The first thing to address in this story is that most "bone cysts" are not typically "cysts," by strict definition. The medical dictionary defines a cyst as, "a structure lined with epithelium (a special cell type) and generally filled with fluid." The key part is that there is a lining of cells that secrete the fluid. With respect to a "bone cyst," there usually is not a secretory cell lining, and, therefore, it does not qualify as a true cyst; there are many authors and researchers who will call these bone lesions a "cyst-like" lesion. Now, with the pure terminology and definitions out in the open, I will take the liberty and refer to these lesions as cysts--some medical dictionaries will define a "bone cyst" as "a solitary bone lesion."
A surgical instrument has been inserted into the cyst shown at left during treatment. Courtesy Dr. Michael Ball.
It would be prudent to review some anatomy and growth specifics regarding bone in an effort to better understand the development of these cyst lesions. Bone is considered to be a special form of connective tissue and is made up of microscopic crystals of calcium and phosphate within a matrix of collagen. Remember, collagen is a protein structure that is also a major structural substance of skin and tendons. Within the collagen fibers are the bone crystals, which are made up primarily of a substance called hydroxyapatite (crystals of calcium, phosphate, water, and hydroxide).
In addition, sodium, magnesium, and carbonate also are present in bone.
One major misconception is that bone, once it has developed and become full grown, is a fixed structure--solid, rigid, just there, right? Wrong. Bone is actually an extremely active tissue. When I was an undergraduate at Cornell, I had an animal nutrition professor that once called bone "as mobile as a tub full of frogs." Having never seen a tub full of frogs, I only had my imagination to visualize this phenomenon, but the message was clear. There are many chemicals that affect the metabolism of bone within the body.
Bone, in fact, acts as the body's store for blood calcium. There are hormones (a chemical released from one part of the body that has an effect on another part of the body) that serve to increase or decrease the release of calcium from bone as needed. One such relationship that can cause bone disease is the decrease of estrogen in older women or younger women who have had an ovariohysterectomy (removal of the ovaries and uterus), causing a weakness of bone--osteoporosis.
Nutrition also can play a vital role in bone development and maintenance. A dietary deficiency of calcium can cause a weakening of bone, a disease called rickets. In addition, an excess of dietary phosphorus can "compete" with the absorption of calcium and cause a weakening of bone. In horses, excessive dietary phosphorus can come from feeding large quantities of bran (high in phosphorus and low in calcium), hence the name "bran disease." One of the physical manifestations of this disease is the softening and enlargement of the skull bones--this disease is also called "big head." These are just a few of the factors that affect the growth, development, metabolism, and remodeling of bone throughout life.
The bones of the forelimb include (starting from the top or proximally) the humerus, radius, seven bones in the carpus (knee), the cannon bone (third metacarpus) and two associated "splint" bones (second and fourth metacarpus), two sesamoid bones, and the three phalanges (P1 or long pastern bone; P2 or short pastern bone; and P3 or coffin bone). The horse essentially stands on its middle finger if compared to a human with the horse's carpus (often called the knee) analogous to the human wrist. Eohippus, the modern horse's 28-million-plus-year-old ancestor, actually stood on three digits, but over the years the outer and inner digit regressed and became the two splint bones. The modern horse's ulna also has largely regressed, with the upper portion remaining fused to the radius and making the point of the elbow.
The bones of the hind limb include, starting proximally, the femur, the tibia, six bones within the tarsus (hock), the cannon bone (third metatarsus) and two associated splint bones (third and fourth metatarsus), two sesamoid bones, and the three phalanges (P1 or long pastern bone; P2 or short pastern bone; and P3 or coffin bone). When comparing the horse's hind limb to a human's leg, the horse stands on its middle toe with the point of its hock analogous to the ball of our foot; the stifle is analogous to our knee. The fibula, which is distinctly associated with the tibia in a human, has largely regressed in the modern horse and exists only as small remnants (it is vestigial).
The joints (articulations) are areas where two bones meet. The soft tissue surrounding a joint forms a pouch, per se, that is lined with tissue that produces a viscous fluid (synovial fluid) that serves to lubricate and cushion the joint. The surface of bone in an articulation is covered by a white, smooth, and shiny tissue--the cartilage. The cartilage serves to provide a smooth gliding surface for the bones to move over as the joint is flexed or extended.
During bone growth in the young animal, many of the long bones have specialized areas at their ends called the epiphysis; the center of the bone is called the diaphysis, and the junction between the epiphysis and diaphysis is called the epiphyseal plate or "growth plate." The growth plate is an area of actively growing cartilage (several inches from the surface of bone in the joint) that is converted to bone; it is this process that in-creases the length of growing bone. As the animal ages and bone growth slows, the growth plate "closes" and the band of cartilage then becomes mostly bone.
So with the development, anat-omy, and physiology of bone having been discussed, where do the bone cysts enter the picture?
