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by Susan Thorpe-Vargas Ph.D., John Cargill MA, MBA, MS

Limping and periodic lameness could be
signs of one of several joint diseases; get
the latest diagnosis and preventive measures

You don't know exactly when it began, but your trusted companion, jogging partner and tennis ball retriever has started to limp. Something is hurting him, but you can't tell what it is.

You tried moving his legs, and he didn't seem to object, but when he stands and moves by himself, he sometimes seems to be in obvious pain. The condition is frustrating, however, because the symptoms seem to come and go, sometimes appearing with exercise, but more often seemingly appearing unrelated to physical activity.

His hips have been X-rayed and the evaluation came back "excellent." What could possibly be wrong?

When a dog starts to drag itself around as if in pain, especially if it starts to limp, the cause may not be hip dysplasia, which can manifest similar symptoms. Other weight-bearing joints of the body also can be extremely painful and cause limping. Some examples are all the joints of the foot and leg, the shoulders and the elbows. Joint disease and arthritis in any joint can become crippling or certainly create a serious limp.

A cursory diagnosis of hip dysplasia can miss the real cause of the problem. Because lameness is so often linked to developmental diseases such as dysplasias and osteochondroses, even the professionals sometimes overlook other types of joint disease when considering a diagnosis. Especially important in this task are owner observations of duration and timing of symptoms, the history of the dog and how the dog reacts to treatment. The informed owner, who is familiar with his or her dog, the joint conditions that can afflict it and the preventive measures available can make a real difference.

If we first look at the different types of joints, perhaps we can better understand why some of the symptoms of joint disease occur. There are three types of joints: synovial (articular), fibrous and cartilaginous.


The pain and stiffness most often associated with joint disease are usually found within the synovial joint. By definition, joints or articulations are physical structures that unite two or more bones. It is the articulation of synovial joints that makes it possible for us to bend fingers, elbows and knees; thus, these joints are known as "true" joints.

The progression of disease in this type of joint depends on whether the join is freely moving or not. The structure of a synovial joint consists of two opposing surfaces covered with a hyaline cartilage membrane. Directly underlying this cartilage is the subchondral bone. The joint capsule, which is composed of a synovial membrane that lines a fibrous outer structure, surrounds the articular surfaces and the joint cavity. We will come back to this joint capsule later, but for now think of it as similar to the rubber boot or grease bladder around a ball joint in the front suspension of your car, or around the CV joint in a front wheel drive vehicle. Take note that this structure is necessary for proper joint functioning.

The synovial membrane lines the inside of the joint capsule, providing additional isolation of the joint space. The synovial membrane is further divided into two layers. The inner layer varies from one to several cells thick and contains synoviocytes. The "B" synoviocyte cells produce hyaluronic acid, which forms an essential gelatinous substance that functions both as a lubricant and as a shock absorber. The outer layer is directly adjacent to the fibrous capsule and is composed of nerves, elements of the lymph system and the reticuloendothial system (the system of macrophages found in bone marrow) along with the blood vessels that supply the joint.

The fibrous portion of the joint capsule is contiguous with both ends of the adjoining bones. In addition, along with other accessory structures such as ligaments, it helps to stabilize the joint by holding it securely together and by helping to maintain a force-dampening hydrostatic pressure when the joint is compressed.

Essential to the health of the synovial joint is the synovial fluid. The joint capsule forms a barrier that when breached can allow various pathogens and contaminants into the joint. Note that septic joints are especially dangerous in the young animal because some pathogens can actually kill bone growth plate and cartilage cells, resulting in a shortened limb in a fixed nonmovable joint.


  • Sutures - The first of these are called sutures and are formed from fibrous tissue that permits the continued growth of bones that eventually ossify (bone formation). The easiest way to remember them is that they are the ones that unite the bones of the skull.
  • Syndesmosis joints - More important clinically are the syndesmosis joints. This kind of fibrous joint joins skeletal structures that are located relatively far apart and are united by ligaments. As we age or after a trauma, these fibrous tissues tend to ossify and form bonelike structures that link two bones that are not supposed to be joined. Examples of this fibrous union can occur after a fracture between the radius and the ulna (the bones of the forearm) as well as the tibia and fibula (the bones of the leg between the knee and the ankle).
  • Gomphoses joints - The third type of fibrous joint is called gomphoses. Although they are not important for our purpose here (they join the teeth to the tooth socket), their status is useful for evaluating periodontal disease.


