Medical Disclaimer
The information on this page is for educational purposes only and is not intended to replace professional medical advice, diagnosis, or treatment.
Always seek the advice of your doctor or other qualified health professional with any questions you may have regarding a medical condition.
π¨Emergency? If you have severe symptoms, difficulty breathing, or think it's an emergency, call 000 immediately.
How Osteoarthritis Develops
Patient-friendly explanation of how osteoarthritis develops - from healthy cartilage to worn joints - including what happens inside the joint, why it causes pain, and what drives disease progression
πWhat is How Osteoarthritis Develops?
Patient-friendly explanation of how osteoarthritis develops - from healthy cartilage to worn joints - including what happens inside the joint, why it causes pain, and what drives disease progression
π¬What Causes It?
- MECHANICAL STRESS - excessive or abnormal loading damages cartilage cells (chondrocytes) and extracellular matrix
- CARTILAGE BREAKDOWN - death of chondrocytes leads to loss of proteoglycans and collagen, cartilage loses ability to withstand load
- INFLAMMATORY CASCADE - damaged cartilage releases inflammatory molecules (cytokines) that further accelerate breakdown
- SUBCHONDRAL BONE CHANGES - bone underneath cartilage thickens (sclerosis) and develops cysts, losing shock-absorption capacity
- SYNOVIAL INFLAMMATION - joint lining becomes inflamed (synovitis), producing more inflammatory molecules and causing pain and swelling
- OSTEOPHYTE FORMATION - bone spurs grow at joint margins attempting to stabilize joint but causing pain and stiffness
β οΈRisk Factors
You may be at higher risk if:
- AGE - strongest risk factor: 10% prevalence under age 45, 50% over age 65, 80% over age 80 (cartilage repair capacity declines with age)
- OBESITY - doubles knee OA risk, triples hip OA risk (every 5kg weight loss reduces knee OA risk by 50%)
- PREVIOUS JOINT INJURY - fracture involving joint surface increases OA risk 7-fold, ACL tear increases knee OA risk 5-fold
- GENETICS - 40-65% of OA risk is hereditary (specific genes affecting cartilage metabolism, collagen structure)
- GENDER - women more prone to knee and hand OA (especially post-menopause - hormonal factors), men more prone to hip OA
- OCCUPATION - jobs requiring repetitive kneeling/squatting double knee OA risk, heavy lifting increases hip/spine OA risk
- JOINT MALALIGNMENT - bow-legged (varus) or knock-kneed (valgus) deformity concentrates load on one side of joint
- MUSCLE WEAKNESS - quadriceps weakness increases knee OA risk 3-fold (muscles normally absorb shock and protect cartilage)
- INFLAMMATORY ARTHRITIS - previous rheumatoid arthritis or septic arthritis damages cartilage, predisposes to secondary OA
π‘οΈPrevention
- βMaintain healthy weight throughout life - obesity in 20s-40s increases OA risk in 50s-70s
- βRegular low-impact exercise to maintain muscle strength and joint mobility (walking, cycling, swimming)
- βAvoid high-impact activities and sports injuries when possible - previous ACL tear increases knee OA risk 5-fold
- βPrompt treatment of joint injuries - anatomic reduction of fractures, ligament reconstruction if needed
- βCorrect joint malalignment early (bow-legged or knock-kneed) before arthritis develops
- βOccupational modification if job requires repetitive heavy lifting, kneeling, or squatting
- βGenetic counseling if strong family history (40-65% of OA risk is hereditary) - can't change genes but can modify risk factors