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Senile osteoporosis
Senile osteoporosis, formerly known as osteoporosis type II, has been recently recognized as a geriatric syndrome with a particular pathophysiology.
It has been pointed out that senile osteoporosis is the product of a skeleton in an advanced stage of life and also due to a deficiency caused by calcium, but physicians are also coming to the conclusion that multiple mechanisms in the development stages of the disease interact together and the product is an osteoporotic bone, regardless of age.〔(An overview on Osteoarthritis ) MedicineNet. Retrieved on 2010-03-05〕
==Cause==
Most of the etiologic considerations regarding senile osteoporosis are not very clear for physicians yet. But based on the current evidence attached to clinical experimentation, it has been determined that the pathogenesis of the disease is clearly related to a deficiency of zinc. Such deficiency is known to lead to an increment of endogenous heparin, which is most likely caused by mast cell degranulation, and an increase in the bone resorption (calcium discharge in the bones) reaction of prostaglandin E2, which constrain the formation of more bone mass, making bones more fragile. These co-factors are shown to play an important role in the pathogenetic process attached to senile osteoporosis as they enhance the action of the parathyroid hormone.〔National Center for Biotechnology Information. ("Etiology of senile osteoporosis" ) 2010-03-05.〕
The intake of calcium in elder people is quite low, and this problem is worsened by a reduced capability to ingest it. This, attached to a decrease in the absorption of vitamin D concerning metabolism, are also factors that contributes to a diagnosis of osteoporosis type II.
抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』
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