Osteoarthritis (OA) is a degenerative joint disease, also known as proliferative arthritis or degenerative arthritis, and is a common and frequent disease in the middle-aged and elderly population. It is also one of the major diseases affecting the quality of life of middle-aged and elderly people and is classified as primary or secondary. Clinical manifestations include pain, dysfunction and deformity. Joint cartilage degeneration and wear; subchondral bone sclerosis and cystic change, fatty change; osteophytes, bone superfluous formation; synovial tissue hyperplasia, joint effusion; meniscal degeneration, injury; cruciate ligament wear; in severe cases, joint deformity, lower limb force line change. It is generally seen in people who are aging, overuse of joints, obese, and women.
The pain of osteoarthritis of the knee is related to the amount of activity, usually manifested as a certain period of time with high activity, appearing or inducing pain, and there is inconsistency with the imaging performance, often with the phenomenon of lighter pain on the heavier side of the imaging, and heavier pain on the non-heavy side of the imaging, with a rotation phenomenon.
In those with predominantly patellofemoral joint changes, pain is manifested on stairs, but not on stairs and walking on level ground; in those with predominantly medial and lateral compartment changes, pain is manifested on stairs and walking on level ground; related to the degree of pain tolerance, it often appears that the imaging is heavier and the pain is lighter, or vice versa; related to the mechanism of pain production, most of the pressure points on the medial side of the knee are obvious, related to the medial side being low in the joint and the accumulation of inflammatory mediators.
In the mechanism of knee osteoarthritis, the alteration of articular cartilage is the cause, the result, and the root, and the mechanical factors are the most important ones. Increasing age leads to a decrease in cartilage proteoglycan content and water content, resulting in biomechanical changes in cartilage, reduced viscoelasticity and creep. Exercise, obesity, and localized stress concentration in cartilage lead to disposable overstress or fatigue wear on cartilage, resulting in cartilage damage and various secondary pathological damages.
Mechanical pain
1, abnormal stress perception of subchondral bone caused by broken cartilage rings such as exfoliation, delamination, softening, etc. (cartilage is not innervated, while subchondral bone has rich nerve endings, abnormal stress can cause changes in intraosseous pressure, subchondral bone microfracture, etc.).
2.Local joint stress changes caused by flap-like cartilage pieces, cartilage fragments, etc. that are peeled off during joint activities.
3.Destruction of cartilage leads to joint instability and pain caused by abnormal stress in intra-articular ligaments and peri-articular muscles.
4.Repair reaction – pain caused by synovial hyperplasia and bone formation. The hyperplastic synovial membrane is richly innervated and can cause pain when stuck between structures in the joint during movement; the joint instability caused by cartilage destruction can cause the body’s repair response, which can produce bone redundancy to increase the contact surface to increase stability, but the bone redundancy is rich in nerve sensation.
5.The degeneration of meniscus and articular cartilage are causal and aggravate each other, while the red area of meniscus has a large number of innervation.
6, joint effusion leads to increased intra-articular pressure, which stimulates sensory fibers and structural receptors in the joint capsule causing pain.
Chemical pain is often an inflammatory response caused by cartilage debris, cartilage wear or fragmentation debris stimulate synovial proliferation to engulf and wrap debris, resulting in synovial inflammatory response, producing a variety of inflammatory mediators, causing pain, while further aggravating cartilage destruction, especially in the lower side of the joint medial, inflammatory mediators accumulate, pressure pain is often heavier.
With the aging of the population, reasonable and effective pain management or pain control for patients with knee osteoarthritis is an important part of improving people’s quality of life and reducing medical expenditures. The overall strategies for pain control in osteoarthritis of the knee are
1.Drug control
2.Physical therapy
3.Intra-articular injection and lavage
4.Arthroscopic cleaning
5.Cartilage repair
6.High osteotomy
7.Arthroplasty
There is no satisfactory treatment for the cause of knee osteoarthritis pain control by medication.
