Degenerative joint disease

Introduction to degenerative joint disease Degenerative arthritis, also known as degenerative arthritis, proliferative arthritis, osteoarthrosis, etc., is the result of years of wear and tear on the joints. This disease occurs mostly in weight-bearing joints such as cervical vertebrae, lumbar vertebrae, knee joints, hip joints. , heel, etc., so long-term or excessive weight should be avoided. Cold and humid are important factors in the disease. The incidence of cervical degenerative diseases is particularly high in long-term workers, poor sleep postures, and inappropriate pillows. This is due to the imbalance of the ligaments and joints of the paravertebral muscles, and the side with large tension is liable to cause different degrees of strain. basic knowledge The proportion of illness: 0.005% Susceptible people: no specific population Mode of infection: non-infectious Complications: synovitis

Degenerative joint disease etiology

Hereditary (15%)

Epidemiological studies have shown that osteoarthritis is a systemic manifestation of a systemic change caused by hereditary metabolic abnormalities. Heberdens nodules can be genetically influenced by a single antosomal gene. Sexual inheritance, recessive inheritance in men, penetrance varies with age, the highest incidence of exogenous women is 30%, in older men, due to recessive hereditary exogenous incidence rate of 3% The precise genetic model is still unclear.

Hormone effect (26%)

Acromegaly articular cartilage changes significantly, and growth hormone (samototrophin) stimulates chondrocytes, which accelerates and enhances the metabolic activity of chondrocytes. When animals age, the growth hormone deficiency is obvious, causing chondrocyte degeneration, chondrocytes Reduced metabolism, diabetes shows progressive abnormalities of chondrocytes, and is highly susceptible to osteoarthritis.

Repeated intra-articular bleeding (20%)

In patients with defective clotting factors, repeated bleeding in the joint may cause serious damage to the articular cartilage and subchondral bone structure. The ionic pigment in the cartilage matrix may change the physicochemical properties of the cartilage, or the chondrocytes engulf a large amount of ionic pigmentation. In the cytoplasm, it can cause lysosome release of degrading enzymes, decrease of protein sugar (PG) concentration, decrease of chondrocyte synthesis activity, and one or occasional intra-articular hemorrhage, without serious problems.

The cause of primary osteoarthritis is unclear. The relevant factors are:

Age

The human body began to degenerate at the age of 20, but it was not obvious until middle age. About 85% of X-ray examinations at 55 to 65 years old showed changes in bone and joint.

2. Gender

The sick male and female are equal. Until the age of 54, male and female were similar in form of illness, and then the female degeneration process was more serious and more extensive than male.

Obesity

Degenerative joint disease doubled in the incidence of obese people, mainly involving weight-bearing joints, and obese men with degenerative joint disease showed more common systemic changes in women.

4. Lesion range

People and people, joints and joints have different degeneration performances. Moreover, there are several types of examinations by the crowd. Before the age of 54 years, the joints were affected and the form was male and female. Women often showed degenerative joint involvement. The carpometacarpal joint and the distal interphalangeal joint often change. In men, the hip joint is more common and can involve any synovial joint. However, the joint that is vulnerable to great pressure is most severely degenerated. The lower spine, the hip joint and the knee joint, due to the strong repetitive muscle strength, the first metacarpophalangeal joint, the first carpometacarpal joint (most angular bone and wrist joint) and the middle cervical vertebra joint, one joint develops osteoarthritis Change, basically non-stress area, Trueta check for different ages, from 14 to 100 years old femoral head showed cartilage degeneration, 71% of femoral head only limited to non-pressure zone degeneration, only 3% degeneration occurred in the pressure zone, the rest 26% of cartilage degeneration occurs in both pressure and non-pressure areas.

5. Inciting factors The cause of primary osteoarthritis is unclear. The cause of secondary osteoarthritis in the joint is determined by the previous state of health and various diseases that alter articular cartilage. It may be a contributing factor to the rate of progression of the degenerative process that already has clinical manifestations or no clinical manifestations.

