Treatment of OA
Etiological treatment.
1. targeting the underlying disease process.
2. inhibiting cartilage degeneration and increasing synthesis.
3, Active exploration.
Symptom treatment
1.relief of pain.
2.Improve function.
3.Prevent disability.
Basic principles of OA treatment
Pyramidal model of OA treatment options for the treatment of osteoarthrosis
1.Medication
2.Surgical treatment
3.Adjunctive treatment
Classification of drugs for the treatment of osteoarthritis
1.Non-specific drugs
1) Antipyretic and analgesic drugs: aspirin, acetaminophen, etc.
2) Non-steroidal anti-inflammatory drugs: ibuprofen, diclofenac, anti-inflammatory pain, etc.
(3) steroidal (hormonal) anti-inflammatory drugs.
2.Specific drugs (symptom relieving drugs, disease ameliorating drugs)
1) Glucosamine.
2) chondroitin sulfate.
3) Hyaluronic acid (mucus supplementation therapy) medication for osteoarthritis.
What are NSAIDs?
NSAIDs are defined as drugs other than adrenocorticotropic hormones that are used to treat inflammation, especially rheumatoid arthritis. NSAIDs are currently used routinely in the treatment of osteoarthritis. NSAIDs inhibit the synthesis of prostaglandins by inhibiting the action of cyclooxygenase, thereby achieving anti-inflammatory pain relief. For osteoarthritis, a degenerative disease of the articular cartilage, treatment with NSAIDs lacks specificity. Long-term use of certain NSAIDs can even aggravate the pathological progression of osteoarthritis (e.g., anti-inflammatory pain).
Effects of NSAIDs drugs on articular cartilage
In vitro studies: can affect the metabolism of articular cartilage proteoglycans
In vivo studies: can accelerate the destruction of articular cartilage in animal models of OA Inhibition of osteoarthritic cartilage is significantly higher than normal cartilage LINK test (1993): long-term administration of anti-inflammatory pain can accelerate the narrowing of joint spaces NSAIDs Side effects: older patients, especially long-term administration of NSAIDs, side effects are greater
Peptic ulcer is 4 times higher
1) Increased mortality due to ulcers
2) interactions with multiple drugs.
3) water and sodium retention l renal insufficiency steroidal (hormonal) anti-inflammatory drugs intra-articular closure: anti-inflammatory, anti-swelling For patients with concomitant synovitis, this method can be used, but long-term application has the potential to aggravate the condition.
Specific drug therapy – glucosamine
Glucosamine is a physiological substance necessary for the biological metabolism of chondrocytes. Chondrocytes use glucosamine to synthesize large molecules of mucopolysaccharides, and these proteoglycans form an important part of the cartilage matrix, maintaining the morphology and function of cartilage together with type II collagen fibers.
Domestic and international clinical studies on the efficacy of glucosamine have shown that compared to traditional drugs used to treat osteoarthritis, such as NSAIDs, glucosamine is equal to or better than the latter in improving symptoms in patients with osteoarthritis in the short term, while being more than 10 times safer than the latter.
Unlike NSAIDs, the therapeutic effect of glucosamine does not disappear rapidly after discontinuation, but is maintained for a considerable period of time.
The results of domestic studies suggest that after 5 weeks of treatment with glucosamine, the therapeutic effect lasts for 4-6 months in 2/3 of patients.
The latest foreign studies on the efficacy of glucosamine suggest that after 3 years of continuous use of glucosamine, the gap in the affected joints remained unchanged compared to the control group, where the gap was significantly narrower, decreasing by 1 mm per year.
Specific Drug Therapy – Hyaluronic Acid Intra-articular Injection Therapy Viscoelastic Supplementation
In the 1970s, Balazs et al. were the first to propose the use of exogenous HA supplementation to restore the lubricating function of synovial fluid, promote cartilage repair, and improve joint function.
VS therapy, which maximally meets the four principles of OA treatment.
1) relief of pain, improvement of function, resolution of disease progression, and improvement of quality of life.
2) Protecting cartilage: lubricating joints, inhibiting inflammation, relieving pain, and promoting the physiological function of endogenous HA secretion of sodium vitrate in the joints.
3) Lubricating joints, cushioning stress and reducing friction.
