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The word arthritis is derived from the Greek word arthron (joint) and suffix -itis (inflammation). For people who have arthritis, the word variously signifies pain, swelling, redness, and heat that may be caused by tissue injury or disease in the joint.

Osteoarthritis is the most common type of arthritis. It is called a degenerative joint disease because it results from the deterioration of the bones and cartilage that make up the joints. The second most common type of arthritis, rheumatoid arthritis, is an inflammatory disease that affects the lining of multiple joints, especially in the hands and feet. Although it affects only one-tenth as many people as osteoarthritis, it can be far more debilitating. The other rheumatic diseases discussed in this report — gout, pseudogout, ankylosing spondylitis, reactive arthritis, psoriatic arthritis, enteropathic arthritis, and infectious arthritis — are also characterized by inflammation.

The musculoskeletal system

All types of arthritis affect the musculoskeletal system in some way, although the joints involved and the means of damage may vary.

The arrangement of bones and muscles in the body is a marvel of engineering. A model of a skeleton may look rickety and frail, but bones have a compression strength equaling that of cast iron or oak. Although incredibly light — the average adult skeleton weighs only 20 pounds or so — bones are capable of bearing tremendous weight. Their strength is necessary to withstand the forces of movement. When you walk at a leisurely pace, each foot strikes the ground with a force about three times your weight. At a brisk walk or run, the pressure increases to five to six times your weight. In other words, a 150-pound person's lower extremities are subjected to 450–900 pounds of force during normal activity.

The arrangement of muscles helps hold the skeleton together and, at the same time, provides a means of moving individual bones. Tendons and ligaments, the structures that bind bone and muscle, are made of connective tissue. The main proteins that make up connective tissue are collagens and elastins, which imbue it with tensile strength and elasticity.

Types of joints

There are three basic types of joints (see Figure 1). Fixed joints, or sutures, are thin bands of fibrous tissue that connect the platelike bones of the skull, allowing the skull to expand and accommodate the growing brain. When brain growth is complete, these fibrous joints disappear as the skull bones fuse together.

Figure 1: Types of joints Types of joints There are three basic types of joints. Fixed joints connect the platelike bones of the skull. Cartilaginous joints, such as intervertebral disks or the sacroiliac joints, contain tough cartilage-like plates that bend. The most mobile are synovial joints. They are surrounded by a loose fibrous capsule lined with a thin membrane called the synovium.

Cartilaginous joints contain tough cartilage plates. In the pelvis, these joints permit slight movement of the pubic bones and the sacroiliac joint, where the sacrum (part of the spinal column) and pelvis meet. The disks between the vertebral bones in the spine are thicker and accommodate greater mobility.

The most mobile joints are the synovial joints of the shoulders, elbows, wrists, fingers, hips, knees, ankles, and toes. Surrounding each of these joints is a loose fibrous capsule lined with a thin membrane called the synovium. Synovial joints are designed for a variety of movements that make possible all manner of activity, from playing tennis to playing piano. Some — for example, the outermost joints of the fingers — are limited to flexion and extension (bending and straightening) within a single plane. Others, such as the shoulder, wrist, and hip, are capable of complex movements in multiple planes.

Joint design

Synovial joints, like machines with moving parts, are vulnerable to friction. If a machine's moving parts come in contact with one another, friction will scratch the surfaces and cause pitting, distortion, and eventually breakage. As any do-it-yourselfer knows, you can prevent such friction in two ways: Apply a lubricant, or insert a cushion, such as a rubber gasket. Human joints are protected in both ways (see Figure 2).

Figure 2: Joint anatomy Joint anatomy Ligaments bind the bones together and keep them in proper alignment. Muscles and their tendons stabilize the joint as well as move it. Cartilage, a tough and somewhat elastic tissue, provides a smooth, slippery surface for movement and cushions the joint. The synovium produces viscous fluid that lubricates the joint to provide frictionless movement. The bursae allow the soft tissues around the joint to move smoothly as the joint moves.

Synovial fluid is a viscous, yellowish, translucent liquid. Produced by the synovium, it oils the joint and minimizes friction. It also helps protect joints by forming a viscous seal that enables abutting bones to slide freely against each other but resist pulling apart. When a joint is moved quickly or forcefully, this seal breaks, making a popping sound. Places where tendons and muscles cross a bone or other muscle are also subject to friction. These sites are protected by bursae, sacs which not only contain lubricating fluid but also act as cushions.

Articular cartilage, a tough and somewhat elastic tissue that covers the ends of bones, provides joint cushioning. Because it's about 75% water, cartilage compresses under pressure (as occurs with jumping or even walking) and resumes its original thickness when the force is released, much like a very tough sponge. Because the articular cartilage can assume a shape or mold, the opposing surfaces of a joint are perfectly matched.

Several things maintain stability through a joint's range of motion so that the joint can function normally. One is the contour and fit of the joint surfaces themselves. The hip, for example, is a ball-and-socket arrangement. With each stride, the head of the femur (thighbone) pushes deep into the cup-shaped cavity of the pelvis, providing maximum stability during walking. Most other joints are more like hinges.

Also helping to maintain bone alignment are the ligaments — tough, slightly elastic, fibrous bands that bind the bones together. For example, ligaments on either side of the finger joints prevent side-to-side bending, while ligaments stretching across the palm keep the fingers from bending too far backward.