(1) Inflammatory process

As in rheumatoid diseases, inflammation around the joints and synovial tissue destroys articular cartilage.

(2) metabolic disorders

For example, gout urate precipitation, pigmentation of black uric acid brown brown disease, accumulation in articular cartilage, the characteristics of articular cartilage are prone to destruction, hemochromatosis is similar.

(3) Biomechanical factors

The tendency of cartilage to fatigue (for example, repeated stress and repeated action, cartilage fatigue), therefore, repeated stress, not only produces collagen fiber breakage, but also consumes proteoglycan on the cartilage surface, bone deformity can increase cartilage This repeated stress, due to joint fracture, dislocation, acetabular dysplasia, osteophyte spondylolisthesis and structural abnormalities caused by Perthes disease, will increase the contact pressure due to the reduction of the support load area, osteonecrosis caused by osteonecrosis Collapse, resulting in pathogenic high load pressure.

Joint deformity (such as knee valgus or knee varus), the load is unbalanced, the side is distributed, and the cartilage is destroyed. The abnormal force of the body can cause internal disturbances of the joint, such as using the envisaged joint for a moment. The force transmission center method measures the direction and speed of the joint force. The line connecting any point on the joint surface and the instantaneous joint force transmission center perpendicular to the action surface can be found to be normal under normal and abnormal conditions. The velocity of the joint contact joint surface is parallel to the articular surface. The patient with the medial meniscus tear is generated as a momentary force conduction center. The tendency to reach the cheekbones, this huge contact force caused a meniscus tear, which later resulted in a degenerative joint disease.

The relative compression of the articular surface causes dystrophies of the articular cartilage, leading to necrosis of chondrocytes, followed by the consumption of matrix protein (PG) polysaccharides, so that the articular cartilage can not withstand the pressure and shear of the joint movement, and degenerative changes occur.

Some experimental animals whose knees are fixed by long-term flexion force, the parts that are not in contact with the articular surface, and the adhesion between the articular cartilage and the synovium may be degenerative changes due to cartilage dystrophy.

(5) Chemical damage

The use of chemical drugs systemically or locally damages the vitality and metabolic activity of chondrocytes.

Intra-articular injection of corticosteroids, resulting in greatly reduced synthetic activity, duration from a few hours to a week or more, when the systemic use of corticosteroids, the amount of immunosuppressive agents, also caused by decreased anabolism, loss of PG (glycoprotein), histological changes Known as focal chondromalacia or early osteoarthritis, injections of alkaline drugs (such as nitrogen mustard or mustipipethiotape) can damage articular cartilage.

(6) Changes in ageing

Some researchers believe that fibrosis on the surface of articular cartilage is age-related, and some special parts are asymptomatic (hip: femoral head depression in the femoral head, tibia (medial articular surface) sometimes causes osteoarthritis, age of articular cartilage Aging changes: There are some changes in the articular cartilage of normal people with age, and those age-related changes in immature cartilage also occur during the process of skeletal maturation and adult age, and it is important that these changes The course of the disease, especially those of osteoarthritis, varies.

1 cell change

The number of immature sputum sputum cells is higher than that of adults. The mitotic activity is obvious in the two regions. Cell division is the reason for the gradual increase of osteophyte cartilage. The cell proliferation of basal cells of iliac cartilage is a sign of cartilage ossification. The small tarsal ossification center of the epiphysis, as the animal ages, usually in the first few months after birth, the cell mitosis is progressively reduced before the age of 2, and the whole cell structure of the adult does not change. It is important to find out with age. Increased, the number of cells on the surface of chondrocytes did not change. When the intact articular cartilage was found to have a decrease in surface cells, the increase in the number of cells in the middle layer was an early manifestation of osteoarthritis.

