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Aseptic Necrosis of the Femoral Head
Source: unknown, chapter titled: Radiology in Veterinary Orthopedics, Miscellaneous Diseases; pp. 353-355.
Submitted by Vandra Huber 3/1/96
Aseptic necrosis occurs in the femoral head as a result of (1) idiopathic (primary) necrosis of the capital femoral epiphysis in growing dogs of small breeds, (2) following fracture of the femoral neck in an adult animal, (3) following capital femoral epiphyseal slippage in a young animal. The radiographic changes may be similar although usually the history or the age and breed of the animal are characteristic. The radiographic changes are best understood in the dog.
Aseptic Idiopathic Necrosis of the Femoral Head in the Dog
(Coxa Plana, Legg-Calve-Perthes Disease, Malum Deformans, Juvenilis Coxae)
Aseptic necrosis of the capital femoral epiphysis in the dog affects members of small breeds with the age of onset of clinical symptoms appearing at 4 to 11 months. No sex predisposition has been shown in dogs (Ljunggren, 1967).
Earliest bony changes in idiopathic aseptic necrosis in the dog are not demonstrated radiographically, since they are limited to subtle increases in bone density of the affected femoral epiphysis. Thickening of the bone trabeculae and formation of almost compact subchondral bone continues until there is gross radiographic evidence of the slight increase in density of the femoral head. Ljunggren (1969) described the irregular density in the femoral head, plus a widening of the joint space, as Grade I changes. The acetabulum and contour of the femoral head and neck remain normal. Grade II changes include flattening of the femoral head as a result of the osteonecrosis, especially at the junction between the articular cartilage and epiphyseal bone. A moth-eaten appearance of the head and neck is obvious and early change to the acetabulum in the form of acetabular spurs may be noted. Grade III describes an accentuation of the changes listed in Grade II. The radiographic changes in Grade IV include loss of the normal outline of the femoral head with minor fragmentation. Secondary change causes a thickening of the femoral neck and the joint space is widened. The typical uneven density always seen in this stage of the disease is prominent. Soft tissue atrophy in the hind leg may be evident at this time. Clincal signs are noticeable at this point, and the first radiographic study made of a case is often not until this stage. In Grade V, extensive fragmentation of the femoral head and resulting discontinuity of the articular surface are characteristic. Remodeling of the acetabulum is marked at this time with secondary joint disease due to marked incongruity of the articular surfaces. Lee (1970) describes a similar pattern of radiographic changes.
Radiographic changes typical of aseptic necrosis of the femoral head are usually only noted unilaterally. Ljunggren (1969) reported only 12.2 per cent of her cases had radiographically demonstrable bilateral involvement. However, histologic examination demonstrates clearly that bone necrosis occurs in the contralateral femoral head, and careful evaluation of the radiographs may suggest the increase in bone density.
Legg-Calve-Perthes disease has also been reported in cattle (Diplock, 1962).
Original Doc: lcp.doc
Calve-Perthes Disease (Legg-Perthes Disease)
By Unknown Author
Source: Cairn Clearing House, Article 7-A
Reference: CTCA Genetic Survey, Sept. 1989
"Legg-Perthe's disease is rare in the breed. Twenty-six people reported dogs with this, for a total of 34 dogs. The condition is very rare, but still warrants selection against it."
Reference: CTCA Newsletter, Dec. 1990, On CMO and Other Genetic Diseases of Cairn Terriers, Geo. A. Padgett, DVM
"Disease Mode of Prevalence Guesstimate of
Inheritance Gene Frequency
_________ ___________ __________ (% Carriers)
1. Legg-Perthes Poly. 1.6/200 Un 17.6%
Reference: Genetics Of The Dog, Malcolm B. Willis, 1989, pg. 130
"This disease is a relatively common problem in small breeds of dog and a similar condition occurs in children. It is a very similar disease to hip dysplasia and in many of the earlier reports there is some confusiion (sic) between the two. Both involve some necrosis of the hip joint. However, whereas in hip sysplasia the essential problem stems from a shallow acetabulum, in Calve-Perthes disease the main area of necrosis is the femoral head. There is enlargement of the femoral neck, loss of minerals and some degree of collapse of the bony support of the head. If the process is halted then the femoral head my be flattened and degenerative joint disease may result. It is at this stage that confusion between the two diseases often occurs. Generally, though not inevitably, hip dysplasia is bilateral with both hips similarly affected whereas in 90 % of cases Calve-Perthes disease is unilateral. The sequence of events which occur once necrosis of the femoral head has occured was reported by Lee (1970) but the original cause of the necrosis is uncertain.
It does appear that hip dysplasia is a feature of large breeds while Calve-Perthes disease is generally confined to small breeds. Most early authors who lump the two together (for example Wamberg 1961, 1963) would appear to be in error and the view of Burns and Fraser (1966) that the two are manifestations of the same genetic abnormality would seem to ber (sic) outdated.
