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Senesence and Osteoporosis

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According to some recent studies, both the sexes undergo an accelerated bone loss at later stages. The exact mechanisms are still not much understood, but several factors related to age-dependent changes have been implicated. Some of these are:

In addition to old age, gender difference plays a major role in the determination of this disease. Osteoporosis in females is directly related to the hormonal changes in the body. Menopause occurs at an age of about 50-52 years, following which, levels of circulating estradiol and estriol significantly decrease by about 25% and 75% respectively.Among several theories, the most accepted one is the one describing direct action of the estradiol on avian osteoclasts. Bone resorption is the unique function of osteoclasts. In the avian model, there is a direct action of estradiol in decreasing the development and function of osteoclasts and increasing the activity of osteoblasts. Estrogen deficiency enhances the activity of osteoclasts, leading to the perforation of bone trabeculae, thus increasing the fracture risk. The life span of functional osteoclasts may also increase following the estrogen deficiency.

Another clear evidence is that women undergoing early menopause, or oophorectomy have an accelerated bone loss and show a higher incidence of bone fractures. Women experiencing early menopause usually have prolonged periods of oligomenorrhea, a trait that has a strong genetic predisposition. Thus these patients are exposed to repeated periods of increased bone loss and low bone mass.

Growth hormone is important in the regulation of longitudinal bone growth. Its role in the regulation of bone metabolism in humans is not completely understood yet. However, its importance in both bone formation and bone resorption is proven by many in vivo and in vitro studies. There are two ways by which the growth hormone increases bone formation:

1. Via a direct interaction with the growth hormone receptors on osteoblasts, and&nbsp.

2. By induction of endocrine and autocrine IGF-1.