In order to understand the causes, symptoms, and treatment of osteoarthritis in animals, it is important to have a general idea of how a healthy joint is structured and how it functions. All your pet's movements, from sitting to jumping on the bed to playing with you or another dog, depend on the precise and coordinated movement of joints. Although we tend to take such flexibility and movement for granted, when joints become injured or inflamed, this delicate and amazing interplay of moving parts is more fully appreciated.

Although humans and other mammals have certain similarities in their skeletal structure, the most obvious difference is that most animals are four-footed, which means their weight is more broadly distributed among the joints. This may be a gift of Mother Nature, since it allows lame animals to continue to move about more easily than a two-legged human with a similar problem.

That difference aside, animal joints are made up of the same basic elements that are found in humans: cartilage, joint capsules, the synovium, ligaments, tendons, muscles, and bursae.

Cartilage: A glistening, bluish white, spongy substance, articular cartilage — the medical term for the kind of cartilage found in joints — covers the ends of bones. Cartilage consists primarily of water, sugars, proteins called proteoglycans, and a tough, fibrous substance called collagen.

The combination of these substances makes healthy cartilage resilient enough to spring back into shape after it has been under pressure, such as when an animal is running. In a healthy joint, the spongy cartilage cushions and protects the bones during activity, serving as a "shock absorber" while providing a smooth, friction-free surface that enables the joint to move properly. When cartilage is in its prime, this surface is so smooth that it is actually more slippery than ice!

Cartilage is highly absorbent, and it is this feature that helps it remain healthy by soaking up nutritious synovial (see below) fluid that fills the joint space. A fine example of an incredibly efficient design, cartilage fills and empties itself of this fluid through normal joint movement. In this way, it is able to take in nutrients and cleanse itself of waste products as the animal goes through the normal motions of everyday life.

Joint capsule: At the ends of a bone, there is an area known as the subchondral bone, where the cartilage is attached. The subchondral bone and cartilage are both encased in a sealed cap-sule, called the joint capsule, or synovial sac. The joint capsule is made up of a tough, fibrous outer layer and a smooth, pliable inner layer, called the synovial membrane. The outside of the capsule consists of thick, cordlike fibers called ligaments. These are anchored to the bone on either side of the joint, where they help to keep the joint stable and hold the bones in correct alignment.

Muscles control joint movement and are attached to the joint bones by tendons, which are tough, dense cords of connective tissue that transmit the force of muscle exertion.

Synovial membrane: The lining inside the joint capsule is the thin, velvety smooth synovial membrane. Only one or two cells thick in a healthy joint, the membrane contains plentiful blood vessels and nerve endings, and produces a clear, viscous fluid resembling raw egg white that fills the capsule. The synovial fluid lubricates the joints and nourishes the cartilage, which has no blood vessels, and therefore no source of nutrients of its own.

Bursae: Lying outside the joint are small, fluid-filled sacs called bursae. These too produce a lubricating liquid and help protect the tendons and ligaments from injury.

As osteoarthritis develops, the fundamental change that occurs is a breakdown of cartilage at the site of the joint. Cartilage becomes softer and starts to lose its elasticity, and the surface can become worn or thin in spots. The cartilage slowly loses its ability to absorb sufficient supplies of synovial fluid to keep it healthy. As the cartilage deteriorates, there is less and less of it between the two bones that meet at the joint. Eventually the cartilage may become so thin that the bones rub together, and fissures, tiny pits, and cracks in the bones can develop. An animal's body attempts to repair the damage, often making the situation worse. The end of the bones may thicken, or bone spurs can form, creating bony enlargements around the joint. In addition, sometimes pieces of cartilage or bone break off and float in the joint fluid, irritating and inflaming the delicate synovial membrane lining the joint.

As osteoarthritis progresses, the animal's cartilage wears away. Joints become painful and stiff, making movement so difficult that it is sometimes avoided unless absolutely necessary. This tendency not to use an arthritic joint can make the problem worse by weakening the muscles and ligaments around the joint and making it even stiffer. In the last stages of arthritis, the cartilage may be completely worn away and the bone fully exposed.

The effects of osteoarthritis are not limited to the cartilage, however. The disease also affects tissues in and around the joints, including the subchondral bone, the joint capsule, and the muscles surrounding the joint.

Why do these changes occur? What happens within the body that makes some — but not all — animals develop osteoarthritis? Over the years a number of theories have been advanced, many of which have turned out to be inaccurate. For example, there is a common assumption that age-related arthritis in animals is an inevitable consequence of growing older. Even many veterinarians believe that most animals are doomed to develop the disease and end their lives as frail, pain-ridden, decrepit shadows of their former selves.

