Saturday, 19 December 2015

Primary[edit]

A number of studies have shown that there is a greater prevalence of the disease among siblings and especially identical twins, indicating a hereditary basis.[14] Although a single factor is not generally sufficient to cause the disease, about half of the variation in susceptibility has been assigned to genetic factors.[15]
As early human ancestors evolved into bipeds, changes occurred in the pelvis, hip joint and spine which increased the risk of osteoarthritis.[16] Additionally genetic variations that increase the risk were likely not selected against because usually problems only occur after reproductive success.[17]
The development of OA is correlated with a history of previous joint injury and with obesity, especially with respect to knees.[18] Since the correlation with obesity has been observed not only for knees but also for non-weight bearing joints and the loss of body fat is more closely related to symptom relief than the loss of body weight, it has been suggested that there may be a metabolic link to body fat as opposed to just mechanical loading.[19]
Changes in sex hormone levels may play a role in the development of OA as it is more prevalent among post-menopausal women than among men of the same age.[20][21] A study of mice found natural female hormones to be protective while injections of the male hormone dihydrotestosterone reduced protection.[22]

Secondary[edit]

lateral
front
Secondary osteoarthritis (due to an old injury with fracture) of the ankle in a woman of 82 years old
This type of osteoarthritis is caused by other factors but the resulting pathology is the same as for primary osteoarthritis:

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