Arthritis: Hope, But No Miracles
Arthritis treatment seems to attract charlatans peddling "miracle cures," folk remedies, and superstition. Over the years, people with arthritis have been advised to cover themselves with horse manure, wear copper bracelets, sit in abandoned radium mines, and swallow any number of magic elixirs. Although we still do not know precisely what causes this collection of disorders, nor in most cases how to halt its course, modern medicine has an arsenal of treatments available that attempt to make life easier. With better understanding of the immune system's role in the spectrum of arthritis, more treatment options may become available.
Common Types of Arthritis
The result of any arthritis is painful joints, but the conditions have a variety of symptoms that make them distinguishable from one another.
This most common form of arthritis is also known as degenerative joint disease, or simply the "wear-and-tear" disease, because it tends to affect older people. Even so, osteoarthritis can appear earlier as the result of a metabolic disorder, congenital or hereditary disorders, or injury or trauma. Triathlete Jay Lehr attributes his arthritic knees to old football injuries. However, findings in a variety of studies that relate osteoarthritis to prolonged occupational or sports-related stress have been inconsistent. In osteoarthritis, the smooth cartilage on facing bone ends wears away, and new bone forms on the exposed ends. This bony overgrowth is a criterion for diagnosis, along with pain when joints move and a grating sensation called "joint crepitus" when the dry, exposed bone ends rub against each other. Osteoarthritis is not usually associated with inflammation.
Darwin J. Prockop, M.D., and his co-workers at Jefferson Medical College in Philadelphia recently uncovered a clue to the underlying cause of osteoarthritis. They examined an extended family of 19, spanning three generations, in which nine members developed osteoarthritis in the fingers, elbows, hips, and knees by their 20s or 30s--far younger than the usual onset of the disorder after age 40 or 50. The researchers zeroed in on a protein called type II pro-collagen. This protein forms coils that intertwine in groups of three to build the cartilage that protects bone ends and reduces the friction in joints. Because of a glitch in the gene that instructs cartilage cells to manufacture collagen, the triple fibrils in the arthritis sufferers in this family unravel after 20 to 30 years. As a result, the cartilage wears down and no longer offers its protective cushion.
Rheumatoid Arthritis - Introduction
In rheumatoid arthritis, the immune system attacks the joints as if they were an enemy to be vanquished. This autoimmune response is a chain reaction of sorts, for as the synovial joints themselves become inflamed, the swelling weakens ligaments, pushes fingers away from thumbs, and throws muscles out of alignment. This can lead to deformity and disability. Holding a pencil, opening a can or bottle, and even shaking hands become monumental tasks requiring the person to use both hands, often in awkward positions.
Rheumatoid arthritis can progressively worsen or stay the same for years before worsening. Rheumatoid arthritis progresses through five distinct stages.
Rheumatoid Arthritis - Stage 1
Stage 1 generally has no symptoms, but deep in certain joints, the cells forming the synovial membrane begin to attract T cells, a specialized type of white blood cell. The T cells and synovial lining cells stick to each other when proteins on their surfaces fit together like interlocking puzzle pieces. Once attached to the joint lining cells, the T cells turn on B cells (another type of white blood cell that makes antibodies that attack the joint) and release small proteins called cytokines. In rheumatoid arthritis, cytokines called interleukin-1, tumor necrosis factor, and gamma interferon are released. Inflammation is detectable by lab results showing elevated numbers of white blood cells in the synovial fluid.
Rheumatoid Arthritis - Stages 2 and 3
In stage 2, the immune assault gears up. The cytokines attract more white blood cells to the joints, and cause the malaise and fatigue, mild joint stiffness, and swelling that are the earliest signs of the disease. At this stage, more than a billion white blood cells a day collect in a knee joint. The joint capsule begins to fill with scaffolds built of new blood vessels. By stage 3, in response to all this activity, the cells forming the synovial membrane begin to proliferate. Symptoms intensify, and drug therapy must start now to prevent irreversible cartilage loss and joint deformity.
Rheumatoid Arthritis - Stage 4
In stage 4, the disease process extends to the cartilage, tendons, and, finally, the bone. Joint swelling is far more pronounced. As a result of increased cell numbers and connective tissue, the synovial membrane can weigh 100 times its normal weight. However, the destruction of the cartilage, tendon and bone is by far the most important consequence of the inflammatory process at this stage.
Rheumatoid Arthritis - Stage 5
By stage 5, overgrowth of cartilage and destruction of bone are so great that the ligaments surrounding the joint are thrown out of position. The destruction that results is irreversible.
The diagnosis of rheumatoid arthritis is based on the presence of all of the following four symptoms, for six or more weeks:
- joint stiffness upon awakening that lasts an hour or longer
- swelling in specific finger joints or wrist joints
- swelling in the soft tissue around three or more joints
- swelling of both sides of the joint.
The swelling can occur with or without pain. Additional diagnostic signs include x-ray evidence of bone erosion, nodules under the skin, a blood test that reveals a "rheumatoid factor" antibody (found in 80 percent of sufferers), or other key signs of the disease.