How is osteoarthritis diagnosed and treated?

  I. Background
  On January 13, 2000, the World Health Organization (WHO) launched a worldwide “Bone and Joint Decade” to raise awareness of bone diseases among governments, medical research institutions, the public, and society at large. This includes Osteoarthritis (OA).
  OA is a common disease that is increasing in its impact on the health of people and in the cost of medical care. On October 12, 2001, the Ministry of Health (MOH) organized a campaign to promote World Arthritis Day and decided to establish the MOH Arthritis Prevention and Control Education Program Fund. With the support of this fund, a draft guideline for the diagnosis and treatment of osteoarthritis was drafted by domestic orthopedic and rheumatologic experts, which provides standardized guidance for the diagnosis and treatment of OA by physicians nationwide.
  However, it has been more than 4 years since the publication of the draft guideline, especially in recent years, with the in-depth understanding of the occurrence and development mechanism of OA, there are many contents in the guideline that need to be updated, therefore, on the basis of foreign OA guidelines 1-12 and literature 19-23, the previous version of the guideline was revised, taking into account the specific situation of China. This guideline is only an academic guideline, and its implementation must still depend on the patient and the specific medical situation. Before taking any preventive and therapeutic measures, you should refer to the relevant product descriptions.
  II. Overview
  OA refers to a joint disease caused by a variety of factors that lead to fibrosis, cracking, ulceration, and loss of articular cartilage. The cause is not clear, its occurrence is related to age, obesity, inflammation, trauma and genetic factors. Its pathology is characterized by degenerative destruction of articular cartilage, subchondral osteosclerosis or cystic changes, osteophytes at the joint edges, synovial hyperplasia, joint capsule contracture, ligamentous laxity or contracture, and muscle atrophy and weakness.
  OA is more common in middle-aged and elderly patients, with more women than men, and the prevalence can reach 50% in people over 60 years of age and 80% in those aged 75 years. OA occurs in joints with high load and high activity, such as the knee, spine (cervical and lumbar spine), hip, ankle, hand and other joints.
  Three, classification
  OA can be divided into two categories: primary and secondary. Primary OA occurs mostly in the middle-aged and elderly, no clear systemic or local causes, and genetic and physical factors have a certain relationship. Secondary OA can occur in young adults, can be secondary to trauma, inflammation, joint instability, chronic and repeated cumulative strain or congenital diseases.
  IV. Clinical manifestations
  (A) symptoms and signs
  1. Joint pain and pressure pain: Initially, it is mild or moderate intermittent hidden pain, which improves at rest and worsens after activity, and the pain is often related to weather changes. In the late stage, there may be persistent pain or nocturnal pain. There is localized pressure pain in the joints, which is especially obvious when accompanied by joint swelling.
  2. Joint stiffness: stiffness and tightness of the joints when waking up in the morning, also known as morning stiffness, can be relieved after activity. Joint stiffness is aggravated when air pressure decreases or air humidity increases, and the duration is usually short, often a few minutes to ten minutes, rarely more than 30 minutes.
  3. Enlarged joints: The joints of the hands are obviously enlarged and deformed, and Heberden’s nodes and Bouchard’s nodes may appear. Some of the knee joints may also be enlarged due to the formation of osteoid or joint effusion.
  4. Bone rubbing sound (sensation): Due to the destruction of articular cartilage and uneven joint surface, bone rubbing sound (sensation) appears when the joint moves, mostly in the knee joint.
  5, joint weakness, activity disorders: joint pain, decreased mobility, muscle atrophy, soft tissue contracture can cause joint weakness, walking with soft legs or joint locking, can not be fully straightened or activity disorders.
  (B) Laboratory tests: blood routine, protein electrophoresis, immune complexes and serum complement are generally within normal limits. Patients with synovitis may have mildly elevated C-reactive protein (CRP) and hematocrit (ESR). Patients with secondary OA may have abnormal laboratory tests of the primary disease.
  (C) X-ray examination: asymmetric joint space narrowing, subchondral bone sclerosis and/or cystic changes, joint edge hyperplasia and bone redundancy formation or with varying degrees of joint effusion, some of the joints can be seen in the free body or joint deformation.
  V. Diagnostic points
  It is generally not difficult to diagnose OA based on the patient’s symptoms, signs, X-ray manifestations and laboratory tests, and the diagnosis can be made by referring to the diagnosis and assessment process of OA in Figure 1. This guideline proposes diagnostic criteria for knee and hip OA for reference (Table 1, 2). The diagnostic criteria are basically based on the criteria developed by Altman and discussed by some orthopedic experts.