2 collagen

Aging is related to the increase of the mature quantity of collagen fibers. The diameter of the whole fiber area increases, and fragments often appear. The adjacent degenerative cell group often contains a calcification center. At the time of birth, the collagen fiber area runs in the tangential direction except for the superficial fibers. Arranged in a row, except that the deepest fibers adjacent to the bone have a vertical orientation, which is always the same during normal ageing. The surface fibers are often not bundled, but remain perpendicular to the articular surface, in the aged fibrous tissue layer. Replaced by stored non-morphological fragments.

3 protein and aminopolysaccharide, synthesis of mucopolysaccharide (GAG)

The synthesis rate is still absolutely constant, in order to maintain the balance of destruction decomposition and synthesis. The half-life of protein sugar in adult rabbit articular cartilage is short, most of the half-life is about 8 days, other 10,000 points include collagen, and the half-life is very slow. The ratio changes, and the synthetic activity increases significantly in certain osteoarthritic states and after tear injury.

4 chemical composition

6-chondroitin sulfate is an aminopolysaccharide, the basic component of mucopolysaccharide (GAG), which accounts for 45% to 75% of the total composition. In immature cartilage, aminoglycan (Glycosaminoglycan), mucopolysaccharide, and the remaining components are mainly 4 sulfuric acid. Chondroitin and a small amount of keratin sulfate, when the animal ages, the concentration of 4 chondroitin sulfate decreases in adult animals by about 5% of the total mucopolysaccharide GAG. In addition, the amount of keratin sulfate increases with age, and the concentration in adult animals is as high. 50%, normal, only found more chondroitin sulfate in immature cartilage, in the process of compensatory reaction of injury and disease (such as osteoarthritis), chondrocytes recovered a large amount of synthetic 4 sulfate cartilage The role of chondrocytes in the growth of this glycosaminoglycan GAG increased.

After the animal measurement observation, the observation of the articular cartilage of the mature corresponding normal person showed little change, and the articular cartilage moisture, collagen, hexosamine, chondroitin sulfate, total nitrogen, sulfur and the like were changed with age. There is no obvious change in the amount of bone ash. In the process of human aging, whether the collagen fiber morphology changes or the human aging affects the biochemical properties of the collagen fibers of the articular cartilage is not clear, and the number of collagen fiber joints cross-links to the articular cartilage aging. The role is not understood.

5 physics changes

As the permeability of aging articular cartilage decreases, the permeability of articular cartilage is maximized between 10 and 40 years old, and this change in permeability is more pronounced in the superficial part of articular cartilage than in the deep layer.

The elasticity of articular cartilage in normal people does not change with age. When the articular cartilage is loaded with weight, an instantaneous deformity occurs, followed by a creep state (gradual change state). The weight is removed, and the articular cartilage is restored to its original thickness with time. After removal, about 90% of the instantaneous deformity recovered. In addition, after the fibrocartilage load, the deformity was extremely large, and the recovery was slow and incomplete.

Joint tension stiffness refers to the force parallel to the articular surface, and the secondary compression effect produced. The effect on the facial tension of the aging joint needs further study. The osteoarthritis lesions are mainly in the surface of the articular cartilage. Stiffness and weakness are not obvious, but the joint stiffness increases as the lesion deepens.

6 joint cartilage nutrition

Only in the embryo and a short time thereafter, the blood vessels pass from the metaphyseal end of the bone to the various parts of the articular cartilage, and directly enter the epiphysis from the periphery of the articular cartilage, the immature articular cartilage, the epiphyseal plate has not been closed, and therefore the tarsal plate The spheroidal fluid secreted by the lower metaphyseal vessels and joints gains nutrition. After the articular cartilage matures, the calcification zone forms a clear sign. At this time, the epiphyseal plate is closed, and almost all nutrients are obtained by the synovial fluid diffusion. Under pathological conditions, For example, osteoarthritis or complete destruction of articular cartilage, a significant compensatory response, the metaphyseal vessels pass through the subchondral tarsal plate and re-pass the deep calcification zone of the cartilage.

