Osteoporosis

Introduction Osteoporosis is a group of bone diseases caused by a variety of causes. The bone tissue has normal calcification, a normal ratio of calcium salt to the matrix, and metabolic bone lesions characterized by a decrease in the amount of bone tissue per unit volume. In most osteoporosis, the reduction in bone tissue is mainly due to increased bone resorption. The incidence is slow, individual is faster, characterized by bone pain and easy fracture. The biochemical examination is basically normal. Pathological anatomy showed that the cortical bone was thin, the trabecular bone was sparsely atrophied, and the bone-like layer was not thick.

Cause

Etiology classification

(a) idiopathic (primary)

Juvenile, adult, menopausal, and senile.

(2) Secondary

Endocrine

Hypercortisolism, hyperthyroidism, primary hyperparathyroidism, acromegaly, hypogonadism, diabetes, etc.

2. Pregnancy and breastfeeding.

3. Nutritional

Protein deficiency, vitamin C, D deficiency, low calcium diet, alcoholism, etc.

4. Hereditary

Osteogenesis imperfects, chromosomal abnormalities.

5. Liver disease

6. Kidney disease

Chronic nephritis, hemodialysis.

7. Drugs

Corticosteroids, anti-epileptic drugs, anti-tumor drugs (such as methotrexate), heparin, etc.

8. Disuse

Systemic osteoporosis is seen in long-term bed rest, paraplegia, space flight, etc., localized after fracture. Sudecks muscle atrophy after muscle spasm) and so on.

9. Gastrointestine

Absorption, stomach removal.

10. Rheumatoid arthritis

11. Tumor

Multiple myeloma, metastatic cancer, monocytic leukemia. Mast-Cell disease, etc.

12. Other reasons

Smoking, osteopenia, transient or migratory osteoporosis.

mechanism

First, senile and postmenopausal osteoporosis

After men are 55 years old, women are seen after menopause. Senile osteoporosis may be associated with low levels of sex hormones, weakened synthetic metabolic stimulation of proteins, and decreased osteoblast function and decreased bone formation. Estrogen inhibits osteoclast activity, reduces bone resorption and promotes osteoblast activity and bone formation, and has anti-cortisol and thyroid hormone effects. After menopause, estrogen is reduced, so bone resorption accelerates and osteoporosis gradually occurs. Estrogen also stimulates la-hydroxylase to produce 1.25-(OH)2-D3. Lack of sex hormones after menopause, 1-a-hydroxylase is less sensitive to the stimulation of parathyroid hormone (PTH) hypophosphatemia, 1.25-(OH)2-D3 biosynthesis is low, and is also involved in osteoporosis. As we age, the osteoblasts gradually die, and the bone matrix changes in both quantity and quality. Therefore, senile osteoporosis is actually the performance of the body's aging process, especially the bone tissue is the most prominent.

Second, nutritional osteoporosis

Lack of protein, poor formation of bone matrix, vitamin C deficiency affects matrix formation, and impairs collagen tissue maturation; long-term calcium deficiency in diet (less than 400mg daily) can cause secondary hyperparathyroidism, promote Bone absorption can also cause disease.

Third, disuse osteoporosis

Disuse of various reasons, less movement, no weight, etc., weakened mechanical stimulation of bones, can cause muscle atrophy, reduced bone formation, enhanced bone resorption, and osteoporosis.

Fourth, youth idiopathic osteoporosis

The reason is unknown, more common in young people, it is also known as young osteoporosis.

5. Endocrine osteoporosis

(a) hypercortisolism

Because glucocorticoids inhibit osteoblast activity, affect the formation of bone matrix, inhibit intestinal calcium absorption, increase urinary calcium excretion, and inhibit protein synthesis, increase decomposition, leading to negative calcium and negative nitrogen balance, resulting in bone formation disorders, but Mainly increased bone absorption.

(two) hyperthyroidism

A large number of thyroid hormones have a direct effect on bones, which enhances bone resorption and bone formation at the same time, but the absorption of bone is more prominent, resulting in a decrease in bone mass. Hyperthyroidism in patients with hypermetabolism, insufficient protein matrix in the bones, calcium deposition barriers, is also the cause of bone density reduction. 1.25-(OH)2-D3 is a vitamin D active hormone that increases intestinal absorption of calcium and phosphorus, stimulates bone growth and bone mineralization. Due to the large amount of thyroid hormone affecting renal 1-a-hydroxylase activity, 1.25-(OH)2-D3 catabolism is interfered. When thyroid function is hyperthyroidism, the level of 1.25-(OH)2-D3 is decreased, and the absorption of calcium in the intestine is reduced, the excretion of fecal calcium is increased, the calcium absorption in the kidney is reduced, and the calcium excretion in the kidney is increased. Collagen tissue breakdown is enhanced, and urinary hydroxyproline excretion is increased, resulting in a negative calcium balance. Therefore, the decrease in bone mineral density in patients with hyperthyroidism may also be related to the decrease in 1.25-(OH)2-D3.

