“Joint disease is very common. It is estimated that 60% of lameness is attributable to the joint,” says Professor C. Wayne McIlwraith, Director of the Orthopedic Research Center at the College of Veterinary Medicine and Biomedical Sciences, Colorado State University in Fort Collins, Colo. Indeed, whether you’re talking humans or horses, you can hardly go a day without hearing joint-related lingo: arthritis, capsulitis, DJD, glucosamine, cartilage, etc. But, what does it all really mean? What goes on in there, and what are we talking about when we discuss joint disease?

Joints are grouped into three categories classified on the basis of range of motion: synarthroses (immovable joints), amphiarthroses (slightly movable), and diarthroses or synovial joints (movable). But for the purposes of this article, “joint” will refer to the last category, the synovial joints. We will examine the joint as an organ — a group of tissues working together to perform a specific set of functions.

The synovial joint is not unlike a piece of machinery, and like a machine, in order to understand how it works and what can go wrong, we need to take it apart.

Anatomy — Structures and Function

Loosely speaking, synovial joints are the hinges of the body — flexible points where two or more bones meet and interact. Looking at the joint, from the deepest part outward, we have:

• The bone ends: Covered by the articular cartilage.
• The articular cartilage: The Teflon coating over the ends of bone,” says McIlwraith.
• Ligaments: Fibrous bands connecting bone to bone. Ligaments stabilize the joint.
• Synovial fluid: The lubricant of the joint. Constant levels of synovial fluid produce a negative hydrostatic pressure, “suction,” that contributes to joint stability.
• Synovial membrane: A thin membrane lining the thicker joint capsule that surrounds the joint. The cells of the synovial membrane produce the synovial fluid and also can produce enzymes and inflammatory mediators designed to fight infection within the joint.
• Joint capsule: The tough, fibrous outermost layer of the joint. The joint capsule protects and stabilizes the joint.

Some rather specific terminology accompanies these specific pieces of the joint. Words (and word fragments) that will help in deciphering joint-speak include:

• -itis: Inflammation. In the joint, arthritis, capsulitis, synovitis.
• Chondro-: Cartilage. Usually referring to the articular cartilage.
• Subchondral bone: The bone beneath the articular cartilage.
• Chondrocytes: Cells of the articular cartilage
• Articulation: Refers to the meeting of two (or more) movable parts; also used to refer to the joint itself.
• Intra-articular: Within the joint.
• Arthro-: Joint.
• Arthrodesis: Fusion of the joint.
• Arthroscopy, Endoscopy: Internal examination of the joint.
• Osteo-: Bone.
• Osteoarthritis (OA): Inflammation of the joint leading to bony changes.

Joints, particularly in the limb, are subjected to multiple forces.2 However, force attenuation (shock absorption) in the joint is not accomplished by the cartilage and synovial fluid but by the bones and the peri-articular soft tissues.3

Pathogenesis

Oops, there’s another specific term. This one is simple: pathos — badness; genesis — start. How does the badness start? Let’s take a look at what can go wrong in the joint. What do we mean by joint disease? And, how does it progress?

Joint disease can stem from multiple causes: infection; acute, severe trauma to one or more of the structures in the joint; or cyclic trauma. Of these causes, the most common, according to McIlwraith is “cyclic trauma, leading to inflammation, which eventually progresses to OA (osteoarthritis).”

“Day-to-day wear and tear leading to problems is a fact of life for athletic horses,” says McIlwraith. “It is also a problem of aging — just as in humans.” That being said, McIlwraith stresses that exercise is good for joints. However, the problems occur when stresses are placed upon the joints that go beyond what is physiologically normal.

According to McIlwraith, the common scenario of cyclic trauma goes like this: repetitive stress and trauma to the synovial membrane and joint capsule produces inflammation (synovitis and capsulitis); with this inflammation comes the release of inflammatory mediators from the synovial membrane into the synovial fluid; these inflammatory mediators cause degradation of the cartilage. Cartilage degradation in turn causes increased friction within the joint and greater inflammation. And the cycle continues.

