Where your DNA places you among other people, and the studies behind it.
Not tailored to your result, and not medical advice
Maintain a Healthy Weight: Excess body weight is the strongest modifiable risk factor for knee OA, partly because each extra kilogram adds several kilograms of force across the knee with every step. Losing 5-10% of body weight is associated with meaningful reductions in pain and disability. In the IDEA randomized trial, combining diet and exercise produced greater improvements in knee pain and function than either approach alone. JAMA
Strengthen Muscles Around Joints: Strong muscles, particularly the quadriceps for the knee, help support and stabilize joints. A Cochrane review of land-based exercise for knee OA found that resistance and neuromuscular training produce moderate reductions in pain and improvements in physical function, with benefits in the range reported for common analgesics and few side effects. Cochrane Database of Systematic Reviews
Stay Physically Active: Structured exercise is a core, first-line treatment for hip and knee OA in the OARSI guidelines, alongside education and weight management. Low-impact activities such as walking, cycling, and swimming improve pain, stiffness, and function. Contrary to the fear of 'wearing out' joints, current evidence does not show that appropriate exercise accelerates OA in otherwise healthy joints. Osteoarthritis and Cartilage (OARSI)
Prevent Joint Injuries: Joint injuries, especially in sports, substantially raise lifetime OA risk: a complete ACL tear with a meniscal tear is associated with roughly a 34% lifetime risk of symptomatic knee OA versus about 14% in uninjured people. Proper technique, appropriate footwear, and neuromuscular warm-up programs can lower injury rates. If an injury does occur, completing rehabilitation before returning to activity is important. Arthritis Care & Research
Address Metabolic Health: Beyond the load of extra body weight, metabolic factors appear to play a role in OA: diabetes, abnormal blood lipids, and low-grade systemic inflammation are associated with cartilage damage, and metabolic syndrome often co-occurs with OA. Managing metabolic health through diet, exercise, and appropriate medical care is a sensible part of an overall joint-health strategy. Current Obesity Reports
How much of this is genetic?
Genetics explains 45% of why people differ in this trait. The rest is environment, daily habits and chance.
Heritability estimate: Boer et al. 2021, Cell
Background and further reading
Osteoarthritis (OA) is the most common joint disease worldwide. The Global Burden of Disease study estimated that 595 million people - about 7.6% of the global population - had OA in 2020, and it ranks among the leading causes of disability in older adults.[2] The disease involves breakdown of articular cartilage along with synovial inflammation, subchondral bone remodeling, and osteophyte (bone spur) formation. It produces pain, stiffness, and reduced range of motion, mainly in the knees, hips, hands, and spine, and is the leading reason for joint replacement surgery. The old 'wear and tear' label is misleading: OA is now understood as an active disease of the whole joint, driven by inflammation and failed tissue repair rather than simple mechanical erosion. There is no cure, but clinical guidelines recommend exercise, weight management, and education as core, first-line care.[3]
Genetic Basis: Twin and family studies put OA heritability at roughly 40-65% for hand and hip OA and somewhat lower, around 37-40%, for knee OA - and the genetic factors differ from joint to joint. A genome-wide study of 826,690 people identified 100 risk variants across 11 OA phenotypes, implicating cartilage and skeletal development, joint shape, and bone-forming pathways.[1] One of the strongest and best-characterized signals sits near GDF5 (growth differentiation factor 5), a gene involved in limb and joint formation; risk variants lower GDF5 activity in ways thought to affect cartilage. Many OA-associated genes are most active during fetal joint development, which suggests that part of a person's susceptibility is laid down early in life rather than arising only from later joint use.
Modifiable Risk Factors: Excess body weight is the strongest modifiable risk factor for knee OA; in the Framingham study, roughly each 5 kg of weight gain was linked to about a 35% higher risk. Joint injury is another major driver - a complete ACL tear combined with meniscal damage raises lifetime risk of symptomatic knee OA to about 34%, compared with roughly 14% in uninjured people.[5] Weak muscles, especially the quadriceps, offer the joint less support, while heavy or repetitive occupational and recreational loading shapes which joints are affected; targeted strengthening and exercise can reduce pain and improve function.[4][6] Metabolic conditions such as diabetes and abnormal blood lipids are also associated with OA beyond their effect on body weight, though how much they independently cause the disease is still being worked out.
The published research behind your score, and the variants it draws on.
11 published scores from 5 studies
The osteoarthritis score combines 11 polygenic scores drawn from 5 published studies.
These traits are influenced by some of the same genes and variants as this one
Back Pain: Chronic or recurrent pain in the lower back, the leading cause of disability worldwide.
Body Mass Index: A measure of body weight relative to height, used as a proxy for overall adiposity.
Height: Adult standing height - one of the most heritable and polygenic human traits.
Content updated August 2026.
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