alkaline calcium phosphate crystal deposition disease
Introduction
Introduction to alkaline calcium phosphate crystal deposition disease Alkaline calcium phosphate crystal deposition disease is a group of diseases including hydroxyapatite (apatite), octacalcium phosphate, tricalcium phosphate and other crystals deposited around the joints and joints, often complicated by osteoarthritis and destructive joint disease. Common calcification deposits in the scapular scapula ligament, called calcific tendinitis; these substances can also be deposited in the joints, especially tendons, causing recurrent episodes of inflammation, so it is also called para- calcification, joints Phosphorus-like rheumatism, calcified para-articular inflammation, etc. This clinical syndrome is currently summarized as an alkaline calcium phosphate crystal deposition disease. basic knowledge Sickness ratio: 0.05% Susceptible people: more common in the elderly Mode of infection: non-infectious Complications: uremia, hyperthyroidism
Cause
Causes of alkaline calcium phosphate crystal deposition
(1) Causes of the disease
Alkaline calcium phosphate crystal deposition in the para-articular tendons has been thought to be secondary ectopic calcification due to tendon injury, so the classic description of the disease often associates it with excessive use or trauma of the shoulder joint. However, cases of bilateral calcification of bilateral or multiple lesions are not uncommon. It is now clear that the disease can be secondary to some basic diseases of abnormal calcium and phosphorus metabolism in the body, such as chronic renal failure, diabetes, rheumatism, thyroid or parathyroid diseases and tumors. Alkaline calcium phosphate deposition disease secondary to uremia is more common. Patients often have metastatic soft tissue calcification, often combined with joint inflammation or para-articular inflammation, and other types of crystals, such as calcium oxalate crystals, are often found. And calcium pyrophosphate crystals, etc., which further suggests that secondary alkaline calcium phosphate deposition disease is closely related to abnormal calcium and phosphorus metabolism. However, the predilection of this disease seems to have no obvious relationship with these underlying diseases. The related research on genetic factors or HLA typing of this disease has not been determined yet.
(two) pathogenesis
1. Structure and function of alkaline calcium phosphate crystals
Alkaline calcium phosphate crystals are a general term for a large class of crystals. The main mineral hydroxyapatite deposited in normal bone tissue is one of alkaline calcium phosphates, which form normal bone tissue, dentin and enamel. It is said to be essential, but it is clear that the alkaline calcium phosphate extracted from normal bone tissue is significantly different in composition from the mineral extracted from the lesion.
The chemical formula of hydroxyapatite is Ca10O(PO4)2OH, and the hydroxyl group in the molecular formula can be substituted by other groups, especially by carbonate. In normal bone tissue, hydroxyapatite is often partially carbonated, with a small crystal grain of about 50 nm as the main mode of existence. Sometimes these irregular fine grains will pass through some intermediate transition forms (such as phosphoric acid Calcium) forms larger crystals. In the deposited calcium lesions beside the joints, it is easy to see a large number of crystals with multi-focal distribution under the light microscope. These crystal accumulations are often isolated from each other by the fibrous collagen tissue and can also be seen under the projection electron microscope. In a similar scenario: a crystal "block" that accumulates in a cluster is floating in the matrix of collagen fibers, and these crystal agglomerates look like large stones in a mortar under scanning electron microscopy. The chemical composition of these crystal agglomerates differs not only from patient to patient, but even from different lesions of the same patient. Usually they consist of a wide variety of crystals, ranging from random alkaline calcium phosphates to crystal structures in teeth or bone tissue that are well-formed and structurally stable. In addition, the degree of carbonation of hydroxyapatite in the para-articular calcification is much higher than in bone tissue, and sometimes it can be seen under high-resolution electron microscopy that the crystal is covered by an electron dense substance. Compared with the calcifications around the joints, little is known about the alkaline calcium phosphate crystals deposited in the joints, but some studies on joint synovial fluids show that these crystals are also composed of various components. These include hydroxyapatite and calcium pyrophosphate, which are chemically closer to the components of the para-articular calcification compared to normal bone tissue, suggesting that they are likely to be from calcification rather than cartilage. The lower bones fell off.
