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.

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. Two strategies can prevent such friction: applying a lubricant, or inserting a cushion, such as a rubber gasket. Human joints are protected in both ways (see Figure 2).

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 sticky seal that enables abutting bones to slide freely against each other but resist pulling apart. Places where tendons and muscles cross a bone or another muscle are also subject to friction. These sites are protected by bursae, sacs that 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 mold to its surroundings, 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.

Ligaments, which are tough, slightly elastic, fibrous bands that bind the bones together, also help with alignment. For example, ligaments on the sides 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 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 — including toxins and infectious microbes — that might enter your body. When there’s a breach to one of these barriers, 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 invaders enter 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 hormones and related substances and additional cytokines. These and other chemical mediators are responsible for intense reactions that include inflammation, which is marked by pain, redness, swelling, and heat. After the attackers have been eradicated, the immune system is no longer stimulated, and the symptoms of inflammation subside.

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.

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 a spot where tendons or ligaments attach to bone, known as an enthesis. The different patterns of tissue damage account for the symptoms that are unique to each of these ailments.

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, many people with rheumatoid arthritis have a genetic marker called HLA-DR4.

Rheumatoid arthritis

Rheumatoid arthritis is a chronic autoimmune disease in which the body’s immune system attacks healthy tissue lining the joints. It affects an estimated 1.5 million American adults. Although the disease usually first appears during middle age, onset may occur as early as a person’s 20s and 30s.

The chronic inflammation of rheumatoid arthritis begins in the synovium, where an unknown event triggers an inflammatory reaction. As a result, synovial and other cells produce a variety of chemical mediators, including cytokines and proteolytic enzymes, which together can destroy all the components of the joint. The synovial tissue also begins to proliferate, causing the normally smooth synovium to form pannus—a rough, grainy tissue that grows into the joint cavity and erodes cartilage (see Figure 1). If the tendons become inflamed, they may shorten and immobilize the joint, which can cause bone fusion and loss of mobility. If the tendons rupture, the joint may become loose or floppy.

Rheumatoid arthritis attacks multiple joints and is usually symmetrical, affecting joints on both sides of the body, particularly the finger joints, base of the thumbs, wrists, elbows, knees, ankles, or feet. It nearly always involves the wrists and the middle and large knuckles, but seldom the joints nearest the fingertips (see Figure 2). At times, joint pain may be constant, even without movement. Morning stiffness that lasts for an hour or longer is a hallmark of the disease and one of the main ways doctors gauge the severity of inflammation.

The course of rheumatoid arthritis is unpredictable. Early on, the symptoms frequently abate or even disappear, only to flare up weeks or months later. Occasionally, complete remission occurs, usually within the first year. But for some people the process is destructive, ending in severe disability within a few years.

People with rheumatoid arthritis often develop eye conditions, including keratoconjunctivitis sicca (dry eye), which causes redness, burning, itching, reduced tearing, and sensitivity to light. Other complications include respiratory, heart, and neurologic disorders. In rare cases, the ligaments that tether the uppermost vertebrae (which support the skull) are damaged, allowing the vertebrae to slip out of alignment and pinch the spinal cord.

At advanced stages, rheumatoid arthritis can limit a person’s ability to carry out normal daily activities such as dressing, bathing, and walking. Those affected often experience feelings of depression and helplessness as the disease progresses. However, medications are now helping to slow the progression of rheumatoid arthritis and make a dramatic difference in the lives of many of those affected.

One of the most important steps you can take if you are diagnosed with the disease is to become an active participant in your own care. This includes working with your doctor so that you can learn to recognize flare-ups and drug side effects, take medication as prescribed, and engage in activities to maintain joint function in order to prevent disability. Balancing rest with activity, dealing with the emotional impact of rheumatoid arthritis, and using assistive devices to protect your joints against overuse are among the most helpful coping strategies. The ultimate goals in managing rheumatoid arthritis are to prevent or control joint damage, prevent loss of function, and reduce pain.