Having said this, the genetics of Calve-Perthes disease is not at all clear. In humans Wynne-Davies and Gormley (1978) could detect no genetic involvement though they did show an association with parity and parental age as well as underdevelopment in the child. The most recent attempt to examine the genetics of the disease in the dog was undertaken by Pidduck and Webbon (1978) using four cases in a Toy Poodle kennel. They concluded that the condition was caused by a simple autosomal recessive gene, but as the authors point out, the view can only be regarded as tentative in view of the limited number of cases and the absence of test matings. The difficulties of diagnosis do not aid genetic studies but it is clear that miniature breeds, where this is likely to occur, need to begin collection of data for genetic studies to be made if the disease is to be controlled. More recently Wallin (1986) has undertaken a study in the West Highland White Terrier in Sweden. Over the period 1976-82 has showed a frequency of 4% of animals affected by this disease. In a study of 39 litters which contained 144 animals there were 51 affected dogs, more or less equally divided by the sexes. The data were indicative of a simple autosomal recessive but further breeding tests were being undertaken."
Reference: Understanding and Reducing Genetic Disease in West Highland Terriers, Watch Bulletin II, June 1991, page 9
Description: Legg-Calve Perthes Disease (synonyms: Legg-Perthes, osteochondritis deformans juvenilis, avascular necrosias, coxa plana) is a noninflammatory avascualr necrosis of the femoral neck and head that usually occurs in small breeds of dogs. The first sign of the disease may be irritability, which progresses to a chronic hind limb lameness of apparent sudden onset. The lameness may decrease as the dog ages. Pain can be elicited when the hip joint is manipulated. Leg motion is reduced, and some muscle atrophy may occur. Either one rear leg or both rear legs may be affected.
Age of Onset: The age of onset is typically 3-11 months.
Diagnosis: Typical clinical signs and radiographs of the hip are diagnostic.
Treatment: There is no specific treatment. Some dogs recover reasonable function without treatment. In severe cases, removal of the head of the femur eases pain and helps restore function. Cage rest has been effective in fewer than 25% of the cases.
Mode of inheritance: Breeding studies in Westies and Poodles have shown the mode of inheritance to be complex, probably polygenic."
Editor's Note: The Westie Watch group is doing a survey on the disease in their breed. They are setting up a registry and will counsel breeders on an individual basis. Subscription to the Watch Bulletin in order to get entire Bulletin II - cost $20. (Patron status)
Editor Comment:Judy Irby - Helen Hislop spoke to Legge-Perthes in her presentation to the C.T.C.A. 10/91. I believe she said it was sometimes self-limiting. Therefore, it behooves breeders to determine conclusively the cause of any chronic lameness before the animal is considered for breeding. Otherwise, one could breed a dog affected with this. Helen is due to lecture for the C.T.C.A. again this year at Montgomery.
Comment: Dr. Geo. A. Padgett, Michigan State University
Legg-Perthes disease is a common disorder of terriers and other small breeds of dogs. The disorder is clearly inherited. Crosses between affected Westies (Legg-Perthes X Legg Perthes), affected Miniature Poodles (Legg Perthes X Legg Perthes) and affected Minature (sic) Pinschers (Legg Perthes X Legg Perthes) yielded both affected and normal offspring in about equal numbers. In addition a cross between an affected Miniature Pinscher and an Affected Miniature Poodle yielded both affected and nonaffected offspring. From this data we can conclude that Legg-Perthes is not a simple autosomal recessive trait. Other data in all three breeds allows us to rule out autosomal dominant and both sex linked dominant and recessive modes of inheritance. The cross between the Pinscher and Poodle allow us to conclude that the genes for Legg-Perthes are the same at least in these 2 breeds of dogs.
The most likely mode of inheritance is polygenic and thus it is inherited in the same manner as Hip Dysplasia.
The disease is a common one occurring in Cairns throughout the world. With a guesstimated gene frequency of 17.6% if you do not have this trait in your line at the present time you will pick up the gene within 5-6 outcross matings.
Original Doc: PERTHES.WPD
Canine Hip Dysplasia: An Overview
By Michael G. Conzemius, DVM
Department of Orthopedic Surgery
Veterinary Hospital at the University of Pennsylvania
Dr. Conzemius received the DVM degree from Iowa State University in 1990. After an internship in small animal medicine and surgery at Rowley Memorial Animal Hospital, he completed a 3 year residency in orthopedic surgery at the University of Pennsylvania.
acetabulum - a large cup-shaped cavity on both sides of the pelvis that helps hold the femoral head in place (the socket of the ball-and-socket joint)
Canine hip dysplasia CHD - abnormal development of the hip joint in a dog
crepitation - a dry, crackling sound or sensation, such as that produced by the grating of two pieces of bone
dysplasia - an abnormality of development
laxity - not tense or firm; relaxed; in canine hip dysplasia, refers to looseness of the femoral head
osteoarthritis - degeneration of the joint and its associated structures, accompanied by pain and stiffness but not inflammation
subluxation - less than a dislocation; in this article, subluxation specifically refers to the femoral head sitting outside of its normal place, the acetabulum
Hip dysplasia (HD) , an abnormal development of the hip joint, 1,2 is a common disorder that affects most breeds of dogs and some cats and humans.1,3 Canine hip dysplasia (CHD) can be caused by many factors; it has been shown to be hereditary, but the frequency and severity of disease are influenced by environmental factors.2 Regardless of cause, however, CHD clinically affects each dog in a somewhat unpredictable manner (i.e., some dogs that appear to have severe disease [based on radiographic evaluation] do not display signs of being affected, yet others with a mild case of CHD are extremely lame and exhibit signs of pain). This article reviews normal canine hip anatomy and explains methods of diagnosing and treating CHD.