These joints are of two types. Although both forms consist of a joint formed by cartilage between apposing bony surfaces, the synchondrosesform ultimately is converted to bone while the symphysesdoes not. In the dog, the most clinically important cartilaginous joint of the latter type is the disc between the vertebrae.

Degeneration of the intervertebral disc due to disease or trauma may cause symptoms not related to the spine, so this is sometimes a difficult diagnosis to make. Examples of this include difficulty chewing or the appearance of a unilateral (appearing on only one side) subluxation as seen in dysplasia.

An example of a synchondroses is found within the pelvic bones. These joints are united by a hyaline and/or a fibrocartilage that with age tends to ossify with a predictable pattern seen in X-rays. Disruptions of this pattern may have clinical implications that may not be easily recognized by the owner and possibly not by the veterinarian unless sequential X-rays are taken over time to determine the degree of ossification.


Generally joint disease could be considered as any abnormality of the joint, but it is easier to understand the different forms of articular disease if we organize them onto several different categories (see the sidebar, "Joint Affairs").

When dealing with joint problems, the issue is often compounded by what condition or disease occurred first. For example, osteoarthritis may occur because of congenital disease (developmental skeletal disease) or because of acquired diseases. In degenerative osteoarthritis, degeneration of articular cartilage is the prominent feature. In inflammatory osteoarthritis, various infectious or immune-mediated conditions result in synovitis (inflammation of the synovial membrane) and cartilage damage.

For sure, degenerative osteoarthritis is the most common form of arthritis recognized in dogs being well-represented by hip dysplasia and osteochondritis dissecans. Degenerative osteoarthritis is a slowly progressive condition characterized by two significant pathological processes: articular cartilage degeneration and new bone proliferation. Very commonly, a low-grade synovitis occurs simultaneously.

The function of nutrition in degenerative joint disease is unclear; however, we do know that nutritional imbalances can result in developmental skeletal disease, which can subsequently/concurrently result in degenerative joint disease. It appears that we are juggling several chickens and several eggs! See Figure 1, "The Paths of Joint Disease."


The first types of joint disease to be considered are congenital anomalies that are present at birth. Whether they are genetic or the result of "birth defects" is often not clear, but the determining factor of a congenital defect is that it immediately demonstrates its effect on the skeleton. Short-limbed dwarfism characterized by an abnormality in the conversion of cartilage to bone is an example of this type of defect.


Occurring sometime after birth, but before the skeleton matures, developmental joint disease is a common type most often seen in dogs as elbow and/or hip dysplasia. The severity of expression depends on several factors. These include age of onset, the amount of damage or remodeling that the articular surface undergoes, the ability of the body to repair the damage (there is a nutritional component here) and how important the joint is in locomotion. Another example is metabolic acidosis that will leach calcium out of bones, resulting in overall loss of bone density and multiple fractures of varying significance.


In the absence of other signs, the sudden onset of clinical symptoms often indicates damage to the joint due to trauma. The injury may be caused by overextension (subluxation) of the joint out of its normal range of motion, intra-articular fractures or cracking of the cartilage. Unfortunately, the onset of chronic osteoarthritis at the injury site is often seen as the animal ages. There is an old adage among athletes and trainers: Most injuries, even those initially recognized as soft-tissue injuries, develop into arthritic conditions. It is the same with our dogs and their joints.


This type of joint disease is one side effect of blood-borne bacterial infections. For example, Lyme disease is notorious for its painful impact on joints. In the young animal, infectious inflammatory joint disease affects many joints and can lead to an infectious polyarthritis. One very serious concern regarding the joints of growing animals is that if the growing surface of the bone is killed by the infection, the bone cannot get any longer.

The older animal frequently presents with only a single joint involved but often has a concurrent infection in the body. One of the most common infectious inflammatory joint diseases is chronic peridontal disease. Other factors to consider are puncture wounds or soft-tissue truama, infection occurring at injection sites or post-surgical infections.


