Proliferative osteoarthropathy

Introduction to proliferative osteoarthrosis The clinically common proliferative osteoarthrosis can have multiple names, including degenerative arthritis, osteoarthritis, and hypertrophic arthritis. This disease is caused by the degeneration of the joints, resulting in the destruction of articular cartilage. Arthropathy. basic knowledge The proportion of illness: 0.006% Susceptible people: no specific population Mode of infection: non-infectious Complications: traumatic synovitis of the knee joint Synovitis

Causes of proliferative osteoarthrosis

Age factor (35%):

About 80% of people over the age of 60 have joint degeneration and show proliferative changes on X-ray films, but this group does not necessarily have symptoms.

Familial inheritance (20%):

The Heberden nodules on the dorsal aspect of the distal interphalangeal joint may be gender-affected autosomal monogenic genetic diseases. Most women are dominant, and the penetrance rate of older women is 30%. Men are mostly recessive, and the penetrance rate is only 3%, which is 1/10 of the former.

Joint weight (15%):

Clinical findings: When the body is too obese, especially when the load on the lower limbs and the spine is too large, it will inevitably impede the nutrition of the articular cartilage. Therefore, the incidence of this type of population is doubled compared with the general population.

Secondary factors (10%):

The so-called secondary osteoarthrosis refers to cartilage destruction or joint structure changes caused by a known cause, such as trauma, surgery or other obvious factors, due to joint surface friction or pressure imbalance, etc. Degenerative changes, in most cases, anatomical or qualitative abnormalities can be found, so some people think that osteoarthrosis is secondary.

Trauma of various joints, inflammation, abnormal metabolites, massive iron deposits after repeated bleeding, and intra-articular injection of adrenal corticosteroids and alkylating agents can directly damage articular chondrocytes or matrices, or It is caused by the destruction of the nutrition of the cartilage, which is gradually worn out, resulting in secondary osteoarthrosis, which is relayed to the latter, called traumatic arthritis. In addition, certain endocrine abnormalities, such as diabetes, can be Abnormal chondrocytes, prone to secondary osteoarthrosis; abnormal joint structure, especially for poor line, so that the corresponding joint surfaces are not well-contacted, uneven contact, resulting in loss of the tube due to pressure imbalance, so that Normally ordered cartilage nutrition exchange procedures are destroyed, and over time, secondary osteoarthrosis occurs.

Pathogenesis

The early changes of chronic osteoarthrosis occur first in the articular cartilage. The cartilage surface of the joint bearing area appears dry, tarnished, pale yellow, and the elasticity is reduced. The surface is fibrillar and has a fluffy sensation. Further, the cartilage surface can be broken. Vertical fissures appear, and then, as the surface of the cartilage wears out, it becomes thinner, and horizontal fissures gradually appear, so that the surface cartilage splits into small fragments and can fall into the joint cavity. At the most stress and friction, the cartilage gradually becomes full. The layer is destroyed, so that the cartilage calcification layer and even the subchondral bone are exposed, the blood vessels and fibrous tissue in the submedullary cavity are proliferated, new bones are continuously generated, deposited under the bare bone surface, forming a hardened layer, and the surface thereof is polished like ivory. It is called dentin, and the site with the least compressive stress can have osteoporosis, and the new bone grows in the direction of least resistance. This naturally forms the epiphysis at the edge of the joint. The bone with the greatest stress is under pressure. Effects of microfracture, necrosis, formation of mucinous bone, necrotic trabeculae, cartilage-like fragments and fibrous tissue cysts, later, The subchondral bone collapses and deforms, and the surrounding hyperplastic bone bulges, making the joint surface more incompletely occluded, and further restricting joint activity and aggravating symptoms.

Joint synovial membrane and joint capsule are stimulated by detached cartilage fragments and become congested, edema, hyperplasia, hypertrophy, increased synovial fluid, secondary serous inflammation, pain, muscle spasm and other symptoms, joint capsule contracture and fibrosis Leading to fibrous ankylosis, Weiss believes that the above series of changes indicate articular cartilage degeneration, it can be said that this is the failure of the human body to repair the degenerative cartilage.

