Chips of bone, on the other hand, may be seen in young horses’ diets. Among domesticated horses, Osteochondritis dissecans (OCD) is a frequent condition, characterized by loose cartilage and/or bone pieces in the joints. Within a few months, many OCD lesions spontaneously resolve. This is a “germ of bliss.” Those who don’t can, on the other hand, inflict long-term damage if not properly addressed.
There are a wide range of ways in which the illness expresses itself in horses, joints, and even lesions. Researchers believe that breed, genetics, and environmental factors may have a role in the severity and recurrence rates of the disease. We’ve gathered the most current research and perspectives from the world’s greatest experts on this condition to help you better grasp this difficult growth problem.
Using the Correct Slang
The first step is to obtain a better understanding of OCD and other growth-related disorders.
Osteochondrosis, a condition that affects the cartilage and bone of developing horses’ joints, is essential to our knowledge of OCDs. This is known as OCD when a lesion reaches the stage where it separates from the bone.
A family of disorders known as juvenile osteochondral diseases includes these two problems as two of its most prevalent manifestations (JOCC). Jean-Marie Denoix, DVM, PhD, head of the Centre d’Imagerie et de Recherche sur les Affections Locomotrices Equines, in Normandy, coined the term JOCC to describe all developmental abnormalities that affect juvenile horses’ joints and growth plates.
These problems fall under a wider umbrella term, developmental orthopedic illness (DOD). Dr. Wayne McIlwraith, an orthopaedic surgery professor and head of Colorado State University’s Orthopaedic Research Center, coined this word in 1986.
The DODs include not just JOCC, but also Wobbler syndrome and limb abnormalities that are connected to development.
As far as joints go,
A disorder of bone development, osteochondrosis can only be seen in the joints. To put it another way, this is about the way bones develop and harden via endochondral osteosis. Epiphyseal cartilage develops at the extremities of bones where they connect other bones as they grow in length.
The ossification process gradually transforms epiphyseal cartilage into real bone. Only a thin layer of cartilage covers the articulating ends of the bones in the joint of adult animals in the form of cartilage. What you see here is known as articular cartilage. Osteochondrosis and other debilitating disorders may be caused by problems in the ossification process.
Naturally, horses have a large number of joints that connect various bones. Osteochondral lesions may occur in any of these joints, and they each have their own unique features.
Dr. Cathy Carlson, professor of veterinary population medicine at the University of Minnesota in St. Paul, states that “the effects, development, and outcome may be varied depending on the place at which lesions originate.” Dr. Carlson adds this.
A professor of equine sciences at Utrecht University in the Netherlands, René van Weeren, DVM, PhD, Dipl. ECVS emphasizes the wide range of lesions. It’s difficult to compare the responses of joints and even places within joints, according to him.
That is why Denoix developed a new osteochondrosis grading system with weighted severity indices (0, 1, 2, 4 and 8) for specific lesions. Reorganizing the scoring system was an important part of this process. He claims that these new rankings assist vets keep track of the progression of lesions and make better treatment and prognosis choices.
Osteochondrosis is most frequent in which parts of the horse? A lot depends on your age and the breed of your dog. According to Denoix, 28 percent of foals born to Warmbloods, Thoroughbred and Standardbred racehorses in France suffer from osteochondrosis in the rear fetlock.
Standardbred trotters’ hocks and stifles were most often found in Thoroughbreds and Warmbloods, while the front fetlock was most frequent in the latter breed.
Failed Vascularization is the main issue.
Osteochondrosis is caused by a lack of blood supply. This means that epiphyseal cartilage and nascent bone have a lot of blood capillaries, pushing nutrients into the tissue and removing waste.
Osteochondrosis may occur if epiphyseal cartilage does not get enough blood flow, according to Carlson.
Cell death and matrix (internal bone structure) deterioration occur as a result of a lack of blood supply, she says. Because of this, articular cartilage may not be able to sustain it and may collapse under pressure, leading to the production of a cartilaginous flap, which may cause discomfort.
Is there a reason for this vascular failure? Carlson has been working with Kristin Olstad, DVM, PhD, of the Equine Section of the Norwegian University of Life Sciences’ veterinary school in Oslo, to address that issue. As of right now, it seems to be an issue of missing connections.