Fortunately, this point of view is quickly being replaced by recent medical and technological developments in diagnosing and treating osteoarthritis. As a result, many animals now lead long, healthy lives in spite of arthritis.

Among the many misconceptions about osteoarthritis is the long-held belief that joints become stiff and painful because of wear-and-tear caused by normal, everyday activity. In fact, this theory underlies the traditional medical opinion that says there is nothing much that can be done about osteoarthritis in your pet, since once cartilage has deteriorated, it is gone forever.

But in the early 1980s several articles appeared documenting evidence of cartilage regeneration. These findings caused a fundamental shift in the way osteoarthritis is viewed. In fact, a recent article in the Journal of the American Medical Association acknowledged the popularity, as well as the effectiveness, of nutritional therapies. "There may well be biological mechanisms by which some nutraceuticals influence processes in OA [osteoarthritis]," said Dr. Timothy McAlindon of the Boston University School of Medicine. "Both glucosamine and chondroitin sulfate resemble molecules present in cartilage, suggesting that these substances could provide substrate for repair of cartilage damaged in OA."

Then on January 13, 1997, Jane Brody, the New York Times health columnist, reported on her experience with giving two supplements, glucosamine and chondroitin sulfate, to her dog:

Fourteen months ago, following my arthritic spaniel's dramatic improvement upon taking a supplement containing two substances that play a role in the formation of cartilage, glucosamine and chondroitin sulfate, I decided to try the stuff myself. . . . Now a year later my dog and I are still taking the supplement, though at lower daily doses. My dog, who will be 13 in June, is free of pain and stiffness. He walks two hours a day, goes up and down stairs easily and regularly climbs a mountain road with me.

The March 8, 1998, broadcast of Dateline NBC devoted a full segment to Jane Brody and her dog, totally mobile and, in all visible respects, fully cured of the disease.

In addition to changes on the cellular level, the correlation between exercise and symptoms of osteoarthritis has also been studied. Again, the wear-and-tear theory was found to be out-dated. The most important finding is that moderate, consistent exercise does not promote osteoarthritis. In fact, such activity improves the functioning of an animal's joints by strengthening surrounding muscles and stabilizing the joint. As a result, the cartilage is less likely to be harmed during everyday activity or exercise.

There are two exceptions. The first involves a joint that has been injured — if an animal has been hit by a car, for example. The second is the result of repetitive impact loading, like repeatedly taking a horse over fences or playing long sessions of Frisbee catch with a dog. These types of joint injuries or abuse can lead to "secondary" arthritis, in which a specific event or frequent repetition of a particular activity is the primary cause. Obesity can also bring on secondary arthritis, simply because the excess weight puts additional pressure on the joints and cartilage. But regular, moderate exercise is now accepted as a means of improving arthritis symptoms, rather than making them worse.

In fact, several studies have specifically examined the effect of jogging on the risk of developing osteoarthritis. Researchers have found that far from damaging joints, regular jogging in middle age is likely to help maintain physical function. Only among long-distance runners did there seem to be an increased risk of developing osteoarthritis in the knee and hip.

Other recent investigations, including one at the University of Iowa College of Medicine, have demonstrated that lifelong moderate — and probably even strenuous — joint use does not cause cartilage degeneration in normal animal joints with proper alignment, stability, articular surfaces, innervation, and muscle control.

Interestingly, in the Iowa study the researchers noted that a lack of "loading or static loading activity"— in other words, inactivity — produced more degeneration of the cartilage "matrix," the area where cartilage is created, and could eventually lead to loss of joint function. What this means to a pet owner is that an animal that spends long days housebound or sleeping appears to be at greater risk of developing osteoarthritis than a pet that is regularly taken for walks or engages in play during its waking hours.

In a study of osteoarthritis in humans, researchers have concluded that lifelong moderate use of normal, healthy joints does not increase the risk of cartilage degeneration. In other words, osteoarthritis is not the result of aging, although, as the authors state, there is a strong correlation between increased age and the prevalence of the disease.

The same authors are quick to point out, however, that repeated high-impact activities and torsional loading (movements that twist or wrench the joints, such as the fast turns made by many herding dogs) can damage normal joints. Furthermore, joints are more susceptible to arthritis when they are not correctly formed or are unstable, when they receive inadequate support because nearby muscles are weak, or when the joint or muscle nerves are not functioning properly.