The primary functions of the canine hip are to provide flexion and extension.1 The hip joint is a ball-and-socket joint that allows for a wide range of motion. The femoral head is the “ball” and the acetabulum is the “socket”. The acetabulum is part of the pelvis; it functions as a deep pocket to cover the femoral head. The hip joint is enclosed by a joint capsule that extends from the acetabulum to the neck of the femur. The ligament of the head of the femur runs from the fovea capitis (part of the femoral head) to the acetabular fossa (part of the acetabulum). This ligament and the joint capsule provide the greatest amount of stability to the hip joint.1 In addition, many muscles in the hip area affect range of motion and stability, most importantly, the gluteal muscles (deep, middle, and superficial) and the thigh muscles (biceps femoris, semitendinosus, semimembranosus, gracilis, and adductor). All of the structures associated with the hip joint affect normal range of motion and contribute to both passive and functional joint stability.
Before diagnosis of CHD can be made, a variety of clinical information must be evaluated, including the age and breed of dog (signalment), history of the patient, any abnormalities noted during the physical examination, and radiographic findings. Signs such as hind limb lameness, pain in the rear quadrant, reluctancy to rise or to climb stairs, or exercise intolerance can all be associated with hip dysplasia. Although this clinical information is certainly consistent with a diagnosis of CHD, many other problems or disease processes could cause identical signs.
Physical examination provides additional information regarding the possibility of CHD. The veterinarian will pursue answers to several questions:
· Does the dog exhibit any lameness when walking?
· Does the dog have disuse muscle atrophy in the real legs; that is, are the muscles smaller than normal because the dog has not been using the legs as much?
· Do the hip joints have a normal range of motion (especially in flexion and extension)?
· Does the patient exhibit signs of pain when the hips are put through a normal range of motion?
· Is the remainder of the physical examination normal, especially with respect to the neurologic function in the rear legs?
· Is there palpable crepitation in the hip joints?
· Does the hip have passive laxity; that is, does the femoral head fail to sit deep inside the acetabulum when the dog is at rest?
· Finally, if the dog does have CHD, is its quality of life affected?
Radiographic examination of the hip joints contributes significantly to the diagnosis of CHD. The veterinarian should consider two things: First, what technique should be used to radiograph the hips, and second, what does the radiographic interpretation mean. Currently, two different radiographic techniques are commonly used in the clinical setting to evaluate the hip joint.
The hip extended view is a radiographic technique that has been employed for decades by veterinarians around the world. This method originated in human medicine with physicians who radiographed their patients in a standing position. When humans stand, the femurs are parallel to the spine and the structures around the hip joint are in a neutral position. When an extended view of the hip is taken in a dog, the patient is positioned on its back with the rear legs pulled into full extension so that the femurs are parallel to the spine. The radiographs are then evaluated for signs of femoral head subluxation and/or osteoarthritis, thus indicating CHD.
Advantages of the hip extended radiographic method are that:
· It is easy for the veterinarian or technician to learn and perform; however, no certification program has been initiated to improve quality control of the radiographic technique.
· The radiograph can be taken without the veterinarian or technician being exposed to ionizing radiation.
· The positioning of the dog allows evaluation of the hip joint for osteoarthritis.
· A radiographic diagnosis of osteoarthritis correlates well with actual pathologic changes in the hip joint.
· The hip extended view is the standard position required by the Orthopedic Foundation for Animals (OFA) Dysplasia Control Registry. The OFA has reported that careful breeding programs based on the registry have decreased the prevalence of CHD in certain breeds.4 The OFA, however, has not conducted studies, to my knowledge, to determine the heritability of CHD in specific breeds.
Disadvantages of the hip extended radiographic method are that:
· Passive laxity (hip looseness during joint relaxation) in the dog is not optimized. The hip of a dog is in a neutral position when the femurs are perpendicular to the spine. Pulling the rear legs into full extension therefore twists the joint capsule, the ligament of the head of the femur, and the muscles of the hip, making the hip joint 50% tighter than normal.5,6
· Interpretation of the radiograph is based on opinion (i.e., degree of subluxation or presence of osteoarthritis). To minimize this problem, the OFA requires that each film be evaluated independently by three radiologists. Recent research, however, has shown great variability between OFA and non-OFA radiologists.7
· The dog needs to be 2 years of age before the hip extended view can be reliably used to detect CHD. Dogs cannot receive an OFA breed registry number unless they are at least 24 months old at the time of radiography.
· A radiographic diagnosis of CHD does not predict the clinical course the disease will take in the dog.
· Functional laxity (hip joint looseness during weight bearing) is not measured. I think that functional laxity is the key in predicting both the clinical and radiographic course the disease will take in the dog.
The compression/distraction method (C/D method) is relatively new to the veterinary community. The dog is positioned on its back for the technique, but the rear legs are positioned perpendicular to the spine in a neutral orientation. A small, harmless, distractive force is applied to the hips while the radiograph is taken so that hip joint laxity is optimized on the radiograph. The amount of looseness in the dog’s hips is measured and compared with that of other dogs of the same breed. This technique is based on the concept that the degree of hip joint laxity/looseness is directly related to whether a dog has, or will develop, CHD.8-11
Advantages of the C/D method are that:
· The legs are in a neutral position when the radiograph is taken, which allows the method to more accurately measure passive hip joint laxity.
· The interpretation of the radiograph is quantitative rather than subjective, which allows for more consistent interpretation.
