see also:

• arthritis - clinical patterns

• a “degenerative” disorder of joints arising from the biochemical breakdown of articular (hyaline) cartilage
• 80-90% of individuals older than 65 years have evidence of radiographic primary osteoarthritis

• historically divided into:
  • primary OA:
    • usually refers to OA involving DIP joints of fingers resulting in Heberden's nodes
  • secondary OA:
    • refers to all other OA, particularly the weight bearing joints

• age
  • prevalence increases dramatically among persons older than 50 years
• obesity
  • particularly, hip, knee and ankle OA
• type II diabetes
• genetics
  • genes in the BMP (bone morphogenetic protein) and WNT (wingless-type) signaling cascades have been implicated, in particular, GDF5 (growth and differentiation factor 5) and FRZB (frizzled related protein)
  • MCF2L gene is associated with large joint OA
• dietary fats
  • long term use of animal fat, butter, and palm oil can weaken the cartilage in rats but lauric acid may be protective ¹⁾
• women are more prone to:
  • OA of the DIP joints of the fingers
  • OA of the knees (1.7x risk)
  • erosive OA (12x risk)
• ethnic differences
  • knee OA is very common in China
• reduced levels of sex hormones
• muscle weakness
  • reduces protection of joint, and increases joint movement range to risk damage to the joint
• repetitive use
  • microtrauma may also cause damage, especially in individuals whose occupation or lifestyle involves frequent squatting, stair-climbing, or kneeling
• malalignment such as varus deformity of knees
  • weight bearing forces passing through higher risk parts of the joint
• secondary to other bone conditions such as gout, intra-articular fractures, infections

• symptom relief:
  • simple analgesics such as oral or topical non-steroidal anti-inflammatory drugs (NSAIDs) (with cover of proton pump inhibitors (PPIs) if at risk as this reduces dyspepsia relative risk by 67% and absolute risk by 9%)
  • topical capsaicin reduces pain by 50% and 0.025% is better tolerated than 0.075%
  • i/articular steroid injections may have a role BUT:
    • should not be given more often than every 4 months as risk of cartilage and joint damage
    • risk of joint sepsis
  • NB. paracetamol (acetaminophen) is no longer 1st line Rx as for chronic pain of OA, it does not appear to be better than placebo, and recent studies suggest chronic use may have significant adverse effects such as GIT, RR 1.4x of cardiovascular events (although this is similar to NSAIDs) ²⁾
  • whilst effective in short term, long term use of opiates and opioids is problematic resulting in fractures (RR 4.5), cardiovascular events (RR 1.8), all cause mortality (RR 1.9), constipation, and dependence and tolerance
  • duloxetine appears to be a useful adjunct to NSAIDs, but does cause nausea, constipation, fatigue, dry mouth and anorexia.
• weight reduction if obese
• knee braces if knee OA
• maintain muscle strength
• joint replacement is a last resort as these generally only last 10-15yrs in younger patients, particularly total knee replacements (TKR)
• daily glucosamine and chondroitin supplements for 2 years in 45-75 yr olds appears to slow joint space narrowing but no evidence of reduced pain vs placebo³⁾