Epidemiology
Through a preliminary epidemiological survey, the prevalence of osteoarthritis of the knee in our population is about 9.56%. the occurrence of this disease over the age of 60 may be related to the following factors.
I. Obesity
The increase in weight and the onset of osteoarthritis of the knee are directly proportional. Obesity is also an aggravating factor. Weight loss in obese people can reduce the onset of osteoarthritis of the knee.
Bone density
When the subchondral bone trabeculae become thin and stiff, their tolerance to pressure decreases, therefore, the chance of osteoarthritis increases in people with osteoporosis.
Third, trauma and force bearing
Abnormal state of the joint, such as in the post-patellar resection link in an unstable state, when the joint withstand muscle force imbalance and coupled with local pressure, there will be degenerative changes in the cartilage. Normal joints and activities or even after strenuous exercise are not osteoarthritis.
Fourth, genetic factors
The involvement of joints varies from race to race, 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 the incidence of osteoarthritis in women with Heberden’s nodes is 2-3 times higher in their mothers and sisters than in their families without the disease. The above reaches 78.5%, similar to, but not as severe as, those in Western countries.
Pathogenesis
Articular cartilage is made up of 1-2mm thick collagen fibers, glycoproteins, and hyaluronate aggregates that act as a cushion-like layer when hydrated to absorb and disperse the weight bearing and mechanical forces. Under physiological conditions, articular cartilage relies on periarticular and thermal contraction and the subchondral bone to perform the above tasks completely. The contraction of the muscles, in addition to driving joint movement, also acts as a rubber band, absorbing a large amount of incoming impulse and protecting the joint.
When an accident occurs (such as a fall), because the muscles do not have a protective response to this sudden shock in a timely manner and make the joint heavier, it can cause damage to the joint. In addition, muscle aging, peripheral neuropathy, muscle energy absorption function is also greatly reduced. Another factor that helps the cartilage to bear the weight is the bone mass under the cartilage showing a reticular distribution, whose texture is softer than the bone cortex although it should be more cartilage, so it has a high degree of elasticity and is conducive to bearing pressure.
Osteoarthritis can be seen in the following two situations: first, when there are abnormalities in the articular cartilage, subchondral bone mass and periarticular muscles, such as senile degeneration, osteoporosis, inflammation, metabolic diseases, etc.; second, when the articular cartilage, subchondral bone mass and periarticular muscles are normal but are subject to excessive pressure, such as obesity, trauma, etc.
Pathology
The deformation of articular cartilage occurs earliest and has characteristic lesions. When the cartilage matrix loses glycoprotein, the cartilage on the surface of the joint softens and fractures at the site of pressure, leaving the cartilage surface in the form of a fine filamentous fleece. Later, the cartilage is gradually shed in sheets and the cartilage layer becomes thin or even disappears. Small fractures and necrosis of the subchondral bone occur, and the osteophytes in and around the joint surface constitute osteosclerosis and bone arthrosis and bone cystic changes on X-ray.
The synovial membrane of the joint may show mild proliferative changes including proliferation of synovial cells and infiltration of lymphocytes due to destruction of cartilage and bone and shedding of metabolites such as the joint cavity, which is much less pronounced than in rheumatoid arthritis. In severe osteoarthritis, there is fibrosis of the joint capsule wall and damage to the surrounding tendons.
Diagnosis
There are no specific laboratory tests for this disease, but they can be used to further differentiate it from other diseases. Blood sedimentation is normal in most patients, C-reactive protein is not elevated, and rheumatoid factor is negative. The joint fluid is yellow or straw yellow with normal viscosity and a normal coagulation test, and its leukocyte level is less than 2 × 109/L. The sugar level is rarely less than 50% of the blood glucose level.
X-rays of the joints are useful for the diagnosis of the disease. The affected joints show the following changes on X-rays according to the severity of the disease.
1. narrowing of the joint space.
2. sclerosis of the subchondral bone.
3. formation of bone artefacts at the joint margins.
4. Cystic changes in the subchondral bone and, in rare cases, ship chisel-like bone changes; 5. Bone deformities including flattening of the femoral head and/or subluxation of the joint.
It should be noted that many of those with the above-mentioned radiographic changes do not have the clinical symptoms of the disease osteoarthritis should be differentiated from the following diseases.
I. Rheumatoid arthritis
Both accumulate finger joints, knee joints, etc. However, rheumatoid is prominent with lesions in the proximal finger joints and metacarpophalangeal joints, and joint swelling and pain, synovial inflammation is much more obvious than in osteoarthritis, Heberden’s nodes rarely appear, and rheumatoid factor is positive, and blood sedimentation is increased.
Psoriatic arthritis
Psoriatic arthritis is also prone to involve the distal finger joints but the x-ray presentation is different from that of osteoarthritis. The patient has a psoriatic skin rash.