Articular cartilage is a matrix — think of cables running through a mattress to reinforce it. Collagen is the scaffolding of cartilage, providing tensile strength. Proteoglycans provide the compressive strength, says McIlwraith. And the enzymes released in the inflammatory process degrade both.

Inflammation of the joint not only deteriorates the articular cartilage, but also causes changes in the nature of the synovial fluid. Remember, the synovial fluid provides lubrication and the proper fluid pressure provides the “suction” that helps to stabilize the joint. In a severe synovitis, the viscosity of the joint fluid decreases (think low-grade motor oil vs. high), and the amount of fluid will increase, distending the joint and destroying that negative hydrostatic pressure. The increased friction and instability that results from the synovitis contributes to the cyclic damage.4

In cases of sudden, severe trauma, such as an articular fracture or ligament tear leading to instability, or infection as with a puncture or neonatal sepsis, the inflammatory cycle is accelerated and the joint undergoes rapid degeneration.

Regardless of the inciting cause, progressive deterioration of the cartilage becomes accompanied, in the end stages, by changes to the bone itself and to the soft tissues of the joint. Here, we have reached osteoarthritis (OA).

Timing Matters

Looking at the vicious cycle of inflammation and cartilage degradation, it becomes readily apparent how important proper and timely intervention can be in managing the progression of joint disease.

“Half of the problem that we have,” says McIlwraith, “is that joint disease isn’t treated immediately. (Often) the client brings the horse into the vet after trying adjunct treatment for 4 months.”

While a wide variety of therapies (some requiring the services of a veterinarian and some not) are available for joint disease, “unless you have a diagnosis,” McIlwraith says, “all your therapy is just shooting in the dark.” From both a legal and a practical standpoint, only a veterinarian is qualified to make a diagnosis.

As we all know, like humans, horses vary in their pain tolerances. A horse with severe cartilage damage and even chip fractures may show little lameness while a horse with a mild capsulitis limps around like someone has tried to cut off his leg. It is critical to identify the source and extent of the joint damage in order to know how best to intervene. Indeed, failure to promptly diagnose a septic joint or an articular fracture could have catastrophic, even life-threatening effects.

Diagnostic Techniques

Although imaging technology continues to advance, diagnosis of joint disease still begins with an old-fashioned examination. Palpation, joint flexion, diagnostic anesthesia, and gait evaluation may help the veterinarian to pinpoint the problem joint(s). Once the affected area is located, any one or more of the following imaging techniques may be used: radiographs (X-ray), MRI, CT, ultrasound, or even diagnostic arthroscopy. Radiography is best for revealing bony changes — defects in the subchondral bone as seen with OC, fractures, and remodeling due to OA. MRI, CT, and ultrasound can all pick up changes in the soft tissues. Though often thought of as a therapeutic technique, arthroscopy can be useful for identifying cartilage and synovial membrane damage that may not be seen through less invasive techniques.

However, these diagnostic techniques are generally most useful in the horse that is displaying clinical changes in the joint. McIlwraith identifies a second, and increasingly pressing, issue in the athletic horse, “diagnosing the horse at risk of a catastrophic injury.” Wouldn’t it be great to identify horses that are being pushed beyond their physiologic limits before disaster strikes? For this approach, McIlwraith points to analysis of “fluid biomarkers” as the “big hope.” Biomarkers are molecular products released into the bloodstream during bone and cartilage turnover. McIlwraith states that research has shown that in studies of racehorses, changes in the fluid biomarkers of horses that sustained injuries could be seen months before the injury itself. “If you can identify the horse at risk, then you can get that horse into imaging,” says McIlwraith. However, “we’re not there yet, but we’re working on it.”

When And How To Intervene

As stated earlier, joint therapies abound: medications, nutraceuticals, compounds that mimic the components of joint fluid, steroids, biologic treatments, laser, shock wave, ultrasound, physical therapy, acupuncture, chiropractic, farriery — the list seems endless.

Some questions that should be asked of any therapy include:

• Is it safe?
• Is it effective?
• When is it effective?
• Is it cost-effective?
• What are the long-term risks or benefits?

