Skeletal fluorosis

Introduction to skeletal fluorosis Fluorosis (bone) refers to a chronic invasive systemic bone disease caused by long-term intake of excessive fluoride and causing fluorosis and involving bone tissue. Fluorosis involves teeth and is called dental fluorosis. In 1901, Eaqer first reported dental fluorosis. In 1932, Denmark's Motlev and Gudijonsson named "fluorosis" and believed that the disease was accompanied by osteosclerosis. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: bone hyperplasia

Cause of skeletal fluorosis

Food factor (20%)

For example, the water content of spring water, especially hot spring water is too high, and the fluoride concentration of edible water is safe below 1×10-6. Long-term consumption of more than 1×10-6 fluorine-containing water may cause chronic fluorine poisoning. To save fuel, there are often hot spring water for cooking, burning soup, brewing tea, removing chicken for chickens, ducks, and steaming vegetables to semi-cooked, etc., all causing pollution.

Drug factor (20%)

Fluoride can stimulate bone growth and is therefore used to treat osteoporosis. Osteoporosis patients can increase their bone mineral density after treatment with fluoride, which has attracted the attention of the medical community. However, the use of fluoride to treat osteoporosis is controversial. The results are summarized as follows: 1 Although the BMD increased after treatment with fluoride in patients with osteoporosis, it has not been proven that this treatment can reduce the occurrence of fractures. The mineralization of new bone formation caused by 2 fluoride is abnormal. This abnormality is more serious in low calcium intake. Even if calcium and vitamin D are used as adjuvant therapy, this abnormality cannot be completely prevented. 3 Due to the imbalance of mineralization due to the production of bone matrix (bone softening), some patients have lower extremity pain and may even increase the fracture.

Environmental factors (15%)

Due to the fluorine content of coal, some industrial raw materials contain fluorine, which causes air pollution during the smelting process.

Pathogenesis

After the fluorine enters the human body through the digestive tract or the respiratory tract, it spreads throughout the body through blood circulation, causing various changes.

1. In combination with calcium ions and magnesium ions in plasma, the concentration of calcium ions and magnesium ions in the blood can be lowered, so there are symptoms such as hand and foot spasm, muscle spasm, muscle pain, etc. Further, it depends on calcium ions or magnesium ions to help. The enzymes that act on the side are all inhibited, so many metabolic processes are affected.

2. The influence of fluoride ion The ion is a poison to the cytoplasm, which can affect the function of the cell, and can act on the apatite of the bone, replacing its hydroxyl group, thus affecting bone metabolism, making osteoporosis, osteosclerosis, or two The mixed type causes bone pain, fracture, deformation, and the teeth are susceptible to fluorine during growth, causing dental fluorosis.

Skeletal fluorosis prevention

The skeletal fluorosis is mainly caused by the high fluoride content of drinking water. Therefore, as long as you change to drink low-fluorine water or remove fluoride from high-fluorine water, skeletal fluorosis is completely preventable. In addition, the kidneys are reduced after fluoride intake. There is still a strong ability to fluorinate, and after the blood level is lowered, the excess fluoride accumulated in the bone tissue and teeth can be released into the blood and excreted by the kidneys, so that the symptoms and signs of the patients with skeletal fluorosis are improved, so Prevention and treatment of skeletal fluorosis by reducing the fluoride content of drinking water is not only necessary but also feasible.

Avoid drinking high-fluorinated water: In high-fluorine areas, residents should try not to drink high-fluorine water, and find low-fluoride water sources, such as deep well water, tap water, rain or snow water, and also regularly measure water quality.

The removal of fluorine from water by drugs includes the following measures:

1. Aluminum sulfate plus an appropriate amount of lime can produce aluminum hydroxide precipitation, and fluoride ions are adsorbed on the precipitate to be removed.

2. Activated alumina has a large surface area and strong ion exchange, and has a strong adsorption effect on fluoride ions.

