Senile osteoporosis

Anomalously high Ca concentrations in hair samples (up to 8285 (xgg-1) which correlate with high P concentrations (up to 4720 jxg g-1) from a group of women from Rio de Janeiro were detected by ICP-MS measurements.87 These abnormal hair compositions were related to endocrinological pathologies affecting calcium/bone metabolism. Very low Ca concentrations were observed in older women and were related to senile osteoporosis.87... 

Anabolic effects Anabolic steroids can be used to treat senile osteoporosis and severe burns, to speed recovery from surgery or from chronic debilitating diseases, and to counteract the catabolic effects of externally administered adrenal cortical hormones. 

Osteoporosis is a disease characterized by a reduction in bone mass and a deterioration in bone microarchitecture, which leads to enhanced fragility. This is a very common disorder, and it is becoming more common with the increase of life expectancy thus, it is a major public health issue. Osteoporosis is caused by an increase in bone loss and at the same time a decrease in bone formation. With increasing age, bone formation is slowed down, especially in women after the menopause, although it is also seen sometimes in men, usually aged over 70 years (senile osteoporosis). 

Type 1 osteoporosis, also known as postmenopausal osteoporosis, involves loss of trabecular bone in the vertebrae, leading to crush fracture with minimal trauma. It is essentially a condition affecting postmenopausal women, with a femaleimale ratio of 10 1. Type 11 osteoporosis (senile osteoporosis) is osteoporotic hip fracture. It shows only a 2 1 excess of females over males and a geometric increase in incidence with increasing age. The two types of osteoporosis are not exclusive, and type 1 patients are more susceptible to hip fracture, whereas many hip fracture patients have asymptomatic vertebral crush fractures. 

The combined effects of vitamin D, calcium, and anabolic steroids in the treatment of senile osteoporosis have been investigated (71). Neither methandienone nor vitamin D3 alone but only the two together seemed to increase coronary morbidity and mortality, and possibly in women only. Simultaneous use of these two drugs should be avoided. 

Osteoporosis is of two forms- primary i.e. idiopathic and secondary. Primary osteoporosis is classified into type I and type II osteoporosis. Type I is referred to post menopausal osteoporosis which is the main type affecting women, characterized by rapid bone loss and affects women after the menopause, mainly in trabecular bone and is associated with vertebrae and distal radio fractures whereas type II also termed as senile osteoporosis occurs due to chronic deficiency of calcium, increase in parathormone activity and decrease in bone formation and is associated with aging. On the other hand secondary type results from inflammatory processes, endocrine changes, multiple myeloma, sedentariness and the use of drugs such as heparin, corticoid and alcohol [3]. Prevention is the main treatment of osteoporosis, for which bone mass peak and the prevention of postmenopausal reabsorption are critical elements. The common treatment of osteoporosis includes calcium consumption as calcium salts, vitamin D supplements, and hormone reposition [4], the use of calcitonin to modulate serum levels of calcium and phosphorous [5], the use of bisphosphonate, mainly alendronates [6], use of ipriflavone and sodium fluoride [7], besides physical activity to strengthen muscles, stimulate osteoblasts formation and prevent reabsorption. 

Type II, involutional or senile osteoporosis occurs later in life than type I, has a closer ratio between sexes, results in both trabecular and cortical bone loss and is related to increased PTH secretion (26). Under these circumstances, osteoporosis may essentially be a side-effect of IHPT or 2HPT (15.26,46-48). Type II osteoporosis is managed, therefore, by correcting the underlying cause of the HPT. 

Kruger, M.C., Coetzer, H., de Winter, R., Gericke, G., and van Papendorp, D.H. (1998) Calcium, Gamma-Linolenic Acid and Eicosapentaenoic Acid Supplementation in Senile Osteoporosis, Agmg 10, 385-394. 

A primary determinant of fracture risk resulting from either postmenopausal or senile osteoporosis is the mass of bone accumulated during growth and early adulthood. Cortical bone continues to accumulate after closure of the epiphyses until about the middle of the fourth decade, i.e., for about half of the life span. Skeletal homeostasis is maintained for only about one decade thereafter before aging bone loss ensues. Differences in susceptibility to osteoporotic bone fractures clearly are related to genetic differences in maximal adult bone mass, as manifested in the greater susceptibility of whites compared to blacks and of families with small bones. 

Whether true facsimiles of human postmenopausal and senile osteoporosis occur in other primates is unclear. Thinning of cortical bone between the ages of 10 and 20 yr has been observed in a cross-sectional sample of pigtailed macaques (Bowden et ai, 1979). However, thinning apparently occurs in premenopausal females at a rate similar to that seen in postmenopausal women, and the influence of the menopause on bone loss in this species is obscure. 

The process of deposition of calcium in bone is not fully understood, but alkaline phosphatase, vitamin D, vitamin C, and probably other factors are of great importance. Removal of mineral from bone and maintenance of normal serum calcium concentration is dependent largely on the activity of the parathyroid hormone. Albright considers that the primary effect of the parathyroid hormone is an increase in phosphorus excretion (Chapter 21). This is followed by a decrease in serum phosphorus and resorption of phosphorus and calcium from bone. Other hormones also influence utilization of calcium and phosphorus (Chapter 21). In hyperthyroidism, excretion of calcium and phosphorus is increased and osteoporosis may develop. The steroid hormones, e.g., estradiol and testosterone, decrease calcium and phosphorus excretion and may therefore be useful in the therapy of postmenopausal and senile osteoporosis. 

Vinther-Paulsen N (1953) Calcium and phosphorus intake in senile osteoporosis. Geriatrics 9 76-79. 

Schwartzman MS, Franck WA. Vitamin D toxicity complicating the treatment of senile, postmenopausal, and glucocorticoid-induced osteoporosis. Four case reports and a critical commentary on the use of vitamin D in these disorders. Am J Med 1987 82(2) 224-30. 

Osteoporosis is a skeletal disease that is characterized by loss of bone mass as well as microarchitectural deterioration of the bone tissue. This disease is associated with increased bone fragility and susceptibility to fracture. It is a condition that is characterized not by inadequate bone formation but, rather, by a deficiency in the production of well-mineralized bone mass. Whereas no medical cause typically is evident in primary osteoporosis (3), secondary osteoporosis classically stems from medical illness or medication use. There are two types of primary adult osteoporosis, type I, or postmenopausal, and type II, or senile (Table 35.1). In type I osteoporosis, there is an accelerated rate of bone loss via enhanced resorption at the onset of menopause. In this form of the disease, the loss of trabecular bone is threefold greater than the loss of cortical bone. This disproportionate loss of bone mass is the primary cause of the vertebral crush fractures and the wrist and ankle fractures experienced by postmenopausal women. In type II osteoporosis, which is associated with aging, the degree of bone loss is similar in both trabecular and cortical bone (5) and is caused by decreased bone formation by the osteoblasts. 

Silberberg, M., and Silberberg, R., 1962, Osteoarthritis and osteoporosis in senile mice, Gerontologia 6 91. 

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