(3) Diabetes

Due to the relative or absolute deficiency of insulin, protein synthesis disorders, negative nitrogen balance in the body, poor formation of bone organic matrix, decreased bone amino acids, collagen tissue synthesis disorders, reduced intestinal calcium absorption, and reduced bone calcification. Diabetes patients with high urine glucose permeability diuretic, leading to increased urinary calcium, phosphorus and renal tubular calcium and phosphorus absorption barrier, leading to negative calcium balance in the body, causing secondary hyperparathyroidism, and then increased PITll secretion, bone Decalcification. When diabetes is poorly controlled, it is often accompanied by hepatic malnutrition and kidney disease, resulting in a decrease in active vitamin D, a decrease in a hydroxylase activity, and aggravation of bone decalcification.

(four) acromegaly

This disease often has adrenal enlargement, cortical hypertrophy, hyperthyroidism, and at the same time, hypogonadism is inhibited. Growth hormone, cortisol, thyroid hormone can increase urinary calcium excretion, reduce blood calcium, increase blood phosphorus, thereby stimulating PTH secretion and increasing bone resorption.

(5) Primary hyperparathyroidism osteoporosis

PTH affects various tissues of tissues: interstitial cells, osteocytes, pre-osteocytes, osteoclasts, pre-osteoblasts, osteoblasts, and bone cells. Acute experiments have shown that the ground first activates a large number of bone cells, exerts its osteolytic absorption, and promotes a small number of inactive pre-osteocytes to become active osteoclasts, accelerating osteolytic absorption, at this time from osteoclasts The transformation process of pre-osteoblasts and osteoblasts is inhibited by the decrease of inorganic phosphorus levels in the cytoplasm, and the osteoblasts are small and small, causing bone calcium outflow and serum calcium to rise. Chronic experiments have shown that in addition to promoting the bone resorption of bone cells and osteoclasts already existing, PTH also promotes the passage of stromal cells through primitive bone cells, and the pre-osteocytes become osteoclasts, thereby increasing the number of osteoclasts. The number of osteolytic absorption processes is further enhanced. The degree of bone change varies from disease to stage, and cystic changes can occur in some cases, but subperiosteal absorption of the cortical bone is characteristically altered.

(6) Hypogonadism as described above.

(7) Hereditary pathological tissue disease

1. Osteogenesis imperfecta is an autosomal dominant disease, because osteoblasts produce less bone matrix, just like osteoporosis.

2. Semi-deacetylated urine is mainly caused by the lack of proline synthase.

(8) Others

Rheumatoid arthritis with osteoporosis, accompanied by atrophy of connective tissue, including bone collagen tissue, there are serious disuse factors, and ship hormone therapy also promotes osteoporosis. Long-term heparin treatment affects collagen structure and can cause osteoporosis.

an examination

Related inspection

CT examination of bone and joint and soft tissue serum osteocalcin (BGP) urinary hydroxyproline calcitonin urinary hydroxyproline (HYP)

(1) Physical examination

The bone pain in the whole body is mainly caused by the spine, pelvic area and fracture. It is persistent pain and parallel with the degree of osteoporosis. Especially when the floor or posture changes. Long-term disease lower limb muscle atrophy, vertebral compression fracture, shortened body length; thoracic deformity, decreased lung capacity, can affect cardiopulmonary function.

(2) Laboratory inspection

Blood calcium, blood phosphorus, blood alkaline phosphatase (AKP) and urinary phosphorus are normal, plasma osteocalcin is elevated, urinary calcium can be high, and urinary hydroxyproline may be elevated. If accompanied by rickets, blood and urine biochemical indicators may change accordingly.