3. Alkaline aluminum chloride can be directly added to drinking water to produce a colloidal polymer. The fluoride ion precipitates with the polymer, and the supernatant liquid is low-fluorinated water.

There are many methods for reducing fluoride in drugs, but they are not ideal enough, and the cost is also large. It is difficult to adhere to the application for a long time.

4. Eat clean water and food, do not eat high-fluorine water and fluoride-contaminated foods to strengthen publicity and education, improve the understanding of the harm of fluorosis and its prevention methods, in the south, especially the consumption of high-fluorinated hot spring water Local, deep wells, and consumption of non-high fluoride water are an important measure to improve poor food storage and cooking habits and avoid fluoride-contaminated food.

Chromosome complications Complications

The clinical symptoms of skeletal fluorosis are characterized by persistent pain in the spine joints of the extremities, no migratory, unrelated to the weather, and thus joint movement disorders, muscle atrophy, limb numbness, stiffness and even paralysis. Chronic cough, lower back and lower limbs are often present in the late stage. Pain, osteosclerosis, tendon, ligament calcification and joint capsule hypertrophy, bone hyperplasia, joint deformation, etc., patients died of chronic dystrophies or other serious complications.

Symptoms of skeletal fluorosis Common symptoms Joint stiffness, joint pain, bone sclerosis, muscle atrophy, bloating, diarrhea, persistent pain, nausea, osteoporosis, osteomalacia

The main clinical manifestations of skeletal fluorosis are pain in the joints of the lower back and legs, joint stiffness, skeletal deformation, and symptoms and signs of compression of the nerve roots and spinal cord.

Patients often complain of persistent pain in the spine and limbs joints, aggravation at rest, remission after activity, no swelling and heat in the joints, and pain in the nerve root compression, such as knife-cutting or lightning-like pain, refusal to touch or support When the condition is serious, the joints, the spine are fixed, the scoliosis is curved, the hunchback or the limbs are stiff, and the life is difficult to take care of themselves. The spinal cord or nerve roots are numb in the limbs or lower limbs, the trunk is restrained, the pain can be accompanied by the limbs. Paraplegia, resulting in distortion in the bed, coughing and turning over caused severe pain, patients died of chronic dystrophies or other serious complications.

Patients often have generalized muscle pain, dizziness, palpitations, weakness, drowsiness and loss of appetite, nausea, vomiting, bloating, diarrhea or constipation, muscle atrophy, electromyography changes, involving the thyroid, adrenal glands, gonads and lens and center. In the nervous system, it can cause the corresponding symptoms and signs. The serum free fluoride, thyroid hormone and TSH concentration of 37 patients were observed in our hospital. It was found that the serum T4 and T3 of patients with fluorosis were significantly lower than the normal control group, and the TSH was significantly higher than the normal control. Group. T3 concentration and T3/T4 ratio were significantly negatively correlated with serum free fluoride concentration. Therefore, it is believed that fluorosis can reduce thyroid function and is related to blood fluoride content.

In general, the symptoms of women with skeletal fluorosis are heavier than those of men. In areas where the fluoride content of drinking water is above 10 mg/L, women with spinal stiffness can reach 50%, men only 7%, and women with scoliosis, hunchback or sputum are 22.2. %, male is 7%. This gender difference may be related to pregnancy, childbirth, breastfeeding, etc., and women have more exposure to coal-burning air. The course of skeletal fluorosis can last for several decades.

Examination of fluorosis

Laboratory inspection

1, blood, urine fluoride measurement:

(1) About 85% of the fluoride in the human body is excreted in the urine. The blood and urine concentration of patients with fluorosis will rise, especially the increase of urinary fluoride concentration is an important basis for the diagnosis of skeletal fluorosis. The normal urinary fluoride range is 1.0. ~3.0mg/24h, the normal range of blood fluoride is 0.15~1.0mg/L. If the blood and urine fluoride concentration in the high fluoride area exceeds the normal range, the possibility of skeletal fluorosis should be considered. It must be pointed out that there are many Factors can increase urinary fluoride, especially some foods with high fluoride content, so the accidental urinary fluoride should not be used as a basis for the diagnosis of skeletal fluorosis. In addition, the urinary fluoride content will fluctuate at different times in a day. In the first half of the night, the amount of urinary fluoride is the highest. The urine content of urine and morning urine in the morning is close to the average daily urinary fluoride content. Therefore, morning urine measurement can be used as a reliable indicator for the diagnosis of skeletal fluorosis.