2. Calcified joint inflammation
Calcified para-articular inflammation usually occurs in the "relative blood supply deficiency critical area" about a few centimeters wide at the attachment of the scapular ligament, while the other parts of the tendon's calcareous deposition area are often the part of the muscle supply that is relatively lacking. Two hypotheses have been proposed: 1 hypothesis of ectopic calcinosis secondary to ischemic necrosis; 2 hypothesis that local hypoxia leads to cartilage-like metaplasia and secondary calcification in tendons. These hypotheses are supported by pathology, and it is indeed possible to find chondrocytes surrounded by fibrocartilage in the tendon and tendon sheath tissues of the lesion, and in the cytoplasm of these cells there is also deposition of alkaline calcium phosphate crystals, and during deposition. Calcification will occur afterwards and will be absorbed secondaryly.
Pathological or X-ray findings of calcium deposition and the absence of significant inflammation or other clinical manifestations in most patients have not been satisfactorily explained. Some people think that this is related to the material wrapped on the surface of the crystal. This layer may have The highly selective absorption of the surface, as to whether it causes inflammation or inhibition of inflammation, is related to the nature of the protein bound by this substance. For example, if the surface of the crystal is covered with a layer of defatted lipoprotein, the latter can suppress immunity. Globulin-mediated inflammatory response. The acute phase manifestations of calcified para-articular inflammation may be related to the inflammatory response caused by detachment of crystals into cells or blood-rich areas after rupture of calcification. The nature of the potential inflammatory response of hydroxyapatite itself has been demonstrated in many experiments: in vitro, when hydroxyapatite is engulfed by inflammatory cells, it can lead to the release of certain inflammatory mediators; In the experiment of volunteers subcutaneous injection of hydroxyapatite crystals, a strong inflammatory reaction was observed. It is currently believed that phagocytosis of inflammatory cells may be the primary means by which the body removes locally deposited crystals.
3. Relationship with osteoarthritis and destructive arthritis
There is a lot of morphological evidence that there is deposition of hydroxyapatite crystals in the articular cartilage involved in osteoarthritis, and these crystals appear to be secreted by chondrocytes into the surrounding matrix. However, both the chemical composition and the spatial structural diversity of these crystals suggest that there are multiple sources of crystals. For example, damaged subchondral bone may become a potential source of crystals. At present, one thing is certain, that is, the deposition of crystals in the joint can cause the destruction of the joint bone, and the destruction of the joint can further lead to the release of crystals deposited in the bone or cartilage, resulting in more serious joint damage. The effect forms a gradual "magnification" cycle, as shown in Figure 1.
For the elderly, the degree of joint damage caused by hydroxyapatite-related destructive arthritis is varied. Hydroxyapatite crystals can cause damage to both bone and cartilage tissue, both mechanical and biological. An in vitro mechanical test showed that hydroxyapatite can accelerate the wear rate of cartilage surface, while in the test tube, hydroxyapatite crystal can activate synovial cells and phagocytic cells to produce many inflammatory mediators, including collagenase and cells. Factors such as prostaglandins. This is consistent with an increase in collagenase and protease levels found in synovial fluid from patients with Milwaukee shoulder/knee syndrome, and suggests that this crystal-induced inflammatory response plays an important role in accelerating joint destruction. However, some people disagree with this. They think that the material that has fallen off the subchondral bone itself contains some inflammatory mediators, and it is not surprising that these media can be found in synovial fluid.
4. Pathology
The pathogenesis of alkaline calcium phosphate crystal deposition disease is still not fully understood. In vitro studies have shown that inorganic pyrophosphate, proteoglycan polymers and non-collagen proteins in normal human connective tissue have a role in preventing calcification. The following conditions will promote the occurrence of abnormal calcification.
(1) Metabolic disorders cause an increase in local solute concentration.
(2) Normal inhibition of calcification is attenuated due to aging and/or tissue damage.
(3) There are nucleating substances in the tissue or basal vesicles rich in alkaline phosphatase in the cells, which promote the calcification of cartilage.
Most patients have idiopathic or secondary local tissue damage; a few are familial and metabolic. Such as hypercalcemia and hyperphosphatemia, vitamin D poisoning, diabetic kidney dialysis, concomitant connective tissue disease and other crystal deposition diseases.
Most people with calcification deposited on the tendon are asymptomatic, with histological calcifications being concentrated pellets or cheese-like substances. Severe pain occurs only when the sediment increases compression or trauma, and the burs rupture, causing inflammation. It is also possible to deposit inflammatory sacs adhesions by calcification, causing pain, limited mobility and systemic symptoms.
