What Is the Difference Between Osteomalacia and Rickets?

Osteomalacia and rickets are a type of skeletal disease characterized by newly formed disorders of mineralization of the bone matrix. As a result, non-mineralized bone-like tissue (osteoid) accumulates and the bone softens, resulting in a series of clinical symptoms and signs such as bone pain, bone deformity, and fracture.

Basic Information

Visiting department: orthopedics
Common causes: Vitamin D nutritional deficiency, deficiency of vitamin D's metabolic activity, lack of minerals in bone mineralization sites, and disorders of bone cells and bone matrix

Common symptoms: Bone pain, bone deformity, fracture, etc.
Contagious: no

Causes of osteomalacia and rickets

The etiology of the disease is diverse and can be divided into four categories:

1. Vitamin D nutritional deficiency.

2. Deficiency of the metabolic activity of vitamin D.

3. Deficiency of minerals in bone mineralization sites.

4. Bone cells and bone matrix disorders.

Rickets occurs before puberty, that is, before the long bone growth plate is closed to the closed period. In adults, bone mineralization after the epiphyseal growth plate is closed is called osteomalacia.

Clinical manifestations of osteomalacia and rickets

Rickets

Its pathological basis is mineralization disorder, a large amount of osteoid accumulation, resulting in softening and deformity of bone. Due to different causes, the time of onset of rickets varies, and the performance varies. Nutritional rickets occur mostly in infants between 6 and 24 months; hereditary pseudovitaminal deficiency of vitamin D is usually 2 to 3 months after birth; and simple hypophosphatemic rickets usually occur only 2 to 5 years after birth. which performed.

Rickets is more pronounced in areas where bone growth and rapid bone turnover occur. In the first year after birth, the fastest growing areas are the skull, wrist and ribs. It is characterized by soft skull, which can be sunken after finger pressure, and has a ping-pong-like elastic feel. The osteoid accumulation of the four ossification centers of the skull bulges to the surface to form a square skull. Patients with severe rickets and infants with rickets can develop hand-foot convulsions due to severe hypocalcemia, and can even cause systemic convulsions, laryngeal spasms, suffocation and death.

2. Osteomalacia

Because only 5% of the adult epiphysis is newly added bone each year, it must take a considerable time to form new bone with insufficient mineralization, causing osteomalacia. With the increase of osteomalacia, bone deformity caused by long-term weight-bearing or muscle stretching during activity, or the sensory nerve terminal that touches the periosteum causes obvious bone pain. Onset or intermittent, obvious in winter and spring, intensified in late pregnancy and lactation.

After a few months or years, it becomes persistent, and develops into severe and severe generalized bone pain. He becomes more active during walking and walking, and may have lameness and duck gait. It is difficult to bend, comb, and turn over. In severe cases, the bone is further softened, and thoracic invagination and sternal protrusion can form chicken breasts, which affects heart and lung function.

Long-term bed rest and sitting can shorten the cervical spine, lumbar lordosis, and thoracic kyphosis, leading to scoliosis, kyphosis, and shortened height. Bone becomes soft and bears weight for a long time, making the promontory sink and lordosis, the pubic protrusion protruding into a bird's beak shape, two acetabulums invading, the pubic bone arch forming an acute angle, the pelvis showing a chicken heart or trilobate deformity, which can cause dystocia. Myasthenia is also a prominent symptom, especially in patients with marked hypophosphatemia. Hands can not hold heavy objects or lift up, can not stand up independently after squatting with legs, often need to support or rely on others, can not turn over to sit up, or the above actions require a lot of effort to complete slowly. Loss of long-term activity can lead to atrophic muscle atrophy, more muscular weakness, and is easily confused with primary myopathy. In patients with such osteomalacia, minor trauma can lead to pathological fractures, especially rib fractures.

3. Lesions

It is obvious at the ends of the long bones and at the junction of the bone and cartilage of the ribs. It can also be seen at the wrists, ankles, etc. Due to insufficient mineralization of cartilage and new bone, a large amount of osteoid tissue accumulates and swells to the periphery, forming a beaded deformity.

The skull can be thinned due to inadequate calcification, which is similar to a softened table tennis but rebounds. Due to the softening of the ribs, the ribs at the attachment site of the diaphragm are pulled to form depressions, forming transverse grooves. This is called the two rib grooves or Harrison, and is found on both sides of the front of the chest wall.

The limbs can form a ring-shaped hump due to the thickening of the metatarsus, which is called a gauntlet or ankle bracelet. The lower limbs form "O" -shaped legs or "X" -shaped legs due to weight bearing, which are more common in the former. Scoliosis, pelvic deformation, etc. can still occur. Osteomalacia can cause the pelvis to become smaller. Because the pelvic bone is soft, it cannot effectively support the spine, causing the pelvic organs to move down and causing pelvic stenosis.