(2) Blood biochemical measurement: As fluoride can stimulate osteoblasts, increase the formation of new bone, leading to bone hyperplasia and osteosclerosis, so that the activity of serum alkaline phosphatase AKP reflecting osteoblast activity is increased due to fluorine energy and Calcium, magnesium, and phosphate combine to form a poorly soluble complex, which makes serum calcium, magnesium, and phosphorus lower than normal. However, if long-term calcium is low, it can induce hyperparathyroidism and promote intestinal calcium and bone calcium absorption. It can increase serum calcium and phosphorus.

2, renal function determination: excessive fluoride intake has a direct toxic effect on the kidney, can produce varying degrees of renal dysfunction, so that blood urea nitrogen increased, creatinine clearance decreased, urine protein positive, urine visible cells and cast Wait.

3, nail and hair fluoride determination: nail and hair quantitative fluoride content is an indicator that can accurately represent the body's fluoride content, is of great significance for the diagnosis of endemic skeletal fluorosis.

4, tibia biopsy: bone tissue non-decalcification biopsy can be found in trabecular bone thickening, decalcification after the slice shows bone plate alignment disorder, bone chemical analysis results show that fluoride, calcium, magnesium content increased, bone phosphorus and blood Phosphorus is in the normal range.

Film degree exam

X-ray changes in skeletal fluorosis include osteoporosis, osteosclerosis, osteomalacia, peri-osseous bone hyperplasia, soft tissue calcification or ossification, joint degeneration, bone developmental disorders, and deformities.

1.X-ray performance

(1) Osteoporosis: The coarse and sparse bone texture can be the only manifestation of early skeletal fluorosis.

(2) Osteomalacia: obvious in the spine and pelvis, its bone density is reduced, the texture is blurred, the scoliosis, hunchback, vertebral body bi-concave deformation, pelvic constriction and pseudo-fracture line formation, osteomalacia and osteoporosis Osteosclerosis and soft tissue calcification occur simultaneously and are mixed.

(3) osteosclerosis type: osteosclerosis often occurs in the spine, pelvis, ribs and skull. The bone texture is as thick as sackcloth or gravel sand. In severe cases, the bone texture is fused, the structure is fuzzy, the X-ray is low and the ivory is like bone. Hardening is often accompanied by osteoporosis of the bones of the extremities. When there is insufficient calcium intake, there may be secondary hyperparathyroidism. At this time, the bones of the extremities are manifested as fibrocystic osteitis.

2. CT manifestations: the spine is bamboo-like, with obvious chest and upper lumbar segments, increased density of vertebral attachments, hyperosteogeny, ossification of ligaments, and osseous spinal stenosis.

3. MRI findings: vertebral body morphology and signal changes have abnormal MRI, vertebral body has a uniform or uneven low signal intensity, uneven signal is plaque or needle in the vertebral body, the same as normal bone marrow In the signal area, the low signal area of the edge of the vertebral body is thickened, and the ligamentum flavum with small joint hyperplasia and hypertrophic ossification is stepped, the spinal canal is narrowed, the dural sac is compressed, and the bone marrow can be compressed and edema. , the T2 weighted image is high signal.

4. SPECT performance: The radioactive signal of the proliferative part is strong, the range is wider, but there is no specificity.

5. Bone biopsy: After decalcification, the slices showed disordered bone plate arrangement, bone fluoride, calcium and magnesium content increased, bone phosphorus and serum phosphorus were normal, and ultrastructure also had specific changes.

