improve muscle mass, strength, balance, and physical function. Weight loss without adequate protein intake and muscle-strengthening activity may be accompanied by a loss of lean tissue, particularly in older adults.
Pain management may be required to enable physical activity and participation in exercise. When medication is necessary, it should complement rather than replace non-pharmacological treatment. Current NICE guidance recommends topical non-steroidal anti-inflammatory drugs for knee osteoarthritis. Oral non-steroidal anti-inflammatory drugs may be considered when topical treatment is ineffective or unsuitable, but gastrointestinal, renal, hepatic, and cardiovascular risks must be assessed. Medication should be used at the lowest effective dose for the shortest appropriate period. (NICE)
Joint replacement may be considered when pain, loss of function, stiffness, or progressive deformity substantially impairs quality of life and appropriate non-surgical treatment has been ineffective or is unsuitable. Overweight or obesity alone should not be used as a reason to exclude a patient from referral for joint-replacement assessment. However, the potential surgical risks and benefits should be evaluated individually. (NICE)