Understanding Osteoarthritis
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Understanding Osteoarthritis

Osteoarthritis results from deterioration or loss of the cartilage that acts as a protective cushion between bones, particularly in weight-bearing joints such as the knees and hips

Post by on Monday, October 4, 2021

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Osteoarthritis (OA), which is also known as osteoarthrosis or degenerative joint disease (DJD), is a progressive disorder of the joints caused by gradual loss of cartilage and resulting in the development of bony spurs and cysts at the margins of the joints. The name osteoarthritis comes from three Greek words meaning bone, joint, and inflammation. 
OA is one of the most common causes of disability due to limitations of joint movement, particularly in people over 50. Men tend to develop OA at earlier ages than women. OA occurs most commonly after 40 years of age and typically develops gradually over a period of years. Patients with OA may have joint pain on only one side of the body and it primarily affects the knees, hands, hips, feet, and spine. 
Causes and symptoms 
Osteoarthritis results from deterioration or loss of the cartilage that acts as a protective cushion between bones, particularly in weight-bearing joints such as the knees and hips. As the cartilage is worn away, the bone forms spurs, areas of abnormal hardening, and fluid- filled pockets in the marrow known as subchondral cysts. As the disorder progresses, pain results from deformation of the bones and fluid accumulation in the joints. The pain is relieved by rest and made worse by moving the joint or placing weight on it. In early OA, the pain is minor and may take the form of mild stiffness in the morning. In the later stages of OA, inflammation develops; the patient may experience pain even when the joint is not being used; and he or she may suffer permanent loss of the normal range of motion in that joint. 
Until the late 1980s, OA was regarded as an inevitable part of aging, caused by simple “wear and tear” on the joints. This view has been replaced by recent research into cartilage formation. OA is now considered to be the end result of several different factors contributing to cartilage damage, and is classified as either primary or secondary. 
Primary osteoarthritis 
Primary OA results from abnormal stresses on weight-bearing joints or normal stresses operating on weakened joints. Primary OA most frequently affects the finger joints, the hips and knees, the cervical and lumbar spine, and the big toe. The enlargements of the finger joints that occur in OA are referred to as Heberden’s and Bouchard’s nodes. Some gene mutations appear to be associated with OA. Obesity also increases the pressure on the weight-bearing joints of the body. Finally, as the body ages, there is a reduction in the ability of cartilage to repair itself. In addition to these factors, some researchers have theorized that primary OA may be triggered by enzyme disturbances, bone disease, or liver dysfunction. 
Secondary osteoarthritis 
Secondary OA results from chronic or sudden injury to a joint. It can occur in any joint. Secondary OA is associated with the following factors: 
Trauma, including sports injuries 
Repetitive stress injuries associated with certain occupations (like the performing arts, construction or assembly line work, computer keyboard operation, etc.) 
Repeated episodes of gout or septic arthritis.
Poor posture or bone alignment caused by developmental abnormalities.
Metabolic disorders.
History and physical examination 
The two most important diagnostic clues in the patient’s history are the pattern of joint involvement and the presence or absence of fever, rash, or other symptoms outside the joints. As part of the physical examination, the doctor will touch and move the patient’s joint to evaluate swelling, limitations on the range of motion, pain on movement, and crepitus (a cracking or grinding sound heard during joint movement). 
Diagnostic imaging 
There is no laboratory test that is specific for osteoarthritis. Treatment is usually based on the results of diagnostic imaging. In patients with OA, x rays may indicate narrowed joint spaces, abnormal density of the bone, and the presence of subchondral cysts or bone spurs. The patient’s symptoms, however, do not always correlate with x ray findings. Magnetic resonance imaging (MRI) and computed tomography scans (CT scans) can be used to determine more precisely the location and extent of cartilage damage. 
Treatment of OA patients is tailored to the needs of each individual. Patients vary widely in the location of the joints involved, the rate of progression, the severity of symptoms, the degree of disability, and responses to specific forms of treatment. Most treatment programs include several forms of therapy. 
Patient education and psychotherapy 
Patient education is an important part of OA treatment because of the highly individual nature of the disorder and its potential impacts on the patient’s life. Patients who are depressed because of changes in employment or recreation usually benefit from counseling. The patient’s family should be involved in discussions of coping, household reorganization, and other aspects of the patient’s disease and treatment regimen. 
Patients with mild OA may be treated only with pain relievers such as acetaminophen. Most patients with OA, however, are given nonsteroidal anti-inflammatory drugs, or NSAIDs. These include compounds such as ibuprofen, ketoprofen and flurbiprofen. The NSAIDs have the advantage of relieving inflammation as well as pain. They also have potentially dangerous side effects, including stomach ulcers, sensitivity to sun exposure, kidney disturbances, and nervousness or depression.
Some OA patients are treated with corticosteroids injected directly into the joints to reduce inflammation and slow the development of Heberden’s nodes. Injections should not be regarded as a first-choice treatment and should be given only two or three times a year. Most recently, a new class of NSAIDs, known as the cyclo-oxygenase-2 (COX-2) inhibitors have been studied and approved for the treatment of OA. These COX-2 inhibitors work to block the enzyme COX-2, which stimulates inflammatory responses in the body. They work to decrease both the inflammation and joint pain of OA, but without the high risk of gastrointestinal ulcers and bleeding seen with the traditional NSAIDs. This is due to the fact that they do not block COX-1, which is another enzyme that has protective effects on the stomach lining. 
Physical therapy 
Patients with OA are encouraged to exercise as a way of keeping joint cartilage lubricated. Exercises that increase balance, flexibility, and range of motion are recommended for OA patients. These may include walking, swimming and other water exercises, yoga and other stretching exercises, or isometric exercises. Physical therapy may also include massage, moist hot packs, or soaking in a hot tub. 
Surgical treatment of osteoarthritis may include the replacement of a damaged joint with an artificial part or appliance; surgical fusion of spinal bones; scraping or removal of damaged bone from the joint; or the removal of a piece of bone in order to realign the bone. 
Protective measures 
Depending on the location of the affected joint, patients with OA may be advised to use neck braces or collars, crutches, canes, hip braces, knee supports, bed boards, or elevated chair and toilet seats. They are also advised to avoid unnecessary knee bending, stair climbing, or lifting of heavy objects. 
Alternative treatment 
Food intolerance can be a contributing factor in OA, although this is more significant in rheumatoid arthritis. Dietary suggestions that may be helpful for people with OA include emphasizing high-fiber, complex-carbohydrate foods, while minimizing fats. Plants in the Solanaceae family, such as tomatoes, eggplant, and potatoes, should be avoided, as should refined and processed foods. Foods that are high in bioflavonoids (berries as well as red, orange, and purple fruits and vegetables) should be eaten often. 
Nutritional supplements 
In the past several years, a combination of glucosamine and chondroitin sulfate has been proposed as a dietary supplement that helps the body maintain and repair cartilage. Studies conducted in Europe have shown the effectiveness of this treatment in many cases. These substances are nontoxic and do not require prescriptions. Other supplements that may be helpful in the treatment of OA include the antioxidant vitamins and minerals (vitamins A, C, E, selenium, and zinc) and the B vitamins, especially vitamins B6 and B5. 
(Author is Medical Practitioner and can be reached at mir.muzaffar@yahoo.com)

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