OA refers to a joint disease caused by a variety of factors that lead to fibrosis, cracking, ulceration, and loss of articular cartilage. The etiology is not clear, and its occurrence is related to age, obesity, inflammation, trauma, and genetic factors. The pathology is characterized by degeneration and destruction of articular cartilage, subchondral bone sclerosis or cystic changes, osteophytes at the joint edges, synovial hyperplasia, contracture of the joint capsule, ligament relaxation or contracture, muscle atrophy and weakness, etc. OA is more common in middle-aged and elderly patients, more women than men, with a prevalence of up to 50% in people over 60 years of age and up to 80% in people aged 75 years. OA is more likely to occur in joints that are heavily loaded and active, such as the knee, spine (cervical and lumbar spine), hip, ankle, hand and other joints.
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 and can be secondary to trauma, inflammation, joint instability, chronic and repeated cumulative strain injury or congenital diseases.
Clinical manifestations
1, joint pain and pressure pain at the beginning of the mild or moderate intermittent hidden pain, better at rest, aggravated after activity, 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 is a stiffness and tightness in the morning when waking up, also known as morning stiffness, which 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 and deformation of the hand joints are obvious, and Heberden’s nodes and Bouchard’s nodes may appear. Some of the knee joints may also become enlarged due to the formation of bone redundancy 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 and activity impairment Joint pain, decreased mobility, muscle atrophy, and soft tissue contracture can cause joint weakness, soft leg or joint strangulation when walking, inability to fully straighten or activity impairment.
Diagnostic points
According to the patient’s symptoms, signs, x-ray manifestations and laboratory tests, it is generally not difficult to diagnose OA, 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 joints. These diagnostic criteria are basically based on the criteria developed by Altman and discussed and determined by some orthopedic experts.
No. Conditions
(1) Recurrent knee pain within the last 1 month
(2) Radiographs (standing or weight-bearing) showing narrowing of the joint space, subchondral bone sclerosis and/or cystic degeneration, and bone redundancy at the joint margin
(3) Clear, viscous joint fluid (at least 2 times), WBC <2000/ml
(4) middle-aged and elderly patients (≥40 years old)
(5) Morning stiffness ≤ 3 minutes
(6) Bone friction sound (sensation) during activity
Treatment
The overall treatment principle of OA is a combination of non-pharmacological and pharmacological treatment and, if necessary, surgical treatment, which should be individualized. Combined with the patient’s own situation, such as age, gender, weight, their own risk factors, the location and degree of lesions, etc. to choose the appropriate treatment plan.
1. Non-pharmacological treatment is the basis of pharmacological treatment and surgical treatment. For patients with OA who are first-time patients and do not have severe symptoms, non-pharmacological treatment is the preferred treatment modality, with the aim of reducing pain, improving function and enabling patients to have a good understanding of the nature and prognosis of the disease.
(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 strength training (such as hip OA should pay attention to the training of abductor muscle groups) etc.
(2) 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 reduces the weight-bearing of the affected joints, and 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 brace or orthopedic shoes to balance the load on each joint surface.
2.Pharmacological treatment If non-pharmacological treatment is ineffective, drug treatment can be selected according to the joint pain situation.
(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 medications can effectively relieve mild to moderate joint pain with mild adverse effects.
(2) Systemic analgesic drugs According to the route of administration, they are divided into oral drugs, injections and suppositories.
(2) Systemic analgesics Treatment guidelines?
(1) Medication principles.
(1) Risk assessment should be conducted prior to drug administration, paying attention to the risk of potential medical diseases.
(2) Individualize the dose according to the patient’s condition.
(2) Individualize the dose according to the patient’s condition.
(3) Use the lowest effective dose as much as possible, avoid overdose and repeated or superimposed use of similar drugs.
(4) 3 months of medication, check blood and stool routine, fecal occult blood and liver and kidney function according to the condition of choice.
(2) Medication method.
① Patients with OA generally choose acetaminophen, and the maximum daily dose should not exceed 4000mg.
②Acetaminophen
OA patients who are not well treated with acetaminophen may use NSAIDs on a case-by-case basis after weighing the risk of gastrointestinal, hepatic, renal, and cardiovascular disease in patients with
NSAIDs (Table 3). The efficacy and adverse effects of oral NSAIDs are not identical in individual patients and should be evaluated by referring to the drug’s instructions and assessing the risk factors for NSAIDs (Table 3).
Risk factors for NSAIDs (Table 4) should be evaluated before selective dosing. If the patient is at high risk for gastrointestinal adverse reactions, nonselective
NSAIDs plus H-receptor antagonists, proton pump inhibitors or gastric mucosal protectors such as misoprostol, or selective COX-2 inhibitors.
(3) 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
(1) Sodium hyaluronate, if oral medication is not effective, joint cavity injection of sodium hyaluronate-based viscoelastic supplements can be combined, and joint fluid should be aspirated before injection.
②Glucocorticoids, intra-articular injection of glucocorticoids is feasible for those with severe OA or those who cannot tolerate NSAIDs drug treatment for 4-6 weeks, persistent pain and obvious inflammation. However, if used for a long time, it may aggravate the damage of joint cartilage and aggravate the symptoms. Therefore, intra-articular glucocorticosteroid injections are not recommended, and repeated use is not recommended, but at most three to four times a year.
(4) Improving the condition of drugs and chondroprotective agents, including diacetin, glucosamine, avocado soybean unsaponifiables (ASU), doxycycline, etc.. These drugs can delay the course of the disease and improve the patient’s symptoms to some extent. Diacerein has a structural modulating effect.
3.Surgical treatment OA surgical treatment is aimed at.
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; part of comprehensive treatment.
The main methods of OA surgical treatment are.
① free body removal.
② joint debridement.
③ Osteotomy.
④ Joint fusion; arthroplasty (artificial joint replacement), etc. Surgical treatment is mainly through arthroscopy (speculum) and open surgery.