An example of noninfectious inflammatory joint disease would be some type of autoimmune condition such as rheumatoid arthritis. Although extremely rare in dogs, immune-mediated joint disease is more often seen in the smaller breeds. In some cases, the inflammatory process appears to cause degeneration of mature cartilage cells, resulting in erosion, which can be considered a function of the severity of the disease. Other forms of noninfectious inflammatory joint disease can be caused by intestinal parasites as seen with leishmaniasis. Another form is the inflammatory connective tissue disease systemic lupus erythematosus.


Although tumors of the joint are rare, nonetheless neoplastic (cancerous) joint conditions do exist, with the most common type being the synovial cell sarcoma. These tumors grow slowly and typically present with multiple destructive sites within the bone, the presence of soft-tissue masses and minimal new bone formation. The tumors originate within the soft tissues and invade the cartilage and bone on both sides of the affected joint creating lesions described as similar to those made by a mouse nibbling on cheese.


Many genetic diseases are the result of inborn errors of metabolism, and metabolic joint diseases are often hard to describe. They usually affect all the joints, with the greatest damage occurring on the weight-bearing surfaces during periods of growth. improper diet, including excess vitamin A or calcium, can precipitate or exacerbate pathological, hormonal or metabolic conditions. These include hypothyroidism, hyperparathyroidism, mucopolysaccharidosis and hemophilia. Even metabolic acidosis can result in bone density loss.


If there is severe destruction of the joint but clinical signs are minimal, neuropathic joint disease is a possibility to be considered. In some cases, the apparent absence of pain may not be neuropathic but instead due to the dog wanting to remain athletically active. It is more likely, however, that the dog actually feels little or no pain if join destruction has occurred but symptoms are not present.

Two types of neuropathic joint disease have been identified - one is associated with the disappearance of bone (atrophic) with little evidence of repair; the other is characterized by rapid bone growth (hypertrophic) and is extremely mutilating. The possible underlying causes could be diabetes, a condition secondary to elbow or hip dysplasia, or hyperextended carpal or tarsal joints.


Although they appear similar, there are actually three different types of osteoarthrosis: primary, secondary and senescent (occurring in old age). The underlying cause may very widely, but osteoarthrosis is still the most common form of noninflammatory joint disease seen by veterinary practitioners. Some other names for this condition include degenerative joint disease, hypertrophic degenerative joint disease, osteoarthritis and arthritis.

  • Primary or idiopathic arthrosis is seen in young or middle-aged dogs in which the underlying cause is not obvious, although high levels of physical activity or obesity have been implicated.
  • The most frequent type of arthrosis seen is the secondary form, so named because it appears secondary to a previous injury or infection, congenital defect, developmental defect, or conformational anomaly that ultimately affects the joints by disrupting normal pressure and weight-bearing forces.
  • Senescent arthrosis is described in older dogs that have had no previous condition to explain its appearance and is considered a part of the aging process, i.e., the cartilage simply wears away. An extremely painful condition, the disease follows a particular progression: 1) noninflammatory wearing away of the articular cartilage followed by 2) excessive new bone growth that remodels the underlying bony surface, which induces 3) abnormal forces on the joint, speeding up the progression of the disease.


Given the various types of joints and the numerous pathologies of join disease, it shouldn't be surprising that diagnosis of joint conditions can be a tricky undertaking. The following factors are among those that should be considered to pinpoint a specific condition in your dog.


The width of the space between the joint is a major factor in ascertaining the progression of most joint pathologies. Unfortunately, it is very difficult to determine radiographically because most X-rays are taken with the dog in a nonweight-bearing position.

Normally, the width of the joint space depends on the condition of the articular cartilage and the amount of synovial fluid. Excess intracapsular fluid, as seen in infectious processes, will lead to widening of the joint. This can happen with a neoplastic condition, but a simultaneous destruction of the subchondral bone is also seen.

Narrowing of the joint space will occur with osteoarthritis; however, this is usually accompanied by an increase in bone density and build up of the subchondral bone. A unique situation occurs with chronic disuse of a limb where the joint space collapses but there

are no other radiographic signs present. See Table 1, "Disease and Joint Space."


Fragile and delicate on one hand, but robust enough to accommodate tremendous pressures, the articular cartilage is a marvel of design. The vertical orientation of the molecular strands from which it is composed gives cartilage a special ability to compress without breaking and, under pressure, to "wick" out synovial fluid, which then acts as a hydrostatic bearing surface on top of the cartilage. So effective is this system that the friction in a well-functioning articular joint is less than that of ice skate blades on smooth, hard ice.

