Postmenopausal osteoporosis

Postmenopausal osteoporosis (POP) is a common aging-related disease mainly affecting postmenopausal women. Estrogen deficiency causes reduced bone mass and changes in bone microarchitecture, increasing bone fragility and fracture risk, as well as fracture-related pain, skeletal deformity, complications and even death, seriously affecting the health and quality of life of the elderly, even shortening life, and increasing the financial and labor burden on the country and family. Postmenopausal osteoporosis is an important health concern. In 1993 the WHO defined osteoporosis as a systemic disease of reduced bone mass accompanied by altered bone microarchitecture, leading to increased bone fragility and thus increased fracture risk. Its pathological feature is proportional reduction of bone mineral content and bone matrix, thinning of the cortex, reduction and thinning of trabeculae, and trabecular fracture in postmenopausal osteoporosis.

Common Symptoms

Elevated serum calcitonin; Lai Xin; calf cramps; kyphosis; osteoporosis; bone pain; amenorrhea

Causes

Estrogen enhances liver 25-hydroxylase and renal 1-alpha-hydroxylase activity, raises 1,25-dihydroxy vitamin D levels, promotes intestinal calcium absorption, deposits calcium and phosphate salts in bone, and promotes bone matrix synthesis. Estrogen also antagonizes parathyroid hormone and, together with it, maintains blood calcium-phosphate balance; parathyroid hormone stimulates bone resorption, so when estrogen decreases its antagonism weakens, accelerating bone dissolution and gradually causing osteoporosis; calcitonin inhibits osteoclast activity, and estrogen promotes calcitonin secretion. After Komm showed estrogen receptors in osteoblasts in 1988, Ernst found that exogenous estrogen promotes IGF-I production by rat osteoblasts; enhanced IGF-I overexpresses estrogen receptors, and estrogen also promotes TGF-beta in osteoblasts, showing these growth factors promote bone formation. Experiments show that with estrogen deficiency, IL-1 from bone marrow monocytes and IL-6 from stromal cells both increase; Pacifici et al. found TNF-alpha and GM-CSF produced by cultured peripheral blood monocytes; ovariectomized patients have elevated TNF-alpha and GM-CSF, which normalize with estrogen treatment; these cytokines promote bone resorption, and estrogen inhibits it by suppressing them. Since komm found estrogen receptors on osteoblasts in 1988 and Penlser found them on osteoclasts in 1990, the direct action of estrogen on bone cells is clearer: estrogen binds estrogen receptors on osteoblasts and osteoclasts, directly inhibiting osteoclast lysosomal enzyme activity and their ability to create resorption pits. In 1996 Shevde showed in castrated rats that estrogen directly inhibits the recruitment and differentiation of osteoclast precursors (bone marrow hematopoietic stem cells) through receptor binding, inhibiting osteoclast activity, and morphologically proved this is achieved by affecting the cell cycle and inducing apoptosis; in 1997 kameda reached similar conclusions with highly purified mature mammalian osteoclasts; Ernst confirmed estrogen enhances proliferation of rat primary calvarial cells and expression of intracellular collagen and IGF-I mRNA. I. Etiology. Divided into primary and secondary osteoporosis by cause. Type I osteoporosis, also called postmenopausal osteoporosis, is mainly due to estrogen deficiency, occurs in women aged 50~70, shows rapid bone loss more marked in cancellous bone, with fractures mostly in cancellous-bone-rich vertebral bodies, proximal femur and distal radius. Type II osteoporosis, also called senile osteoporosis, has more male patients than type I, though the male-to-female ratio is still 1:2; onset is mostly over 70, shows slow bone loss at roughly equal rates in cancellous and compact bone, and, besides the same sites as type I, has increased hip fractures. In 1983 Riggs compared type I and type II osteoporosis. Secondary osteoporosis is caused by other conditions: chronic disease such as chronic renal failure, gastrectomy, intestinal bypass, calcium malabsorption syndrome and multiple myeloma; endocrine disease such as hyperprolactinemia, hyperthyroidism, excess adrenal cortical hormone, diabetes and hyperparathyroidism; iatrogenic factors such as long-term antiepileptics, aluminum-containing antacids, excess thyroxine or long-term glucocorticoids, and GnRH agonists. Postmenopausal osteoporosis is multifactorial, related to heredity, lifestyle and nutrition. Those at high risk: white and Asian women, family history of osteoporosis, or women with special genes affecting bone mass; insufficient calcium intake; lack of physical activity; heavy smoking and drinking; early menopause or bilateral oophorectomy before menopause. Whether osteoporosis occurs depends on peak bone mass and rate of bone loss: those with high peak and/or slow loss are less likely, while low peak and/or fast loss are more likely. 1. Peak bone mass. Peak bone mass is the highest bone mass in a lifetime, generally reached at 25~35 years; many factors affect it, heredity being most important, with some influence from nutrition and habits. (1) Genetic factors determine 70%~80% of peak bone mass; for example blacks have higher BMD than whites and Asians with fewer osteoporotic fractures; osteoporosis runs in families; MZ twins have smaller BMD differences than DZ twins; males have higher peak bone mass than females; in some countries polymorphisms of the vitamin D receptor, estrogen receptor or collagen genes relate to BMD, all proving genetic influence on peak bone mass. (2) Nutrition: high calcium intake in adolescence gives higher peak bone mass, up to 6% effect on mature BMC; WHO recommends 1000mg elemental calcium daily in adolescence. (3) Lifestyle: exercise increases BMD; those exercising daily above the mean by 1 SD have bone mass 7%~10% higher than those below the mean by 1 SD, but excessive exercise causing hypogonadism and amenorrhea lowers bone mass; heavy smoking and alcohol before peak formation lower it. (4) Those with primary hypogonadism and delayed puberty have lower peak. 2. Bone loss rate. Female bone loss relates to age and menopause. (1) Age-related loss: spinal bone loss generally starts at 40~50 at 0.8%~1.2% per year, while limb bone loss starts about 10 years later, at 50~60, at 0.3%~0.6% per year, both linear; mechanism unclear, possibly related to reduced bone formation; the result is thinner trabeculae without perforation. (2) Menopause-related loss: regardless of age, once menopause occurs estrogen drops sharply and bone loss increases logarithmically, trabeculae becoming thinner then fractured (perforated); after bilateral oophorectomy, all ovarian sex hormones vanish and loss is faster, with spinal loss twice that of limbs, up to 4%~5% per year, slowing only after 5~10 years; limb loss is slower and lasts longer. Animal and clinical studies confirm that estrogen supplementation in ovariectomized animals or postmenopausal women lowers bone turnover and prevents loss, proving estrogen deficiency is the main cause. II. Pathogenesis. Normal bone is renewed by remodeling: osteoclasts excavate resorption pits, then osteoblasts migrate in and synthesize and secrete collagen and bone-forming polypeptides; after calcium deposition bone matrix forms, the pit is repaired, completing a remodeling unit of about 3~4 months. Bone turnover is the rate of old-bone resorption and new-bone formation; postmenopausal estrogen decline increases turnover and loss, giving high-turnover osteoporosis. Estrogen affects osteoporosis mainly through the following pathways.

