On October 12, 2001, the Ministry of Health, with the support of the Arthritis Prevention Education Program Foundation, organized domestic experts in orthopedics and rheumatology to draft a guideline for the diagnosis and treatment of osteoarthritis (draft), and he provided standardized treatment for physicians nationwide to perform OA.
Osteoarthritis is a common and frequent chronic joint disease in clinical practice. It is an osteoarthrosis caused by fibrosis, chafing, ulceration and loss of articular cartilage due to various causes.
The main clinical manifestations are deformation and destruction of articular cartilage, subchondral bone sclerosis or cystic changes, osteophytes at the joint edges, synovial pattern hyperplasia, joint capsule contracture, ligamentous laxity or contracture, and muscle atrophy and weakness (i.e., chronic joint disease characterized by degenerative changes of articular cartilage and secondary osteophytes).
Epidemiology of OA to the middle-aged and elderly, more women than men, now 30 years old is often present, the prevalence rate of 50% in people over 60 years of age, and up to 80% in people over 75 years of age, the disability rate of the disease can be as high as 53%, OA occurs in joints with a large load, more activities, such as the knee, spine (cervical and lumbar spine), hip, ankle, fingers and other joints.
Classification According to the presence or absence of local and systemic pathogenic factors, osteoarthritis is divided into two categories of primary and secondary causes. The commonly referred to osteoarthritis is primary.
Primary OA mostly occurs in middle-aged and elderly people, with no obvious systemic or local causative factors, and is related to genetic and physical factors.
Secondary OA can occur in young adults and can be secondary to trauma, inflammation, joint instability, chronic recurrent cumulative strain or congenital disease.
Etiology Primary OA is an osteoarthropathy of unknown etiology, without genetic defects, systemic metabolic and endocrine abnormalities, trauma, infection, or congenital deformities. The primary etiology is unknown, and cartilage damage is caused by eight speculative theories.
(i) Abnormal cartilage metabolism Cartilage is composed of collagen, proteoglycan, and water. Basal cells show increased metabolic activity after damage to the cartilage surface, as evidenced by isotopic studies: increased uptake of deuterated-thymidine nucleotides, suggesting increased DNA synthesis and replication. The regulation of this repair mechanism is influenced by the endocrine system in the body. Disruption of regulatory mechanisms can contribute to the development of osteoarthritis. For example, insulin promotes the entry of 35S04 into cartilage and facilitates the synthesis of proteoglycans. Inadequate insulin in diabetic patients may be one of the causes of osteoarthritis. Growth hormone has a stimulating effect on cartilage, and the deficiency of growth hormone can lead to degenerative changes of cartilage. Androgens have a promoting effect on osteoarthritis, while estrogens have an inhibiting effect on it. But no single abnormality of the endocrine system can perfectly explain the development of osteoarthritis.
(ii) Degradation of cartilage matrix by enzymes Osteoarthritis is often associated with synovial inflammation, and experiments have shown that synovial inflammation can increase intra-articular pressure, and when the pressure rises by 5-10 mmHg, it can cause impaired blood circulation in synovial veins, resulting in a decrease in oxygen partial pressure, which in turn leads to an increase in alkaline phosphatase and granulolytic enzymes produced by periosteal cells, which can further digest the chondroitin sulfate chain in proteoglycans, causing cartilage mechanical properties are compromised, leading to arthritis generation.
(iii) Alteration of biochemistry The physical properties of cartilage are mainly generated due to the presence of highly hydrated macromolecular proteoglycans and collagen fibrous cells together. In animal experiments, it is shown that the earliest physicochemical property of osteoarthritis is the increase of water in cartilage, which is due to the damage of collagen network in cartilage after the proteoglycan chains open and bind a large amount of water, thus changing the physical properties.
(iv) Altered nutrition: cartilage is not vascularized and synovial fluid is the only way to supply nutrients and process metabolites. When nutrition is inadequate, the proliferation of chondrocytes is affected, thus failing to repair cartilage defects and making cartilage weak, resulting in degeneration.