Degenerative joint disease prevention

This disease occurs in middle-aged and old friends who have major joints, so it should be done for middle-aged and elderly people:

1. Control weight or lose weight:

Obesity is an important cause of this disease, so middle-aged and elderly friends should control their body weight and prevent obesity. Once they exceed the standard weight, there is no doubt that weight loss is the most important. After weight loss, it can prevent or reduce joint damage and reduce the disease. The pressure on the joints contributes to the treatment of this disease.

2. Avoid standing for long periods of time and walking long distances:

Because they increase joint tolerance and accelerate joint degeneration.

3. Timely and proper treatment of joint trauma, infection, metabolic abnormalities, osteoporosis and other primary diseases.

4. Calcium supplement:

Should be based on food supplement, pay attention to the balance of nutrition, more dairy products (such as fresh milk, yogurt, cheese), soy products (such as soy milk, soy flour, tofu, yuba, etc.), vegetables (such as day lily, carrots, cabbage) , small rapeseed) and seaweed, kelp, fish, shrimp and other seafood, at the same time should see more sun and vitamin D to promote calcium absorption, if necessary, appropriate amount of calcium supplements, such as calcium gluconate, giant energy calcium is a common clinical price Cheap calcium supplements, but care should be taken to supplement calcium under the guidance of a doctor.

5. Adhere to moderate physical exercise to prevent osteoporosis:

Regular exercise can help protect the joints and prevent the occurrence of osteoarthrosis by strengthening the support of muscles, tendons and ligaments.

6. Pay attention to the joints to keep warm:

This is also important for the prevention of osteoarthrosis, which is often caused by cold joints.

Degenerative joint disease complications Complications Synovitis

The degenerative process of this disease begins with articular cartilage, and the surface articular cartilage changes progressively to the full layer of articular cartilage. With the change of biochemistry, the pressure and tension tolerance are reduced, a large amount of fibrous tissue is formed, and the deep tissue is broken. Crack, finally the cartilage is completely eroded, the subchondral bone is exposed, and the cartilage surface is changed early, while the subchondral bone vessels are increased, the blood vessels are deep into the calcified layer, and the lesion is penetrated. Because the articular cartilage is eroded, the subchondral bone layer and its adjacent The trabecular bone is thickened and thickened. The pathological changes are mainly characterized by degenerative changes of focal articular cartilage, subchondral bone sclerosis, marginal osteochondral callus formation and joint deformity. Clinical manifestations of recurrent pain Joint exudative synovitis, limited stiffness and progressive activity.

Degenerative joint disease symptoms Common symptoms Joint pain Joint stiffness

The disease can occur in all joints of the whole body, but it occurs in the knee joint, hip joint, spine and finger joints with heavy weight, especially knee and hip joint lesions.

Almost all cases have different degrees of pain. As the disease progresses slowly, the pain is obvious when the joint starts to move. The pain is relieved after a little activity. However, when the weight and joint activity are too much, the pain will be aggravated. This is the characteristic of osteoarthrosis. Sometimes the pain can be radioactive. For example, hip pain can be radiated to the inner side of the thigh. Near the knee joint, joint stiffness can be seen early. If the knee joint is in a certain position for a long time, the conscious activity is unfavorable, the starting is difficult, and the joint instability gradually occurs. The range of flexion and extension of joints is reduced and the walking ability is reduced. Especially the lower steps, lower jaw, running, jumping and other ability declines are more obvious. Some patients with advanced osteoarthrosis may also have some lower extremity deformities, and knee inversion is the most common, commonly known as "Road legs".