Treatment

Medication, supportive treatment, rehabilitation therapy

Prevention

After menopause, bone density progressively decreases with age, sharply raising osteoporosis and fracture risk; the main goal is to control risk factors throughout a woman's life. 1. Avoid high-risk factors from youth to old age, including heavy smoking, alcoholism, a sedentary lifestyle, anorexia and certain drugs (corticosteroids, heparin, some antiepileptics); emphasize outdoor activity, sunlight, nutrition, moderate weight-bearing exercise and fall prevention. 2. Ensure calcium supplementation in youth; combined with regular moderate exercise it helps women achieve ideal peak bone mass. 3. Prevent estrogen loss after menopause; hormone replacement therapy in the first 5~10 years after menopause is effective in prevention, but with its indications and contraindications it should be used under medical supervision. 4. Supplement calcium and vitamin D in old age; this partly prevents bone loss and osteoporotic fractures, and combined with antiresorptive drugs (estrogen, calcitonin, bisphosphonates) is markedly therapeutic. Although some risk factors such as early menopause and family history are unchangeable, these interventions benefit high-risk groups and reduce osteoporosis and fracture incidence. 5. Prevent falls in the elderly. It is reported that over 1/3 of people over 65 fall each year, half repeatedly; about 1 in 10 falls causes serious injury such as pelvic or other fracture, subdural hematoma, severe soft-tissue or head injury. Osteoporotic fractures in the elderly are hard to treat; prolonged bed rest slows circulation, impairs drainage of pulmonary and tracheal secretions, and predisposes to cardiovascular disease and lung infection, raising mortality. Preventing falls and fractures improves quality of life. Fall-related factors include arthritis, depression, orthostasis, cognitive/vision/balance/gait/muscle deficits, and polypharmacy; drugs linked to increased fall risk include SSRIs, tricyclic antidepressants, tranquilizers, librium, anticonvulsants and some antiarrhythmics. Doctors should take a fall history, identify risk factors and give targeted advice; common measures are removing loose rugs, using safer shoes (enclosing the foot, low-heeled, thin-soled and well-fitted), non-slip bath mats, night lighting and stair rails; these can reduce fall risk by about 20%. Professional balance and gait training, muscle strengthening, and gradual reduction of psychotropic drugs also reduce falls; those with eye disease, syncope or arrhythmia should see ophthalmology or cardiology to find and treat causes.

Recommended Department

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Warm reminder: The above information is provided for health education reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek care at a regular hospital in time.