Says McIlwraith, “the guide to integrated therapy is not a simple one.” Ultimately, the decision whether, when, and how to treat a horse should be made by the veterinarian and owner together and be based upon the needs of the individual horse. However, questions and confusion over the array of equine therapies are common, and farriers are often at the frontlines of the owner quandary. So, here is an overview of some of the joint therapies available:

NSAIDs: Non-steroidal anti-inflammatories are often the first line of treatment for acute or mild joint disease. This category includes drugs such as: phenylbutazone (Bute), flunixin meglumine (Banamine), acetylsalicylic acid (Aspirin), firocoxib (Equioxx), naproxen (Equiproxen, Naprosyn), and diclofenac (Surpass). NSAIDs are exactly what the name implies: non-steroidal anti-inflammatory drugs. These compounds typically inhibit the COX enzymes in the inflammatory cascade.

While often given in oral form, several NSAIDs are available in an injectable form, and one (Surpass) is even applied topically. The COX inhibition by NSAIDs is a double-edged sword. While NSAIDs act against inflammatory enzymes, they also can block “good prostaglandins,” compounds that promote blood flow to vital organs. Side effects of NSAID use can include: gastric ulcers, liver and kidney damage.

Systemic: Intravenous and intramuscular injections have the advantage of targeting the whole horse, useful if more than one joint is suspected to be affected. As mentioned above, NSAIDs can be administered systemically; though long-term NSAID injection is rare. More commonly administered systemics are hyaluronins (HA) and polysulfatedglycosaminoglycans (PSGAGs) – Legend and Adequan, respectively.

These drugs are often administered both as treatment for joint disease and as a preventative. However, while intravenous (IV) Legend has been shown to have value in treating OA, according to McIlwraith, intramuscular (IM) Adequan “does nothing in experimentally induced OA.” Intra-articular Adequan, however, does have benefit ( see below). These two drugs are often touted for the prevention of OA. However, says McIlwraith, there is not data to either prove or disprove any purported prophylactic benefit. Unlike with “prophylactic” intra-articular injections, with systemic medications used preventively, at least, says McIlwraith, “while they haven’t shown value, the only thing they will harm is your pocketbook.”

Intra-articular medication: This is not a drug class, but a route of administration. “Joint injections” as intra-articular therapy is more commonly called, can involve a variety of compounds: steroids, hyaluronic acid (HA) (Legend, Hylartin), polysulfated glycosaminoglycans (PSGAGs)(Adequan), and biological therapies such as IRAP, PRP and stem cells.

While McIlwraith calls intra-articular injection “good” in the case of a clinical joint, citing its usefulness “even in low-grade synovial effusion,” he calls the practice of so-called prophylactic joint injections “very questionable.”

The joint, remember, is exquisitely susceptible to bacterial infection and while a needle-stick may seem minimally invasive, the risk of introducing an infectious agent is always present and thus unwarranted where no pre-existing disease is present.

In a clinical joint, with the proper diagnosis, however, intra-articular therapy can be a valuable tool in the arsenal against joint disease. Corticosteroid use has long been a staple of joint therapy, and the effects of intra-articular HA and PSGAGs are well documented. Knowledge of the newest category of intra-articular therapy, the biologics, is still evolving. Also called regenerative medicine, this category of treatment uses the horse’s own cells to attempt repair.

James N. MacLeod, VMD, Ph.D, of the University of Kentucky’s Gluck Equine Research Center, calls regenerative medicine “the most exciting thing happening in OA,” adding that. “Articular cartilage is well positioned to benefit from regenerative medicine going forward.” Because articular cartilage is one of the tissues in the body with an extremely limited ability to repair itself, MacLeod suggests that future progress will come from developing therapies directed toward facilitating cartilage repair and achieving full restoration of the tissue’s structure and function.