· The method can be safely and effectively employed when the dogs are 16 weeks of age, thereby possibly providing earlier detection of excessive passive laxity that predisposes dogs to later osteoarthritis.8 The amount of passive hip joint laxity remains relatively constant over time unless severe arthritis occurs.8 The same study showed that laxity measured by the Norberg Angle from the conventional hip extended view was far less consistent.
· National training and certification programs have been instituted to assure consistency in the radiographic method and to increase availability.
· Heritability of passive laxity measured from the distraction radiograph has been shown to be considerably higher (0.47 to 0.52) than estimates of heritability from the subjective hip extended method (0.24).8,12 Heritability is an important factor in determining the expected rate of genetic change by application of selection pressure (i.e., selected breeding). A heritability of 0.52, when compared to 0.24, indicates expected genetic change to occur at approximately twice the rate for the higher number.
Disadvantages of the C/D method are that:
· The veterinarian and/or animal technician currently must be in the room while the radiograph is taken. This exposure to ionizing radiation can be minimized with protective lead vests, gloves, thyroid collars, and dosimeters.
· This method, although not difficult to learn, is not widely available.
· Although this method has increased accuracy in measuring passive hip joint laxity, like the OFA method, it does not address functional laxity.
· Because this method is new, radiographic signs characteristic of osteoarthritis have not been identified.
· A radiographic diagnosis of CHD does not necessarily predict the clinical course of disease in a dog.
· The C/D method has not stood the test of time. Early results showed that passive laxity as measured on the distraction view is the single most important factor in predicting the risk of developing osteoarthritis.8 Similar relationships between laxity and osteoarthritis were found in a smaller study of Labrador retrievers.9
To diagnose CHD it is important that all the components of the work-up (i.e., history, physical exam, and radiographs) be completed. This will increase the veterinarian’s chances of making the correct diagnosis. Although CHD is very common in dogs, most do not have the clinical signs associated with the disease (lameness, pain, etc.) And do not need to be treated.
An old saying regarding CHD is, “Dogs don’t walk on their radiographs.” This means that a radiographic diagnosis of CHD, regardless of severity, may not correlate with the clinical prognosis. Many dogs have radiographic evidence of CHD, however, only those with clinical signs of disease should be treated. Dogs that experience clinical problems generally have an excellent prognosis for return to good pet quality function following treatment.
Most dogs with CHD can be successfully treated using medical methods.13 Antiinflammatory drugs are one popular and effective method for treating CHD. Drugs such as aspirin, phenylbutazone (Butazolidin® - Coopers Animal Health Inc., Mundelein, IL), piroxicam (Feldene® - Pfizer Inc, New York, NY), and others are classified as nonsteroidal antiinflammatory drugs (NSAIDs) and their effectiveness for problems similar to CHD is well documented. These drugs have been used as the first line of treatment for dogs exhibiting problems associated with CHD. Although NSAIDs are commonly used, it does not mean they do not have potentially dangerous side effects. Many NSAIDs used in humans can cause severe gastrointestinal bleeding or even kidney failure in dogs. A veterinarian should be consulted before NSAID use is initiated.
A second treatment option that is frequently indicated is weight loss. Research has shown that if two dogs have the same genetic predisposition for CHD but one is heavier than the other, the heavy dog will be affected earlier, more frequently, and more severely.2 Hip joints of the heavier dog must carry more load when doing the same amount of work compared with the hip joints of the lighter dog.
Another way to treat CHD is to rest the dog when it displays signs of pain and to allow it to get daily exercise when it appears to be free of pain. There is little argument that rest is initially beneficial, as it gives the pain and inflammation in the joint a chance to decrease. The effect of daily exercise on CHD, however, is still somewhat controversial. Nonabusive exercise, such as swimming and leash walking, are generally recommended.
Another method of treating CHD is through the use of polysulfated glycosaminoglycans. Drugs in this group work as antiinflammatories and are hypothesized to be chondroprotective (i.e., slowing of cartilage degradation.14 The use of these drugs has had some success in the treatment of cartilage injures in horses.14 Their use in the canine population is just now being explored, and many questions are still unanswered. In my opinion, drugs in this group certainly have potential to help dogs with CHD; however, more scientific evidence should be presented before they are widely accepted in veterinary practice.
Dogs with CHD that do not respond to medical therapy may require surgery. Three main surgical options exist. Prognosis for the patient is good for each of these techniques, but much debate remains as to which method is best. Young dogs that display signs of pain associated with subluxation of the femoral head but have either no or very little hip joint osteoarthritis may be considered for a triple pelvic osteotomy (TPO).3 This procedure involves cutting the pelvis in three different places so that the acetabulum can be rotated over the femoral head. This allows for imported coverage of the femoral head and, in theory, greater stability.3 It is believed that this procedure stops the progression of arthritis by reducing the hip joint laxity.3 The clinical results from this procedure appear to be very good; however, recent reports have shown that arthritic changes continue in spite of the surgery.15 The TPO may turn out to be the best way to treat dogs with little or no hip joint osteoarthritis, but more research and case follow-up is needed before such a determination can be made.