Bone cysts often are called "subchondral bone cysts" because in most cases these cysts are found just under the cartilage surface within a joint. The term subchondral means "under the cartilage." Bone cysts in horses are typically associated either with a developmental bone anomaly and/or trauma to the cartilage surface, with the former thought to account for the majority. In addition, a more rare cause of bone cyst formation can be infection or neoplasia (cancer).
It is difficult to discuss subchondral cysts without bringing up the subject of osteochondrosis, as this is thought to cause the majority of bone cysts. Often referred to as OCD, which stands for osteochondrosis dissecans, the disease process is one of young growing animals and relates to an abnormal development of growing cartilage. Dissecans describes an area of cartilage that is affected with osteochondrosis, in which the cartilage actually has become detached from the underlying bone and has formed a flap--it has "dissected" away from the bone.
An extremely comprehensive review article entitled "Subchondral cystic lesions (osteochondrosis) in the horse" by C. Wayne McIlwraith, BVSc, MRCVS, PhD, from the Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, was published in a 1982 edition of the Compendium of Continuing Education for the Practicing Veterinarian and will be used as a general source of information for this article. McIlwraith is a noted expert in equine orthopedic disease and has published numerous scientific articles and book chapters on the subject of osteochondrosis and degenerative joint disease.
Osteochondrosis is a complex disease process that is multifactorial in nature. The explanation presented here is an extreme oversimplification of this disease, but will give you the basic idea.
Osteochondrosis is one of the most heavily studied orthopedic disease areas in the horse. There is evidence of heredity and genetic predisposition that might be influenced by rapid growth in large-framed horses, nutrition relating to calcium and phosphorus concentrations in the feed, deficiency of dietary copper or excessive dietary zinc, and abnormal hormonal influence of bone metabolism. These factors culminate in a failure of normal mineralization of cartilage, degeneration of deeper layers of cartilage, and thickening and retention of the growth cartilage on joint surfaces.
The areas of abnormal cartilage also are influenced by mechanical trauma produced when these animals are exercised; the lesions of OCD occur somewhat predictably in locations where the weight-bearing on the surface of bone, and therefore cartilage, is greatest within the joint. The lesions associated with OCD include cartilage flap development, inflammation of the cartilage and joint tissue, softening of the cartilage, the development of cracks in the cartilage and miniature fractures in the underlying bone, and the development of subchondral cysts.
Subchondral bone cysts were first reported to occur in the horse in 1968. In 1970, a case series reported on the presence of 69 cysts observed in 64 horses. Subchondral cystic lesions have been reported to occur in the shoulder, hip, and in multiple locations within the carpal, fetlock, pastern, coffin, stifle, and tarsal joints. The most common anatomical location for subchondral cyst-like lesions is in the medial femoral condyle (the inside of the lower part of the femur), where the incidence is highest in horses under three years of age. It has been reported, in one study group, that 38% of stifle lameness in the horse was caused by subchondral bone cysts; 90% of those cases involved the medial femoral condyle with the cyst located immediately above the weight-bearing area of the bone within the joint. It is thought that in most incidences, the development of subchondral bone cysts is related to OCD. When diagnosed in older horses, they are still probably related to OCD.
In most cases, it is difficult to ascertain how long the cyst was there prior to the observation of clinical signs. It is possible that these cysts could be subclinical (not causing observable problems) for some period of time before the circumstances are right for the manifestation of lameness. In some cases, certain types of trauma to the cartilage surface might lead to the development of a bone cyst. In a 1996 issue of the Journal of the American Veterinary Medical Association, I reported on one horse where there was strong evidence for such a scenario leading to the development of cystic lesions in the lower tibia of an adult pony.
Clinical Signs And Treatment: The Stifle
As previously mentioned, the distal end of the femur within the stifle joint is the most common location for the development of subchondral bone cysts. The veterinary literature indicates that horses between the age of five months and 13 years have been diagnosed with subchondral bone cysts in this location. Again, 70% of reported horses were less than three years of age and 75% were less than four years of age.
The most common presenting clinical sign for these horses is lameness with an associated shortened stride. The lameness is typically intermittent in nature and often is coincidental with the start of training a young horse or increase in exercise program. The joint usually does not have any gross enlargement related to excess synovial fluid production (joint distension or effusion). The use of local anesthetics placed into the joint (intra-articular anesthesia) has a reported variable effect and, therefore, might not always be useful in assisting in the diagnosis.
There is some evidence that a percentage of the pain associated with bone cysts is caused by the actual pressure buildup inside of the cyst--this is supported by the observation that many horses have an immediate and obvious decrease in lameness after the cyst has been surgically "decompressed."
The definitive diagnosis of stifle bone cysts, as well as cysts in all other locations, is made by radiographic observation of a cyst-like lesion. The cavity of the cyst typically is filled either with fluid and/or soft connective tissue, both of which are less dense than bone; these lesions appear as lucent areas within the bone. In one study, performed at the University of Pennsylvania School of Veterinary Medicine, 68% of 18 horses radiographed had a cyst-like lesion in the perceived to be "normal" stifle as well as the stifle that was clinically isolated to be abnormal. Due to the incidence of cystic lesions occurring in both stifles concurrently (bilaterally), the opposite stifle should be radiographed if a cystic lesion was observed in the opposite limb.