Prevention
Prevention of alkaline calcium phosphate crystal deposition disease
Population prevention
With the prolongation of life expectancy and the improvement of detection methods for patients with chronic renal failure, the detection rate of this disease has an increasing trend. The bone biopsy and radionuclide scanning can be used to diagnose the disease early.
Population control measures include controlling high blood phosphorus, correcting hypocalcemia, supplementing vitamin D, preventing hyperthyroidism, hemodialysis or kidney transplantation, but the key is to control hyperphosphatemia early.
2. Personal prevention
(1) Primary prevention:
1 control of high blood phosphorus: first should control the intake of phosphate in the diet, phosphate is mainly from protein in food, patients with advanced renal failure such as daily phosphorus intake >1.2g, and not taking phosphorus binder, then Hyperphosphatemia can occur, followed by the use of phosphorus binders as appropriate, and the use of small doses of calcium carbonate or calcium lactate under strict monitoring of blood calcium is currently the first recommended method.
2 correct low blood calcium: maintaining normal calcium balance is conducive to bone mineralization, inhibition of hyperparathyroidism, calcium absorption in patients with advanced renal failure, and the intake of calcium in the diet is only 400 ~ 700mg per day, so should Daily supplementation of elemental calcium 1 ~ 2g, to supplement calcium acetate, calcium gluconate and so on.
3 application of active vitamin D: kidney produces l, 25. dihydroxyvitamin D failure, plays an important role in the occurrence and development of renal osteopathy, 1,25-dihydroxyvitamin D3 can make blood calcium in uremic patients The level of blood is significantly increased, and the level of blood parathyroid hormone is significantly decreased. Currently, vitamin D preparations commonly used include vitamin D2, alfacalcidol and calcitriol (Rosin Calcium).
4 Dialysis and kidney transplantation: Dialysis can partially replace renal function, while kidney transplantation can completely replace renal function, thereby treating renal bone disease.
(2) Secondary prevention:
The incidence of renal osteopathy is concealed, and there are often no symptoms, blood calcium is lowered, and elevated blood phosphorus and alkaline phosphatase can be used as the basis for early diagnosis. Tibial biopsy, photon absorption bone mineral density measurement and 99ECT scan can make early diagnosis. Rate increase, diagnostic points:
1 diagnosis basis of renal failure;
2 children are rickets, adults are mainly bone pain, and the lower limbs bear heavy bones;
3X line examination showed specific bone disease performance.
Once renal osteopathy is discovered, the above preventive measures should be implemented immediately. Subtotal thyroidectomy should be performed for patients with obvious secondary hyperparathyroidism, persistent hypercalcemia, metastatic calcification and severe itchy skin. .
(3) Level 3 prevention :
In the case of fractures and significant skeletal deformities, surgical procedures may be considered for correction, but preoperative preparation should be sufficient, such as correcting the patient's anemia, nutritional status, etc., and performing intraoperative monitoring.
Complication
Basic calcium phosphate crystal deposition disease complications Complications uremia hyperthyroidism
Common complications of this disease: 1. Pain. 2. Uremic disease. 3. Hyperthyroidism.
Symptom
Alkaline calcium phosphate crystal deposition disease symptoms Common symptoms severe pain parathyroid hyperthyroidism calcium deposition hypersensitivity calcification spur formation
Alkaline calcium phosphate crystal deposition disease is more common in the elderly, and its prevalence increases with age, mainly affecting the weight of the large joints, the most common is the shoulder joint sac, tendon, ligament, to the right, Others are hip, elbow, wrist and knee joints. Clinically, when alkaline calcium phosphate crystals are deposited in different parts of the body, they can cause different symptoms or syndromes.
1. Calcified joint inflammation
Calcified para-articular inflammation can usually have no clinical manifestations, but often begins with an acute attack. About 70% of patients have calcified para-articular inflammation around the shoulder joint, and some seizures can be secondary to trauma, but most patients There is no incentive or aura before the onset. The typical symptom at the onset is sudden pain. It is often described as allergic. As the disease progresses, the pain gradually worsens with severe tenderness. There may be an increase in redness and skin temperature. If it occurs around the shoulder joint, the pain is mainly concentrated in the subacromial region and radiated to the ipsilateral upper limb. The ankle joint movement is obviously affected. This serious condition can last for several days. Then the symptoms gradually relieved, and the entire acute course takes 2 to 3 weeks to relieve. Some patients have different degrees of stiffness in the shoulder joint after the acute phase.