1.Chondroprotective drugs
Hyaluronic acid, chondroitin, type II collagen, etc., is the initial means of OA treatment, early and mid-term effect is good, and the effect is not good for those with severe symptoms in the later stages. However, chondroprotective drugs are the basic measures and should be actively applied as early as possible.
Mechanism of action: the destruction and repair of cartilage is a dynamic process of change, these drugs themselves are the main components of the composition of cartilage, but also the main substances of cartilage repair, but perhaps no analgesic effect itself.
2.Non-steroidal anti-inflammatory drugs (NSAIDs)
NSAIDs are currently one of the most used drug classes in the world. They are used by approximately 30 million people worldwide every day and are indicated for patients with chronic pain in all periods of osteoarthritis.
They can be divided into 3 categories: the first category of aspirin; the second category of other NSAIDs for pain relief; and the third category of acetaminophen.
Oral dosage forms: aspirin, acetaminophen, indomethacin, naproxen, naproxen, diclofenac, ibuprofen, nimesulide, rofecoxib, and celecoxib.
Topical dosage forms: creams (such as fotarine ointment, ibuprofen ointment, etc.); patches (piroxicam patches, etc.).
Mechanism of action: mainly by inhibiting COX enzyme to reduce the synthesis of inflammatory mediators such as PG and produce peripheral analgesic effects.
Two kinds: COX-1 basic enzyme, COX-2 enzyme-inducing enzyme. Arachidonic acid is converted to PG by the action of COX enzymes.COX-1 enzymes, present in most tissues, are involved in the synthesis of physiological PG synthesis required for normal cellular activity.PG protects the gastric mucosa, maintains normal platelet function, and participates in regulatory roles in the kidney and vascular endothelium.COX-2 enzymes, which are inducible enzymes, are normally present in small amounts and are mainly induced by cytokines in local inflammatory response and is present in most inflammatory tissues. Conventional NSAIDs, which inhibit both COX-1 and COX-2, disrupt the protective effect of PG on gastric mucosa and platelets while providing anti-inflammatory and analgesic relief. In contrast, selective COX-2 inhibitors, at normal doses, do not inhibit COX-1, but mainly inhibit COX-2, thus avoiding damage to gastric mucosa and platelets. Selective COX-2 inhibitor stands for celecoxib.
Advantages and disadvantages: non-addictive; more adverse reactions (mainly gastrointestinal reactions, gastric bleeding, etc.), topical application of topical preparations should be chosen as much as possible; there is a capping effect, that is, beyond the maximum effective dose, the analgesic effect no longer increases, so the simultaneous use of two similar drugs and overdose should be avoided, but one drug treatment is ineffective when another drug can be switched. the application of NSAIDs is purposeful and planned. The course of treatment should be emphasized, usually in 10-14d (can be extended to 9 weeks if necessary).
3.Opioid drugs
There are three main classical opioid receptors, namely μ, κ and δ receptors. Opioid receptors belong to the broad category of G protein-coupled receptors Among these three classical opioid receptors, μ-opioid receptors are the main acting receptors of most opioids currently in use, and are also the key target site factors for exerting effects including analgesia, tolerance and dependence.
Opioids can be divided into two categories, weak opioids and strong opioids. Weak opioids are used for mild to moderate pain, such as codeine and caffeine. Strong opioids are used for moderate to severe pain, such as morphine and oxycodone.
There are two types of dosage forms: oral and topical. Oral dosage forms include immediate release and extended and controlled release dosage forms. The immediate release form has a short duration of action, generally 3 to 4 hours, such as morphine, dihydromorphone, codeine, hydrocodone, fentanyl and oxycodone. Extended and controlled release dosage forms have a long duration of action, generally lasting 8 to 12 hours, such as controlled release morphine tablets, oxycodone hydrochloride controlled release tablets, tramadol hydrochloride extended release tablets, etc. The effect of fentanyl transdermal patch reaches 72 hours.