A second surgical option for management of CHD is a femoral head and neck excision. This surgery requires the surgeon to remove the head and neck from the femur on the affected side.1 As a result, there is no longer a connection between the acetabulum and the femur - the hip joint is removed. After healing, the animal will form a pseudoarthrosis, or “false joint.”1 This procedure works well in most dogs regardless of the degree of osteoarthritis in the hip joint. There are times, however, when this procedure should be avoided, especially in dogs having a great degree of disuse muscle atrophy. Because the hip joint has been removed, the muscles of the hip joint must carry the work load when the animal walks. If the muscles of the hip joint are small, recovery can be prolonged. Additionally, large or giant breeds of dogs may have a less-than-optimal response to this surgery. The larger the dog, the greater the weight that must be transmitted through the hip joint during work. Because the hip joint has been removed, the muscles of the hip may have difficulty bearing the load created by a large breed.
Total hip replacement is another treatment option for dogs with CHD. Dogs that have total hip replacements generally have an excellent prognosis for resolution of the lameness. The favorable prognosis results from the extensive amount of research that has been completed to address potential complications during and after surgery. Total hip replacements can be performed in most adult dogs that need surgery for treatment of their CHD. The procedure, however, is usually reserved for those older patients that show disability from severe osteoarthritis. The main disadvantages of total hip replacement are cost, the surgical expertise necessary to do the procedure, and the strict requirement for operating room sterility.
Canine hip dysplasia is a very common disease that affects both large and small breeds of dogs. The majority of dogs with CHD do not need to be treated for the disease. In fact, most dogs probably never have a clinical problem and may go undiagnosed. Many factors contribute to the cause of CHD and the significance of each needs to be studied closely. Dogs that are affected by CHD usually can be treated successfully without surgery, although some will require surgery to make their lives more comfortable.
1. Hauptman J: Orthopedics of the hindlimb, in Slatter D (ed): Textbook of Small Animal Surgery, Philadelphia, WB Saunders, 1985, pp 2153-2179.
2. Kealy RD, Olsson SE, Monti KL, et al: Effects of limited food consumption on the incidence of hip dysplasia in growing dogs. JAVMA 201(6):857-863, 1992.
3. Slocum B, Devine T: Pelvic osteotomy in the dog as treatment for hip dysplasia. Semin Vet Med Surg 2(2):107-116, 1987.
4. Corley EA: Role of the Orthopedic Foundation for Animals in the control of canine hip dysplasia. Vet Clin North Am Sm Anim Pract 22:579-594, 1992.
5, Heyman SJ, Smith GK, Cofone MA: Biomechanical study of the effect of coxofemoral positioning on passive hip joint laxity in dogs. JAVMA 54(2):210-215, 1993.
6. Smith GK, Biery DN, Gregor TP: New concepts of coxofemoral joint stability and the development of a clinical stress-radiographic method for quantitating hip joint laxity in the dog. JAVMA 196(1):59-70, 1990.
7. Smith GK, et al: Hip dysplasia diagnosis: A comparison of diagnostic methods and diagnosticians. Proc 19th Annual VOS Conference, Keystone, CO, p 20, 1992.
8. Smith GK, et al: Coxofemoral joint laxity from distraction radiography and its contemporaneous and prospective correlation with laxity, subjective score, and evidence of degenerative joint disease from conventional hip-extended radiograph in dogs. Am J Vet Res 54:1021-1042, 1993.
9. Lust G, et al: Joint laxity and its association with hip dysplasia in Labrador retrievers. Am J Vet Res 54:1990-1999, 1993.
10. Smith GK, McKelvie PJ: Current concepts in the diagnosis of canine hip dysplasia, in Kirk RW (ed): Current Veterinary Therapy, Philadelphia, WB Saunders, in press.
11. Popvitch CA, Smith GK, Gregor TP, Shofer FS: Factors affecting the risk of developing hip degenerative joint disease and comparison of hip dysplasia susceptibility in Rottweiler and German Shepard Dog breeds. JAVMA, in press.
12. Jessen CR, Spurrell FA: Heritability of Canine Hip dysplasia. JAVMA 162:53-60, 1973.
13. Barr ARS, Denny HR, Gibbs C: Clinical hip dysplasia in growing dogs: The long-term results of conservative management. J Small Anim Pract 28:243-252, 1987.
14. Yovich JV, Trotter GW, McIlwraith GW, Norrdin RW: Effects of polysulfated glycosaminoglycan on chemical and physical defects in equine articular cartilage. Am J Vet Res 48:(9):1407-1414, 1987.
15. Koch DA, Hazewinkel HAW, Nap RC, et al: Radiographic evaluation and comparison of plate fixation after triple pelvic osteotomy in 32 dogs with hi dysplasia. VCOT 6:9-15, 1993.
Original Doc: hip.doc
Canine Hip Dysplasia
VETERINARIAN IN ATTENDANCE
By Samuel Hodesson, D.V.M., MPH
Part I - A Review
Source: Dog News, issue unknown, pp. 42,130,134.
Abnormal hips, first described as a rare disease, became a major problem for many breeds of dogs in the 1960s. A group of competent, interested veterinarians founded the Orthopedic Foundation for Animals (OFA) and devised a plan to control the rapid spread of hip dysplasia. Members of the organization standardized x-ray techniques that received universal recognition.
In 1993 Roger C. Penwick, a veterinarian with a special interest in orthopedic surgery, addressed a meeting of Southern Arizona veterinarians. He introduced us to a new method for diagnosing and eventually eliminating hip dysplasia. The veterinarians at the University of Pennsylvania who developed the program called it the Pennsylvania Hip Improvement Program (PennHIP).
Part I will consist of a review of progress made and not made in determining cause, treatment, and elimination of Canine hip Dysplasia. Part II, scheduled for a later issue of Dog News, will shed some light on the objectives of PennHIP.
