|
|
|
1. Anatomy of a Rupture by Rachel Peeples, DVM 2. Interview with Dr. Peter Muir, researcher in Cranial Cruciate Ligament Rupture by Rachel Peeples, DVM Most of the major joints in the canine body are constructed such that the shape and arrangements of the bones that meet in the joint prevent excess or abnormal movement. Examples of this include the ball and socket construct of the hip joint, or the hinge construct of the elbow joint. The primary exception to this is the canine stifle (analogous to the human knee) in which the femur and tibia/fibula meet. Because the bones are not arranged in such a fashion as to prevent excess or abnormal movement, the stifle must rely solely on the soft tissue structures in and around the joint to protect it. There are many structures that help perform this task for the stifle including the cruciate ligaments. Figure: Close up of the Ruptured Cranial Cruciate Ligament. With knee cap resected for a clearer view. The cruciate ligaments are so named because the form an "X" in the interior of the stifle joint. These two ligaments run in opposite directions (see Figure ). One is the caudal cruciate ligament and the other is the cranial cruciate ligament. The function of each is to prevent excess movement in their respective directions. Thus, the function of the cranial cruciate ligament is to keep the tibia from moving too much cranially (forward) during use of the stifle. Rupture of this ligament eliminates this safeguard on stifle movement and allows the tibia to move excessively in the forward direction. This disrupts the joint capsule and other soft tissues surrounding the stifle joint. As a result, irritation and inflammation occur in these soft tissues, leading to pain, swelling, and lameness. Over time, the body tries to protect the joint by laying down additions to the bones in the joint. Unfortunately, all this does is accelerate the irritation as bone forms where bone is not meant to form. The whole process continues to cyclically snowball until the affected stifle has developed permanent degeneration of the joint All Figures Courtesy: Hill's Atlas of Veterinary Clinical Anatomy. Reprinted with permission of the copyright owner, Hill's Pet Nutrition, Inc. This interview was conducted by e-mail from questions taken directly from ACA member submissions on June 17, 2003. Q: Can you tell us a little about yourself and what got you interested in studying CCL rupture in dogs? Dr. Muir received his veterinary degree from Bristol University in 1985. After a period of time in private veterinary practice, from 1987 to 1990 he was a graduate student at Bristol University and was awarded a PhD in Veterinary Medicine in 1990. From 1990 to 1992, he was a Resident in Small Animal Surgery at the University of Sydney, and earned a Master of Veterinary Clinical Studies degree in 1992. From 1992 to 1995, he was a Resident in Small Animal Surgery at the University of Wisconsin-Madison and became a Diplomate of the American College of Veterinary Surgeons in 1995. After periods of time as a faculty member in Small Animal Orthopaedics at the University of California, Davis and The Royal Veterinary College, University of London, he joined the Department of Surgical Sciences as Assistant Professor in Small Animal Orthopaedics in 1999. Dr. Muir's research interests are focused on connective tissue remodeling or adaptation in bone and ligament. In ligament adaptation, the expression and regulation of proteinases involved in ligament remodeling and adaptation is being studied, with the long-term goal of gaining a fundamental understanding of the disease mechanism for cruciate rupture in dogs and suspensory ligament desmitis in horses Cruciate disease is the most important orthopaedic disease of dogs and this is the basis for our interest in this condition. Q: Is CCL injury usually caused by structural deficiencies, or weakness in the CCL itself? The disease mechanism for cruciate disease is not known. Current information suggests that the majority of cruciate ruptures are pathological and are not due to accidental trauma. The key factors that lead to eventual rupture of the ligament are not known. Therefore the importance of breed and conformation as risk factors for cruciate disease and pathological cruciate rupture are not known. Q: If CCL rupture is linked to structural deficiencies, have weight - to - height or weight - to - bone density, hock/stifle conformation been identified as risk factors? The importance of conformation as a risk factor for cruciate disease and pathological cruciate rupture is not known. Q: How would you describe what happens preceding the actual injury? The majority of cruciate ruptures are due to pathological rupture and are not due to traumatic injury. Our work in this field suggests that excessive release of degradative protease enzymes in the tissues of the stifle (knee) joint leads to weakening of the cruciate ligament as the collagen within the ligament is degraded. This precipitates progressive rupture of the ligament during normal activity. This is why cruciate disease usually affects both stifle joints. Please refer to the following reference for more detailed information: Muir P, Hayashi K, Manley PA, Colopy SA, Hao Z. .Evaluation of tartrate-resistent acid phosphatase and