Equine Joint Health for the Long Run

Osteoarthritis might not be completely avoidable as a horse ages, but early diagnosis and conscientious care can slow its advance and minimize pain.

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Equine Joint Health for the Longrun
While originally defined as the painful degeneration of the articular cartilage lining the ends of bones inside joints, OA is now recognized as a whole joint disease. | Photo: Photos.com

Why wait for the inevitable? Take charge of your horse’s joint health from the very first step

Osteoarthritis (OA)—the painful loss of articular cartilage and bone together with soft-tissue changes associated with the joint—dominates the long list of important conditions affecting horses. Despite massive research efforts in this field, there’s no cure for OA, and it continues to limit horses’ ability to perform and negatively affects their quality of life. All too often, OA results in early retirement, financial losses, and even euthanasia when the pain associated with the disease becomes unmanageable.

Researchers and veterinarians have amassed a wide array of OA therapies that fit into the currently accepted paradigm of “multimodal therapy.” This includes everything from the tried-and-true everyday anti-inflammatories (e.g., phenylbutazone, or Bute) to advanced technologies such as stem cell therapy and platelet-rich plasma.

But what if we could spare ourselves all the expense associated with diagnosis and treatment, as well as the disappointment that comes with failed attempts to relieve our horses of the pain associated with OA? What if, from the very first step, we could protect every joint from daily wear and tear to massively slow the rate at which OA develops?

“OA may not be completely avoidable as a horse ages, but early diagnosis and conscientious care can certainly slow its advance and profoundly minimize pain and disability associated until the horse reaches a ripe old age,” says Mandy Peffers, BSc, MPhil, PhD, BVetMed, FRCVS, of the Faculty of Health and Life Sciences at the University of Liverpool, in the U.K.

How OA Develops

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“While originally defined as the painful degeneration of the articular cartilage lining the ends of bones inside joints, OA is now recognized as a whole joint disease,” says Peffers.

Joint trauma and inflammation initiate a complex series of events that ultimately damages all associated joint tissues: the articular cartilage lining the ends of joint bones, the synovial fluid bathing the cartilage, the inner and outer linings of the joint (the synovial membrane and joint capsule, respectively), and that subchondral bone lying beneath the articular cartilage.

In simple terms, two processes can initiate the inflammatory cascade and cause OA: normal forces placed on abnormal musculoskeletal tissues and abnormal forces placed on normal musculoskeletal tissues.

Normal forces on abnormal musculoskeletal tissues.

This first category refers to horses that have defects as foals (e.g., poor conformation) that result in joint inflammation during weight-bearing.

Foals can be born with conformation defects such as flexural deformities—­abnormal joint angles from the front to the back of the limb. Examples include a carpal or fetlock flexure where the foal’s knee or ankle is bent abnormally and cannot straighten. A club foot is another example of a flexural deformity. 

Other foals, as they grow, might develop a slight (or even profound) outward or inward deviation of the lower limb. For example, when the inner aspect of the forelimb at knee level begins to grow more quickly than the outer aspect, the foal appears knock-kneed. This is called carpal valgus. The same can happen at the fetlock joint (fetlock valgus), or the outer aspect of the limb can grow faster than the inside, making the foal appear bow-legged due to carpal or fetlock varus.

As you can imagine, the forces normally placed on these joints during weight-bearing will not be normal. Certain parts of the joint will be subject to excess forces that can cause trauma. With carpal valgus, for example, the foal will essentially “crush” the small bones that make up the inner knee during weight-bearing. And if a foal has a flexural deformity, he will place excessive forces on the bones at the back of the joint.

“Many of these conformation defects can result in inflammation in the joint, which as we know initiates the series of events that can lead, rather slowly, to OA,” says Scott Anderson, DVM, a sports medicine veterinarian with Woodside Equine Clinic, in Ashland, Virginia. “Correcting these anatomic defects early in life can allow a foal to bear weight normally on normal joints, thereby preventing the development of OA.”

Anderson, who primarily works on performance horses, says that by the time he sees his population of patients, their conformation “is what it is.”

“It is important to recognize when a horse has conformation predisposing to abnormal joint function,” says Anderson. “Making decisions as to what level of performance is the least likely to predispose her to joint stresses potentially leading to OA would be ideal. Monitoring the horse’s comfort and outward signs of joint inflammation can allow for adapting its training regimen as necessary. We can also shoe the horse to best support its weaknesses.”

Abnormal forces placed on normal musculoskeletal tissues.

Any horse with a normal joint can still develop joint inflammation due to excessive forces or other insults.

We know that a certain level of training is needed for bone and cartilage adaptation to occur. This remodeling and strengthening allows joints to become accustomed to the work a horse is being asked to do. In some cases a performance horse might experience overtraining, and inflammation of the joint can develop when a horse is asked to do more than his musculoskeletal system is prepared for. 

“How young horses are brought along will affect joints in the future,” says Anderson. “Repetitive motion and forces beyond the level the horse is ready for lead to inflammation of the joint. Over time this can cause degradation of the cartilage. The outward signs of inflammation are often apparent acutely as lameness and poor performance.” 

If enough injury has occurred, the affected joint can be permanently damaged. 

To prevent OA and prolong a horse’s career, the owner, trainer, and veterinarian should work together to adjust the animal’s training regimen. Take, for instance, a young horse with a large frame that doesn’t yet have the conditioning and maturity to support himself properly in work. First he needs to strengthen the muscles supporting the stifle, sacroiliac, back, and neck joints. The owner can achieve this through exercises such as trotting hills and ground poles.

