What Is Metabolic Bone Disease?

Osteoporosis

Metabolic bone disease

Metabolic bone disease refers to a bone disorder that occurs when the body destroys or interferes with normal bone metabolism and biochemical conditions due to congenital or acquired factors, leading to bone biochemical metabolic disorders. The pathogenesis of metabolic bone disease includes abnormalities in the three aspects of bone resorption, bone growth, and mineral deposition. The X-ray changes caused are mainly osteoporosis, softening of the femoral index and osteoporosis. Typical symptoms are rickets.

Classification of metabolic bone disease

Osteoporosis
2. osteochondrosis
3. Primary hyperparathyroidism
4. Primary hypoparathyroidism
5. Toxic bone disease (vitamin D, fluorine, lead, phosphorus and other poisoning)
6. Others such as abnormal mucopolysaccharide metabolism, Marfan's disease, Paget's disease. [1]

Bone Structure and Function of Metabolic Osteopathy

Metabolic bone disease (1) Structure

Bone is different from cortical bone and cavernous bone. Cortical bone is mainly the backbone of tubular bone with high hardness, while cavernous bone is short bone and flat central part such as spine, and the rigidity of long tubular bone and diaphysis is relatively high. Low and vulnerable to pressure loss. During development, there is a growth cartilage band between the bone end and the trunk end of the tubular bone, which promotes the growth in the long direction. The primary cavernous bone at the end of the bone becomes a mature cavernous bone through bone absorption and new bone deposition. . This kind of cavernous bone is composed of more bone beams and bone marrow tissues, has abundant blood vessels, and is in contact with fluid, which is far more vigorous and active than cortical bone metabolism. Cortical bone has a periosteum on the outside, and its inner layer has a nutritional osteogenesis effect, which can promote the growth of the bone in the transverse direction. The inner surface of the cortical bone has an endosteal membrane. During growth, a certain thickness of the cortical bone is maintained due to the osseous absorption of the inner surface. The cortical bone has a Harvers tube that develops in the long axis direction, and a Volk-mann tube connected to it in the vertical direction. Among them, the blood vessels and hematopoietic tissues of vegetative bones have concentric circular lacunae around the Havers tube. There are bone cells inside. The connection between the Havers tube and the bone cavity is the canaliculi for nutrition.