Consequently, it is important to realize that even young dogs can develop osteoarthritis from repetitive jumping or overexertion. Good examples are dogs that jump high into the air when playing catch. The wear-and-tear on joints and muscles from jumping several times the animal's body height and then landing, especially on hard surfaces, can sometimes cause premature deterioration. One recent study shows a slight increased risk of developing osteoarthritis in weight-bearing joints when there is very frequent and heavy exercise over many years. For the majority of less active dogs, however, routine recreational physical activity neither decreases nor increases the risk of developing arthritis.

Understand, though, that the debate over the consequences of exercise on joints is not over yet. Researchers at the University of Kuopio, in Finland, examined the effects of running in a controlled study of mice. Those mice in the runner group exercised daily from the age of two months to eighteen months, and were sacrificed at intervals within this period. Examination of the knee joints in the runners, as compared with mice in the control group, which did not exercise, showed that moderate, long-lasting running accelerates the development of osteoarthritis in the knee joints. Even so, no one knows yet if these findings apply only to mice or to mammals in general.

While we wait for the final word on whether physical stress is a factor in the development of osteoarthritis, scientists can say for certain that the origins of the disease are rooted in metabolic changes in the cartilage itself. The progressive deterioration of joints occurs when chondrocytes, special cells in the cartilage that create new collagen and other cartilage ingredients, go awry. When this happens, the chondrocytes produce cartilage-destroying enzymes, like metalloproteinases, as well as nitric oxide. Nitric oxide not only causes oxidative damage to tissue but also con-tributes to a process called apoptosis, which kills chondrocyte cells. As a result, existing cartilage degenerates faster than new cartilage can be produced. Antioxidant vitamins and nitric oxide inhibitors are being studied as means of fighting this aspect of the disease. Meanwhile, other experts are approaching treatment from the opposite perspective, by examining ways of creating more cartilage. For reasons that are not yet clear, changes in the tissue and cell chemistry cause existing cartilage to degenerate faster than new cartilage can be produced.

At the Department of Veterinary Pathology and Department of Veterinary Clinical Science and Animal Husbandry at the University of Liverpool, researchers conducted a study of how cartilage changes with osteoarthritis. Cartilage from seven dogs with osteoarthritis was compared with healthy cartilage from five other dogs. Researchers examined a substance called type VI collagen, which is an essential element in the cartilage matrix. In healthy cartilage, the type VI collagen was concentrated in the capsule next to chondrocytes. In the osteoarthritic cartilage, however, researchers found that this form of collagen was present throughout the cartilage matrix and was greatly increased in the region surrounding chondrocytes.

As the study authors point out, here is evidence that cartilage can regenerate. The higher concentration of type VI collagen in the chondrocyte area, where cartilage production takes place, is a sign that the body's own natural healing process is under way. Researchers have concluded that these collagen fibers, which organize and stabilize other major collagen fibers, are part of an active process designed to repair damaged osteoarthritic cartilage.6

Other studies also provide evidence of cartilage regeneration and repair. In one study that explored this process, scientists examined osteoarthritic cartilage and found primitive forms of proteoglycans, large molecules made up of protein and sugars that are one of the essential ingredients of cartilage. This primitive proteoglycan is typically found in immature cartilage. From this discovery, the researchers concluded that the healing process occurring in articular cartilage is similar to the process that takes place in other damaged connective tissue, such as skin and tendons. This immature cartilage appears soon after injury and throughout the mending process, thereby supporting the theory that the body produces it specifically as a means of repairing cartilage.

These same researchers also report that in dogs, osteoarthritis increases collagen synthesis. But unlike the proteoglycans production, the collagen is not a primitive form, but a mature version primarily responsible for cartilage growth.

With this growing body of evidence to support cartilage regeneration, the wear-and-tear theory of osteoarthritis is definitely on the wane. So too is the notion that osteoarthritis is inevitable and that once a beloved pet develops this condition, there is nothing that can be done.

The new understanding of osteoarthritis has also opened up the possibility of new avenues of healing. One focus is on how healthy cartilage may be affected by three major factors — heredity, poor nutrition, and injury. Subsequent chapters look at each of these points in greater detail.

Other researchers are also finding ways to repair and maintain normal cartilage structure and function, for instance, healing with supplements of glucosamine and chondroitin sulfate.

Studies from around the world amply demonstrate the potential of these supplements when it comes to osteoarthritis. Clinical research from Europe, South America, and Asia has demonstrated the healing value of glucosamine and chondroitin sulfate in people. In years past, public acceptance of such treatments would have been difficult without widespread support from veterinarians. Today strides in the treatment of osteoarthritis in animals are being made in the United States, where research and clinical reports attest to the benefits of glucosamine and purified chondroitin sulfate. Progressive veterinarians herald glucosamine and chondroitin as the wave of the future, and success stories are everywhere, from pet magazines to the Internet.