(v) Injury, trauma is one of the most important conditions that cause osteoarthritis. Superficial damage to cartilage is caused by violence and frequent blunt, repetitive injuries. This produces chondrocyte division, basal synthesis, and increased activity of catabolic enzymes, such as deep surface damage to articular cartilage, subchondral bone hematoma, mechanization, granulomatous proliferation, new bone formation and fibrosis, and bone hardening, which reduces the ability of articular cartilage to produce deformation during impact loading. This further aggravates the cartilage damage, and if the joint is continuously braked after the injury, especially in joints that are relatively cartilage-dense and maintain a certain pressure, osteoarthritis can quickly develop.
It is also suggested that cartilage is best preserved where the joint surface receives a certain amount of pressure intermittently, because this intermittent pressure promotes the entry of certain nutrients from the synovial fluid into the cartilage.
(vi) Obesity: Weight gain is directly proportional to the development of valgus arthritis. Obesity is also an aggravating factor. Weight loss in obese individuals may reduce the incidence of knee osteoarthritis
(vii) Bone density: When subchondral trabeculae become thin and stiff, they are less tolerant to stress and therefore have a greater chance of developing osteoarthritis in people with osteoporosis
For example, osteoarthritis of the hip and carpometacarpal joints is more common in Caucasians, but less common in people of color and nationalities, and gender also has an effect, with the disease being more common in women. Data show that in women with heberden’s nodes, the incidence of osteoarthritis in their mothers and sisters is 2-3 times higher than in family members without the disease.
The development of osteoarthritis is a long-term, gradual process that involves many systemic and local factors. Therefore, its development may be a combination of factors.
Secondary osteoarthritis is caused by congenital malformations, trauma, intra-articular fractures, ischemia, joint instability, or long-term application of glucocorticoids with.
Pathology
1 Cartilage: articular cartilage – softening, erosion, bone exposure
2 Bone: bone densification – surrounding cystic changes – resorption – cystic enlargement – surrounding generation of reactive sclerotic wall.
3 Synovial membrane: due to the stimulation of exfoliated cartilage fragments and proliferated bone, the synovial membrane undergoes ① proliferative synovitis: a large amount of synovial value-added, edema, and increased synovial fluid, showing grape bunch-like changes. In fibrous synovitis, the synovial fluid decreases and most of the grape bunch-like changes disappear and are replaced by fibrous tissue proliferation forming strips.
4 The joint capsule and surrounding muscles: the joint capsule also has fibrous hyperplasia, thickening, muscle spasm, joint movement is limited, and flexion deformity occurs.
Clinical manifestations
1: Pain and pressure through: early mild dull pain, gradually aggravated, pain aggravated by activity, alleviated by rest, some patients catch pain at rest or in the morning, alleviated by slight activity, called rest pain. Excessive activity can also cause pain, which can be aggravated by cold and moisture, and limping.
Hip pain sites are in the anterior, lateral, and medial thighs, and can often be reflected to other sites, such as: the sciatic nerve travel area, near the knee joint.
The point of pressure pain is at the attachment point of the ligament.
2: Stiffness: Another complaint of hip osteoarthritis is stiffness and tightness of the joint after waking up in the morning or after resting during the day, which disappears after activity, and the stiffness of the joint is aggravated when the air pressure decreases or the air humidity increases, and the duration is generally short, often a few minutes to ten minutes, rarely more than 30 minutes, which is the point of differentiation from other diseases.
3 Bone rubbing sound (sense): Due to the destruction of articular cartilage and uneven joint surface, bone rubbing sound (sense) appears when the joint moves, mostly in the knee joint. Or a popping sound when moving.
4: Joint swelling, joint effusion: With synovitis is possible to have joint swelling, hand joint enlargement and deformation is obvious, Heberden’s nodes (and Bouchard’s nodes) may appear. Some knee joints may also be enlarged due to bone formation or joint effusion. Arthritis sometimes has effusion present, and knee effusion is more pronounced, and the floating patella test may be positive.
5: Dysfunction: Due to muscle atrophy and soft tissue contracture can cause joint weakness, soft fade or joint strangulation when walking, inability to fully straighten or impaired movement.
The hip joint is flexed, externally rotated, and internally retracted position to reduce intra-articular pressure and relieve pain, and Thomas sign is positive.
In the knee joint, there is a feeling of instability when walking, inability to fully extend the knee, or even a contracted flexion deformity, coarse knee joint due to muscle atrophy, inversion and valgus deformity, etc.