Metabolic bone disease (b) bone metabolism

Bone tissue is composed of cells and extracellular matrix, the latter contains 35% organic matter and 65% inorganic matter. Cells occupy only a small volume. The role of cells is to regulate and distribute inorganic components and help maintain the concentration of serum calcium in a very narrow range. Second, bone reconstruction is performed, and the bone tissue is continuously formed and absorbed, so that it can bear weight. Respond to the mechanics of exercise to maintain the internal balance of the bones.
Inorganic salt of bone
The inorganic salt of bone is bone salt, which accounts for about 65% to 70% of the backbone weight, and the rest is the matrix part. Bone contains 99% of total calcium in the body, followed by carbonic acid, fluorine, and chlorine. The total weight of human bone calcium is about 1.2 to 1.5 kg, and phosphorus accounts for 50%. Inorganic calcium and phosphorus in bone salts are mainly distributed in organic matter in the form of crystalline light apatite and amorphous colloidal calcium phosphate.
2. Bone Organic Matrix
Collagen tissue accounts for the vast majority of the matrix, 90% to 95% are type I collagen, and the rest are non-collagenous. Polymetabolic bone disease is a systemic body with calcium and phosphorus, vitamin D metabolism, and abnormal parathyroid function. Bone disease. Sugar, lipid and glycoprotein complexes such as osteonec-tin, osteocalcin and osteolpon-tin. After the collagen fibers mature, they are bundled and arranged regularly, and bone salt is deposited in the gap. Vitamin C, auxin, parathyroid, and heparin can all affect collagen synthesis and metabolism.
3. Cell components
The process of osteogenesis and bone resorption mainly depends on the role of osteoblast, osteoclast and osteocyte. Undifferentiated mesenchymal cells can be transformed into osteoclasts or directly into osteoblasts after being stimulated by vitamin D and parathyroid hormone, but calcitonin inhibits this transformation. Osteoclasts can transform into osteoblasts under the action of calcitonin, but parathyroid hormone inhibits this transformation. Osteoblasts contain specific bone-type alkaline phosphatase (AKP), receptors for parathyroid hormone and 1,25 (OH) zD, and can synthesize specific matrix proteins such as type I collagen, osteocalcin, and bone phosphate protein. Osteoblasts synthesize proteins first in the rough endoplasmic reticulum pool, then in the Golgi complex, and finally outside the cell. Recent studies have found that some secretory components may be directly produced from the cell matrix. The final product unit is a soluble tropocollageii macromolecule, which is secreted extracellularly. Osteoblasts can produce bone in tissue culture. Concentrates collagen-containing amino acids. Once osteoblasts are embedded in the surrounding bone matrix during osteogenesis, they become osteoblasts. Bone cells maintain the integrity of the bone as a sign of bone survival. After osteoblasts make bone matrix around them, they are confined in the matrix and turn into stationary bone cells. Osteoblasts and bone cells make up the vast majority of cells in the bone. Osteoclasts are more common at the edge of the bone resorption site, and they are foreign-type multinucleated giant cells. The bone surface is covered by a layer of osteoblasts and is connected to osteoblasts in the bone fossa to form an osteoblast-osteocyte complex that separates bone fluid and extracellular fluid. These cells respond to hormonal and mechanical stress stimuli and are very active in metabolism.
The function of osteoblasts is to synthesize collagen fibers, glycoprotein complexes and RNA, and to transport calcium ions from extracellular fluid through bone fluid to bone matrix. Although osteoblasts, osteocytes and osteoclasts have higher dehydrogenase and acid phosphatase, osteoblasts contain higher AKP, but the mechanism of action during osteogenesis is unknown. In hypophosphataemia lacking A KP, calcification is affected. Bone mechanical stress, such as weight-bearing physical activity, can strengthen the vitality of osteoblasts. Viability of auxin and sex hormones, transforming factor (3 (TGF- (3) type I and II, acidic and basic fibroblast growth factor, platelet-derived growth factor and insulin-like growth factor I and n) on osteoblast It is also very important.
Bone cell function: Bone cells act as physiological mineral pumps, exchange bone ions and calcium in blood through bone tubules, and have osteolytic effects.
The function of osteoclasts is: osteoclasts mainly promote bone resorption. Osteoclasts contain many enzyme systems, including oxidase and collagenase, which are related to osteolysis and absorption. Both parathyroid glands (PTH) and osteoclast activating factor (OAF) can affect the formation of osteoclasts and strengthen the activity of osteocytes. Calcitonin (CT) and bisphosphonates have inhibitory effects. In addition, some factors such as interleukin I, tumor necrosis factor, and interferon can promote bone resorption through osteoclasts.
4. Bone formation
Bone formation is closely related to the role of chondrocytes and osteoblasts, and the product of calcium and phosphorus in plasma also plays an important role. Osteoblasts can synthesize and secrete matrix components such as collagen and glycoprotein, and then the matrix undergoes bone salt deposition to form bone. Bone salt deposition has been found to be associated with stromal vesicles. The surface of chondrocytes and osteocytes can protrude into matrix vesicles surrounded by a membranous structure, which can tightly bind to calcium ions. The vesicles also contain more AKP, which can decompose a variety of phosphates and pyrophosphates, eliminate the effect of inhibiting the formation of bone salt, promote the deposition of bone salt, and form bone. The product of calcium and phosphorus in the plasma is also important for the deposition of bone calcium. When it is lower than the normal value of 35 to 40, it is not conducive to bone calcium deposition or decalcification. If the product is too high, ectopic calcification may occur. Matrix vesicles accumulate a large amount of calcium and phosphorus, and gradually form light apatite crystals, which gradually increase as crystal nuclei, so that bone salt is deposited on collagen fibers and in the interstices, and becomes complete bone.
The formed bone is continuously absorbed and dissolved for metabolic renewal. This mainly depends on the role of osteoclasts. Some hydrolytic enzymes are secreted from the lysosome to break down the collagen fibers in the bone and release the unique collagen tissue. Light proline, osteoclasts simultaneously dissolve the light apatite crystals in the bone, and increase blood calcium.
During growth and development, old bones are continuously reabsorbed and new bones are constantly formed, which is called bone remodeling. Bone reconstruction begins at the edge of the cartilage. Osteoclasts first absorb the bone into the cavity, and new bone forms and deposits in the bone cavity several months later. If osteogenesis is dominant, the bones become thicker. Although there is no significant increase or decrease in adult bones, 3% to 5% of bone is under continuous reconstruction. Radionuclide studies show that approximately 18% of total bone calcium participates in the reconstruction of bones each year, so bones are very active in metabolism. The organization requires a complete blood supply. In bone metabolism, such as the loss of dynamic balance of bone resorption and bone formation, various metabolic bone diseases can occur. [1]

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