The onset of the acute phase is usually thought to be caused by the rupture of the para-articular calcification, which is caused by the fall of the lens into the surrounding tissue. The crystals in the shoulder joint are most often detached into the subacromial sac and cause acute inflammation in the site. The edge of the calcification is clear on the X-ray film of the anterior shoulder joint, but the boundary of the calcification becomes blurred after the onset, and the density of the calcification is also reduced. Sometimes the calcification will become smaller or even disappear.
In the acute phase, the joints involved in the acute phase often combine with some chronic painful diseases, and because the damaged tendons are more prone to calcification, the two often overlap each other, making the pain in this part often difficult to say for what reason, The nature of this pain during the seizure interval is moderate to severe, with varying degrees of tenderness and local activity disorder. For example, when it occurs in the shoulder joint, the pain can often be radiated to the deltoid muscle, and in severe cases, it can be radiated to the forearm. Patients often avoid lying to the affected side during sleep, and sometimes both shoulder joints can be involved at the same time.
In a few cases, calcified shoulder-shoulder acute inflammation can recur, with intermittent periods ranging from a few months to years, while in intermittent periods it is only chronic pain. These patients are often accompanied by a composition of the shoulder capsule. A set of tendon or muscle damage (especially the supraspinatus and infraspinatus muscles) can cause a complete tear of the rotator cuff.
In addition to the shoulder joints, other commonly involved sites are: the greater trochanter of the femur, the upper jaw of the elbow joint, the wrist joint (especially around the bean bone) and the knee joint, but the misdiagnosis rate of these parts is higher, the clinician is very Major local swelling and tenderness are associated with calcifications in the para-articular tendons.
Second, the joint calcium phosphate crystal deposition disease
Because it is difficult to identify the alkaline calcium phosphate crystals deposited in the joints in the clinic, little is known about the relationship between the deposition of alkaline calcium phosphate crystals in the joints and its clinical manifestations, but it seems that the disease is clinically manifested. The prognosis is not bad, and it has been noted that the deposition of hydroxyapatite crystals in aged cartilage is a fairly common phenomenon.
(1) Acute synovitis: When hydroxyapatite crystals fall from the calcification to the joint capsule or other joint tissues, it can cause acute calcification para-articular inflammation, and sometimes the crystals in the para-articular calcification will fall off directly. In the joint cavity, for example, there are sometimes direct passages between the subacromial and ankle joints of the elderly, and the crystals often enter the ankle joint directly through these channels and cause acute synovitis.
(2) Chronic monoarthritis: The deposition of alkaline calcium phosphate crystals in the joint can also cause chronic monoarthritis, sometimes even erosive, which is rare and generally not easy to make the disease. diagnosis.
(3) Osteoarthritis: Osteoarthritis is not only the most common concomitant disease in the deposition of alkaline calcium phosphate crystals in the joints, but alkaline calcium phosphate crystals can be found in the joint fluid of 30% to 60% of patients with osteoarthritis. This condition is more pronounced in patients who have previously been treated with intra-articular glucocorticoids. It has been found that the severity of changes in the imaging of knee osteoarthritis and the level of hydroxyapatite in the synovial fluid of the knee are positive. Related, but this does not prove the causal relationship between alkaline calcium phosphate deposition and osteoarthritis in the joints, especially the severe lesions of the subchondral bone are often difficult to distinguish from osteoarthritis, in addition, medical scientists have not found There were other significant differences between the two groups of patients with osteoarthritis with intra-articular crystal deposition and without crystal deposition.
Third, Milwankee shoulder / knee syndrome
McCarty studied 30 patients with specific arthritis and named it Milwankee shoulder/knee syndrome, which has a special clinical, X-ray and synovial fluid.
Clinical manifestation
80% are female patients, and the invasion of the shoulder is mainly accompanied by ankle degeneration and significant rotator cuff tear. The patient is 53 to 90 years old, with an average age of 72.5 years. The incidence is slow, from 1 to 10 years. In most years, most patients experience mild to moderate pain, especially after shoulder activity. A few people also experience severe pain during rest. Other symptoms include limited joint activity, stiffness and nocturnal pain. Restricted, unstable, if you push the humeral head to the shoulder, it can produce bone friction and pain. The joint puncture is often bloody, about 30-40ml, sometimes even up to 130ml.