Osteomalacia and rickets

Blood calcium and phosphorus

Rickets and osteomalacia due to different causes and degrees and the presence or absence of secondary hyperparathyroidism, the blood calcium and phosphorus can have the following six changes: decreased blood calcium, normal or low blood phosphorus, such as mild nutritional vitamin D lack of rickets. Blood calcium is normal or low, and blood phosphorus is significantly reduced, such as X-linked hypophosphatemia, renal tubules, and tumorous osteomalacia. Calcium and phosphorus were significantly reduced, such as vitamin D-dependent rickets type and severe vitamin D deficiency rickets with secondary hyperparathyroidism. Hypocalcemia and normal blood phosphorus, such as idiopathic parathyroidism and renal bone disease (uremic bone disease). Normal or elevated blood calcium and normal blood phosphorus, such as familial hypoalkaline phosphatase. Blood calcium and phosphorus are normal, such as axial osteomalacia and bone fibrosis.

2. Urine calcium and phosphorus Ranch

Urine calcium varies from rickets and osteomalacia caused by various causes, but most rickets and osteomalacia have a prominent feature. A small number of osteomalacia and osteomalacia are osteomalacia. Normal or increased. There are many inconsistencies in urine phosphorus, which are related to phosphorus intake and the presence or absence of secondary parathyroidism.

3. Blood alkaline phosphatase (AKP) and urine hydroxyproline (HOP)

Most rickets and osteomalacia are often related to the severity of bone lesions. However, familial hypophosphataemia is reduced, dysplasia at the metaphysis, and axial osteomalacia are normal.

4. Parathyroid hormone

Although the majority of patients with rickets and osteomalacia have compensatory increased parathyroid function, PTH is generally within the normal range measured by radioimmunoassay. A small number of patients with obvious secondary hyperparathyroidism may have PTH levels were mild and moderately elevated. Idiopathic hypoparathyroidism decreases PTH.

5. Vitamin D determination

Vitamin D testing is very important to distinguish the cause and type of rickets and osteomalacia. Changes in laboratory tests for various rickets and osteomalacia.

6. X-ray signs

(1) The main pathological changes of rickets occur in areas with strong growth, and the changes of X-ray signs are also mainly in the fastest growing metaphysis, such as distal femur, proximal humerus, tibia and ulna.

(2) Mild patients with osteomalacia show only a general decrease in bone mineral density. Further development may lead to thinning of the cortex, a decrease in density to a villi-like shape, and a lumbar vertebrae with a double concave shape.

7. Two-photon bone density check

It can be used as an evaluation index of recovery after osteomalacia treatment, and it is more accurate than X-ray detection.

8. Bone metrology examination

This is a method of double-labeling tetracycline to perform bone biopsy in vivo, and then to quantitatively detect osteometric parameters by histomorphology. It is an important method to diagnose rickets and osteomalacia.

Osteomalacia and Rickets Diagnosis

Should be based on medical history, clinical manifestations, blood biochemical examination and X-ray bone examination. The latter two tests are more diagnostic for atypical cases and staging of rickets.

Differential diagnosis of osteomalacia and rickets

It should be distinguished from rickets caused by other causes. For clinical diagnosis of vitamin D deficiency rickets, anti-vitamin D rickets should be considered, often associated with kidney disease.

Osteomalacia and Rickets Treatment

Vitamin D

Cod liver oil or concentrated cod liver oil can be used for mild cases, and heavier patients need direct intramuscular injection of vitamin D ₂ or D ₃ . Unless the patient has severe rickets and osteomalacia or accompanied by severe hypocalcemia, the use of active vitamin D may be effective about one month earlier than the mother's vitamin D.

(1) Vitamin D metabolism deficiency Liver 25- (OH) D ₃ production is reduced. This type of rickets and osteomalacia should be actively treated for primary disease. In addition, daily doses of vitamin D or 25- (OH) D ₃ are administered orally. Cure.

However, in patients with primary biliary cirrhosis, chronic vitamin D depletion is shown, short-term vitamin D is ineffective, and longer-term vitamin D treatment is required. Patients with liver disease are better treated with 25- (OH) D ₃ , and the vitamin D requirement of preterm infants is 3-6 times higher than that of full-term infants. Therefore, the dose of vitamin D to be treated is greater than the recommended dosage for normal children.

(2) Hereditary vitamin D-dependent rickets are ineffective with general doses of vitamin D and 25- (0H) D ₃ , and symptoms can only be relieved by high doses of vitamin D, but life-long medication is required. Once interrupted, performance can reappear It is called vitamin D-dependent rickets.