Degenerative joint disease examination

1, physical examination

Non-inflammatory joints can touch the membrane and hear the dry squeaking of the joints. During the development period, the joints are marginal hyperplasia, the joint capsules are hypertrophy, the joints are enlarged, the movement is limited, the joints are severely damaged, the movement is obviously restricted, and the joints are deformed. Consistent with joint destruction, joint movement never completely loses. When the joint has inflammation, the synovial fluid increases, which can cause limited tenderness in the joint space, no muscle spasm and atrophy. Heberdens nodules are the distal metacarpes of the fingers. A special manifestation of cartilage enlargement, which is usually seen in many fingers, can occur naturally or after trauma, especially in women with menopause, no pain in the nodules or soon after the onset of pain, swelling and tenderness, The mass may be soft and sometimes cystic or sclerotic. The enlarged mass is mainly cartilage, so X-ray examination can not be found, generally no systemic symptoms, age is middle or old, gender: diffuse osteoarthritis women More, after menopause, women develop osteoarthrosis, males only have a heavy relationship and are more common, good hair joints, distal interphalangeal joints, lumbar vertebrae, knees, hips, lower cervical vertebrae The ankle and elbow, the patient's body shape is often obese.

2, laboratory inspection

ESR, blood cell count, normal blood biochemistry, positive heat agglutination test, 10% to 30% of patients with thyroid dysfunction showed dysfunction, can be used for synovial examination for degenerative joint disease and rheumatoid arthritis, identification of infectious arthritis, when acute Inflammatory reaction, joint fluid accumulation is the same as normal synovial fluid when the joint accumulates a large amount of liquid. At this time, the joint fluid is clear, transparent, yellowish, sticky, does not form a clot, and the cell count is normal 60-3000, mainly composed of mononuclear cells. The concentration is the same as blood, and the protein content does not exceed 5.5g/100mL. On the contrary, the synovial fluid of rheumatoid arthritis is thin, turbid and clotted liquid in the case of standing, Ropes test is positive, but osteoarthritis is Is negative, the cell count is often increased by more than 3000, mainly polymorphonuclear cells, total synovial protein is often above 8g, globulin concentration often equals or exceeds albumin, when osteoarthritis with rheumatoid arthritis, slippery Fluid can have the performance of two diseases, therefore, although synovial fluid has a special manifestation of typical rheumatoid arthritis, osteoarthritis cannot be excluded, so Can only be diagnosed by the main cause synovial fluid, addition, osteoarthritis synovial fluid has the characteristics of rheumatoid arthritis in stationary phase may, once the two diseases are in doubt, synovial fluid must be checked repeatedly.

3, X-ray inspection

Early X-ray examination of osteoarthritis was normal, and the joint space stenosis gradually appeared later, reflecting the thinning of the articular cartilage layer covering the cortex. Finally, the osteoarthrosis progressed progressively, the joint space was narrowed, and the joint edge became sharp. Bone spurs or osteophyte formation at the edge, thickening and sclerosis of the subchondral bone, bone cysts occur in the largest part of the subchondral bone compression, X-ray film negative can not rule out osteoarthritis, on the contrary, X-ray examination There is a typical manifestation, and it is not certain that it is primary osteoarthritis. Degenerative changes often have other diseases at the same time. Gout, infectious arthritis and rheumatoid arthritis are worth noting.

Diagnosis and differentiation of degenerative joint disease

diagnosis

Non-inflammatory joints can touch the membrane and hear the dry squeaking of the joints. During the development period, the joints are marginal hyperplasia, the joint capsules are hypertrophy, the joints are enlarged, the movement is limited, the joints are severely damaged, the movement is obviously restricted, and the joints are deformed. Consistent with joint destruction, joint movement never completely loses. When the joint has inflammation, the synovial fluid increases, which can cause limited tenderness in the joint space, no muscle spasm and atrophy. Heberdens nodules are the distal metacarpes of the fingers. A special manifestation of cartilage enlargement, which is usually seen in many fingers, can occur naturally or after trauma, especially in women with menopause, no pain in the nodules or soon after the onset of pain, swelling and tenderness, The mass may be soft and sometimes cystic or sclerotic. The enlarged mass is mainly cartilage, so X-ray examination can not be found, generally no systemic symptoms, age is middle or old, gender: diffuse osteoarthritis women More, after menopause, women develop osteoarthrosis, males only have a heavy relationship and are more common, good hair joints, distal interphalangeal joints, lumbar vertebrae, knees, hips, lower cervical vertebrae The ankle and elbow, the patient's body shape is often obese.