2. Relevant factors
The factors associated with it include:
1 Injury and overuse: including falls, motorcycle accidents, professional wrestlers and recurrent shoulder arthritis dislocation;
2 congenital shoulder dysplasia;
3 neuropathy: such as cervical radiculopathy or syringomyelia;
4 long-term dialysis patients;
5 Unexplained reasons: about one-third.
Milwankee shoulder/knee syndrome, which may be the result of many causes, is very similar to the rotator cuff tear joint lesion described by Neer et al., and may be the same disease.
3. X-ray features
X-ray can be found in the ankle joint degeneration, soft tissue calcification, humeral head up and down dislocation, articular angiography found rotator cuff tear, most patients' humeral head upper edge to the upper edge of the shoulder is less than 2mm, common condyle, shoulder The lower surface of the peak and the acromioclavicular joint injury, the humeral head, the shoulder and the clavicle often form a pseudo joint. The common humeral head is destroyed, but the spur formation is not serious. These X-ray changes are different from the shoulder joint degenerative arthritis. So far, no such cases have been found in China.
4. Joint fluid characteristics
The number of white blood cells in the joint fluid is often less than 1 × 109 / L. Most of the joint fluid can find alkaline calcium phosphate crystals, granular collagen, and collagenase and protease activity can also be found.
5. Knee joint performance
Of the 30 patients reported by McCarty, 16 had knee joint involvement, of which 30% was lateral stenosis. This form of knee degeneration was different from general knee degenerative arthritis. .
Fourth, secondary alkaline calcium phosphate crystalline joint disease
Some diseases, including chronic failure, autoimmune diseases and nerve damage, can produce calcification deposits. Alkaline calcium phosphate crystals can be deposited in the soft tissues of the joints, bursae and joints, and often combined with some rheumatic diseases. symptom.
It has been reported that calcification is found in the joints of patients with scleroderma, and even chalk-like joint fluid can be extracted. It has also been reported that multiple calcification deposits are found in patients with overlap syndrome.
It has been found that after intra-articular injection of glucocorticoids, para-arterial calcification can occur along the way of needle insertion. Calcification can occur several months after injection, and this calcification can gradually occur after several months or years. absorb.
A neoplastic calcification disease is a single or multiple intra-articular or para-articular, gradual enlargement of calcification deposits, which is more common in Africa, rarely seen in North America and Europe, and if the patient has hyperphosphatemia, the treatment is determined. The method is to limit phosphate uptake, which is often family-oriented.
Uremia can also be associated with the deposition of alkaline calcium crystallization in the joint or adjacent soft tissue. Patients with uremia often have metastatic soft tissue calcification, often accompanied by joint inflammation or para-articular inflammation, crystallization-induced arthritis in uremia It is not uncommon in patients to have urate crystals or alkaline calcium phosphate crystals, and crystallization of dihydrate pyrophosphoryl often combined with secondary hyperparathyroidism.
Examine
Examination of alkaline calcium phosphate crystal deposition disease
Laboratory inspection
1. Identification of hydroxyapatite crystals
The identification of hydroxyapatite crystals requires some unconventional techniques and equipment, because a single apatite crystal is invisible under ordinary light microscopy, and can only be seen under the microscope when many crystals are randomly accumulated into agglomerates. Generally, it is spherical or coin-shaped. The general laboratory can only use some calcium dyeing methods, such as the method of using Alizarin red stain to qualitatively determine the crystal agglomerates under the light microscope. The dyed crystal blocks will have a color. The ring changes like this, but this method can only be used as a primary screening method, and the probability of false positives and false negatives is high.
Electron microscopy is often used to observe the crystal morphology of hydroxyapatite, but the final component identification still requires elemental analysis or electron diffraction. If the laboratory can obtain enough crystals, it can also be X-ray crystal diffraction or Infrared spectroscopy is used to determine the properties of crystals. It is often found that hydroxyapatite crystals are combined with other types of crystals by using these high-tech methods. Among them, calcium pyrophosphate crystals or alkaline calcium phosphate such as octacalcium phosphate are common. Crystals, while the hydroxyapatite crystal itself is also carbonated to varying degrees.
2. Calcium and phosphorus metabolism
The deposition of hydroxyapatite crystals is rarely associated with abnormal metabolism of organisms. Multi-focal deposition, especially large-area crystal deposition or crystal deposition in some rare parts, often indicates that the body may be associated with abnormal calcium and phosphorus metabolism. In particular, hyperphosphatemia is more likely to cause calcium deposition than hypercalcemia alone. In this case, it is necessary to monitor the concentration of calcium and phosphate ions in the blood of the patient and the function of the kidney.