OFA believed that x-ray examination of adult dogs would help breeders pick animals with normal hips for breeding programs. They expected dogs without evidence of hip degeneration to produce puppies free of the disease.
Many theories have attempted to explain the cause of hip dysplasia but the first, and most popular one, blamed it on a genetic defect. The answer to the problem seemed obvious: find the defective dogs and bitches and don't breed them. Later studies discovered that the disease appeared most frequently in large, heavy, rapidly growing breeds.
The proponents of the hereditary theory had a logical explanation for its failure to eliminate bad hips. They blamed it on the large number of unknown, defective genes involved.
Others believed conformation contributed to the problem. The German Shepherd Dog with its sloping croup was more susceptible than the Greyhound with its heavy muscled rear quarters. These investigators believed that strong muscles, tendons, and ligaments contributed to healthy hips. Genetics also contributes to all of these qualities.
A third group blamed the problem on loose hip joints, hip laxity. Many veterinarians began to palpate the hip in growing puppies and, by calculating the degree of laxity, predict dysplasia in the adult dog. Most accept loose hips as an important contributor to the developement of osteioarthritis but is difficult to diagnose by palpation unless the condition is severe.
Others blamed hip dysplasia on environmental factors: fast growth, and strenuous growth, and strenuous exercise at too young an age. They also incriminated overfeeding growing puppies and excessive weight.
A group of endocrinologists suspected that a hormone imbalance was largely responsible. Controlled studies failed to support this theory.
Clinical signs of hip dysplasia may appear as early as four weeks but usually owners will notice them at four to six months of age. These signs vary greatly. Pain and lameness may be slight to intense. Some dogs seem quite normal until exercised. A brisk walk can cause pain and lameness in a sedentary dog.
X-rays offer the best diagnostic tool. The OFA method positions the dog with its back on the table and hind legs extended. The objective is to find evidence of arthritis caused by loose hips. For this reason OFA will not certify dogs examined under two years of age. This may not be long enough. The very mild cases may not show evidence of degeration until much later. Good results for most dogs require general anesthesia.
Radiologists classify dysplasia in three different categories: Normal, borderline, or dysplastic but haven't reached a consensus on what is acceptable for breeding. Neither do they always agree on interpretation of the x-rays.
A third problem made it difficult to determine the number of dogs with dysplasia. If the practicing veterinarian doesn't believe the x-rays will qualify, some owners will not submit them for certification. They don't want a negative report that will prevent sale of puppies or stud services.
Some recent studies show that fewer dogs have bad hips since the advent of OFA. Others find the prevalence unchanged. Statisticians can juggle interpretation of data to suit their own agenda.
Improved surgical and medical procedures permit many dogs with abnormal hips to live out their expected life span. It is practical to classify therapy as either medical or surgical.
One would expect the degree of pain and lack of function to increase as the damage to bone and cartilage increases. This isn't so. Some dogs do very well with hips showing advanced stages of arthritis. Others suffer from extreme pain with little evidence of deterioration. Most veterinarians don't treat patients unless they show clinical signs.
The American Veterinary Medical Association (AVMA) journal published an excellent review of treatments for hip dysplasia (July 15, 1992). Four veterinarians, experts on the subject, contributed. They offered the promise of improved therapy in the near future.
Treatment for dogs suffering from osteoarthritis has progressed over the years. Veterinary journals and dog magazines have published nurerous reports on the use of non-steroidal, anti- inflammatory drugs for control of painful joints. The play an important role in management of some cases of hip dysplasia but do not prevent further joint deterioration. Many still use the old standby, aspirin. Veterinarians and owners must carefully monitor dogs on any of these drugs for side effects.
Two products, Adequan and Cosequin, have received much attention. Producers claim their product promotes growth of new, healthy cartilage. Two investigators found Adequan effective in the treatment of osteoarthritis but questionable when hip dysplasia was the cause.
In later studies, scientists agreed with the earlier reports. They learned however, that when they gave Adequan to young dysplastic dogs it slowed the development of arthritis.
Independent studies on Cosequin are underway but are not yet completed. Apparently, neither of these drugs cause any side effects and we can expect to hear more abou them. Controlled exercise has helped many of my patients.
Unsupervised dogs with arthritis, after a good rest, will run and play until they become stiff and sore. The end result is increased damage to the joints. Swimming and leisurely walks with your dog provide beneficial exercise.
Both heat and cold applications claim numerous advocates. Take your pick.
R. D. Kealy, Ph.D. and a group of colleagues reported on the effects of limited food consumption on the incidence of hip dysplasia in growing dogs. (AVMA Journal, September 1992). The divided forty eight, two-month-old Labrador Retrievers into two groups and fed half the dogs all they would eat. the other half received 25% less. When the dogs were two years old the research team examined all of them for the presence of hip dysplasia.
Seven of the 24 dogs on the restricted diet showed signs of the disease in contrast to eighteeen in the conrol group. No one as yet associates nutritional quality with the disease.
Orthopedic surgeons continue to develop new procedures and improve on the extablished ones. Most agree they should spend more time on research to evaluate them. Veterinarians and/or their consultants are best qualified to determine if surgery will help. Demands made on the dog will affect the decision. A placid house pet is less likely than the hunter or agility competitor to need help. If the decision is positive, the surgeon will choose a procedure. The following paragraphs will briefly describe a few frequently used methods.