Differential diagnosis

The disease needs to be differentiated from bone destruction caused by ischemic necrosis. The avascular necrosis of the femoral head and degenerative arthritis of the hip are used as examples to identify the two diseases:

1, avascular necrosis of the femoral head is due to partial or complete ischemia caused by bone and bone marrow cell components necrosis, can be seen after trauma, hormone therapy, blood disease, some metabolic diseases and non-specific arthritis, etc., cause More, the pathology is divided into four phases:

(1) Stage I is a blood supply disorder and partial bone marrow component necrosis;

(2) Stage II is reactive hyperemia and inflammation and partial bone resorption in the infarct area;

(3) Stage III is the formation of new blood vessels and new bone formation during the repair period;

(4) Stage IV is the stenosis and degeneration of joint space.

Because of the different pathological basis of each period, the imaging performance is different. Early X-ray and CT examinations can be found without positive findings, but the sensitivity of magnetic resonance is higher, especially the fat suppression sequence (STIR), for the early femoral head. Necrosis is more sensitive, showing a strong signal, MRI findings of bone marrow edema: T1 weighted low signal, T2 weighted signal or high signal change, fat suppression sequence (IR) is high signal, generally wide range, including stocks The area of bone necrosis, the femoral neck, and even the upper femur and the entire femur, the signal changes to diffuse, and the signal is reduced due to fibrosis and hardening of the bone in the middle and late stages of the lesion.

2, hip degenerative osteoarthritis is divided into two primary and secondary, primary more common after the age of 50; secondary often due to congenital dislocation of the hip, acetabular dysplasia, fracture, Dislocation, as well as avascular necrosis of the femoral head, after the degeneration, articular cartilage becomes brittle, thin and worm-like defects, and bone surface sclerosis, due to high pressure in the joint capsule, cartilage destruction and osteoporosis and sac Change in shape, degeneration and hyperplasia to form bone spurs.

The manifestations of MRI are: the surface of the cartilage is not smooth, the local thinning is an early change after degeneration of the cartilage, the abnormal low signal of the articular cartilage, and the low signal hardening zone in the femoral head and acetabular subchondral bone (T1WI and T2WI) or femoral head morphological changes, further development of T1WI low signal in the acetabulum and femoral head, subchondral cyst and joint cavity effusion with high signal of T2WI, free body in some joint cavity, neck cavity gradually narrowed, even Subluxation occurs, because the viewing angle of the X-ray film is limited, and it is an overlapping image. When the hip joint has a slight morphological change of the femoral head, it can not be judged whether there is bone necrosis change, and early pathological changes can not be reflected, although some Indirect signs can also have certain discriminative value, such as secondary hip degenerative osteoarthritis often originated from congenital hip dysplasia, measuring neck stem angle straightening or Shentong's line discontinuity and acetabular fossa Shallow, etc., contribute to the acquisition of indirect signs, but imaging is a three-dimensional science, and horizontal level images are useful for observing the morphological changes of the femoral head.

Therefore, CT further realizes the detection of bone destruction and saccular light transmission, but magnetic resonance imaging is hydrogen proton imaging, which is more sensitive to the pathological reaction of early femoral head necrosis, and is a true full three-dimensional scan, which is X-ray and CT can not compare the detection means, therefore, because X-ray film and CT for the diagnosis of avascular necrosis of the femoral head and the diagnosis of degenerative osteoarthritis limited information, so early hip joint lesions should be combined with magnetic resonance examination, comprehensive, Accurate clinical diagnosis.

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