3. Examination of synovial fluid and joint capsule fluid
A typical change in the tissue extract of the joint capsule and other joints in patients with acute calcific para-articular inflammation is a "toothpaste-like" or creamy "white-like suspension of liquid, and sometimes even gray-white gravel-like particles are extracted. The synovial fluid extracted from the joint cavity of patients with alkaline calcium phosphate deposition in the joint has no specific appearance. It is usually viscous and the cell count is not high, similar to the change of synovial fluid of osteoarthritis. In addition, the synovial fluid of patients with senile destructive arthritis is often bloody, and some cartilage fragments are often seen, but the cell count is low.
Other inspection
1.X-ray performance
(1) calcified para-articular inflammation: X-ray plain film is the easiest way to find calcareous deposits, and in practice it is often sufficient to photograph the right lateral flat of the joint, but sometimes it is necessary The image of the internal or external rotation of the shoulder joint to further clarify the calcification after the tibia. It is important to emphasize that the positive side of the contralateral joint needs to be photographed regardless of whether the disease involves the other joint at the same time.
Calcification near the shoulder joint is often located on the circumflex sleeve, especially at a few centimeters from the origin of the supraspinatus tendon, which is often involved, although the subacromial sac is often involved, although clinically sometimes resort to CT or magnetic Resonance technology to find some small calcifications or lesions, but the morphology of calcifications is the clearest in dry-slide photography, and its performance can vary from a few millimeters to several centimeters, but within the joints. Contrast is helpful in diagnosing rotator cuff tears. In addition, some clinicians suggest that once calcium deposits along the shoulders are found, they should be expanded to find other areas of the body (such as knee joints, wrist joints, hands and pelvis). Calcification to exclude multifocal lesions.
The imaging findings of calcification are not static. In the acute stage of calcified para-articular inflammation, the calcification tends to become smaller or even disappear, and it will reappear after the attack. Even in asymptomatic patients, the size of the calcification is also Will fluctuate with changes in calcium and phosphorus metabolism in the body. This phenomenon has been confirmed by radionuclide-labeled diphosphates bone scan test, whether the calcification is enlarged or partially absorbed, on the bone scan phase. The performance of calcification is a "hot spot".
Calcium deposits along the joints are sometimes confused with ossification on the X-ray, but the latter may have trabecular bone formation, which can be identified. Another disease to be diagnosed is calcium pyrophosphate deposition. It is mainly deposited in the fibrous cartilage and joint capsule of the joint, and rarely deposited in the tendon tissue next to the joint, which is typically characterized by a thick linear high-density shadow parallel to the subchondral bone, unlike the alkaline calcium phosphate deposit. A coin-shaped high-density shadow is formed (Fig. 2, 3, 4, 5).
(2) Alkaline calcium phosphate crystal deposition in joints: Alkaline calcium phosphate crystals deposited in joints are almost difficult to image by conventional imaging methods, mainly because these deposits in synovial or synovial fluid of joints The crystal particles are very small, the X-ray is easy to pass through and can not leave an image on the film. Different types of calcifications in different parts have clinical misdiagnosis or missed diagnosis.
2. The synovial fluid, needle aspiration or tissue biopsy is difficult to detect under the light microscope because the BCP crystal is small, but sometimes the visible crystal of the visible light under the optical microscope can also be diagnosed by the Alizarin red stain. (Figure 6), further need to be confirmed by electron microscopy, but the clinical can not be promoted.
3. Pathological examination Most of the pathological studies of this disease were obtained by observing the lesions of the shoulder joints. The main manifestations were the granular deposition of calcium in the fibrous connective tissue. The depositional lesions were uniformly changed in milky white, and there was inflammation infiltration around the lesions. With tissue necrosis or lack of fibrous structure, some hydroxyapatite crystal micro-depositions with diameters of 0.1-0.2 mm can be seen in soft tissues such as tendons, ligaments or joint capsules. Muscle calcification is often accompanied by Degenerative changes, and adjacent blood vessels will undergo some changes similar to vasculitis, including thickening of the vascular membrane, stenosis of the lumen and formation of thrombus, and some small blood vessels may also occlude the lumen, other non- Specific inflammatory changes also include cell proliferation, phagocytosis of giant cells, and neovascularization.