Muscles and tendons, the fibrous cords that attach muscle to bone, stabilize joints as well as move them. The best example of how this works is in the shoulder, which has such a wide range of motion that ligaments would impede it. While the large, visible shoulder muscles supply the power to move the shoulder, the small rotator cuff muscles and tendons keep the head of the humerus (upper arm bone) from slipping out of the glenoid fossa, a shallow cuplike indentation in the shoulder blade.

The immune system

Inflammation is the hallmark of a number of types of arthritis, including rheumatoid arthritis, gout, pseudogout, ankylosing spondylitis, reactive arthritis, psoriatic arthritis, enteropathic arthritis, and infectious arthritis. Such conditions all appear to stem, directly or indirectly, from an inflammatory response instigated by the immune system.

In inflammatory rheumatic diseases, the immune system reacts to elements that the body perceives as foreign — be they actual invaders, such as bacteria, or simply cell components wrongly identified as foreign. Research shows that certain people may be more genetically susceptible than others to such inflammatory rheumatic diseases.

The normal immune response

The skin covering your body and the mucous membranes lining your respiratory system and gastrointestinal tract are protective barriers that keep out most of the harmful substances in the environment that might enter your body. When these barriers are insufficient, the immune system activates special cells, proteins, and powerful chemicals to eradicate the invader. Although surveillance and policing go on quietly all the time, major confrontations can result in inflammation and tissue damage.

When bacteria, viruses, or other foreign substances invade the body, specialized cells release cytokines, chemical messengers that increase blood flow to the site and direct an army of white blood cells, microbe-fighters, and other protective substances to flow into the invaded tissue. Here, white blood cells release potent chemicals including leukotrienes, prostaglandins, and additional cytokines. These and other chemical mediators are responsible for intense reactions that include inflammation in the form of pain, redness, swelling, and heat. After the attackers have been eradicated, the immune system is no longer stimulated, and the symptoms of inflammation subside.

In order for this process to occur, however, the immune system must first identify the invaders as "non-self" in contrast to normal "self" cells. This requires a complex interaction of numerous recognition and signaling molecules. In simplified terms, the immune system works via several types of cells. First, cells known as phagocytes encounter the invaders, digest them, and present an antigen (a distinguishing protein or carbohydrate) on their surface (see Figure 3). The antigen binds to a special molecule called a human leukocyte antigen (HLA) complex, which in turn presents it to a second class of immune cells launching an attack on the "non-self" invaders.

Figure 3: Immune response Immune response T cells attack and destroy invaders, then multiply to prepare for a future invasion.

This second cell type includes several classes of lymphocytes (white blood cells). T lymphocytes recognize the antigen signal and recruit killer lymphocytes to destroy the foreign cells. At other times, T lymphocytes stimulate B lymphocytes to make antibodies, proteins that are designed especially to attack the invader. Natural killer cells and macrophages are other white blood cells involved in fighting foreign molecules. The immune system can also target body cells that become abnormal because of injury, cancerous transformation, or invasion by certain viruses.

Given this complexity, it's not hard to imagine how autoimmune injury might occur. Antibodies made against foreign molecules might mistakenly attack normal body proteins; lymphocytes might misidentify "self" and "non-self" cells; or normal cells could get caught up in the immunological crossfire of harmful enzymes and toxic molecules.

When the system malfunctions

Inflammatory rheumatic disease occurs when something goes awry with the immune response, perhaps because B lymphocytes continue producing antibodies or because the "self" tissues are affected in some way by the original attack that makes them seem "foreign." However it occurs, the result is an inflammatory response that continues far longer than it should.

This prolonged inflammation can be devastating. In rheumatoid arthritis, inflammation may involve internal organs as well as joints. And in ankylosing spondylitis and related disorders, inflammation often centers on an enthesis, a spot where tendons or ligaments attach to bone. The different patterns of tissue damage account for the symptoms that are unique to each of these ailments.

It's become clear that for most forms of inflammatory joint disease, the cause isn't a single infectious agent that could affect anyone. Rather, such diseases occur through a combination of several inciting events in an individual who is genetically susceptible or predisposed at a given time by otherwise unrelated factors.

Much like fingerprints, each person's immune response is unique. This is because a group of genes that regulate the immune system can produce responses to a very large array of potential antigens. On the short arm of chromosome 6 lies an area called the major histocompatibility complex (MHC), containing genes that underpin the immune response.

These genes function as a sort of headquarters for the immune system by determining the structure of the HLA molecules that present antigens to T lymphocytes and enable immune cells to distinguish "self" from "non-self." They were first discovered in the 1950s when immunologists were trying to understand why organ transplants were often rejected by the recipient's immune system. This line of research led to the discovery that people who received transplants had a better chance of recovery if certain of their HLA molecules matched the donor's.

A number of HLA molecules are associated with particular types of inflammatory arthritis. For example, a genetic marker for HLA-B27 is present in nearly all people who have ankylosing spondylitis and in most of those with reactive arthritis, which is triggered by bacterial infection elsewhere in the body. Similarly, a genetic marker for HLA-DR4 can be found in many people with rheumatoid arthritis.

Source: from Harvard Health Publications, Copyright © 2008 Harvard University. All rights reserved. Harvard Medical School does not endorse products.
Used with permission of StayWell.
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