But where is regenerative medicine in the joint now? McIlwraith calls the biologic therapies “a bit of a hodgepodge at the moment.” Of IRAP, he says “there is good evidence to its value.” Stem cells, too, “have shown value. They don’t cure everything, but IA treatment can promote cartilage repair.” PRP (platelet-rich plasma), also called Autologous Conditioned Serum (ACS), however, is “still somewhat of a black box,” says McIlwraith. “We don’t know yet if there is harm or good” and “we still need to define benefits versus side effects.”

Surgery

In instances of significant damage to the cartilage, ligaments or subchondral bone, surgery may be the best option. In the equine joint, the most common surgery is arthroscopy — entering the joint with a very small fiber-optic scope through a small incision. With an arthroscope, the surgeon can visualize the interior of the joint, debride damaged cartilage, subchondral bone, or ligament, and remove chip fragments. Other surgeries impacting the joint may involve fixation of large fractures.

Adjunct Therapies

Over the past couple of decades, there has been an explosion of non-traditional therapies in all branches of medicine, but this plethora of complimentary therapies seems particularly noticeable when discussing equine orthopedics. For many of these therapies, data is still being collected, but it is worth reviewing the existing research for a clearer picture.

Nutraceuticals: Not quite food and not quite drug, the nutritional supplements known as nutraceuticals inhabit a regulatory grey area. These supplements are not regulated by FDA for potency or efficacy, and safety is only evaluated if there are indications that the substance is unsafe or if associated with a label claiming a drug use.5 In other words, although as McIlwraith states, “there are some good products out there,” when it comes to nutraceuticals, the motto is “Buyer Beware.”

Riders of performance horses should be particularly cautious about using “natural products” to treat or prevent joint disease. The USEF Drugs and Medications Guidelines states:

“Trainers, owners, exhibitor and their veterinarians are cautioned against the use of medical preparations, tonics, pastes, powders and products of any kind, including those used topically, the ingredients and quantitative analysis of which are not specifically known, as they may contain a forbidden substance. This is especially true of those containing plant ingredients.”

In other words, a “natural” supplement is not necessarily safe from drug regulation. The Guidelines go on to state “Just some of the hundreds and perhaps thousands of examples of herbal/natural or plant ingredients that would cause a product to be classified as forbidden are valerian, kava kava, passionflower, skullcap, chamomile, vervain, lemon balm, leopard’s bane, night shade, capsaicin, comfrey, devil’s claw, hops, laurel, lavender, red poppy and rawuolfia.”6

Laser: While there are anecdotal reports of improved wound healing and lameness scores with “therapeutic laser” technology, there is little data to show actual benefit. In fact, the only study performed in the horse showed no benefit in wound healing.7

Acupuncture: Although the practice of using needles to stimulate particular anatomical points has existed for centuries, there are few consistent controlled studies that document the benefit of current acupuncture practices in equines. Says McIlwraith, “There is no evidence either way.” A few case studies have indicated some benefit to acupuncture, but there is currently a lack of randomized, controlled trials.8 Also, there are licensing concerns regarding both acupuncture and chiropractic in the veterinary field. These practices are increasingly becoming defined as the practice of veterinary medicine, which should limit their use to appropriately trained veterinarians rather than lay practitioners or those certified to work on humans.

Manual Manipulation: Stretching, massage, chiropractic and osteopathic techniques have been appropriated from human medicine into the horse world. However, as with acupuncture, there is still a lack of evidence derived from controlled studies of many of these techniques in the horse.

The bulk of the existing equine research in manual therapies has been centered on chiropractic techniques. The benefit that has been demonstrated is primarily spinal.9 Again, with these techniques as with acupuncture, the skill, training, and licensure status of the practitioner is likely to impact benefit.

Extracorporeal Shockwave Therapy (ESWT): ESWT, or “shockwave,” is the use of acoustic waves generated outside the body on a therapeutic basis. ESWT has been shown to produce significant analgesic (pain relieving) effects in lameness models in the horse.10 Also, a study has shown an increase in biomarkers indicative of bone remodeling in a chip-fragment model of OA in the horse.11

Because of the analgesic effects of ESWT, it is particularly critical to have an accurate diagnosis before beginning treatment. The results of significant pain relief in a horse with an underlying fracture could be catastrophic.