Causes and Diagnosis

Most people will eventually develop some degree of osteoarthritis (OA), but only two-thirds experience symptoms. How to understand, identify and treat a misunderstood condition.

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By  Harvard Medical School Published  February 14, 2006

|~||~||~|By the time they reach 80, most people develop some degree of osteoarthritis (OA). But only about two-thirds experience symptoms. Meanwhile, many people who have joint pain mistakenly attribute it to this prevalent condition, when it is really caused by something else. As a result, osteoarthritis is often misunderstood — and mistreated.

To thoroughly understand osteoarthritis, it makes sense to start by looking at the joint from an engineer’s point of view. To an engineer, every joint is a compromise. Joints have to perform two contradictory functions: They have to be flexible, to allow smooth movement, but they also have to be stable, to support weight and absorb tremendous force without wavering. Different joints meet these challenges in different ways, but they all have some common features.

Joints are found at the junction of two (or more) bones. Muscles attach to the bones through their strong fibrous tendons. To move a joint, some of the muscles contract, pulling on the tendons and bones. For smooth, painless motion, though, the muscles on the opposite side of the joint must relax. For example, the elbow bends, the biceps contract but the triceps relax.

Muscles are essential for movement, but they also have an important role in providing strength and stability; muscle weakness or imbalance puts extra stress on joints. Ligaments also provide strength and stability. These bands of fibrous tissue extend across a joint, attaching one bone to another while still providing enough “give” for motion.

If joints were made up of only bones, muscles, and ligaments, every movement would be painful and we’d all be swollen and deformed. Fortunately, joints have built-in shock absorbers and lubricants. Cartilage is the smooth, shiny tissue that does the job; cooks recognise it as the “gristle” that caps bones. Unlike bones, though, cartilage doesn’t have any blood vessels or nerves. That means if an injury damages just cartilage, it will be painless — but it also means that cartilage cannot heal and repair itself like other tissues.

Cartilage is a living tissue. Because it lacks blood vessels, it gets its nutrition from the joint fluid (synovial fluid) that bathes the joint, providing extra lubrication as well as nutrition. The joint fluid is produced by the synovial membrane, a richly vascular capsule that surrounds the joint.

Osteoarthritis begins in the cartilage. At first, the cartilage is swollen due to an increase in its water content. The collagen fibres that give cartilage its strength get smaller and become disorganised. The cells that produce healthy cartilage begin to produce less of the good proteins and more of the enzymes that break down the tissue. The cartilage thins out, and in advanced cases it wears away completely.

Deprived of normal cushioning, the bones get into the act, producing abnormally dense tissue next to the arthritic joint (sclerosis), often with tiny cysts in the bone. The process can also produce bone spurs (osteophytes), and small fragments of bone or cartilage sometimes break off and float in the joint fluid (see figure 1 below).

In the earliest stages of OA, these changes are so subtle that they can be detected only through a microscope. Soon, though, x-rays begin to reveal a narrowing of the space between the bones as cartilage wears away, then abnormally dense sclerotic bone and bone spurs. Somewhere along the way, patients begin to notice things, too, as their joints become swollen, stiff, and painful. But OA doesn’t always produce pain and swelling. In some people, it doesn’t go beyond the stage of mild x-ray abnormality, with a little stiffness or discomfort from time to time. In others, unfortunately, it progresses to cause severe pain and disability.

What it’s not
OA is the most common form of arthritis, accounting for roughly half the cases. But there are many other types of arthritis, to say nothing of the non-arthritic conditions that cause aches and pains around muscles and joints. Here are some of the problems that are often confused with OA:

l Rheumatoid arthritis (RA). It’s much less common than OA but is often more serious. RA starts in the synovial membrane, not the cartilage. It is an inflammatory condition caused by an overactive, misdirected immune system that attacks the body’s own tissues. Unlike OA, RA can cause fever and disturbances in many organs. Aggressive new treatments that tame the immune system can be very helpful.
l Lupus and other types of “collagen-vascular diseases” have many similarities to RA. Like RA, they are much more common in women than men.

l Gout is much more common in men than in women. Produced by the deposit of uric acid crystals in a joint (typically, a single joint in the big toe), it is abrupt, intensely painful, and produces a swollen, tender, reddened joint, often with fever. In contrast, OA is gradual, less painful, and often affects multiple joints, which remain cool and are not tender. Pseudogout is caused by another type of crystal; it often strikes the knee and can cause chronic pain similar to that of OA.

l Infections of joints begin abruptly, are usually accompanied by fever, and are often accompanied by a rash or other symptoms. Bacterial infections are the most serious; staph and strep are examples. They require drainage of the infected joint fluid as well as high-dose antibiotics. Spirochetes, such as Lyme disease, can be treated with antibiotics alone. Viral infections, such as rubella (German measles), resolve without treatment.

