Osteoporosis

Osteoporosis is a systemic bone disease characterized by reduced bone mass and destruction of bone microarchitecture, showing increased bone fragility and thus greatly increased fracture risk; fractures occur easily even after minor trauma or without trauma. It is a multifactorial chronic disease with usually no special clinical manifestations before fracture. It is more common in women than men, especially postmenopausal women and the elderly.

Common Symptoms

Reduced bone metabolism; thoracolumbar compression fracture; spinal bony changes; kyphosis; bone pain; female low back pain; widened incisor spacing; gastrocnemius spasmodic pain; long-bone and limb muscles; diffuse osteoporosis

Causes

Female osteoporosis is due to estrogen deficiency, and male osteoporosis to testosterone decline from hypogonadism. Osteoporosis is especially common in postmenopausal women, and premature ovarian failure advances it, suggesting estrogen reduction is an important factor; within 5 years after menopause there is a sudden phase of accelerated bone loss, commonly 2%~5% per year; about 20%~30% of early postmenopausal women lose bone >3%/year (fast losers), while 70%~80% lose <3%/year (normal losers). Thin women develop osteoporosis and fractures more easily than obese women, because androgen converts to estrogen in adipose tissue; compared with normal women of the same age, osteoporotic patients show no obvious difference in blood estrogen, so estrogen reduction is not the only factor. Osteoporosis is common in whites, especially Nordics, then Asians, and rare in blacks. Bone density (BMD) is an important diagnostic index, determined mainly by heredity and then environment; DZ twins show 4 times the BMD difference of MZ twins in youth and 19 times in adults. Recent studies link BMD to vitamin D receptor gene polymorphism; in 1994 Morrison et al. reported that the vitamin D receptor genotype predicts BMD differences, accounting for 75% of genetic influence; after adjusting for environmental factors, bb genotypes have about 15% higher BMD than BB, vertebral fracture onset about 10 years later, and hip fracture rate only 1/4 of BB; these show large racial and national differences pending further study; collagen and estrogen receptor genes have also been studied without firm conclusions. Calcium intake in adolescence is directly related to adult peak bone mass; calcium deficiency increases PTH secretion and bone resorption, so low-calcium diets predispose to osteoporosis; vitamin D deficiency impairs bone matrix mineralization and can cause osteomalacia; long-term protein deficiency impairs bone matrix protein synthesis and delays new bone formation, accelerating osteoporosis when combined with calcium deficiency; vitamin C is essential for bone matrix hydroxyproline synthesis, maintaining normal growth and alkaline phosphatase production, and its deficiency reduces matrix synthesis. Mechanical muscle forces affect bone: strong muscles and bones give high BMD. In the elderly, reduced activity weakens muscles, reduces mechanical stimulus and lowers bone mass; weakness and incoordination make falls more likely, and with reduced bone mass fractures occur. Long-term bed rest after stroke causes disuse bone loss and osteoporosis.

Treatment

Supportive treatment, rehabilitation therapy

Prevention

Osteoporosis greatly inconveniences patients and is slow to treat, while fractures can be life-threatening, so three-level prevention is emphasized. Primary prevention: start in children and adolescents; eat a reasonable diet rich in Ca and P such as fish, shrimp, dried small shrimps, kelp, milk (250ml contains 300mg Ca), dairy, bone soup, eggs, beans, coarse grains, sesame, sunflower seeds and leafy greens; avoid risk factors and maintain a scientific lifestyle: exercise, sun exposure, no smoking or drinking, little coffee, strong tea and carbonated drinks, little sugar and salt, not too much animal protein; late marriage, fewer children and limited lactation help preserve calcium; raising peak bone mass to the maximum is the best prevention of later osteoporosis; strengthen basic research and follow up genetically high-risk groups early. Secondary prevention: in middle age, especially after menopause, bone loss accelerates, so check BMD yearly and act early on fast losers; many in Europe and America start long-term estrogen replacement within 3 years of menopause plus long-term preventive calcium supplementation to safely prevent osteoporosis; Japan often uses active vitamin D (rocaltrol) and calcium; actively treat related diseases such as diabetes, rheumatoid arthritis, steatorrhea, chronic nephritis, hyperparathyroidism/hyperthyroidism, bone metastases, chronic hepatitis and cirrhosis. Tertiary prevention: for degenerative osteoporosis, actively use drugs that inhibit bone resorption (estrogen, CT, Ca) and promote bone formation (active vitamin D); strengthen fall, collision, tripping and jolting prevention; for middle-aged and elderly fracture patients, actively operate with rigid internal fixation, early mobilization, physical and psychological therapy, nutrition, calcium, analgesia, bone growth promotion, bone-loss containment and improved immunity and overall fitness.

Recommended Department

It is recommended to visit the orthopedic surgery department; before the visit you may first book an appointment and connect with experts through this platform.

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.