The blood vessels in the bone’s developing end cartilage must connect to the bone’s vessels as it grows. Occasionally, she adds, the hookups simply don’t happen—for unknown reasons.
Vascularization may also fail in other ways. Bacterial infection, frostbite, or trauma may potentially contribute to blood vessel malfunction and degeneration.
The most recent findings on osteochondrosis are shocking: Osseous lesions affect up to half of Standardbred and Dutch Warmblood newborns, according to Carlson.
As she puts it, “It is a major issue, and one that we continue to perpetuate via bloodlines.” Carlson points out that because the disease has a hereditary predisposition, it is particularly relevant to livestock breeders.
According to van Weeren, domestic horses are the only ones susceptible to the disease. In certain locations, the prevalence of wild horses is as low as 2%, while it is as high as 0% in others. He goes on to say that most domesticated ponies are immune to the sickness.
What exactly does it imply to you? Statistics clearly show that we’ve mistakenly selected for the genes causing osteochondrosis by producing bigger, faster-growing creatures.
We’ve heard from our sources that selective breeding isn’t going to help at this stage. Because the condition is clearly polygenic (including numerous genes), “there is little possibility of addressing the issue via breeding tactics alone,” van Weeren argues.
Osteochondrosis genes are present on at least 22 of the horse’s 33 chromosomes, according to McIlwraith, who believes genomic discoveries and molecular genetics “have only offered additional proof of the disease’s intricacy.”
Since it’s so complicated, he adds, it’ll be impossible for humans to ever breed it out of existence because of that. It’s possible that your efforts may lead to the exclusion of other good characteristics.
Environment Plays a Role
As the saying goes, “you’re either doing it or you’re not.” A young foal on a large field is more likely than one in a stall to have an injury. But restricting a kid just stimulates osteochondrosis growth.
INRA researcher Johanna Lepeule, MS, PhD, recently found that foals (especially those younger than two months) moving freely in a reasonably large pasture on a daily basis acquired considerably less osteochondral lesions by six months than foals housed in stalls.
To avoid these difficulties, she explains, “they have to go outdoors and moving.”
Osteochondritis Dissecans – How to Spot It?
One of the most frequent ways veterinarians uncover osteochondral lesions in adult horses is during prepurchase tests, adds McIlwraith. That’s because most of these lesions don’t really create any clinical indications, so owners are usually unaware their horses even have them.
A thorough workup, which may include imaging, is warranted in young horses who exhibit symptoms such as joint effusion (swelling) and lameness. These are typically detected when young horses first start training, on radiography of the effused joints.
MRI exams, which are more detailed but also more costly, are becoming more popular among pet owners. A less costly approach is ultrasonography, which van Weeren believes is showing some positive outcomes in first diagnostic investigations.
A (Mostly) Self-Healing Disease
Most osteochondral lesions are nothing to worry about since they’ll heal on their own. According to Van Weeren, lesions discovered in a horse before its first birthday have a fair chance of healing. There are certain fetlock lesions and stifle joint lesions that Carlson believes are “beyond the point of no return” at about 18 months of age.
The researchers caution that location does make a substantial impact in outcome. Osteochondrosis of the femur (the long upper leg bone) seems to be reversible in the vast majority of patients. Hock lesions showed no clinical development in 60% of patients, according to Denoix and co-authors. And fetlock lesions seemed just as likely to cure as they would develop.
When Osteochondritis Dissecans Surgery Is Necessary?
In certain cases, OCD becomes so troublesome that an arthroscopy procedure is required to remove the growth. McIlwraith says that’s frequently because the horse will have lasting clinical difficulties (e.g., arthritis or lameness despite medication) without surgery or because the high-value horse can’t be sold for a decent price without fixing the lesion.
Horse receiving arthroscopic surgery
Again, lesion location might be the decisive factor. For example, surgery on the hocks and fetlocks may be beneficial. Stifles are a popular surgical location, as well, adds McIlwraith.
Shoulder lesions, however, depend on the position inside the joint. Some problems involving just the glenoid (socket) may be treated without surgery. If they affect the humeral head (the end of the humerus bone that articulates with the scapula), surgery is essential; however, these surgeries only have a 50/50 success rate.