Severing the Pectineus Muscle: Veterinarians found that this simple surgical procedure reduced pain. The pectineus is a small muscle that attaches to the pelvis near the hip joint and extends to the inside of the femur near the stifle. When it contracts it pulls the stifle in. This tends to move the head of the femur out of the hip socket.
No one knows exactly why the surgery works but many veterinarians, dogs, and owners have learned that it does. It doesn't slow development of arthritis and eventually pain returns.
Total Hip Replacement: The surgeon replaces the head and neck of the femur with an artificial one. Veterinary surgeons developed the technique many years agao and physicians quickly borrowed it for humans.
Numerous improvements in the artificial hip and its application have brought wide acceptance in human and veterinary medicine. Surgeions at Ohio State University veterinary college have completed 1,700 total hip replacments with a 95% success rate. Veterinarians accept the method as superior to other types of surgery but it is also the most expensive.
Removal of the Head of the Femur: This is a comparatively simple procedure that is less expensive than hip replacement. Dr. Whitlock (AVMA Journal, July 1992) said, “Only total hip replacement or femoral head (removal) will stop the disease process.” Surgeons prefer to use the artificial hip but will remove the femoral head if the owner can’t afford hip replacement.
New diagnostic procedures promise early detection. These would allow owners to pick breeding stock from younger litters. Methods of treating hip Dysplasia have made considerable progress in the last ten years.
Assurance of finding the precise cause in the near future seems less likely. Some veterinarians believe the answers to this murky problem will take many years. Others think that one or two years of intensive research will bring the desired results. Funding for the study is not yet available.
A description of PennHIP is planned for a future issue of Dog News. Researchers at the University of Pennsylvania veterinary college believe they have developed a better way of measuring hip laxity and predicting dysplasia in offspring.
Origianal Doc: hip01.doc
Causative Factors of Canine Hip Dysplasia (Part 2)
Owners must separate fact from myth when examining theories on genetic, nutritional and environmental factors that influence CHD
By John C. Cargill, MA, MBA, MS and Susan Thorpe‑Vargas, MS
This is the second part in a series of articles on canine hip dysplasia. What follows is written from the perspectivethat the readers of the series are serious and conscientious breeders who are the guardians of the genetic pools that constitute their breeds. While this series of articles will not replace a stack of veterinary and medical texts, it is a relatively in‑depth look at the whole problem of canine hip dysplasia. Furthermore, the series is designed to be retained as a reference. When you finish reading this series you will have a sufficient background to make rational breeding choices and will be able to discuss the subject from an informed basis with your veterinariean. You may not like what you read, but you will be more competent to deal with the problem.
Conclusions from Part I(May 1995 issue): Genetics is the foremost causative factor of canine hip dysplasia. Without the genes necessary to transmit this degenerative disease, there is no disease. Hip dysplasia is not something a dog gets; it either is dysplastic or it is not. An affected animal can exhibit a wide range of phenotypes, all the way from normal to severely dysplastic and funtionally crippled. Hip dysplasia is genetically inherited.
In this article, we will address the issues of genetic, nutritional and environmental factors. We hope to debunk some of the myths and introduce some recently developed theories.
Other diseases, infections or trauma can produce clinical signs suggestive of canine hip dysplasia. In some breeds the animals learn to live with pain and are stoic about letting anyone know of their pain. This stoicism seems to be espceially prevalent in terriers and northern breeds and is the case ‑ not the exception ‑ in the fighting breeds. Those fanciers who participate in pulling, freighting, carting or sledding events with their dogs should always be aware that tendonitis or pulled muscles can cause a gait change reminiscent of hip dysplasia. Anyone involved in lure chasing or coursing for real needs to understand that on occasion, an animal will twist or turn the wrong way while in full chase. In the older dog, trauma from younger uyears may mainifest itself as arthritic deterioration. A little bit more unusual is to have viral penetration or bacterial penetration of the joint capsule with resultant damage to articular cartilage, or the epiphyseal surfaces of the femur. Absent such unusual occurrences, the reality of hip dysplasia is that it is a genetically linked condition ‑ always was, always will be.
The role of growth
In the first article we said that the first six months of a puppy's life seem to be critical time of development. The rate of growth can be astonishing. When one thinks of the number of things that could go wrong as an Akita puppy, for instance, goes form a birth weight of slightly more than 1 pound to 60 to 70 pounds in six months and then adds another 30 to 40 pounds by year end, it is amazing that most dogs mature without serious problems. It is during this period that dogs are most active. There is eveidence to suggest that exercise is necessary to retain the depth of acetabulum. How much exercise and of what type is unknown.
One Norwegian anecdotal study published in England in 1991 concluded that German Wirehaired Pointer, English Setter, Irish Setter, Gordon Setter and Labrador Retriever puppies growing up during the spring and summer had a lower incidence of hip dysplasia than puppies growing up during autumn and winter. Oddly enough, Golden Retrievers and German Shepherd Dogs did not manifest the same seasonal pattern of incidence of hip dysplasia.1
While this study may lack strict experimental protocol, it raises many questions. The first question is whether there was an exercise differential between the dogs due to weather in Norway. The second question was whether there was different availability of sunlight necessary for vitamin D production and utilization. The list of questions could go on, but this study is brought up to show that there may be exercise and diet factors at play, and that various breeds may respond to these factors in different ways. It would be reasonable to conclude that there is probably an amount of exercise during a genotypically dysplastic puppy's rapid growth period where phenotypic expression is mitigated, delayed, or both. Without taking the time, cost and effort to conduct a rigorous scientific study, it is still sometimes possible to glean valuable information from exisiting, i.e., available, data. Therefore, do not shy away from creating working hypotheses from anecdotal studies; conversely, do not lock their findings in concrete as inviolate fact.