Unlike other diagnostics for crystalline arthrosis, since alkaline calcium phosphate crystals have no birefringence properties, they cannot be diagnosed by phase contrast polarized light microscopy.
It is easy to be confused with osteoarthritis, gout, calcium pyrophosphate deposition, traumatic myositis, rheumatism, and various joint calcifications. Pay special attention to tendon calcification and ossification and bone of alkaline apatite crystal disease. The difference between sputum is valuable for differential diagnosis.
Diagnosis
Diagnosis and identification of alkaline calcium phosphate crystal deposition disease
diagnosis
(1) Identification of crystallization
(B) joint synovial membrane around the shoulder joint, tendon, ligament and bursal tissue is the most common calcification deposit site, Bosworth found that the right shoulder is more common than the left shoulder, and about 50% of patients have deposition on both sides, alkali Calcium phosphate can be deposited almost in the joints or tendons of the whole body. Gondos found that the more active joints, the easier it is to find alkaline calcium phosphate deposits, and found that shoulder calcification accounts for about 69%, followed by hip joints, elbow joints. The wrist and knee joint, and the shoulder with the scapular ligament, the most common deposition unit about 1cm from the attachment of the greater tubercle of the humerus. When the shoulder joint is in the inner and outer rotations, It can be clearly seen that the calcium deposits on the scapular ligament, the calcification of the scapular ligament attached to the sacral nodule, is secondary degenerative calcification, and this degenerative calcification is irreversible. The primary para-arterial calcification is different, and the calcification of calcified para-articular inflammation can become larger, smaller, dispersed, or completely disappear with time.
(3) Clinical manifestations
(4) Typical X-ray performance
Differential diagnosis
1. Acute calcified para-articular inflammation
There are severe pain and tenderness in the acute onset, accompanied by increased redness and skin temperature. These need to be differentiated from gout, pseudo-gout and septic arthritis. The disease mainly involves the shoulder joint and the greater trochanter of the femur. The upper jaw of the elbow joint, the wrist joint (especially around the bean bone) and the knee joint, the calcification of the X-ray beside the shoulder joint, often located on the circumflex sleeve, these predilection sites have a good relationship with the above-mentioned disease The big difference is helpful for clinical identification, and if you can dynamically observe the X-ray changes in the patient's attack site, it is more conducive to the diagnosis of the disease, that is, in the acute phase of the attack, the original clear calcification If the lesion suddenly becomes smaller or even disappears, it is highly suggestive of the disease, while other crystalline osteoarthritis is often very obvious in the acute stage of calcification. If the clinical symptoms and X-ray findings of the disease are not typical, it needs to be extracted. The joint fluid looks for a typical crystal under the microscope to make a diagnosis.
2. Chronic parasympathetic syndrome
The chronic phase of the disease is mainly the manifestation of chronic tendonitis. It needs to be differentiated from tendinitis caused by other diseases in clinical practice. In addition to the specific predilection sites of this disease, local X-ray examination often finds more clear calcification. Stove, but in general, local biopsy is not recommended to confirm the diagnosis.
3. Acute and chronic arthritis
As mentioned earlier, the arthritis caused by the deposition of alkaline calcium phosphate in the joints does not give a definitive diagnosis unless the evidence for the presence of alkaline calcium phosphate is found in the joint fluid, and the disease is clinically Often combined with other joint diseases, especially osteoarthritis, the diagnosis of this disease often does not affect the treatment of the latter, some medical experts suggest that in the actual situation can not consider the diagnosis of the disease, but first treat the merger Arthropathy.
4. Destructive joint disease in elderly patients
The disease needs to be differentiated from Charcot arthritis, chronic septic arthritis, advanced rheumatoid arthritis, osteonecrosis and destructive pyrophosphate arthritis, in addition to the special predilection sites (shoulders, knee joints, etc.) of the disease, clinical Without the characteristics of nervous system diseases, the disease can be distinguished from Charcot joint disease; the common microscopic examination and culture of joint fluid can distinguish it from septic arthritis; and the crystal can be found under phase contrast polarized light microscope. It is helpful to distinguish from other crystalline arthropathy; the identification of osteonecrosis requires X-ray filming of the joint. Except for the specific manifestation of joint deterioration, both sides of the joint line of the disease can be involved. Unlike osteonecrosis, several differential diagnosis of crystalline arthritis (Table 2).