6: X-Ray film: no change in the early stage.
Late stage: the joint space becomes narrower, there is bone superfluous formation at the edge of the joint, the joint surface is not smooth, irregular and fractured, the femoral head becomes flattened, the neck becomes shorter, the bone density at the top of the acetabulum increases, the socket fossa becomes deeper, the cartilage bone plate is dense or small cystic changes can be seen, round in shape, the wall of the capsule is dense.
7 Laboratory tests: Blood tests, protein electrophoresis, immune complexes and serum complement are generally in the normal range. Patients with synovitis may have mildly elevated c-reactive protein (CRP) and hematocrit (ESR). Patients with secondary OA may present with abnormal laboratory tests of the primary disease.
Diagnosis (see Tables 1 and 2 below)
Treatment
The goal of treatment for OA is to reduce or eliminate pain, correct deformity, improve or restore joint function, and improve quality of life.
The overall treatment principle for OA is a combination of non-pharmacological and pharmacological treatment, with surgical treatment if necessary, and treatment should be individualized. The treatment should be individualized, taking into account the patient’s own situation, such as age, gender, weight, own risk factors, lesion location and degree, etc. to choose the appropriate treatment plan.
1: Non-pharmacological treatment: It is the basis of pharmacological treatment and surgical treatment, etc. For patients with OA who present for the first time and who do not have severe symptoms, non-pharmacological treatment is the preferred treatment modality, aiming to reduce pain, improve function and enable patients to have a good understanding of the nature and prognosis of the disease.
① Patient education A self-behavioral therapy (reduce unreasonable exercise, moderate activity, avoid poor posture, avoid prolonged running, jumping, squatting, reduce or avoid climbing stairs), B weight loss, C aerobic exercise (such as swimming, bicycling, etc.), D joint function training (such as knee flexion and extension in the non-weight-bearing position to maintain maximum joint mobility), E muscle strength training (such as hip OA should pay attention to the training of the abductor muscle group ), etc.
Physical therapy mainly increases local blood circulation and reduces inflammation, including heat therapy, hydrotherapy, ultrasound, acupuncture, massage, traction, transcutaneous electrical nerve stimulation (TENS), etc.
③ Mobility support Mainly to reduce the weight-bearing of the affected joint, including cane, crutches, walker, etc.
④ Change the line of weight bearing According to the inversion or valgus deformity associated with OA, appropriate braces or orthopedic shoes are used to balance the load of each joint.
Appropriate rest is very important, allowing self-care, body rest for severe cases, and appropriate weight loss for obese people, which can be supported by crutches, canes, walkers, etc.
2: Drug treatment
① Non-steroidal analgesics can be applied for pain (see Table 1 and 2)
② condition improving drugs and chondroprotective agents including diacetin, glucosamine, avocado soybean unsaponifiables (ASU), doxycycline, etc. These drugs can slow down the course of the disease and improve the patient’s symptoms to some extent. Diacerein has structural modulating effects.
Intracavitary injection: Hyaluronate is an emerging drug in recent years, which can lubricate joints, protect joint cartilage, and promote cartilage repair. If the effect of oral drug treatment is not obvious, joint cavity injection of hyaluronane-like viscoelastic supplements can be combined, and joint fluid should be aspirated before injection.
Glucocorticoid application has been gradually eliminated in recent years because it can destroy the production and repair of cartilage. If the pain is particularly heavy, the exudation is particularly large, and the treatment with NSAIDs is ineffective for 4-6 weeks for severe OA or those who cannot tolerate NSAIDs, intra-articular injection of glucocorticoid is feasible. However, if used for a long time, it can aggravate the damage of joint cartilage and worsen the symptoms. Therefore, intra-articular injection of glucocorticoids is not recommended, and it is opposed to repeated use for several times, generally no more than 3-4 times per year.
Chinese herbal medicine: Shujiaozhi and blood-strengthening tablets, Dong Yue consume shake (19), and gun urgently cynical consume according to the inscription (13) base
3: Surgical treatment.
① Early stage: arthroscopic joint cleaning can be performed to clean the synovial membrane and remove the free body.
② Late stage.
A osteotomy
B hip arthrolysis
C arthrofusion (knee, hip)
D artificial hip replacement (knee, hip)