Article

Degenerative joint disease (DJD) or osteoarthritis or arthritis is the NUMBER ONE reason for premature horse retirement in the equine industry, regardless of horse occupation. Arthritis is a natural aging process in animals that live long enough to tell. In other animals it is produced by different reason with TRAUMA (one time or repeated) being the most common. Infection is another common insult that may result in DJD. The joint is composed of:

The road to DJD usually passes through a process call synovitis or arthritis, which is an inflammatory process of the joint without degeneration. The degenerative process (DJD) is better called arthrosis. However the term arthritis is widely used as a synonym.
The suffix….-itis means Inflammation, -osis means Degeneration. The cornerstone process of DJD is degeneration of the articular hyaline cartilage. You can have inflammation without degeneration, but cannot have degeneration without inflammation. From a diagnostic and prognostic point of view it is important to know if you are dealing with –osis or –itis.

Due to the nature of horse’s occupation, trauma is the number 1 cause of joint disease. This could be a one-time event (similar to you twisting your ankle) or a chronic repetitive trauma (e.g. marathon runners). The repetitive trauma is conditioned to: frequency, load (weight and speed), force (ground surface) and distribution of load (shoeing, conformation).

You can have normal load on an abnormal joint or abnormal load in a normal joint. Both of the situations will overload the joint and potentially result in joint damage.Think about a mattress and a boxspring. The mattress would be the cartilage and the boxspring the subchondral bone (the bone directly beneath the cartilage). Repetitive loading of the subchondral bone (box spring) may damage it and cause it to deteriorate (change its biomechanical/physical properties). When this happens, the cartilage (mattress) looses considerable support and is exposed to higher loads resulting in its deterioration. The former (box spring/ subchondral bone damage) can be seen radiographically as something that we called subchondral bone sclerosis. The latter (cartilage damage) leads to the typical radiographic signs of joint disease (narrowing articular space, lipping, ostepophytes (“mouse chips”).

We all wish things would be that simple but as you may have thought already, it is not that way. Subchondral bone is a very dynamic structure (remember is bone!), while cartilage does not have blood supply, nor lymphatic drainage nor nerve endings (and still is a living tissue!). Subchondral bone responds to load by varying its biomechanical characteristics. Basically it tries to get stronger where needed. However, this process also called remodeling, takes some time. If the bone (leg) is loaded faster than it can adapt, it develops what we call non-adaptive remodeling, and this is seen on radiographs as something we call sclerosis. In the horse, this sclerosis may be irreversible such as the one seen in young horses in the 3rd carpal bone in the knee. Once subchondral bone exhibits signs of sclerosis, the horse is well on its way of developing joint disease. Often, sclerosis is a painful condition as the subchondral bone has a generous nerve supply. But what is happening with the cartilage in the meanwhile? Remember I told you that cartilage has no vascular, lymphatic or nerve supply. Your question may be, how can it afford to live? This is explained by the nutrition mechanism of the cartilage. Cartilage is composed mainly of water (95 %). The rest is formed by collagen (type II), very sparse cell population (chondrocytes), and other molecules (sugar, proteins…) some of them of famous names such as polysulfated glycosaminoglycans (PSGAG’s). The chondrocytes float on a watery matrix keeping its shape (despite a high water content) due to a network of collagen fibers, sort of like the Olympic bird’s nest stadium in Beijing. This matrix acts sort of like a sponge, absorbing fluid and creating a highly tensile and compressed surface that has a friction factor of almost 0. It is the matrix which is responsible for the nutrition of the chondrocyte, and the chondrocyte which is responsible for forming most of the matrix. Trauma can mechanically damage the matrix and its sophisticated network of collagen fibers and other molecules, resulting in an abnormal water content, loss of molecules (PSGAG’s), and an ongoing cascade of degenerative events which we call…..you got it! Degenerative Joint Disease! Therefore until you have cartilage degeneration, there is hope. After it occurs…..there is no return, or at least one that we know the road to. Chondrocytes are very sparse and have a very very long turnover time, which is responsible for the minimal healing capacity of the cartilage. HEALING! The magic word! The word that brings peace and solace, confidence, gets into people’s pockets, brings hope, keeps us going…..I invite you to look into health magazines and see how many times this word is abused, misused, overquoted, misrepresented, profanated, desecrated…. Keep in mind these differences: HEALING, REPAIR, REGENERATION…what do they mean? Are they equal?
Cartilage, simply put, does not heal. Or I should say does not heal properly, does not regenerate, but it does repair. Whoever finds the way for cartilage regeneration to occur will have the key to a very very large safe, full of golden coins.
Cartilage has a very limited capacity of intrinsic repair too. This means that if no extrinsic outside) elements are available for the repair process, it just simply doesn’t happen to a large extent. This is why, partial thickness cartilage lesions (do not go into the subchondral bone) never heal. There are three mechanisms as to how the damaged cartilage is repaired: intrinsic (due to chondrocyte’s own abilities…Good luck!), extrinsic (when blood elements have access to the damaged joint and matrix flow (which means that the matrix surrounding the lesion periphery, sort of rolls like when you are kneading bread dough). The ability for matrix flow to cover a defect is limited and there is what we call a critical size defect (about 5 mm), beyond of which matrix flow is not possible. When repair happens it does it in the form of fibrocartilage. Fibrocartilage is NOT hyaline cartilage and has very different and distinct structural and biomechanical properties, inferior to hyaline cartilage. Therefore fibrocartilage is not and ideal repair tissue. Researchers have been trying to re-surface cartilage defects or stimulate cartilage metabolism to HEAL them, but to date this has been unsuccessful. There are grafting techniques, which are very promising, and also techniques involving pluripotential cells (stem cells) that would differentiate into chondrocytes once in the joint. There have also been efforts to modify chondrocyte metabolism by using growth factors and hormones. Although we know way more about cartilage biology than we did just a few years ago, no solution has been found. I remain optimistic however, that you and I, along with our horses will be able to find the fountain of youth.
Ok! What you should know about joint disease and the horse:

Highly prevalent

• Is progressive and degenerative
• Is treatable but not curable
• Drugs are not the only answer

Clinical signs: (these are related to severity of disease but some horses may be more stoic than others, and not always present all together)
• Lameness referable to a synovial cavity (blocks out after intraarticular local anesthetic)
• Positive (pain) flexion test
• Filling of joint
• Decreased range of motion
• Heat around the joint

Radiographs may be NORMAL: Radiographs lag behind clinical joint disease

It is important to differentiate:
• Septic (infectious) arthritis: Acute, very lame, very abnormal synovial fluid– A true emergency!
• Traumatic arthritis: Acute, mild to very lame, mildly abnormal synovial fluid – needs prompt attention
• Idiopathic synovitis: no or very mild lameness, no changes in synovial fluid – very rare

Synovitis is usually diagnosed if the clinical signs are referred to the joint but no radiographic abnormalities are identified. Since radiographs lag behind clinical disease, this process may understimate when degeneration is present. Usually persistance of signs despite treatment would support the presence of degeneration.

If your horse has been diagnosed joint disease how should you proceed?

It depends on:
1) Severity
2) Location
3) Inciting cause
4) What does your horse do for living

STAY TUNED FOR MORE INFO ABOUT THIS TOPIC IN THE UPCOMING WEEKS!