4) Acting as a filler and diffusion barrier
Scavenger function representative drug: Spironolactone Average molecular weight 1.2 million Argi Average molecular weight 800,000.
Non-pharmacological treatment
1) Reducing weight bearing on the joint, avoiding harmful movements, splinting or plaster bracing in the acute stage.
2) Swimming, walking, low-volume aerobic exercise and joint extension range-of-motion exercises, static contraction exercises.
3) Cold and hot compresses: moist heat therapy, hot water baths, paraffin baths, steam baths, hot spring baths. Dry heat therapy. Ice pack to reduce swelling and relieve pain, cold compresses are contraindicated for poor circulation.
4) Transcutaneous electrical nerve stimulation (TENS): subcutaneous electrodes are placed in the painful area and pulsed electrical stimulation. tens blocks nerve signal transmission and improves the perception of pain.
5）Acupuncture: stimulate the brain and nerve center to release natural analgesic substances.
6）Body therapy massage: increase local blood circulation, the masseur should know the disease very well.
Complementary treatment
1）Weight loss and weight control.
2）Physical therapy
physical therapy; braces; canes; walkers.
Chinese herbal medicine: dialectical treatment, expel wind and remove dampness, activate blood circulation, relieve tendon and pain.
Functional exercise
Life lies in exercise. Exercise can maintain the existing joint function and prevent muscle atrophy as well as calcium ion loss from bone.
Adherence to functional exercise maintains joint function, improves quality of life and minimizes disability. Protect the joints from injury, avoid repeated impact or rotational sprains, and minimize ascent exercises.
Exercise program: swimming, walking, cycling, straight leg raise in supine position, or resistance training. Extend and flex in place without weight bearing on the joint.
Functional exercise
(1) Correct incorrect exercise methods: too much weight, too much labor, too much going up and down stairs, too much climbing, should reduce the number of squatting and standing, in the exercise exercise to do the right amount, should not be too tired.
(2) early patients, do leg press exercise is beneficial, method: standing elevated lower limbs, hands in the knee joint up and down pat, so that the knee joint straighten 180 °. This exercise method mainly prevents spasm of calf gastrocnemius and flounder muscles leading to knee flexion deformity.
(3) The intensity of the exercise should be such that the joint pain can disappear at the end of the exercise and after 2 hours of rest.
Surgical treatment in the middle stage: arthroscopic examination, synovectomy, bone removal, free body removal.
Late stage: Artificial total knee arthroplasty.
Indications for minimally invasive arthroscopic surgery: no effect after 2 months of regular medication, X-ray (grade I-III) or MRI (grade II or higher cartilage wear).
Repeated conservative treatment with good and bad results, X-ray (grade I~III) with free body strands, meniscal injury symptoms, more severe synovitis, etc.
1) No contraindications to surgery, such as skin rash, infection, stiffness in the surgical area and other three elements of good surgical efficacy in arthroscopy.
2) selection of appropriate cases and mastery of surgical indications (caution in milder cases or severe cases)
3) Skilled surgical technique, limited and gentle operation (only deal with the painful area, do not advocate carpet cleaning)
4) Systematic postoperative rehabilitation, gradual practice plus adjuvant therapy (postoperative review, guidance on practice and physiotherapy, pharmacotherapy)
Main steps of arthroscopic surgery
1）Joint flushing to remove cartilage debris, small free bodies and pathogenic factors, remove collagen antibodies, slow down autoimmune reactions to reduce synovial inflammation, remove synovial edema cations in the flushing fluid to adsorb negatively charged pain-causing factors, supplement sodium and potassium ions, and alkalize the joint fluid.
(2) Cartilage treatment to remove cartilage in the exfoliated state (cartilage injury is poor self-healing ability, try to preserve cartilage, repair the edge of the defective cartilage), plasma knife solid shrinkage cartilage edge, cartilage smooth and not easy to lift.
(3) Arthroscopic microfracture surgery subchondral bone drilling plays a role in decompression and pain relief, and is effective for persistent bone pain caused by subchondral bone extrusion, bruising, hypoxia, necrosis, cystic degeneration, and increased local bone pressure (clinically effective in some patients).
It has the potential to promote cartilage repair through the aggregation and differentiation of multiple superficial energy cells in the subchondral bone marrow cavity into chondrocytes to repair the defect. (Histological examination with fibrocartilage or calcification formation).