Proliferative osteoarthrosis prevention

Reducing joint burden, reducing weight, avoiding excessive weight bearing, and protecting joints are all ways to prevent bone and joint hyperplasia. However, this is a degenerative disease, so reducing the weight bearing and excessive large-scale activities of the joints, and cherishing the diseased joints is of great significance for delaying the progression of the lesions.

Proliferative osteoarthrosis complications Complications knee traumatic synovitis synovitis

Can be complicated by intra-articular free body and traumatic synovitis.

Symptoms of proliferative osteoarthrosis Common symptoms Joint hard joint pain Joint swelling of the transverse stripes Deepening of the skeletal joint hypertrophy

Depending on the course of the disease, the symptoms vary greatly, but the performance of most patients is not typical, especially in the early cases, only 5% of the people have symptoms, the majority of patients are over 50 years old, elderly patients, the disease is slow onset There is no systemic symptoms, usually multiple joints, and there are single joints. The affected joints may have persistent dull pain. When the activity increases, the weight increases. After the break, the pain is often not serious. When the pressure is reduced, it is aggravated. Therefore, it is related to climate change. Sometimes there may be acute pain episodes and joint stiffness. Occasionally, there may be frictional sounds in the joints. After a long sitting, the joints will become stiffer, but after a little activity, it will be better. Some people call it "rest pain", and the joints are swollen and enlarged. Large and restricted movement, but rarely fully rigid, generally manifested as bone block.

Examination of proliferative osteoarthrosis

There is no abnormal change in blood cell sedimentation rate and blood. The joint fluid is often clear, yellowish and highly viscous. The white blood cell count is usually within 1.0×109/L, mainly mononuclear cells, and the mucin clot is solid.

X-ray film: There was no obvious abnormality in the early stage, and the joint space stenosis gradually appeared after several years. This indicates that the articular cartilage has begun to thin. At the beginning, the joint space is normal when the weight is not heavy, and the stenosis occurs after the weight bearing. There is significant stenosis in the joint space, microscopic fracture under the cartilage, and then bone sclerosis. Finally, the edge of the joint becomes sharp and there is osteophyte formation. Under the cartilage, there may be a bony cavity under the cartilage. Signs of osteoarthrosis.

CT and MRI examination : abnormal changes in articular cartilage and subchondral bone can be found at an early stage.

Diagnosis and differentiation of proliferative osteoarthrosis

According to the chronic medical history, clinical manifestations and X-ray findings, the diagnosis is relatively easy. If necessary, the joint synovial fluid examination can be performed to confirm the diagnosis. The X-ray changes cannot indicate the primary osteoarthrosis. It should be clear from the medical history that the lesion is the original. Hairy or secondary.

Differential diagnosis

Acute rheumatic fever

1 The onset is acute, the systemic symptoms are heavy, and the duration is short.

2 The skin on the joint surface is red hot.

3 affected joint pain, tenderness, severely migratory, no joint dysfunction.

More than 4 with heart disease.

The 5X line inspection has no change.

2. Rheumatoid arthritis

More than 1 in 20 to 50 years old.

2 severe acute attacks, systemic symptoms are lighter and last longer.

3 The affected joint is more symmetrical or multiple, and does not invade the distal interphalangeal joint.

4 early joint swelling was fusiform, late dysfunction and tonic deformity.

5X line examination of local or systemic osteoporosis, articular surface absorption of bone healing and straight deformity.

6 laboratory examination of rapid blood sedimentation, rheumatoid factor positive.

3. Ankylosing spondylitis

1 more than 15 to 30 years old male youth.

2 slow onset, intermittent pain, multiple joint involvement.

3 spinal activity is limited, joint deformity, morning stiffness.

4X-ray examination showed that the ankle joint space was narrow and the ligament of the spine was calcified, which was a bamboo-like change.

5 laboratory examination of rapid or normal blood sedimentation, HLA-B27 is positive, rheumatoid factor is mostly negative.

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