An aging horse or one developing OA from overuse would benefit from a scale down of his work—reducing his level of competition, for example. Excess body weight is another example of an abnormal force placed on normal joints. Harvard researchers suggest that in humans the force on the knees is equivalent to 1.5 times body weight. Thus, a 200-pound individual will put 300 pounds of pressure on their knees. Gain some weight, say 50 pounds, and that individual now has the equivalent to 375 pounds of pressure on the same joint. Going up or down an incline or stairs or squatting will further increase the forces on those knee joints.

Studies in humans show that obese individuals have a four- to fivefold risk of developing knee OA compared to nonobese individuals (National Health and Nutrition Examination Survey, Johns Hopkins Arthritis Center).

Similar data are not available for horses; however, OA is remarkably similar between the two species. Horses likely experience similar trends.

“Studies show that overweight but otherwise healthy individuals secrete inflammatory mediators called adipokines and cytokines that mimic systemic inflammation in nonobese individuals,” says Peffers. “Increases in these inflammatory mediators can contribute to the development of obesity-related inflammatory disorders such as OA.” 

Equine Joint Health for the Long Run
Preventing and managing OA requires a multimodal approach that combines diet, medication, and a variety of therapies.

Can Joint Supplements Prevent OA?

Many horse owners use joint supplements once their horses begin showing signs of OA, such as stiffness at the start of exercise. Researchers have shown that some joint supplement ingredients ameliorate cartilage inflammation in vitro (in the lab), and some studies even support the use of these products to improve lameness in live horses. Only a few scientists have looked at using oral joint health supplements preventively before joint injury or inflammation occur. Those study results were promising, prompting further work in this field. 

Jessica Leatherwood, PhD, an associate professor in equine science at Texas A&M University, and colleagues responded to this call for data and conducted a series of three experiments on the prophylactic effect of nutritional supplements on joint inflammation in young horses.

They supplemented horses with glucosamine HCl, a trace mineral supplement, or a product called conjugated linoleic acid (CLA). The latter is a polyunsaturated fatty acid with anti-inflammatory effects, says Leatherwood.

The researchers used a similar model for each study: They fed horses the nutritional supplement for several weeks. They then injected a single joint with bacterial lipopolysaccharide (LPS)—an inflammatory product meant to mimic an inflammatory insult (e.g., trauma) to the joint. After LPS administration, horses continued to receive their dietary supplement for an additional few weeks. During that time, the team measured various markers of inflammation and cartilage breakdown in the synovial fluid of the affected joints and compared them to the levels found in samples collected from horses in the control group that had not received the nutritional supplement. 

Leatherwood says key findings of these studies included:

  • Dietary glucosamine supplementation results in a significant increase in glucosamine levels in both blood and synovial fluid. These levels continued to increase over time, with higher levels measured in blood and joint fluid at 28 days and 84 days of supplementation;
  • Intra-articular administration of LPS results in significant increases in prostaglandin E2 (PGE2) levels—a marker of inflammation;
  • Administering LPS also resulted in significant elevations of cartilage metabolism markers, including C2C, a marker of cartilage degradation, and CPII, a marker of cartilage synthesis; and
  • PGE2 and C2C levels were significantly lower in horses offered the glucosamine supplement than in control group horses.

“Oral administration of 30 mg/kg glucosamine HCl … twice daily (in) horses for 84 days prior to LPS challenge resulted in a significant decrease in inflammation and cartilage breakdown,” said Leatherwood.

This study also reaffirms that oral glucosamine does reach the joint.

Even though trace minerals play an important role in the normal maintenance and turnover of bone and connective tissue, the team reported no changes in inflammation or cartilage degradation in the trace-mineral-supplemented horses.

Finally, Leatherwood and colleagues found the following in horses supplemented with CLA:

  • CLA levels were undetectable in the control group but evident in the supplemented group;
  • Circulating blood levels of arachidonic acid—an inflammatory mediator—­decreased significantly in response to CLA supplementation. Supplemented horses also had lower arachidonic acid levels in their synovial fluid;
  • Unlike glucosamine, CLA supplementation didn’t decrease joint inflammation determined via PGE2 in joint fluid; and
  • However, supplemented horses experienced a decrease in cartilage degradation and an increase in cartilage synthesis.

Together, these data show that ­nutritional supplements can certainly play an important role in OA prevention. Leatherwood warns owners to not focus too closely on individual supplements.

“It is always important that a diet is balanced,” she says. “While supplements may be beneficial to young horses to prevent OA development, (they) may easily become detrimental if you don’t know what you are giving. It is critical for young, growing horses to receive a diet that is balanced, and supplements may easily cause an imbalance. For instance, if the supplement contains a single mineral, this may result in a toxicity or a deficiency in other minerals. I would suggest to owners to work with an equine nutritionist for their specific horse(s).”

Take-Home Message

Addressing conformation defects, training strategies, and weight go a long way toward reducing joint trauma and inflammation. Nonetheless, the daily wear and tear of being a horse can culminate in joint inflammation and OA. This is where employing preemptive strategies, or products that can protect the joint, might prove invaluable.


Written by:

Stacey Oke, MSc, DVM, is a practicing veterinarian and freelance medical writer and editor. She is interested in both large and small animals, as well as complementary and alternative medicine. Since 2005, she’s worked as a research consultant for nutritional supplement companies, assisted physicians and veterinarians in publishing research articles and textbooks, and written for a number of educational magazines and websites.

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