Osteoarthritis (OA): Causes, Symptoms & Treatment
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| Study In Detail About Osteoarthritis |
Osteoarthritis (OA)
Osteoarthritis is a complex, chronic, progressive disease involving bone, cartilage, and the synovium. It is the most common type of all rheumatological disorder. It is characterized by the loss of articular cartilage primarily in the knees, hips, hands, and spine.
Osteoarthritis not only affects joints but also the tissues around joints. It is due to the breakdown and disintegration of the cartilage and new bones. In osteoarthritis, the space between joints becomes narrow. It is also due to the erosion of articular cartilage.
The risk of osteoarthritis increases with increasing age. Individuals over the age of 65 years are at higher risk for developing osteoarthritis. According to a report by the Centers for Disease Control and Prevention (CDC) in 2005, approximately 26.9 million people older than 65 are affected by osteoarthritis. It accounts for about 0.2 to 0.3 deaths per 100,000. It increases costs to our health care systems.
There are multiple factors responsible for the development of osteoarthritides such as genetic predisposition, local inflammation, mechanical forces, and joint integrity. Another major risk factor of osteoarthritis is obesity. The incidence of osteoarthritis increases with increasing body weight.
The incidence rates of osteoarthritis of the hand have been estimated to be 100 per 100,000 people; hip osteoarthritis has been estimated to be 88 per 100,000 people and knee osteoarthritis to be 240 per 100,000 people per year.
Females are more prone to the development of osteoarthritis. But the reason behind it is not clear. Its symptoms include extreme pain and movement limitations. It is common in both sexes and in older age. In this type of arthritis, the Rh factor is negative.
Causes Of Osteoarthritis
The exact etiology of osteoarthritis is not completely understood.
The morphology and clinical complications are the results of a convergence of risk factors. There are multiple factors responsible for the development of osteoarthritides such as genetic factors, age, mechanical overloading, acromegaly, local inflammation, obesity, joint integrity, previous injury or diseases such as rheumatoid arthritis or gout, and gender.
Chronic repetitive joint injury by occupational, recreational, or major joint trauma will result in cartilage deterioration. Either repetitive or traumatic injury to articular surfaces initiates the cascade leading to the release of inflammatory cytokines (tumor necrosis factor [TNF], IL-1), nitric oxide, and enzymes that break down the extracellular matrix. The breakdown of the extracellular matrix results in less elastic cartilage and less ability to support joint loads, and stiffening of subchondral bone. The cartilage is less able to support forces, with diminished efficacy for providing joint lubrication and weight distribution across the joint.
Cartilage is avascular, however, and contains chondrocytes that under normal conditions are responsible for cartilage breakdown and repair. In early osteoarthritis, chondrocytes attempt to repair joint damage by forming osteophytes, which try to stabilize the joint or alter the biochemical properties of cartilage. The formation of osteophytes may provide an increased surface area over which to distribute the forces across the joint.
Osteophytes or bony outgrowths may be responsible for the patient's reports of pain and limited mobility. It is unclear whether osteophytes are formed as a result of abnormal stress fracture healing of the subchondral bone proximal to the joint margins. Alternatively, osteophyte formation may occur secondary to vascularization of the cartilage that has been altered through etiologies and risk factors mentioned previously.
Early in the disease process, the water content of the cartilage is increased. However, this less viscous cartilage is structurally weaker than normal cartilage. Many structural alterations contribute to the weakened collagen network.
One of the early changes is a smaller diameter of type II collagen, in comparison to that in the more structurally intact disease-free joint. With disease progression, the proteoglycan concentrations diminish with shorter glycosaminoglycan side chains resulting in decreases in net aggregate proteins. Type I collagen within the extracellular matrix increases, and keratin sulfate concentrations decrease.
Some of the biochemical changes are reflective of those produced in culture by immature tissue. The deposition of calcium crystals represents a curious finding. It is unknown whether calcium deposition has a direct involvement or is reflective of increased chondrocyte activity. Eventually, the initial water swelling of the cartilage is replaced by cartilage with a reduced propensity to allow the bone to distribute the force and slide on the bone.
Chondrocytes are unable to maintain the production of essential macromolecules necessary for healthy cartilage. However, the syntheses of those enzymes that break down the matrix are increased by the same chondrocytes. The enzymes that degrade proteoglycans and collagen are called aggrecanases and collagenases, respectively. The control of these enzymes is complicated by the enzymatic activation of latent proteins and inactivation by proteinase inhibitors.
In osteoarthritis, the expression and production of proteinases are increased. Collagen is typically cleaved by matrix metalloproteinase (MMP), MMP-1, MMP-8, and MMP-13. Of the three, MMP-13 may be the most important in OA because it preferentially degrades type II collagen. Bench science has substantiated the increased expression of MMP-13 in cartilage cultures. Upregulated by IL-1 and TNF, MMPs cleave collagen and break down other important elements of the extracellular matrix. Ultimately, the imbalance between cartilage maintenance and degradation leads to erosion and eventual cartilage destruction.
Symptoms Of Osteoarthritis
If you are diagnosed with osteoarthritis, you may have pain (This pain is increased by movement and mechanical overloading on the joints), swelling in the joints, stiffness, and tenderness in joints, motion limitations, and joint grinding.
You may also have symptoms of physical dependence, fever and fatigue, weight loss, morning stiffness for 30 minutes, loss of flexibility, hard lumps around the joints, and warm joints.
Treatment Of Osteoarthritis
The purpose of treatment in osteoarthritis is to provide rapid pain relief and prevent disease progression. Paracetamol and topical NSAIDs are first-line agents used for the treatment of osteoarthritis.
Acetaminophen is proven to be very effective for the treatment of mild to moderate osteoarthritis of the hands and knees. Acetaminophen is given regularly for 2-3 weeks. The dose of acetaminophen should be less than 4 g/day or less than 3 g/day in patients older than 65 years.
Capsaicin, diclofenac gel, and diclofenac topical solution are available in the form of topical products for the reduction of pain and swelling.
If there is no improvement with acetaminophen, then NSAIDs are recommended. Non-steroidal anti-inflammatory drugs (NSAIDs) are used for the reduction of pain and swelling.
The most commonly used topical NSAIDs are tramadol, diclofenac sodium (DSG), and dimethyl sulfoxide solution (D-DMSO). They should be used for a short period at low doses. Your doctor can also prescribe a proton pump inhibitor along with NSAIDs.
Intra-articular steroids and opioids can also be prescribed for the treatment of chronic pain. They provide short-term relief from pain.
If there is no improvement with oral or effective treatments, intra-articular injections serve to be the last choice before medical procedures. Manufactured hyaluronan is given as an intra-articular injection. It ends up being powerful for the improvement of joint function and decrease torment.
Hyaluronan is an endogenous molecule. It is found in the synovial liquid that expands the viscosity of synovial liquid and gives lubrication inside the joint. Nutraceuticals can likewise be suggested for the treatment of osteoarthritis.
In case of osteoarthritis due to obesity or being overweight, you must lose weight. You must exercise regularly to improve muscle strength such as aerobic fitness training.
In the case of osteoarthritis, the role of glucosamine, chondroitin, and combination products have represented such an alternative to many patients. Researchers have found in evaluating the use of glucosamine, chondroitin, and the combination in osteoarthritis of the knee that they were all ineffective in reducing pain.
Another natural product, S-adenosyl methionine (SAMe) was supported by an 8-week trial in patients with osteoarthritis for the reduction of pain and joint stiffness. Vitamin E, ginger, a combination of ginger, and omega-3 fatty acids were not found to have any effects in patients suffering from osteoarthritis.