(3) In the treatment of rickets and osteomalacia (nephrotic bone disease) caused by chronic kidney disease , the primary disease must be actively treated to correct metabolic acidosis. Patients with renal insufficiency should be given phosphate binder aluminum hydroxide gel early to inhibit hyperphosphatemia, which can prevent and delay the occurrence of renal bone disease, and can also reduce soft tissue calcification. It is not effective to give ordinary vitamin D preparations, and alfacalciferol should be preferred. To ordinary vitamin D, large doses should be used.

(4) Hypoparathyroidism and pseudohypoparathyroidism If maternal vitamin D is used, a large dose is required, and blood and urine calcium should be reviewed regularly. Dihydrotachysterol (DHT) has a similar effect to PTH, and has obvious curative effect in the treatment of this disease. When taking the above-mentioned vitamin D preparation, it is necessary to add calcium and pay attention to reducing blood phosphorus. Aluminum hydroxide gel can be used.

(5) Treatment of hereditary vitamin D resistance rickets : When there is a certain sensitivity, use a larger dose of vitamin D than vitamin D-dependent rickets. More severe cases are best treated with high doses of active vitamin D, l, 25- (OH) 2D3, which allows patients to maintain a higher concentration of 1,25- (OH) 2D3 during treatment. Patients who have no calcium response to vitamin D in any form and dose need to be given high-dose oral or intravenous calcium. Elemental calcium solution can be infused intravenously every day or every other day for 12 hours.

(6) Treatment of calcium deficiency syndrome and chronic hypophosphatemia due to mineral deficiencies in bone mineralization sites : Treatment should be based on different causes. The most basic treatment is phosphorus supplementation, which is usually given 4 to 6 times. The daily dosage of infants, children, and adults needs to be respected by your doctor. Phosphorus supplementation can affect intestinal calcium absorption, so calcium supplementation should be strengthened. A large dose of vitamin D ₂ or D ₃ or 1,25- (OH) ₂ D ₃ and 1- (0H) D _{3 should be given} .

(7) X-linked familial hypophosphatemia treatment of mineral deficiencies in bone mineralization sites : Vitamin D or D3 can be given in high-dose vitamin D treatment, but active vitamin D, 1, 25- (OH ) ₂ D ₃ Gradually increase from the appropriate amount, or 1- (0H) D ₃ . The combined treatment of vitamin D and phosphorus preparations not only reduces the amount of vitamin D, but also avoids secondary hyperparathyroidism due to the decrease in blood calcium by simply using phosphate, which aggravates bone lesions. Elemental phosphorus can be given daily to maintain at least 1 mmol / L (3.1 mg / dl) of blood phosphorus, and it is unlikely that fasting blood phosphorus will become completely normal. Simultaneous treatment with vitamin D, calcium and phosphorus can reduce the amount of vitamin D. It is recommended to take small doses of phosphorus orally.

(8) Renal tubular damage Severe renal tubular damage results in rickets and osteomalacia. Treatment includes: The most important thing is to correct acidosis, and you can take sodium bicarbonate. Perchlorate is the first treatment with citrate solution. Alkali is often taken for life. If hypocalcemia, calcium should be added in time before oral alkaline preparations. In patients with renal tubular acidosis, after correcting the acidosis, the bone lesions have not improved or healed significantly, and vitamins are available. Those who have kidney calcification and kidney stones should not take calcium and vitamin D. Fanconi syndrome requires a larger amount of vitamin D.

(9) Magnesium deficiency syndrome rickets osteomalacia accompanied by significant hypomagnesemia. Those who are poorly treated with vitamin D and calcium should be supplemented with magnesium in a timely manner.

(10) Phosphatase deficiency has a certain effect when taken in large doses of oral neutral phosphorus solution. X-rays show that bone calcification has improved, and blood phosphorus has only slightly increased. The use of sodium fluoride drugs (fluoride ion 40mg / d) can increase blood alkaline phosphatase, and bone lesions have improved to some extent.

(11) Treatment of low conversion osteomalacia to remove aluminum sources; intravenous infusion of deferoxamine to chelate aluminum to remove aluminum from tissues.

(12) Metaphyseal cartilage dysplasia. After bed rest for a period of time, there is a tendency to spontaneously heal.

2. Calcium

In addition to vitamin D supplementation, nutritional vitamin D treatment should also be given a certain amount of calcium. One is that many patients have poor absorption of vitamin D accompanied by calcium absorption disorders. Although vitamin D supplementation can promote intestinal calcium absorption, it is difficult to provide a large amount of calcium ions in the ordinary diet. The second is because vitamin D treatment promotes a large number of calcium ions into the bone, resulting in lower blood calcium, and timely calcium supplementation can prevent the occurrence of hand-foot convulsions. No matter what kind of calcium is used, it should be based on the amount of supplemental calcium.

3. Other

Natural sunbathing and artificial ultraviolet irradiation (wavelength 240-315nm) therapy are also methods for treating rickets and osteomalacia.