Risk factors for osteoporotic fracture can be split between nonmodifiable and (potentially) modifiable. In addition, osteoporosis is a recognized<unk> of specific diseases and disorders. Medication use is theoretically modifiable, although in many cases, the use of medication that increases osteoporosis risk may be unavoidable. Caffeine is not a risk factor for osteoporosis. Nonmodifiable Bone density peaks at about 30 years of age. Women lose bone mass more rapidly than men. * The most important risk factors for osteoporosis are advanced age (in both men and women) and female sex; estrogen<unk>  following menopause or surgical removal of the ovaries is correlated with a rapid reduction in bone mineral density, while in men, a decrease in testosterone levels has a comparable (but less pronounced) effect. * Ethnicity: While osteoporosis occurs in people from all ethnic groups, European or Asian ancestry predisposes for osteoporosis. * Heredity: Those with a family history of fracture or osteoporosis are at an increased risk; the heritability of the fracture, as well as low bone mineral density, is relatively high, ranging from 25 to 80%. At least 30 genes are associated with the development of osteoporosis. * Those who have already had a fracture are at least twice as likely to have another fracture compared to someone of the same age and sex. * Build: A small stature is also a nonmodifiable risk factor associated with the development of osteoporosis. Potentially modifiable * Excessive alcohol: Although small amounts of alcohol might be beneficial (bone density increases with increasing alcohol intake, although the link has not been conclusively shown as causal), chronic heavy drinking (alcohol intake greater than three units/day) probably increases fracture risk despite any beneficial effects on bone density. * Vitamin D<unk> : Low circulating Vitamin D is common among the elderly worldwide. Mild vitamin D insufficiency is associated with increased parathyroid<unk>  (PTH) production. PTH increases bone resorption, leading to bone loss. A positive association exists between serum 1,25-dihydroxycholecalciferol levels and bone mineral density, while PTH is negatively associated with bone mineral density. * Tobacco smoking: Many studies have associated smoking with decreased bone health, but the mechanisms are unclear. Tobacco smoking has been proposed to inhibit the activity of osteoblasts, and is an independent risk factor for osteoporosis. Smoking also results in increased breakdown of exogenous estrogen, lower body weight and earlier menopause, all of which contribute to lower bone mineral density. * Malnutrition: Nutrition has an important and complex role in maintenance of good bone. Identified risk factors include low dietary calcium and/or phosphorus, magnesium, zinc, boron, iron, fluoride, copper, vitamins A, K, E and C (and D where skin exposure to sunlight provides an inadequate supply). Excess sodium is a risk factor. High blood acidity may be diet-related, and is a known antagonist of bone. Some have identified low protein intake as associated with lower peak bone mass during adolescence and lower bone mineral density in elderly populations. Conversely, some have identified low protein intake as a positive factor, protein is among the causes of dietary acidity. Imbalance of omega-6 to omega-3 polyunsaturated fats is yet another identified risk factor. * A diet high in protein may be optimal for bone health, as higher protein diets tend to increase absorption of calcium from the diet and are associated with higher bone density. No interventional trials have been performed on dietary protein in the prevention and treatment of osteoporosis A meta-analysis of published medical studies shows that higher protein diet helps slightly with lower spine density but does not show significant improvement with other bones. * Underweight/inactive: Bone remodeling occurs in response to physical stress, so physical inactivity can lead to significant bone loss. Weight bearing exercise can increase peak bone mass achieved in adolescence, and a highly significant correlation between bone strength and muscle strength has been determined. The incidence of osteoporosis is lower in overweight people. * Endurance training: In female endurance athletes, large volumes of training can lead to decreased bone density and an increased risk of osteoporosis. This effect might be caused by intense training suppressing menstruation, producing amenorrhea, and it is part of the female athlete triad. However, for male athletes, the situation is less clear, and although some studies have reported low bone density in elite male endurance athletes, others have instead seen increased leg bone density. * Heavy metals: A strong association between cadmium and lead with bone disease has been established. Low-level exposure to cadmium is associated with an increased loss of bone mineral density readily in both genders, leading to pain and increased risk of fractures, especially in the elderly and in females. Higher cadmium exposure results in osteomalacia (softening of the bone). * Soft drinks: Some studies indicate soft drinks (many of which contain phosphoric acid) may increase risk of osteoporosis, at least in women. Others