Arthritis is all too well-known by most of us as a source of discomfort and pain. There are different forms of arthritis, however, with distinctive symptoms and prognosis.
Osteoarthritis is the most common form. It is the kind that seems to come with the wear-and-tear process of aging, affecting approximately 70 to 80% of the population over age 50. The onset is marked by morning stiffness, crackling joints, and perhaps some pain. As it gets worse it causes discomfort, pain, and disability in varying degrees for millions of people. It also causes an enormous consumption of painkillers and anti-inflammatory drugs that many times have undesirable long-term effects. Does it have to be this bad?
Modern medicine does not have much to offer for these chronic conditions, only symptomatic, temporary relief. Painkillers and the so-called NSAIDs, non steroidal anti-inflammatory drugs, are effective in reducing symptoms quickly but often cause serious side effects such as ulcers and gastrointestinal bleeding, and they do not stop the progression of the disease. In the long run they have actually proven to worsen the condition by accelerating joint destruction.
The last few years of research, however, have brought some hope to this dismal picture. Old herbal remedies such as ginger, nettle, and willow bark, as well as fish oils and the already well-known cartilage constituents glucosamine sulfate and chondroitin sulfate, are about to revolutionize the treatment of arthritis. These substances not only give symptomatic relief but actually intervene at the root of the problem and help the body to rebuild functioning joints.
The Normal Joint
To understand the pathological processes in the joint, we need to take a look at the normal healthy joint. Joints are held together by a joint capsule and designed to allow smooth movement between adjacent bones. In the type of joint commonly affected by arthritic diseases, the highly movable joints, we find the bone ends covered by articular cartilage and the joint space enclosed by a synovial membrane. This thin membrane secretes synovial fluid that lubricates the space between the cartilage-covered joint-forming bones. The cartilage contains no blood vessels or nerves and receives its nutrients by diffusion from the synovial fluid and from the bone.
Joint function depends on the health of the cartilage in the joint. Cartilage is a gel-like substance that acts as a shock absorber, essential for smooth and easy movement in the joint. Cartilage gets its elasticity from collagen fibers and its sponge-like quality from water, held by a structure of big molecules called proteoglycans. Collagen and proteoglycans are produced by special cells, called chondrocytes, in the cartilage. Joints can withstand enormous pressure by slowly releasing water from the cartilage.
As we age, the ability to restore and maintain a normal cartilage structure seems to decrease. The activity of important repair enzymes is reduced, the water content diminished, and the joints become more prone to damage. But the full pathological mechanism for arthritis development is not yet known.
Osteoarthritis/arthrosis is a disease mainly characterized by degenerative processes of the articular cartilage, but changes also involve the synovial membrane and the bone next to the cartilage. It is a gradual decay that most often affects the weight- bearing joints (knees, hips, and spinal joints) and the joints of the hand. A breakdown of the cartilage matrix leads to cracks and ulcers and a thinning of the cartilage with a loss of shock absorption. The underlying bone starts to thicken as a response to the increasing stress, and bone spurs are formed. In the advanced phases of osteoarthritis, an inflammatory reaction in the synovial membrane can be seen. This severe degeneration causes pain, swelling, deformation, and reduced range of motion.
Traditionally, osteoarthritis has been connected to aging, obesity, and repeated mechanical joint stress. Predisposing factors such as trauma or inherited abnormalities are also known to trigger degenerative changes and cause secondary osteoarthritis at even younger ages. New research is beginning to shed light on how osteoarthritis develops at the cellular and molecular levels.
Evidence is accumulating that the culprits may be factors called cytokines together with enzymes that break down the collagen matrix. Cytokines are proteins that carry messages between cells and regulate immunity and inflammation. Two cytokines, tumor necrosis factor alpha (TNF-a) and interleukin one beta (IL-1B), play an essential role in the cartilage destruction and inflammation process (Feldman et al., 1996). They have been found in elevated levels in the synovial membrane, the synovial fluid, and the cartilage of osteoarthritis patients. In animal models it was shown that inhibition of TNF-a results in decreased inflammation, while inhibition of IL-1B effectively prevents cartilage destruction (Plows et al., 1995).
TNF-a has proven to be an even more important factor in rheumatoid arthritis (RA), where it is a key factor in promoting inflammation and damage to cartilage and bone (Bertolini et al., 1986; Saklatvala, J., 1986).
Rheumatoid Arthritis (RA)
Unlike osteoarthritis, rheumatoid arthritis is a so-called autoimmune disease, characterized by chronic inflammation and thickening of the synovial lining in addition to cartilage destruction. In autoimmune diseases the immune system attacks body tissues as if they were foreign invaders. As in most other chronic inflammatory diseases, the etiology and pathogenesis of RA is poorly understood. Contributing factors are thought to include food allergies, leaky gut syndrome, hereditary factors, and microbes.
RA affects approximately 3% of the population, striking women three times as often as men. The typical onset is at 20 to 40 years of age. The clinical picture varies from mild chronic joint inflammation with occasional flare-ups to painfully deformed joints. The disease is often accompanied by low-grade fever, weight loss, and a general feeling of sickness and soreness.
Source: Life Extension Foundation