Primary osteoporosis related to aging has been classified as type II, or senile, osteoporosis. The type I disorder is related to the onset of menopause, and is thus termed postmenopausal osteoporosis. Other causes of osteoporosis can be secondary, such as that caused by long-term corticosteroid use or endocrinopathy.
Peak bone mass is achieved between the ages of 16 to 25 years in most people. After this age, bone mass slowly, but continuously, decreases. The greater the amount of bone achieved during the peak period, the lower the chance that a person will develop osteoporosis later in life. Normal rates of bone loss are different in men and women. In men, bone mass is lost at a rate of 0.3% per year, while for women this rate is 0.5%. In contrast, bone loss after menopause, in particular the first 5 years after its onset, can be as high as 5-6% per year . Because women live longer than men, it is believed that increased longevity places women at higher risk of senile osteoporosis.
Besides the difference in age at onset, types I and II osteoporosis have somewhat different effects on the kinds of bone lost. Type I appears to affect mostly trabecular bone, while type II affects both cortical and trabecular bone . While both types substantially increase the risk of fracture in cancellous bone, such as osteoporotic vertebral compression, distal radius, or intertrochanteric hip fractures, patients with type II disease may be at greater risk of fractures through cortical bone, such as the femoral neck, pelvis, proximal humerus, and proximal tibia.
The cellular mechanism of type II osteoporosis is mul-tifactorial. A major factor is probably progressive dietary calcium deficiency . As patients age, appetite can become suppressed, leading to lower intake of foods rich in calcium. Financial constraints, as endured by many elderly individuals with low fixed incomes, can be a disincentive to purchasing foods that support a well-balanced diet. This factor, by itself, has been known to contribute to states of malnutrition in elderly people. Moreover, the presence of osteoporotic vertebral compression fractures and the resultant alterations in the dimensions of the trunk can lead to early satiety in affected individuals . This would have a self-perpetuating effect on osteoporosis, as this can lead to further calcium deficiency and more profound loss in bone density.
Another contributing mechanism is progressive inactivity. Bone mass is positively affected by mechanical loads (i.e., exercise and activity). With age, most people become less active, which can potentiate progressive bone loss. While osteoporosis itself is painless, profound inactivity from the pain of an osteoporotic compression fracture can lead to a vicious cycle of further bone loss, more fractures, and more pain and inactivity.
While not the primary mechanism as in type I osteoporosis, decreases in estrogen levels have been demonstrated in both elderly men and women and this is thought to be an important cause of senile osteoporosis as well.
The cumulative effect of normal aging, dietary calcium deficiency, and lower activity is the upregulation of bone resorption and downregulation of bone formation. While it is commonly held that these effects are mediated by stimulation of osteoclasts and inhibition of osteoblasts, the exact mechanisms by which they lead to age-related bone loss is still not well understood.
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For centuries, ever since the legendary Ponce de Leon went searching for the elusive Fountain of Youth, people have been looking for ways to slow down the aging process. Medical science has made great strides in keeping people alive longer by preventing and curing disease, and helping people to live healthier lives. Average life expectancy keeps increasing, and most of us can look forward to the chance to live much longer lives than our ancestors.