Osteoporosis occurs in the bones of the extremities. The bones are thick and sparse. The bone sclerosis is more common in the spine, pelvis, ribs and skull base. The bones of the extremities are less common. The main manifestations are gravel-like and coarse-grained bone streaks. Osteoclastosis, but the structure is ambiguous, rarely uniform ivory-like, bone softening with the spine and pelvis as the weight, showing reduced bone density, blurred bone pattern, vertebral body bi-concave deformation, pelvic constriction deformity and false Sexual fractures, sometimes osteosclerosis and osteomalacia can coexist at the same time; peri-osseous bone hyperplasia is common in the limb bones, and the upper part of the humerus is more common, which is characterized by localized bone formation of the bone, which can form a lace-like shape, and often has adjacent bones. Membrane calcification, soft tissue calcification or ossification is mainly found in the interosseous membrane, ligaments and tendons. It is low-density corrugated or plexiform in the early stage, and then rose-like, and finally merges into a lace-like or irregular shape. Start slightly higher than soft tissue, then gradually increase, close to bone tissue, joint degenerative changes found in the spine and limbs, manifested as bone hyperplasia, spur formation, joint space stenosis, articular surface sclerosis, Intra-articular free body and joint capsule calcification; bone development disorder manifested as growth disorder line and bone age retardation, bone deformity manifested as scoliosis and posterior spine, followed by pelvic reclining, knee varus and knee valgus are also common.

Diagnosis and diagnosis of skeletal fluorosis

Diagnosis

In the early stage of chronic fluorosis, the enamel loses its dark color or spotted lime. In the late stage, there are chronic cough, back and lower limb pain, osteosclerosis, tendon, ligament calcification and joint capsule hypertrophy, bone hyperplasia, joint deformation and so on.

There are three types of skeletal fluorosis indexing:

Grade I: Patients with fluorosis who have only clinical symptoms and no obvious signs.

II degree: There are typical clinical manifestations such as bone and joint pain and dysfunction, but they can participate in some laborers.

III degree: patients with fluorosis who have lost their ability to work.

The diagnosis of typical skeletal fluorosis is not difficult: 1. More than two years of endemic skeletal fluorosis in high-fluorine water and drinking or suffering from dental fluorosis.

2. The clinical manifestations are consistent with the symptoms and signs of typical skeletal fluorosis.

3. Radiological examination revealed a change in bone specificity.

4. Those with a diagnostic laboratory test positive.

5. Bone biopsy is consistent with skeletal fluorosis.

6. Grading (degrees) Generally, the indexing can be performed according to the following criteria:

I degree: only clinical symptoms without obvious signs.

II degree: There are typical clinical manifestations such as bone and joint pain and dysfunction, but they can participate in certain physical labor.

III degree: Those who have lost their ability to work.

7. X-ray diagnosis of skeletal fluorosis classification and indexing: X-ray photographs require clear bone lines, including at least the pelvis and lateral anterior wall, and the calf position.

(1) Classification: According to the main changes in bone density and structure, it can be divided into 3 types:

1 hardening type: There are two main types: 1. Increased bone density, thickening of trabecular bone, thickening of cortical bone, narrowing or disappearing of medullary cavity, 2. ossification of interosseous membrane and surrounding ligament.

2 loose type: can also be divided into two cases: 1, bone density is reduced, trabecular bone sparse, bone has different degrees of absorption decalcification or bone deformation, 2, interosseous membrane or periorbital ligament ossification.

3 mixed type: both of the above characteristics (there are different degrees of bone hyperplasia and bone resorption) or cancellous bone reticular or saclike structure, cortical bone structure is loose, the number of trabecular bone per unit area is significantly reduced.

(2) Indexing: There are different degrees of change in the above 3 types, which can be divided into early changes and light, medium and heavy 3 degrees.

