Osteoarthritis (or degenerative joint disease), is one of the most common types of arthritis. Once believed to be due to wear and tear on joints, the medical community is now recognizing osteoarthritis to be an active disease caused by dysregulation of the normal degradation and repair processes of articular cartilage.
Patients with osteoarthritis usually present with pain, swelling, and stiffness of joints that tends to worsen over time. The pain worsens after weight-bearing activities and improves with rest. Morning stiffness is common. On physical examination, patients often have tenderness on palpation, bony enlargement, crepitus on motion, and/or limitation of joint motion. Inflammation is usually mild and localized to the affected joint. The process that leads to these symptoms is not well understood. Once believed to be a disease of the cartilage surface, it is now known that osteoarthritis affects the entire joint causing loss of cartilage, damage to bone, formation of bone spurs, and inflammation of the soft-tissues.
The hips and knees are joints most commonly affected by osteoarthritis. This is believed due to evolutionary factors. (As man evolved into an upright walker, the lower extremity joints failed to develop in a manner that would bear the additional weight/stress. Similarly, osteoarthritis in the fingers is likely attributable to the development of a pincer-like grip placing abnormal stress on the finger joints.) While evolutionary factors may be the primary cause of the condition, local biomechanics ultimately influence the site and severity of osteoarthritis.
Throughout life, the cartilage undergoes a cycle of breakdown and repair. In osteoarthritis, the repair function is slowed or rendered ineffective. As a result, the joint lining wears thin.
There is no known cure for osteoarthritis (says mainstream medicine). Treatment designed for the individual patient can, however, reduce pain, maintain and/or improve joint mobility, and limit functional impairment. While some contributory factors cannot be modified (evolution, genetics), there are many ways in which the progression of osteoarthritis can be addressed. These include physical and psychosocial coping mechanisms, and use of medications.
Physical and psychosocial coping mechanisms include exercises for strengthening the joints, diet and other lifestyle factors, all of which are helpful in relieving the physical and emotional aspects of osteoarthritis. Patients should be encouraged to participate in self-management programs since individuals who participate in these programs report decreases in joint pain and frequency of arthritis-related physician visits, increases in physical activity, and overall improvement in quality of life.
Analgesics and Anti-inflammatories
Nonsteroidal anti-inflammatory drugs (NSAIDs) are a group of drugs commonly used to treat osteoarthritis because of their analgesic, anti-inflammatory, and antipyretic properties. NSAIDs inhibit the enzymes Cox-1 and Cox-2 (cyclooxygenase), which catalyze arachidonic acid to prostaglandins and leukotrienes. Arachidonic acid is released from membrane phospholipids as a response to inflammatory stimuli. The efficacy of NSAIDs differs from patient to patient. This is likely due to the pharmacokinetic differences among the various NSAIDs.
Through their inhibition of Cox-1 enzyme, NSAIDs can cause stomach irritation, bleeding, fluid retention, and decreased kidney function. Since NSAIDs bind to plasma proteins they may be displaced by or may displace other plasma-bound drugs such as coumadin, methotrexate, digoxin, cyclosporine, oral antidiabetic agents, and sulfa drugs. This interaction can enhance the therapeutic or toxic effects of either drug.
NSAIDs (particularly indomethacin) can interfere with the pharmacologic control of hypertension and cardiac failure in patients who take beta-adrenergic antagonists, angiotensin-converting enzyme inhibitors, or diuretics.
The long-term use of NSAIDs may have a damaging effect on chondrocyte function.
Adverse effects of NSAIDs (which can occur at any time), include renal failure, hepatic dysfunction, bleeding, and gastric ulceration.
A relatively new sub-class of NSAID, known as Cox-2 inhibitors, work by blocking cyclooxygenase 2 enzyme which is involved in the inflammation pathway. By sparing cyclooxygenase 1 (Cox-1) enzyme, gastrointestinal toxicity is purportedly reduced. Due to their proclaimed reduction of gastrointestinal side effects, Cox-2 inhibitors have claimed a large share of the osteoarthritis medications market.
Unfortunately, recent studies have indicated that Cox-2 inhibitors can increase the risk of cardiovascular problems including angina, myocardial and cerebral infarction, thrombosis and sudden death, to four times that of traditional NSAIDs. A review of more than 48,000 patients taking rofecoxib revealed that 0.52% of patients taking an inactive placebo pill had a heart attack each year. The annual rate of heart attack was 0.74% for patients taking rofecoxib. One theory for this holds that Cox-1 enzyme plays a role in preventing the clot formation that leads to cardiovascular problems.