Pseudogout
Pseudogout is a painful swelling of local joints (knee is most commonly involved) caused by calcium pyrophosphate crystals deposited in articular cartilage, synovium, periosteum, and ligaments, and X-rays show calcification lines on the cartilage surface of joints, and calcium pyrophosphate crystals can be found in joint fluid. The latter two can be distinguished from osteoarthritis.
IV. Other
The disease is differentiated from hip tuberculosis and aseptic osteonecrosis according to the patient’s age, clinical presentation, and X-ray features.
Treatment of osteoarthritis
1. Non-pharmacological treatment of osteoarthritis: including patient health education, self-training, weight loss, aerobics, joint mobility training, muscle training, and use of mobility aids. Patients with osteoarthritis of the knee often have reduced quadriceps muscle strength, which was previously thought to be caused by disuse atrophy, strengthening quadriceps muscle strength training and aerobic training is beneficial to patients with osteoarthritis. Get more sunlight, pay attention to prevent cold and dampness, and keep warm so that the knee joint can get good rest.
After pain relief, walk slowly on flat ground once or twice a day for 20-30 minutes each time. Try to reduce weight-bearing exercises for the knee joint such as going up and down steps and running to avoid and reduce the wear and tear of joint cartilage. Don’t stay in one position for a long time, and don’t do exercises such as repeatedly flexing and extending the knee joint, rubbing the patella and shaking the knee joint blindly. Exercise the quadriceps to make them strong and powerful to reduce knee pain.
The specific exercise method suitable for middle-aged and elderly people is: sitting or supine position, straighten the knee joint, tense the thigh muscle, foot to the head dorsiflexion, while tensing the calf muscle, each time adhere to three or four seconds, do 10 times per minute, do three or four minutes in a row. You can do it three or four times a day.
2, osteoarthritis drug treatment
(1) Sodium hyaluronate: It is the main component of the synovial fluid of the joint cavity and one of the components of the cartilage matrix, which plays a lubricating role in the joint and reduces the friction between tissues. The injection in the joint cavity can significantly improve the inflammatory reaction of the synovial tissue, enhance the viscosity and lubricating function of the joint fluid, protect the joint cartilage, promote the healing and regeneration of the joint cartilage, relieve pain and increase the mobility of the joint. It is often injected intra-articularly, 25mg once, once a week for 5 weeks, subject to strict aseptic operation.
(2) Glucosamine: It is the most important monosaccharide that constitutes polyglucosamine (GS) and proteoglycan in the cartilage matrix of joints.
Glucosamine can block the pathogenesis of osteoarthritis, promote the synthesis of proteoglycans with normal structure in chondrocytes, and inhibit the production of enzymes (such as collagenase and phospholipase A2) that damage tissue and cartilage, reduce damage to chondrocytes, improve joint movement, relieve joint pain, and delay the course of osteoarthritis. Take 250-500mg orally once, 3 times a day, best taken with meals.
(3) Non-steroidal analgesic anti-inflammatory drugs: can inhibit the synthesis of cyclooxygenase and prostaglandin, counteract the inflammatory response, and relieve joint edema and pain. You can use ibuprofen 200-400mg once, 3 times a day; or celecoxib 200mg once, 1-2 times a day; nimesulide 100mg once, 2 times a day, 4-6 times in a row.
(4) Sodium vitreous acid: Through experiments and clinical applications have proved that sodium vitreous acid is a safe, ideal and effective drug for the treatment of osteoarthritis. It has various physiological functions such as participating in the regulation of electrolytes and water in extracellular fluid, lubricating joints, resisting infection, participating in wound healing, etc. It plays an important role in the protection, nutrition and function of joints, mainly in the lubrication of joint cavities, covering barriers and buffering stress.
Under the action of various pathogenic causes, the synovial membrane composition of the joint cavity changes and the content of sodium vitrate decreases or the joint function decreases, resulting in joint cartilage erosion and destruction, resulting in pain and impaired movement. Supplementation of exogenous sodium vitrate can increase the content of sodium vitrate in the synovial membrane, re-form the natural barrier, and prevent further destruction of cartilage matrix; improve the biological function of the synovial membrane in pathological state, reduce or eliminate joint friction and pain; reduce synovial membrane permeability, increase the production of polymeric sodium vitrate, and reduce intra-articular exudate through its inhibition of leukocyte movement and chemotaxis; cover and protect nociceptive It covers and protects nociceptive sensory apparatus, binds to pain mediators and relieves pain; binds to glycoproteins and prevents the substance from participating in the inflammatory process, while sodium vitrate enters the cartilage matrix and forms aggregates with glycoproteins to repair the damaged cartilage. Therefore, sodium vitrate has good efficacy in mild to moderate osteoarthritis of the knee.