(three) X-ray examination

When the X-ray shows osteoporosis, the reduction of bone minerals is above 30%~50%. The main change is cortical phenanthrene, trabecular bone is reduced, thinned or sparsely atrophied, the bone-like layer is not thick, and the spine and pelvis are obvious, especially the chest and lumbar weight-bearing stages are particularly heavy. Early manifestations of reduced bone density, increased transparency, horizontal trabecular bone is arranged in a vertical grid. Lateral longitudinal trabecular bone was also absorbed, the ability to withstand pressure decreased, and the thoracic vertebrae were wedge-shaped deformed. Because the loose bone of the sponge is more decalcified than the dense bone, the vertebral body is compressed by the intervertebral disc to form a double-sided depression, and a vertebral compression fracture or a pathological fracture of other parts can also be seen. X lines are sometimes not easily distinguished from rickets, or both. In recent years, a variety of new technologies have been applied to the detection of osteoporosis, such as neutron activation analysis for total body calcium, single beam bone densitometry for forearm bone density, dual energy X-ray absorptiometry for spinal bone density, vertebral The body uses computerized tomography (CT) and radiation densitometry. Performing a bone biopsy when necessary is important for early diagnosis and follow-up of osteoporosis.

Differential diagnosis

diagnosis

(1) History and clinical features

Female patients should pay attention to pregnancy, breastfeeding and menstruation. Different causes may have their corresponding symptoms and signs. But the common points are: bone pain in the body, mainly in the spine, pelvic area and fractures, showing persistent pain, and parallel with the degree of osteoporosis, especially when the floor or posture changes. Long-term disease lower limb muscle atrophy, vertebral compression fracture, shortened body length; thoracic deformity, decreased lung capacity, can affect cardiopulmonary function.

(2) Laboratory inspection

Blood calcium, blood phosphorus, blood alkaline phosphatase (AKP) and urinary phosphorus are normal, plasma osteocalcin is elevated, urinary calcium can be high, and urinary hydroxyproline may be elevated. If accompanied by rickets, blood and urine biochemical indicators may change accordingly.

(three) X-ray examination

When the X-ray shows osteoporosis, the reduction of bone minerals is above 30%~50%. The main change is cortical phenanthrene, trabecular bone is reduced, thinned or sparsely atrophied, the bone-like layer is not thick, and the spine and pelvis are obvious, especially the chest and lumbar weight-bearing stages are particularly heavy. Early manifestations of reduced bone density, increased transparency, horizontal trabecular bone is arranged in a vertical grid. Lateral longitudinal trabecular bone was also absorbed, the ability to withstand pressure decreased, and the thoracic vertebrae were wedge-shaped deformed. Because the loose bone of the sponge is more decalcified than the dense bone, the vertebral body is compressed by the intervertebral disc to form a double-sided depression, and a vertebral compression fracture or a pathological fracture of other parts can also be seen. X lines are sometimes not easily distinguished from rickets, or both. In recent years, a variety of new technologies have been applied to the detection of osteoporosis, such as neutron activation analysis for total body calcium, single beam bone densitometry for forearm bone density, dual energy X-ray absorptiometry for spinal bone density, vertebral The body uses computerized tomography (CT) and radiation densitometry. Performing a bone biopsy when necessary is important for early diagnosis and follow-up of osteoporosis.

Differential diagnosis

Extensive osteoporosis is mainly due to reduced osteogenesis. It is a type of osteoporosis whose cause is consistent with the cause of osteoporosis: there are many causes of osteoporosis, and calcium deficiency is recognized as a factor. Clinical manifestations: (1) pain. (2) Shortened length and hunchback. More often after the pain. (3) Fracture. This is the most common and serious complication of degenerative osteoporosis. (4) The respiratory function is reduced. Chest and lumbar compression fractures, posterior curvature of the spine, and thoracic deformity can significantly reduce lung capacity and maximum ventilation. Patients often have symptoms such as chest tightness, shortness of breath, and difficulty breathing.

Ectopic calcification, pathological terminology. Also known as heterotopic ossification. In addition to normal physiological calcification, calcium deposits occur outside of bone tissue. This change usually occurs at the tendon attachment of the bone, ligaments, blood vessel walls, bone fascia, and the like. Calcium ions are precipitated from the skeletal system and often lead to osteoporosis. Therefore, some scholars advocate ectopic calcification as an indirect sign of osteoporosis.

Myeloma (also known as plasmacytoma) is a malignant tumor originating from plasma cells in the bone marrow and is a relatively common malignant tumor. X-ray bone examination: The affected bone shows a circular piercing defect, which is typical of the skull. Diffuse osteoporosis and decalcification can also be seen.

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