The assertion that Cox-2 inhibitors (rofecoxib, celecoxib) do not induce hemorrhage in the upper gastrointestinal tract, is also under dispute. While studies confirm that Cox-2 inhibitors cause fewer gastrointestinal events than traditional NSAIDs in the short-term, it is not yet known what the long-term effects of these drugs will have on the gastric mucosa.
Important News Release September 2004
Vioxx®, the cox-2 inhibitor made by Merck, has been pulled from the market because of severe lethal side effects due to heart attack and stroke.
Acetaminophen is often prescribed to relieve mild to moderate arthritis pain. The drug possesses analgesic and antipyretic properties, but is not an anti-inflammatory. For this reason, it may usually be safely combined with an anti-inflammatory medication to relieve pain.
Overdosing can cause liver damage that may be severe enough to cause liver failure and death. This damage occurs in a dose-related manner and is the leading cause of rapid onset liver failure in the US, Canada and the UK.
Long term use can result in kidney disease.
For the average healthy adult, the recommended maximum dose of acetaminophen over a 24-hour period is four grams (4000 mg) or eight extra-strength pills. (Each extra-strength pill contains 500 mg and each regular strength pill contains 325 mg.) A patient who drinks more than two alcoholic beverages per day, however, should not take more than two grams of acetaminophen over 24 hours. For children, the dose is based on weight and age.
A single dose of 7 to 10 grams of acetaminophen (14 to 20 extra-strength tablets) can cause liver injury in the average healthy adult. (This amount is about twice the recommended maximum dose for a 24-hour period.) In children, a single dose of 140 mg/kg body weight of acetaminophen can result in liver injury. However, amounts of acetaminophen as low as 3 to 4 grams in a single dose or 4 to 6 grams over 24 hours, have been reported to cause severe liver injury, sometimes resulting in death. Certain individuals, for example, those who regularly drink alcohol or those with hepatitis C, are more prone than others to developing acetaminophen-induced liver damage.
Cortisone may be injected directly into the joint to relieve severe inflammation and swelling. A cortisone injection can provide almost immediate relief for a tender, swollen or inflamed joint. However, since corticosteroids can degrade cartilage and demineralize the bone, they should only be used rarely. Chronic use of corticosteroids may result in weight gain, hypertension, susceptibility to infection, capillary fragility, acne, excess hair growth, cataracts, glaucoma, diabetes, muscular atrophy, accelerated atherosclerosis, menstrual irregularities, irritability, insomnia and psychosis. Since steroids appear to cause premature death of osteoblasts and slow their replacement; osteoporosis and bone damage are of particular concern. Long-term use may also affect brain cells, causing memory loss. Certain side effects such as hypoglycemia, edema and hypertension can be minimized by treatment.
Substances That May Help Modify the Disease Process
Nutricol has been developed to improve circulation to tissues, speed repair and slow or halt tissue damage. Available as the OTC supplement Recovery in many pharmacies, Nutricol is proposed to reduce the inflammation that accompanies osteoarthritis. This may reduce the likelihood of progression and diminish accompanying pain. Nutricol (Recovery) is an anti-catabolic agent that works at cellular level to help stabilize joint structures. Biomedica Labs also believes that this proprietary blending of plant nutrients naturally increases the cells' receptivity to hormones such as insulin which are required to speed the repair of joint tissues.
Recovery contains the active ingredient Nutricol, a disease modifying anti-catabolic agent (DMAC), which Biomedica Laboratories is proud to introduce to health care professionals.
Biostructural Medicine goes beyond simply addressing symptoms; it is a cell structure-oriented health science that addresses the pathogenic factors of degenerative and inflammatory conditions.
Nutricol (Recovery) may be safely combined with other medications or taken on its own to help counter inflammation. It does not produce unpleasant side effects.
Glucosamine and Chondroitin
Glucosamine and chondroitin are two popular supplements for arthritis and are often available in combination form. While many studies have indicated that these supplements can bring relief to arthritis sufferers, more research is required to determine the precise mechanism that accounts for pain reduction. The ongoing consumer demand for glucosamine and chondroitin suggests very strongly that many people are deriving measurable benefit from their use.
While glucosamine is produced naturally in the body, its production diminishes with age. Proponents of glucosamine suggest that replacing this glucosamine allows the joint cartilage to repair itself via the following mechanisms:
- contribution to the construction of proteoglycans and glycosaminoglycans
- stimulation of chondrocytes
- regulation of cartilage metabolism.