Acute and chronic cartilage abnormalities are seen in several types of joint disease; however, early damage to the cartilage is difficult to see with X-rays. The status of the articular cartilage is normally evaluated by looking at the underlying subchondral bone and by evaluating the joint for normal joint space. Radiographically noticed narrow joint spaces indicates a loss of cartilage depth and commonly a thickening of the subchondral bone. As tough and resilient as cartilage seems to be at first glance, it is exceptionally delicate with respect to its requirements for specific nutrients and a sterile environment.


The bone directly under the articular cartilage plays an important role in absorbing the pressures associated with locomotion and prevents traumatic damage. The structure of the cartilage provides a natural resilience, but it depends on the subchondral bone for support. In turn, the articular cartilage protects the underlying bone from fractures by providing a more even distribution of stress. Thus, defects in either surface will cause damage to the other.

Several different patterns of change or bone remodeling occur in a diseased joint. For example, with noninflammatory arthrosis there is a subsequent increase in bone density called subchondral sclerosis. This is caused by an alteration of fit between the two articular surfaces, with some areas becoming denser and others losing density as they become no longer weight-supporting. A destructive pattern of change is seen in infectious conditions. Osteolysis or the absorption or destruction of bony tissue is caused by osteoclasts (large, multinuclear cells) that are driven by the inflammatory process. See Table 2, "Bone Changes in Joint Disease."


Entheses are the attachment sites of ligaments. When the join capsules or ligaments undergo chronic strain due to tears or other trauma from an unstable joint condition, reactive bony processes called enthesophytes are formed. These appear as a single spur or ridge of new bone that extends into the affected soft tissue. This condition is extremely painful.


Without the joint capsule, and other stabilizing structures, most joints would literally fall apart. Joints can safely take a lot of pressure when properly aligned and held firmly by the capsule, tendons, ligaments and even skin. The joint has no blood supply for nourishment, and cartilage is fed through osmosis through the synovium and the capsule. If the joint capsule and synovial membrane are breached, a cascade of serious, destructive events begins. White blood cells release enzymes and oxygen radicals (free radicals) that attack and destroy hyaluronic acid. When this occurs, the loss of HA reduces the lubrication that prevents friction and limits erosion of the articular cartilage. Even worse, loss of HA allows the enzymes from white blood cells to join forces with oxygen free radicals and attack the articular cartilage. Thus, free radicals play a major role in degenerative arthritis.


We have already alluded to the diagnosis problem as one of juggling several chickens and a whole lot of eggs. There is tremendous interaction among multiple body systems in joint disease, but the following factors help to rule in or rule our various medical conditions when seeking the cause of lameness in joints.

  • Age - The degree of bone maturation is important in determining the status of the joint, so the age of the animal is a major consideration. In addition, clinical symptoms often occur at specific ages. A swollen stifle joint in a young dog would suggest an infectious arthritis while the same symptom in an older dog would likely be a degenerative disease.
  • Sex - Some developmental diseases are more commonly found in males, while certain types of metabolic disease (hypothyroidism, for example) are seen more often in females.
  • Breed/Genetics - Pain in the hip joints in a German Shepherd Dog would most likely be due to osteoarthrosis secondary to hip dysplasia while the same symptoms in a Toy Poodle would probably indicate aseptic necrosis of the femoral head.
  • Physical Activity - An older dog that experiences joint pain after a weekend hike is more likely to have some type of degenerative disease. With a younger, more athletically fit dog, the clinician would probably consider an acute injury such as a sprain or torn ligament.
  • Affected Joints - Particular patterns of affected joints are often seen with specific disease processes. one of the most obvious would be the coxofemoral joints in hip dysplasia. Others would include osteochondrosis in the humeral head or aseptic necrosis of the femoral head.


Although there is a genetic component to most joint disease (the list of susceptible breeds is a very long one indeed!), there are also contributing environmental factors within the control of the dog owner, including diet.

In their research on restricted food intake as it correlates to joint disease, Dr. Dick Kealy and his colleagues have demonstrated conclusively that overweight and obese dogs suffer far more from joint disease than dogs that are kept in a lean condition all their lives. (See the Journal of the American Veterinary Medical Association, Vol. 201, No.6; Vol. 210, No.2; and Vol. 217, No.11.)