  VI. Treatment
  The purpose 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 of OA is a combination of non-pharmacological and pharmacological treatment, surgical treatment when necessary, and treatment should be individualized. Combine the patient’s own situation, such as age, gender, weight, own risk factors, lesion site and degree, etc. to choose the appropriate treatment plan.
  (i) Non-pharmacological treatment: It is the basis of pharmacological treatment and surgical treatment, etc. For the first visit and the symptoms of OA patients are not heavy non-pharmacological treatment is the preferred treatment modality, the purpose is to reduce pain, improve function, so that patients can well understand the nature of the disease and prognosis.
  1, patient education: self-behavioral therapy (reduce unreasonable exercise, moderate activity, avoid poor posture, avoid prolonged running, jumping, squatting, reduce or avoid climbing stairs), weight loss, aerobic exercise (such as swimming, bicycling, etc.), joint functional training (such as knee flexion and extension activities in a non-weight-bearing position to maintain maximum joint mobility), muscle strength training (such as hip OA should pay attention to the training of the abductor muscle group) etc.
  2. Physical therapy: mainly to increase local blood circulation and reduce 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, cane, crutches, walkers, etc. can be used.
  4. Change the line of negative gravity: according to the inversion or valgus deformity associated with OA, use the corresponding orthopedic brace or orthopedic shoes
  to balance the load of each joint surface.
  (2) Drug treatment: If non-drug treatment is ineffective, drug treatment can be selected according to the joint pain.
  (1) Local drug therapy: For hand and knee OA, it is recommended to choose local drug therapy before using oral drugs. Topical drug therapy can use non-steroidal anti-inflammatory drugs (NSAIDs) emulsions, creams, patches and non-NSAIDs rubs (capsaicin, etc.). Topical topical medications can be effective in relieving mild to moderate joint pain with mild adverse effects. For moderate to severe pain, topical drugs can be used in combination with oral NSAIDs.
  2. Systemic analgesic drugs: according to the route of administration, they are divided into oral drugs, injections and suppositories.
  (1) Medication principles.
  ① Conduct risk assessment before drug administration and pay attention to the risk of potential medical diseases.
  (2) Individualize the dose according to the individual patient’s condition.
  (3) Use the lowest effective dose possible and avoid overdose and repeated or superimposed use of similar drugs.
  ④ Use the drug for 3 months and check blood and stool routine, fecal occult blood and liver and kidney function according to the condition of choice.
  (2) Drug administration method.
  ① Patients with OA generally choose acetaminophen, with the maximum daily dose not exceeding 4000 mg.
  (2) In patients with OA who are not well treated with acetaminophen, NSAIDs are used on a case-by-case basis after weighing the risk of gastrointestinal, hepatic, renal, and cardiovascular disease in patients (Table 3). The efficacy and adverse effects of oral NSAIDs are not identical in individual patients, and selective dosing should be performed after referring to drug instructions and assessing risk factors for NSAIDs (Table 4). If patients are at high risk for gastrointestinal adverse reactions, non-selective NSAIDs plus gastric mucosal protectors such as H2 receptor antagonists, proton pump inhibitors or misoprostol, or selective COX-2 inhibitors may be used.
  ③Other analgesic drugs. patients with OA who are ineffective or intolerant to NSAIDs treatment can use tramadol, opioid analgesics, or a combination of acetaminophen and opioids.
  3.Joint cavity injection.
  ①Sodium hyaluronate, if oral medication is not effective, joint cavity injection of sodium hyaluronate-like viscoelastic supplements can be combined with injection of chilblains in aspirated joint fluid.
  ②Glucocorticoids, intra-articular injection of glucocorticoids is feasible for those with severe OA or those who cannot tolerate NSAIDs drug therapy for 4-6 weeks, persistent pain and marked inflammation. However, if used for a long time, it can aggravate the damage of joint cartilage and aggravate the symptoms. Therefore, intra-articular glucocorticosteroid injections are not recommended, and repeated use is not recommended, generally no more than 3 to 4 times a year.
  4, improve the condition of drugs and chondroprotective agents: including diacetin, glucosamine, avocado soybean unsaponifiables (ASU)
  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.
  (iii) Surgical treatment
  The purpose of OA surgical treatment is to: (1) further assist in diagnosis, (2) reduce or eliminate pain, (3) prevent or correct deformity, (4) prevent further aggravation of joint destruction, (5) improve joint function, and (6) be part of a comprehensive treatment.
  The main methods of OA surgical treatment are: (1) free body removal, (2) joint debridement, (3) osteotomy, (4) joint fusion, and (5) arthroplasty (artificial joint replacement).
  Surgical treatment is mainly through arthroscopy (speculum) and open surgery.

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