4.Group prescription drugs
It is a common prescription drug, which usually combines analgesic drugs with different mechanisms of action to enhance analgesic effect and reduce adverse reactions. For example, Tylenol is a compound preparation of oxycodone and acetaminophen, oxycodone is a strong agonist of opioid receptors with central nerve analgesic effect, and acetaminophen (NSAIDs) has peripheral nerve analgesic effect.
5.Chinese medicine
There are mainly blood activating and pain relieving drugs and herbal pain relieving drugs, “the pass is not painful, the pain is not pass”, pain is paralysis. Therefore, Chinese herbal medicine can play a very good role in relieving pain by activating blood circulation. In addition, Chinese herbal medicines with good pain-relieving effect, such as Cao Wu Jia Su, are often used. The biggest advantage of these drugs is that they do not have the side effects of non-steroidal drugs. There are herbal oral preparations and topical creams.
Traditional medicine and physical therapy
Cupping, acupuncture, ultrashort wave, herbal fumigation, and pain stimulation are all very effective.
For those with altered knee joint force lines, braces or foot pads have a better effect.
Strength strengthening of the medial femoral muscle has a good therapeutic effect on patients with patellofemoral joint degeneration.
Painful point injection (closed treatment): injection therapy is the drug directly to the lesion local, eliminate inflammatory stimulation, stop the occurrence and development of pathological reflexes, eliminate inflammatory exudation hyperplasia swelling, relieve muscle tension, improve local blood circulation stop primary and excitatory pain.
Long-acting glucocorticoids, such as compound betamethasone or tretinoin, are usually used, mixed with lidocaine and injected at painful points.
Intra-articular cavity injection closure therapy: the same as painful point closure therapy, can be performed at the same time joint fluid extraction and lavage.
Intra-articular injection of sodium hyaluronate (HA).
Mechanism of action.
1. HA is an important component of articular cartilage.
2, HA is an important component of synovial fluid, maintaining the biological function of synovial fluid (nutrition of cartilage) and biomechanical function (lubrication, shock absorption, barrier).
3, OA synovial fluid and cartilage matrix in endogenous HA concentration or content is reduced.
Supplementation of exogenous OA facilitates the dynamic damage and repair process of cartilage and improves the biological and biomechanical properties of synovial fluid.
Several issues of intra-articular cavity injection
1, the number of closed
Generally closed 1 to 2 times, generally no more than 3 to 4 times in a row, each interval of 7 to 10 days, increasing the number of times to achieve better results. Clinical findings of some patients only injected once on the phenomenon of local muscle atrophy.
2, the effect of hormone intra-articular injection on cartilage, generally closed only 1 time, glucocorticoids have a clear damage effect on articular cartilage, including chondrocyte damage and reduction of cartilage matrix proteoglycans. Usually a hormone such as Depo-Provera or Trimethoprim is added to the first sodium hyaluronate injection and is not used thereafter.
3. The effects of intra-articular lidocaine injections on cartilage are still controversial. Intra-articular bupivacaine injections have been reported to cause articular cartilage lysis, and there are studies on the toxic effects of 1% lidocaine on chondrocytes at 5°, or cartilage loss >2 mm, or inappropriate age (40-60 y). Without addressing cartilage problems and affecting subsequent joint replacement, not many are actually performed and the selection of indications should be strict.
Arthroplasty
Unicompartmental replacement: patellofemoral joint replacement, unicondylar replacement, total knee replacement; perioperative pain control, severe pain in the early postoperative period, elevation of the affected limb to promote venous return and eliminate swelling, cold ice packs on the knee for 1 to 2 days, continuous postoperative femoral nerve block, lumbar plexus nerve block, continuous epidural anesthesia, analgesic pump (PCA) intra-articular injection of anesthetics (lidocaine, bupivacaine, etc.), oral or intramuscular injection of pain medication.