An overweight dog stresses not only its hips, but also its elbows, shoulders, spine and other joints. The simplest and probably one of the most effective things dog owners can do is to feed their dogs a balanced and complete diet and ensure that the caloric intake is not in excess of caloric requirements.

Especially for the large- and giant-breed puppies, this means avoiding overnutrition. One way to do this is to feed one of the many large-breed puppy foods designed to help control growth rates, because rapid growth rates correlate positively to join disease in later life.

Dog food manufacturers recognize the effects of the rapid growth rate on skeletal development, and the industry as a whole provides the owner with a wide variety of large-breed puppy foods from which to choose. We high recommend their use over standard puppy foods or feeding adult foods to large-breed puppies.

There is a move among manufacturers to produce large-breed adult foods. Our sense of it is that it is a little too early to determine how effective these large-breed adult foods are at reducing the severity of joint disease beyond just helping to maintain the larger dogs at more ideal weights.

We also recommend staying within the Association of American Feed Control Officials' nutrient profiles for calcium and maintaining that all important calcium-to-phosphorus ratio. Unless you are feeding a nutritionally inadequate diet, there is absolutely no reason to supplement with calcium. To do so is to disrupt this ratio and potentially to cause skeletal and joint problems down the road.

Similarly, diets need magnesium and selenium for proper skeletal growth, and AAFCO has established minimums for both. There is a growing recognition that various trace elements such as chromium, fluoride, nickel, molybdenum, silica, vanadium and even arsenic can have a positive impact on bone growth in the right amounts; however, those dietary levels are not well-established and AAFCO has not included these trace elements in its nutrient profiles.

Despite this, a few manufacturers have started to include these trace elements. We do not know yet what good they do or the amounts in which they should be included. For this reason, we recommend that dog owners who wish to feed diets with trace elements added select those foods that have been through AAFCO's live-animal feeding trials protocol to demonstrate nutritional adequacy.

Because obesity is essentially an owner compliance problem that unfortunately is unlikely to change, a number of manufacturers have introduced light, lean and reduced-calorie diets to help keep the weight off chubby pets. Low-calorie diets allow owners to satiate dogs with big appetites without exceeding their necessary caloric intake.


Aside from maintaining a healthy weight, some supplements have also shown promising results for the joints. Ever since Nutramax® Laboratories had great success in clinical trials with Cosequin® (a manganese, glucosamine and chondroitin supplement), a number of manufacturers have started including glucosamine and/or chondroitin in their foods. We have become convinced that many of these products work to preserve joint health; however, we continue to have a preference for Cosequin because of the large number of randomized, double-blind, placebo-control studies in both dogs and humans with the actual product.

With that said, we see many manufacturers are "shirt-tailing" on the Nutramax Laboratories' research efforts and creating what they consider to be similar products. Without clinical trials with the actual product, it is not possible to really know which products are effective and which are not. For example, in a paper out of the University of Maryland School of Pharmacy, 84 percent of the glucosamine/chondroitin products tested did not meet their label claims! (See JANA, Vol. 3, No.1.) Thus, it quickly becomes a caveat emptor situation.

For what should be obvious reasons, given the above, we recommend giving priority consideration to those products that have been tested in clinical trials over those that have not.

* * * * * *

As you can see, there is more to joint disease in dogs than mere hip dysplasia. Symptoms overlap and mimic each other, and it is not easy to diagnose joint problems without having a complete history, which is why an observant owner is so necessary in helping to make a diagnosis.

Sometimes an invasive procedure such as tapping the join for a culture sample may be required because many bacteria are difficult to identify and often cause the same symptoms. Mix in a little Lyme disease with an underlying autoimmune problem, a touch of trauma and a dash of overuse, and it becomes difficult indeed to sort out the problems and how to deal with them directly.

We hope to have imparted an appreciation for not only the function of joints, but also the delicate balance required for them to survive in optimal working condition. We also hope that with some preventive measures, your pet's joint health will keep it up and running for many years to come.

Our sincere thanks to the authors for allowing us to present this ©copyright work on the Mastiff Breeder Web Site.