الفهرس 
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Abstract
Menopause is the term used when women permanently stop having menstrual periods. It can be diagnosed after one year with no periods following the final menstrual period (FMP). Menopause may occur naturally, or may occur due to chemotherapy, surgery, or radiation . Natural menopause occurs when the ovaries stop producing oestrogen, and finish releasing eggs that may be fertilized by sperm to result in pregnancy. The change in hormone levels means the uterus (womb) no longer prepares itself for pregnancy each month, which is why periods no longer occur. This decrease in function of the ovaries occurs gradually, and the timing is due to the genes a woman inherits from her parents. The process usually begins in the mid to late thirties, and the ovaries completely fail to work (signifying menopause) by the time she is in her mid to late forties or fifties. The average age at menopause is 51 years. The physical changes that occur before and during menopause may be bothersome, but they’re a normal part of the menopause transition. However, risk for more serious complications increases after reach menopause—during the postmenopause stage. The complications such as heart diseases, osteoporosis, weight gain and urinary problems are associated with menopause, though menopause isn’t often the sole cause. Normal aging also increases risk of developing these medical problems. Living bone is constantly being remodeled. The state of bones is always close to an equilibrium between bone formation and bone resorption. In childhood and during the teens, bone formation is slightly ahead. We reach peak bone mass in the twenties, and from then onwards, resorption has the upper hand. Skeletal growth velocity and growth plate activities are largely dependent on growth hormone, IGF-1 and thyroid hormone, along with the calcium-regulating hormones, parathyroid hormone and vitamin D. Altogether, the hormonal influence on optimal skeletal growth and peak bone mass is enormously important. As calcium (Ca2+) is one of the main components of our bones, large amounts are present in our body. At the same time, comparatively low extracellular concentrations of Ca2+ are fine-tuned to regulate important functions, not to speak of even far lower intracellular concentrations. This dichotomy is possible due to the low solubility product of Ca2+ and phosphate (PO43-): if one ion is added to a solution of the other, most of it precipitates as calcium phosphate. Parathyroid hormone (PTH) is named for the four parathyroid glands producing it. An increase in the concentration of free Ca2+ activates the calcium-sensing receptor (CaSR) located at the membrane of their chief cells. The cells react by decreasing PTH production. A second means to lower PTH secretion is a high concentration of 1,25 dihydroxyvitamin D. PTH is a small protein of 84 amino acids and has an extremely short half-life of about four minutes. In the kidney, the action of vitamin D parallels that of PTH by increasing reabsorption of Ca2+, although its effect is much weaker. Contrary to PTH, vitamin D also enhances reabsorption of phosphate: both ions are required to promote bone mineralization. Together, these effects of vitamin D raise Ca2+ and phosphate concentrations above their solubility product, inducing their precipitation in osteoid. Growth hormone (GH) is essential for longitudinal bone growth. It is a 191 amino acid protein GH secretion is stimulated by GH releasing hormone (GHRH), inhibited by somatostatin. GH is secreted in short bursts of pulses only during sleep or during exercise (it makes no sense to assay GH levels at daytime in a child at rest). GH has a few fast, direct effects that are almost directly opposed to the more important slow, indirect effects via insulin-like growth factors. The receptor-mediated fast effects are antipodal to insulin action and include lipolysis in fat cells, gluconeogenesis in liver and an inhibition of glucose uptake by muscles. Likewise, the importance of sex steroids for bone metabolism became obvious from clinical observations. Lack of these hormones in various forms of hypogonadism results in osteoporosis. Overproduction of androgens or estrogens during childhood initially accelerates growth (as normally seen around puberty) but results in early epiphyseal closure with reduced final height. Postmenopausal osteoporosis starts with a decrease in estrogen concentrations. Bone mineral density (BMD) loss has been attributed to relative estrogen deficiency in postmenopausal women ,a view reinforced by studies of bone loss after oophorectomy and minimization of bone loss with estrogen replacement .Prospective studies have described a 2–2.5% annual rate of bone loss during the first 5 yr after menopause. Osteoporosis is the most common bone disease in humans and affects both men and women, usually during or beyond the seventh decade of life. Osteopenia is a condition where bone mineral density is lower than normal. It is considered by many doctors to be a precursor to osteoporosis. However, not every person diagnosed with osteopenia will develop osteoporosis. More specifically, osteopenia is defined as a bone mineral density T-score between -1.0 and -2.5. In the past the diagnosis of osteoporosis required evidence of a fragility fracture, then the World Health Organization established operational definitions of osteoporosis and osteopenia in postmenopausal white women based on bone mineral density (BMD) to help researchers and clinicians classify degrees of bone loss. Osteoporosis is diagnosed on the basis of a low-impact or fragility fracture or low bone mineral density, which was best assessed by central dual-energy x-ray absorptiometry.