cathepsin K in ruptured canine cruciate ligaments in dogs, American Journal of Veterinary Research, 2002;63:1279-1284. Q: As a followup to this, are there things that owners can do to prevent rupture? As a followup: How about preventing rupture in the second leg during the recovery period? As the disease mechanism for cruciate disease is not fully understood, the answer to this question is not known. The only thing we would specifically recommend to an owner at present is do not let your dog get overweight and if the dog is overweight, place the dog on a weight reduction diet until body weight is normal. We expect that in time ourstudies in this field will lead to the development of a new treatment that will prevent rupture in the second leg during the recovery period. Q: Is there evidence is there that CCL injury is hereditary in nature primarily or is it more related to diet/environment? If there is a thing as hereditary CCL weakness, what identifying factor (s) would you point to as a dead giveaway for heritable CCL weakness if you were the practitioner evaluating the dog ? The key factors that predispose to cruciate disease and pathological ligament rupture are not understood. Therefore, the answer to this question is not known. Q: How do you see current x-ray screening programs as being useful in eliminating CCL rupture from the breeding population? Do you see a more useful test being developed from your research? This is a very good question. Early detection of cruciate disease before pathological ligament rupture develops is an important goal. We expect that in time our studies in this field will lead to the development of a new diagnostic test for cruciate disease. We expect that this test will be performed on a sample of synovial (joint) fluid that is removed from the joint using a needle and syringe. Radiographic changes are also seen in dogs with early cruciate disease before pathological ligament rupture, but these changes are not specific. Q: What is the one change you would like to see Akita owners or breeders make to reduce the frequency of cruciate injuries within the breed? The key factors that predispose to cruciate disease and pathological ligament rupture are not understood. Therefore, the answer to this question is not known. Q: In your opinion, what is the "best" treatment after CCL injury has occurred? Once pathological rupture has occurred and the dogs stifle (knee) has become unstable, the dog has advanced or end-stage disease. All surgical treatments at this stage have a poor to moderate long-term prognosis and dogs generally get progressively worse over time. Outcome will only be improved with early detection of cruciate disease before pathological rupture of the ligament has occurred and provision of a treatment that will prevent rupture, so that the dog retains a stable stifle. We expect that in time our studies in this field will lead to the development of a new diagnostic test and medical treatment with a drug that will prevent ligament rupture in dogs with early cruciate disease. Q: Is there a statistically significant age risk for non-traumatic CCL ruptures to occur? If so what age(s) seem are most at risk? The answer to this question is not known. Cruciate disease can occur in all ages of dogs, although it is more common in older dogs. Q: Has there been any more scientific evidence linking the following to the CCL ruptures that occur non-traumatically:
This is a very good question. Cruciate disease is a degenerative condition, not a developmental disease. Cruciate disease and pathological rupture of the ligament is associated with inflammation of both the cruciate ligament and the synovial membrane lining the joint. The factors that cause white blood cells to migrate into the joint and ligament tissues during this inflammatory reaction are not known. Therefore, it is not known whether this inflammation is an auto immune reaction. Our studies have shown that degenerative changes to the cells within the ligament (fibroblasts) predispose the ligament to rupture. However, the cause of these degenerative changes is not known. The following publication has more detailed information on this point: Hayashi K, Frank JD, Manley PA, Hao Z, Dubinsky C, Muir P, Histologic changes in ruptured canine cranial cruciate ligament, Veterinary Surgery. 2003;32:269-277. Q: Do you maintain, or could you recommend, a good informational website on CCL rupture? Studies into cruciate disease in the dog are a very important part of our program at this time. We are actively working on a specific diagnostic test for early cruciate disease, and a new drug treatment. How quickly this work will translate into a new clinical treatment for canine patients is dependent on the amount of funding we have to pursue these studies. Our funding from the American Kennel Club as well as other canine foundations will be very helpful. However, a lot more work still needs to be done. We are very excited about our work in this field and we hope that over the next few years we will be able to develop a new way of treating dogs with this disease that will be much more effective than the traditional surgical treatments for dogs with unstable stifles (knees) and advanced or end-stage disease . Thanks very much Dr. Muir ! Updated on 09/18/2008 |