Before discussing the amazing ability of glucosamine and chondroitin sulfate to promote cartilage mending and to reverse osteo-arthritis, let's take a look at some of the other accepted methods of regenerating cartilage. Physicians are currently using some, and researchers continue to experiment with others. Any decision to use these options for your pet should be made with advice from your veterinarian, who can inform you of the short- and long-term benefits and concerns associated with any treatment protocol.

Pharmaceutical Medications

Although it began as a treatment for show and racehorses with orthopedic problems, Adequan, from Luitpold Pharmaceuticals in Shirley, New York, can alleviate arthritis and hip dysplasia pain in dogs too. In addition, studies have shown that it also promotes cartilage healing. Keep in mind, though, that it works best in mild to moderate situations. In advanced stages of the disease, Adequan may not provide enough pain relief to make a difference.

Derived from the tracheae and lungs of cows, Adequan is purified glycosaminoglycan (GAG) polysulfate, part of a family of molecules that serve as precursors in the creation of joint fluid and cartilage. Adequan treatments can enhance the quality of the joint fluid, as well as protect and repair cartilage.

The medication is fairly costly and requires several trips to the veterinarian, since it must be injected into the muscle once or twice a week for anywhere from one to eight weeks. Once the pet improves, monthly maintenance visits are recommended. Side effects are rare.

Rimadyl is a nonsteroidal anti-inflammatory drug that was created especially for relieving pain and inflammation in dogs. Studies have shown that it does provide relief for osteoarthritis symptoms. Although Rimadyl was introduced only in 1997, it is one of the top ten bestselling products in the U.S. animal-health market, with more than 1 million dogs now on the medication. Rimadyl has fewer side effects than other anti-inflammatory drugs, but on rare occasions it can cause digestive upset or liver problems. If your dog takes Rimadyl, follow-up visits to the veterinarian are recommended.

Cartilage Transplantation

In recent years considerable progress has been made with this technique. In animal studies, for example, bone and cartilage cells have been successfully transplanted from one mouse to another.

In humans the technique is known as autologous chondrocyte implantation (ACI) and involves healthy living cartilage that is removed from the patient and used to cultivate a living graft. This graft is then implanted into the damaged, arthritic joint. ACI has proved useful in healing secondary arthritis resulting from injuries, but not primary arthritis.

This technique is also being performed on dogs and horses but is currently in the experimental stage. It is too early to tell whether this alternative form of cartilage can withstand the pressures of normal use.

Scientists have high hopes for a related procedure (being studied at New York's Beth Israel Hospital) that involves removing a portion of cartilage from an inflamed joint and then cloning it in a laboratory. The new growth is reinjected into the joint to stimulate the creation of new cartilage. Although it is expensive now, this technique may be affordable for the average patient someday.

Test tube cartilage: In the laboratories of the Massachusetts Institute of Technology (MIT), scientists are experimenting with growing cartilage in test tubes. Thus far, they have produced a substance that is stiff but flexible and nearly the same as human cartilage. But it is too early to say whether this material can be transplanted into joints to repair cartilage damage associated with arthritis.

Chondrogeneron: This is a combination of fibrinogen, a simple protein commonly found in animal tissues, and a cartilage-regenerating substance called transforming growth factor beta (TGFß). When used together, the fibrinogen helps the TGFß adhere to the injured cartilage. Chondrogeneron may one day be used to treat osteoarthritis in pets, since it has been used successfully to repair cartilage and promote cartilage growth in laboratory animals.

Meniscus transplants: The meniscus is a type of fibrous cartilage found in the knee joint. Experiments are under way in America to use donated meniscal tissue or synthetic material to restore a damaged meniscus. But more studies are needed before this procedure can be considered viable for human or animal osteoarthritis.

The good news is that your animal no longer has to suffer needlessly from the pain and debilitation of arthritis. If you're reading this book, you're obviously concerned about your pet's health and the possibilities for treating osteoarthritis. Damaged cartilage can be repaired and the degenerative process of osteoarthritis reversed. Chapter 4 takes a closer look at the wonders of glucosamine and chondroitin sulfate, and offers stories that will warm your heart and give you and your pet hope.

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Now, let's take a more in-depth look at the disease in animals, including its causes, signs, and symptoms.

Copyright © 2000 by Affinity Communications Corporation
Excerpt posted with permission from http://www.twbookmark.com

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