The specific treatment for subchondral cysts in the stifle is still slightly controversial and can be influenced by specific characteristics of the individual cysts, the age of the horse, the intended use of the horse, the amount of convalescent time that can be invested, and the amount of funds available for treatment.
The two principal therapeutic regimens are essentially surgical and non-surgical in nature. The non-surgical, or conservative, therapy for cystic lesions in the stifle joint involves a rest period of at least six months. The "rest" period can include complete stall rest, turnout to pasture, or light exercise.
There are two studies in veterinary literature supporting the potential for conservative therapy having a positive outcome. One study, reported by Barbara Stewart, VMD, and Charles Reid, DVM, MS, from the School of Veterinary Medicine, University of Pennsylvania, in a 1982 edition of the Journal of the American Veterinary Medical Association, followed 25 horses which had been diagnosed with a subchondral bone cyst in the stifle and reported that 16 of the 25 horses (64%) of the horses became "sound" and "useful" between four months and one year after the diagnosis had been made.
In a second study following 33 cases, the horses were given a six-month rest period followed by pasture turnout. Of the 33 cases, 28 horses had what was considered to be a clearly defined cystic lesion, with 14 of the 28 horses (56%) making what was considered to be a complete recovery.
In both of these studies, horses which were younger and horses with smaller lesions had a better prognosis. Although one report in the veterinary literature indicated that continued moderate exercise during the therapeutic period was not detrimental to the eventual outcome, a specific exercise program shown to maximize benefit and minimize risk of detriment has not yet been defined. It also has been observed that when maximal performance training has been resumed, some horses have a recurrence of the lameness.
Surgical management involves the use of arthroscopy. During the procedure, the joint can be more effectively evaluated for the presence of degenerative joint disease and other factors that might affect the overall prognosis. With respect to the cystic lesion, the procedure involves essentially removing it. The abnormal cartilage over the cystic area is removed as well as all abnormal material within the cavity. Some surgeons prefer to place a bone graft into the remaining cavity in an effort to expedite the healing process.
A study presented by Robert Lewis, DVM, in the proceedings of the 1982 meeting of the American Association of Equine Practioners, reported the results of 99 cases of subchondral bone cysts treated by arthroscopic techniques. He indicated that approximately 70% of the horses had a satisfactory outcome with respect to the horse's intended use.
In addition, a similar success rate of 74% was observed in 41 horses in a more recent study by J. Foland, DVM; C. Wayne McIlwraith, BVSc, MRCVS, PhD; and Gayle Trotter, DVM, from the Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, that was published in a 1992 issue of the Equine Veterinary Journal.
A pertinent fact is that once the abnormal cartilage is removed, it will not heal as normal cartilage. Once cartilage tissue is damaged, it does not regenerate, but in fact heals with an altered type of cartilage. This altered cartilage does not have 100% of the functionality of normal cartilage and could predispose the horse to future or chronic joint problems. This fact has stimulated research that is exploring the value of a type of cartilage "transplant" with respect to the promotion of normal cartilage regeneration. The development of such techniques could further improve the prognosis for this and other OCD lesions treated surgically.
The development of subchondral cystic lesions in the elbow is rare, but has been reported to occur.
In a 1986 issue of the Journal of the American Veterinary Medical Association, Alicia Bertone, DVM, MS; C. Wayne McIlwraith, BVSc, MRCVS, PhD; and others from the Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, reported on conservative versus surgical management of subchondral cystic lesions in the elbow. It was demonstrated that there was a better long-term success, as determined by return of athletic soundness and less evidence of subsequent degenerative joint disease, when cystic elbow lesions were managed surgically as opposed to medically.
Other Anatomical Locations
Bone cysts in other anatomical locations are reported sporadically in veterinary literature. As with the discussed locations, the clinical signs are lameness with or without distension of the affected joint, with the definitive diagnosis made by obtaining radiographs. The prognosis and most appropriate therapeutic regimens are difficult to define for these other sporadic sites of bone cyst formation due to the limited number of cases reported to date.
About the Author
Michael A. Ball, DVM, completed an internship in medicine and surgery and an internship in anesthesia at the University of Georgia in 1994, a residency in internal medicine, and graduate work in pharmacology at Cornell University in 1997, and was on staff at Cornell before starting Early Winter Equine Medicine & Surgery located in Ithaca, N.Y. He is also an FEI veterinarian and works internationally with the United States Equestrian Team.
Ball authored Understanding The Equine Eye, Understanding Basic Horse Care, and Understanding Equine First Aid, published by Eclipse Press and available at www.exclusivelyequine.com or by calling 800/582-5604.
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