Table 1.
Risk factor | Comment |
---|---|
Advanced age | 0.1% prevalence in ages 25–34 [2, 3] 80% prevalence in ages > 55 [2, 3] |
Female sex [4, 5] | Relative risk of 2.6 [5] Higher rates of rapid structural damage [6] |
Obesity/metabolic syndrome | One of the strongest modifiable risk factors [5, 6] Repetitive overloading of cartilage ➔ chondrocyte oxidant-dependent mitochondrial dysfunction ➔ disruption of chondrocyte anabolic responses to mechanical stimuli ➔ cartilage destabilization [7] |
Higher bone mineral density | Especially related to hip OA in older women [8–10] Conflicting evidence in regard to the relationship between estrogen replacement therapy and OA |
Occupation | |
Sports activities [11] | Recreational parachuting (ankle) Ballet dancing (talar joints) Soccer (ankle, talar joints) Football (foot/ankle) |
Trauma | Unilateral amputation via increased contralateral weight bearing stress [12, 13] |
Physical exercise [14–16] | Neuroanatomically normal joints at increased risk with sedentary activity level and repetitive, high-impact activities Neuroanatomically abnormal joints at increased risk with repetitive, low-impact activities |
Proprioceptive deficits (neuroarthropathy) | Diabetic neuropathic arthropathy via diabetes mellitus ➔ peripheral neuropathy ➔ decreased proprioception ➔ ligamentous laxity ➔ increased joint ROM ➔ instability ➔ minor trauma ➔ altered architecture ➔ asymmetric weight bearing ➔ focal trauma |
Genetics | |
Acromegaly | |
Calcium crystal deposition disease | |
Deformity |