1 early changes: one of the following signs can be diagnosed as early skeletal fluorosis: 1, long bone end, pelvic bone only see a spotted texture or thickened disorder bone, 2, long bone cortex edge There are more than two young shoots broken bone-like bones. The humeral ridges are mostly wavy.

2 mild: 1, bone density is slightly higher than normal, the trabecular bone is thick and dense, bone spots appear, the trabecular bone becomes thinner, the density is reduced, 2, the ligament of the muscle ligament is pointed ossification, and the interosseous membrane is obviously proliferated.

3 moderate: 1, bone density increased significantly, cortical thickening, trabecular thickening, partial fusion; or cortical thinning, trabecular bone thin and thin, reduced density, or trabecular sparse, but coarse texture, Increased density, 2, interosseous membrane and periorbital ligament with a large range of ossification.

4 severity: 1, trabecular thickening, most of the fusion into a piece, medullary cavity, cortical boundary is unclear; or osteoporosis is patchy absorption, cortical bone part of the disappearance disappeared, bone deformation is more obvious, 2, bone The membrane and surrounding ligaments are more ossified, can be bridged, and can appear calcification of other soft tissues (such as blood vessels).

8. Diagnostic considerations

(1) There must be a personal history of long-term living in high-fluorine areas, drinking high-fluorine water, eating food contaminated with fluorine or air environment contaminated with fluorine. In addition, gender and renal function are also related to the condition.

(2) The clinical manifestations are osteoarthritis, dyskinesia or deformity of skeletal fluorosis, accompanied by dental fluorosis (patients who have moved to high fluoride area after 12 years of age may have no dental fluorosis).

(3) Skeletal X-ray changes have osteoclastosis, a characteristic change of perivascular soft tissue calcification.

(4) blood, urinary fluoride exceeds the normal range, early skeletal fluorosis may be asymptomatic and X-ray abnormalities, alkaline phosphatase is elevated during this period, blood urinary calcium is low, urinary hydroxyproline excretion is higher than normal, suggesting that fluoride has Excitatory osteoblast activity, damage to collagen, osteoporosis and osteomalacia in patients with skeletal fluorosis secondary to hyperparathyroidism, elevated plasma PTH, elevated blood tartaric acid phosphatase, combined with the above aspects Changes, the diagnosis of typical endemic skeletal fluorosis is not difficult, industrial skeletal fluorosis patients often belong to the osteosclerosis type, the history of fluoride exposure in the living and occupational environment can help diagnose.

Differential diagnosis

In typical cases, there is no difficulty in diagnosis. The following situations should be noted when identifying.

1. Primary osteoporosis: There is osteoporosis in the X-ray, but there is generally no sclerosis. If osteoporosis is seen on the X-ray, and osteoporosis is seen, it does not conform to the primary bone. Osteoporosis (including senile osteoporosis), in addition, primary osteoporosis found in elderly patients, no history of high fluoride intake, blood and urine fluoride is not increased, are available for identification.

2. Osteosis: The causes of osteomalacia are various, most of which are due to vitamin D deficiency or abnormal metabolism, or abnormal calcium and phosphorus metabolism. If there is no history of high fluoride intake, blood and urine do not increase. It can rule out chronic fluorosis.

3. Other metabolic bone diseases: Although it can cause bone pain, fracture or bone deformity, but no history of high fluoride intake, blood and urine fluoride does not increase, can be identified.

4. Stone osteopathy: visible bone density increases, there are transverse strips on the tubular bone, and multiple layers of wavy dense shadows in the tibia and fibula. These images are clearly distinct from skeletal fluorosis.

5. Osteogenic metastatic carcinoma: The general distribution of sclerosing changes is not uniform and often causes changes in bone structure.

6. Renal osteopathy: very similar to some fluorosis, the bone is generally dense and (or) loose, the trabecular bone is rough and fuzzy, etc., often difficult to distinguish from X-ray signs, combined with epidemiology, clinical manifestations Identification with renal function tests.

None of the above disorders have ligament calcification.

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