suggest soft drinks may displace calcium-containing drinks from the diet rather than directly causing osteoporosis. * Proton pump inhibitors (such as lansoprazole, esomeprazole, and omeprazole), which decrease the production of stomach acid, are a risk factor for bone fractures if taken for two or more years, due to decreased absorption of calcium in the stomach. Medical disorders The body regulates calcium homeostasis with two pathways; one is signaled to turn on when blood calcium levels drop below normal and one is the pathway that is signaled to turn on when blood calcium levels are elevated. Many diseases and disorders have been associated with osteoporosis. For some, the underlying mechanism influencing the bone metabolism is straightforward, whereas for others the causes are multiple or unknown. * In general, immobilization causes bone loss (following the 'use it or lose it' rule). For example, localized osteoporosis can occur after prolonged immobilization of a fractured limb in a cast. This is also more common in active people with a high bone turn-over (for example, athletes). Other examples include bone loss during space flight or in people who are bedridden or use wheelchairs for various reasons. * Hypogonadal states can cause secondary osteoporosis. These include Turner syndrome, Klinefelter syndrome, Kallmann syndrome, anorexia nervosa, andropause, hypothalamic amenorrhea or hyperprolactinemia. In females, the effect of hypogonadism is mediated by estrogen<unk> . It can appear as early menopause (1 year). Bilateral oophorectomy (surgical removal of the ovaries) and premature ovarian failure cause deficient estrogen production. In males, testosterone<unk>  is the cause (for example, andropause or after surgical removal of the testes). * Endocrine disorders that can induce bone loss include Cushing's syndrome, hyperparathyroidism, hyperthyroidism, hypothyroidism, diabetes mellitus type 1 and 2, acromegaly, and adrenal insufficiency. * Malnutrition, parenteral nutrition and malabsorption can lead to osteoporosis. Nutritional and gastrointestinal disorders that can predispose to osteoporosis include undiagnosed and untreated coeliac disease (both symptomatic and asymptomatic people), Crohn's disease, ulcerative colitis, cystic fibrosis, surgery (after gastrectomy, intestinal bypass surgery or bowel resection) and severe liver disease (especially primary biliary cirrhosis). People with lactose intolerance or milk allergy may develop osteoporosis due to restrictions of calcium-containing foods. Individuals with bulimia can also develop osteoporosis. Those with an otherwise adequate calcium intake can develop osteoporosis due to the inability to absorb calcium and/or vitamin D. Other micronutrients such as vitamin K or vitamin B12<unk>  may also contribute. * People with rheumatologic disorders such as rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus and polyarticular juvenile idiopathic arthritis are at increased risk of osteoporosis, either as part of their disease or because of other risk factors (notably corticosteroid therapy). Systemic diseases such as amyloidosis and sarcoidosis can also lead to osteoporosis. * Chronic kidney disease can lead to renal osteodystrophy. * Hematologic disorders linked to osteoporosis are multiple myeloma and other monoclonal gammopathies, lymphoma, leukemia, mastocytosis, hemophilia, sickle-cell disease and thalassemia. * Several inherited or genetic disorders have been linked to osteoporosis. These include osteogenesis imperfecta, Multicentric carpotarsal osteolysis syndrome, Multicentric Osteolysis, Nodulosis, and Arthropathy, Marfan syndrome, hemochromatosis, hypophosphatasia (for which it is often misdiagnosed), glycogen storage diseases, homocystinuria, Ehlers–Danlos syndrome, porphyria, Menkes' syndrome, epidermolysis bullosa and Gaucher's disease. * People with scoliosis of unknown cause also have a higher risk of osteoporosis. Bone loss can be a feature of complex regional pain syndrome. It is also more frequent in people with Parkinson's disease and chronic obstructive pulmonary disease. * People with Parkinson's disease have a higher risk of broken bones. This is related to poor balance and poor bone density. In Parkinson's disease there may be a link between the loss of dopaminergic neurons and altered calcium metabolism (and iron metabolism) causing a stiffening of the skeleton and kyphosis. Medication Certain medications have been associated with an increase in osteoporosis risk; only glucocorticosteroids and anticonvulsants are classically associated, but evidence is emerging with regard to other drugs. * Steroid-induced osteoporosis (SIOP) arises due to use of glucocorticoids – analogous to Cushing's syndrome and involving mainly the axial skeleton. The synthetic glucocorticoid prescription drug prednisone is a main candidate after prolonged intake. Some professional guidelines recommend prophylaxis in patients who take the equivalent of more than 30 mg
complications of Growth hormone deficiency
complications of Kallmann syndrome
medical cause of Precocious puberty
onset of Kallmann syndrome
complications of Klinefelter syndrome
complications of Turner syndrome
medical cause of Hyperdontia
complications of XYY syndrome