I. Background
On January 13, 2000, the World Health Organization (WHO) launched the Bone and Joint Decade, a global initiative to raise awareness of bone diseases among governments, medical research institutions, the public and society at large. This includes Osteoarthritis (OA), a common disease with increasing health consequences and medical costs. On October 12, 2001, the Ministry of Health (MOH) organized a campaign to raise awareness of 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 urgent updates in the guideline, therefore, based on foreign OA guidelines 1-12 and literature 19-23, combined with the specific situation in China, the previous version of the guideline has been revised. 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.
Third, the 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. Joint enlargement: The joints of the hands are 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 strangulation, inability to fully straighten or activity disorders.
(B) Laboratory tests: blood routine, protein electrophoresis, immune complexes and serum complement are generally within normal limits. Patients with concomitant 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, and free bodies or joint deformation visible in some joints.
V. Diagnostic points
It is generally not difficult to diagnose OA based on the patient’s symptoms, signs, X-ray performance 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 OA of the knee and hip 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 treatment of OA aims 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 the non-weight-bearing position to maintain maximum joint mobility), muscle 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 OA associated inversion or valgus deformity, use the corresponding orthopedic support or orthopedic shoes, to
to balance the load of each joint surface.
(B) Drug therapy: If non-drug therapy is ineffective, drug therapy can be selected according to the joint pain.
1. Local medication: For hand and knee OA, it is recommended to choose local medication first before using oral medication. Topical medication can be used in the form of emulsions, creams, patches and non-NSAIDs rubs (capsaicin, etc.) of non-steroidal anti-inflammatory drugs (NSAIDs). Topical topical agents 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: risk assessment before medication and attention to potential medical disease risk. Individualize the dose according to the individual patient’s condition. Try to use the lowest effective dose and avoid overdose and repeated or superimposed use of similar drugs. For 3 months of drug administration, check blood and stool routine, fecal occult blood and liver and kidney function according to the condition of choice.
(2) Dosing: Acetaminophen is generally used in OA patients, with a maximum daily dose of no more than 4000 mg. For OA patients with poor results with acetaminophen, NSAIDs may be used on a case-by-case basis after weighing the risk of gastrointestinal, hepatic, renal, and cardiovascular disease in patients. The efficacy and adverse effects of oral NSAIDs vary among individual patients, and selective use of NSAIDs should be based on drug instructions and assessment of risk factors for NSAIDs.
If patients are at high risk for gastrointestinal adverse effects, non-selective NSAIDs may be used in combination with H2 receptor antagonists, proton pump inhibitors, or gastroprotective agents such as misoprostol, or selective COX-2 inhibitors. Other 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: sodium hyaluronate, such as oral drug therapy is not significant, can be combined with joint cavity injection of sodium hyaluronate-like viscoelastic supplements, injection of chilblains in the aspiration of joint fluid. Glucocorticoids, intra-articular cavity injection of glucocorticoids is feasible for severe OA that is not effective with NSAIDs drug therapy for 4-6 weeks or for those who cannot tolerate NSAIDs drug therapy, persistent pain and significant 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), 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.