Sometimes, McIlwraith adds, it’s a “question of your pocketbook,” since, again, it’s possible to simply wait things out to see how they evolve. It is possible to reduce secondary osteoarthritis and boost selling prices by having clean X-rays taken. Surgery may also improve performance and help prevent secondary osteoarthritis from forming.
But if you choose not to operate, seldom is it a welfare problem. “The only time OCD would be a welfare concern is with particular shoulder lesions, or a severe OCD lesion in the stifle, which we see relatively seldom today, since that parents know how to feed their foals better,” McIlwraith explains.
How to Approach Osteochondritis Dissecans with a Balanced Perspective?
Yes, OCD is severe in that it affects a considerable percentage of horses, notably Warmbloods and Thoroughbred and Standardbred racehorses. But all in all, we could well be overdoing it when we worry too much about osteochondrosis in our young horses.
There’s no necessity, for example, to regularly scan our adolescents to check on their osteochondrosis status, say our sources. “Due of the various predilection sites in horses and the fact that different sites are impacted at periods throughout development, it would not be logical or cost-effective to X ray horses at several time points
” Carlson says. Resting the afflicted joint is typically not an option with horses since they are usually standing or moving around a lot. Additionally, we have no current treatments for subclinical lesions (those that do not exhibit clinical indications).
That being said, there are circumstances where OCD produces enough discomfort that it becomes a significant concern—again, depending on the lesion’s location. “Some OCD lesions in the stifle and shoulder in horses have a guarded prognosis, and some of these horses have to be euthanized,” Carlson explains.
Osteochondritis Dissecans Elbow
OCD of the elbow is less prevalent than FCP and occurs most commonly in retrievers and other big breeds of dog (Figure 21-7). (Figure 21-7). OCD of the elbow appears as a loose cartilage flap most typically on the medial region of the humeral condyle.
It may be diagnosed preoperatively as a minor defect on the medial humeral condyle on the craniocaudal radiographic projection or on a pronated craniocaudal radiographic projection. Arthroscopic therapy of OCD of the elbow consists of excision of the cartilage flap, debridement of the bed, and microfracture of the full-thickness cartilage defect.
Arthroscope and instrument portals are the same as in arthroscopy for an FCP, except that the arthroscope may be placed somewhat more proximal to provide better view of the cartilage flap. A 180-degree rotation of the scope, after it has entered the joint and the coronoid process has been seen, will allow one to see the whole lesion in the medial humeral condyle.
Once detected, the flap is removed using graspers, and the bed of the lesion and any residual loose cartilage is removed with a curette or the shaver. Microfracture is conducted in the bed of the lesion as in arthroscopy for an FCP. The joint is subsequently irrigated, and the skin incisions are closed.
The prognosis for soundness with elbow OCD is dubious since many of these dogs subsequently acquire substantial osteoarthritis of the elbow joint. Postoperative care is the same as with FCP patients, and many dogs will need osteoarthritis treatment for the rest of their lives.
Several innovative cartilage resurfacing treatments, such as the osteochondral allograft transfer system (OATS), have been successfully done on a few dogs with elbow OCD. These procedures may be suitable for elbow OCD patients.
Fetlock horse Osteochondritis Dissecans
The sagittal ridge and condyles of the distal third metacarpus/metatarsus of the fetlock joint are often affected by osteochondritis dissecans (OCD). Osteochondrosis-based pieces also develop on the proximal dorsal surface of the proximal phalanx.
Clinical indications are consistent with fetlock disease and attention must be given in examining all four fetlock joints since it is not unusual for this condition to be visible in several fetlock joints. Clinical indications in horses with radiographic appearance of lesions are not always obvious, but radiographs are utilized to confirm their existence.
Radiographs of yearlings destined for sale are the most typical source of these. Sagittal ridge lesions may be one of three forms. There are three types of OCD lesions: Osteochondritis Dissecans type 1 occurs when just the sagittal ridge flattens or defects, type 2 when the flattening region is fragmented, and Osteochondritis Dissecans type 3 when free or loose bodies in the joint are present.
Type 1 lesions are generally treated conservatively and clinical symptoms normally disappear.
7 Type 2 and type 3 lesions with fragmentation should have surgical debridement performed by arthroscopy. Prognosis for type 1 lesions is favorable with conservative therapy but guarded for arthroscopic surgery required for type 2 and type 3 lesions. Secondary articular cartilage injury worsens the prognosis.