l Other forms of arthritis. Many diseases that focus on other organs can produce joint inflammation and pain. Examples include psoriasis (a skin disease) and ulcerative colitis and Crohn’s disease (intestinal diseases).

l Other pains. A wide range of disorders can produce pain in the vicinity of joints without actual arthritis. Examples include bursitis, tendinitis, sprained ligaments, and muscles that are stretched, torn, or in spasm. A pinched nerve can cause pain that is referred to a joint. Fibromyalgia produces muscle and joint aches without any inflammatory or structural abnormalities. Polymyalgia rheumatica causes stiffness and pain, especially in older adults, and is often mistaken for arthritis of the shoulder, neck, or hips. And the list goes on — which is why rheumatology is a separate specialty of internal medicine.

l Osteoporosis is a disease of bones, not joints. It’s caused by a deficiency of bone calcium (“thin bones”). It increases the risk of fractures but is painless until a fracture occurs. The only reason to confuse it with OA is the similarity of the two names.

Causes and risk factors
Until recently, doctors blamed OA on “wear and tear,” implying that simple overuse causes the cartilage to wear away. It’s a logical theory, but it’s wrong. Time and mechanical stress do contribute to OA, but the process is really much more complex. In fact, scientists still don’t understand all the mechanisms involved, but they have identified the major OA risk factors, including:

l Age. Time takes a toll on the whole body, and joints are no exception. In fact, age is the strongest risk factor for OA. Although the disease can sometimes start in the 30s, it usually surfaces between the ages of 50 and 65, becoming more prevalent (and more prominent) with each passing year. Advancing age does mean more cumulative wear and tear, but age-related changes in the body’s metabolism, circulation, and elastic tissue may be even more important.

l Heredity. OA tends to run in families. Heredity is particularly important in early-onset OA, in OA of the hands (see figure 2) or hips, and in an uncommon form of the disease that strikes many joints at once.

l Obesity. It’s an important risk factor, and it’s one of the few that’s correctable. Extra weight makes joints work harder; every 10 pounds of excess weight, for example, produces about 40 pounds of extra stress on the knee with each step. A study of young men suggested that each 18 pounds of extra weight increases the lifetime risk of painful knee OA by 70%.

l Mechanical abnormalities. Neurological or orthopedic problems that produce faulty body mechanics, such as an abnormal gait, increase the stress on joints. The joints that bear the brunt of such stress are the most likely to develop OA.

lInjury. It’s the reason retired football players appear in advertisements for arthritis medication. A joint injury can seem to heal completely, but residual damage can slowly progress to produce OA later in life. A study of 1,321 Johns Hopkins Medical School graduates proves the point. Nearly 14% of doctors who suffered hip injuries during their student years developed hip OA by age 65, while only 6% of those without hip injuries developed OA. A knee injury in youth was even more significant, producing a fivefold increase in the risk of OA of the knee in maturity.

l Occupation and sports. Does running cause arthritis of the knees and hips? Most nonrunners would answer yes, but most studies of runners say no. Repetitive use, such as long distance running, has been linked to a slight increase in x-ray abnormalities but not to an increase in clinical OA (unless a significant injury has occurred along the way). Contrary to expectations, long-distance runners have fewer musculoskeletal complaints over the years than sedentary people. But occupations that involve frequent knee bending increase the risk of knee OA, and those that require frequent lifting appear linked to hip OA.

l Nutritional factors. Diet affects the metabolism of many tissues. The Framingham Knee Osteoarthritis Study linked low levels of vitamins C and D to an increased risk of OA. Unfortunately, there is no evidence that vitamin supplements can relieve the symptoms of OA or slow its progression. Still, a good diet is important for health, and weight control is particularly important for OA.

l Diagnosis. OA is difficult to understand, and it can be hard to treat — but it’s usually easy to diagnose. Blood tests are not necessary unless doctors need them to rule out other forms of arthritis. The symptoms and clinical findings of OA are quite characteristic, and ordinary x-rays are usually all that are needed to confirm the diagnosis. Typical x-ray findings include joint space narrowing, sclerosis (areas of increased bone density), bone cysts and osteophytes (spurs).

Advanced imaging techniques such as CTs and MRIs can be very helpful for OA of the spine, but they are rarely needed for other joints. And although joint taps can be crucial to diagnose infections and some other types of arthritis, they are rarely helpful for OA, since the joint fluid is normal. It’s important to diagnose OA correctly, but only an understanding of the symptoms of OA and the treatments that can bring relief will actually help patients feel better.

This article is provided courtesy of Harvard Medical International.
© 2005 President and Fellows of Harvard College||**||

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