With respect to the published scientific literature, we found nothing in Medline (an online listing of medical and biological articles) referencing any journal article addressing the subject of surfaces and their effects on the incidence of hip dysplasia. While we know of breeders who write into their sales contracts that animals must be kept on a specific surface and fed a specific feed, these demands seem to be without scientific basis.
There is some evidence that preventing rapid growth reduces the extent to which the adult dog will manifest hip dysplasia. Decreasing the dog's food consumption during its growth period seems to correlate well with normal hips.2 The Kealy study published in 1992 was based upon 48 8‑week‑old Labrador Retriever puppies. These puppies were sex‑matched littermates randomly assigned to two groups: the first group was fed ad libitum (as much as they wanted, when they wanted to eat); the second group was fed the same feed until they were 2 years old, but in amounts only 75 percent of what the first group consumed ad libitum. Thus for every puppy fed ad libitum, there was a same‑sex littermate on a restricted diet. This rigid protocol gives this study great respectability and credence. The accompanying chart gives the findings in tabular form. Note the tremendous increase in normal animals at 2 years of age when kept on a restricted diet for those two years. This ought to more than suggest that overweight animals are at risk for phenotypic expression of canine hip dysplasia.
Many researchers conclude that early fusion may lead to bone and cartilage deviations which then could predispose the animal to future dysplasia. An important point that these studies illustrate is that it is possible to improve the individual phenotype of dogs whose parents carried the gene for hip dysplasia (genotypically dysplastic).
In the fist article we alluded to joint laxity as being present whenever there is canine hip dysplasia. Given that joint laxity is at least one of the factors governing the onset of hip dysplasia, then any process that retards this condition could possibly minimize the severity of the disease. It also is conceivable that retardation of joint laxity could delay the onset of the physical appearance of the disease.
Feed for health
A recent study (1993) showed that coxofemoral joint stability was improved in dogs that were fed increased levels of chloride and decreased levels of sodium and potassium.3 In the eight‑part "Feed That Dog!" series (DOG WORLD, July 1993 through February 1994) we emphasized repeatedly the importance of the ratio of sodium and chlorine, with a ration of 1.5 sodium to chlorine being accepted as the dietary requirement.4 We noted also that "sodium chloride deficiency is manifested by fatigue, decreased utilization of protein, decreased water intake, inability to maintain water balance, retarded growth, dryness of skin and loss of hair."5 Potassium deficiency "results in poor growth, restlessness, muscular paralysis, a tendency toward dehydration, and lesions of the heart and kidney."6 We cautioned that "prednisone, a steroid commonly prescribed for various skin allergies and coat allergies, causes a loss of potassium and retention of sodium, and retention of sodium can cause further loss of potassium."7
Calcium (Ca), sodium (Na) and potassium (K) are the electrolytes considered most important, as they are necessary to many biological functions. Electrolytes are atoms or molecules that carry either a negative or a postive charge. Anions have an extra electron, and thus they carry a negative charge. Cations are missing an electron, thus they carry a positive charge. In the study cited, Kealy et. al. introduced the theory of "dietary anion gap" or DAG.8 The researchers explained DAG as the amount of chloride ion subtracted from the sum of sodium ion and potassium ions:
DAG = [ (K+ + Na+) ‑ Cl- ]
This experiment, consisting of the raising of 167 puppies, included puppies from five different breeds. They were placed on three different diets that varied only in their DAG content. Examples of low DAG ingredients are rice with a DAG of 6 and corn gluten meal with a DAG of 5. The result of this experiment showed that except for some breed‑specific exceptions, those dogs that were fed a lower DAG diet had better hips at 30 weeks than those fed a diet with a higher DAG content. Differences in DAG balance did not result in different rates of weight gain. This is important, for it allowed elimination of weight gain as a causative factor in the study. Hips were evaluated by their degree of subluxaion as measured by the Norberg angle. The Norberg angle is the "angle included between a line connecting the femoral head centers and a line from the femoral head center to the craniodorsal acetabular rim."9 The greater the Norberg angle, the less the subluxation. Norberg angles are commonly measured as <90 degrees for loose hips and >105 degrees for tight hips. Those dogs with better hips at 30 weeks also had good hips at 2 years of age.
Unfortunately, the researchers were unable to explain the mechanism or the "why" of how they got the results they did. One of the theories proposed was that a lower DAG somehow affected the pH or "acidity" of the synovial fluid. This in turn affected the osmolality or "thickness" of the synovail fluid. The osmolality of a fluid depends upon the number of dissolved particles in it, and is the measure of the osmotic pressure. In previous studies, a higher osmolality was associated with the greater synovial fluid volume found in dysplastic dogs. Note, of course, that there is a normal range of DAG values in a balanced diet. Leaving that range while formulating a dog food, for example, could cause serious problems.
The question of calcium supplementation, while controversial among breeders, is fairly easy to answer: don't do it. It is not necessary to add extra calcium to your dog's diet. Not only is calcium an essential skeletal component, it is also necessary for blood coagulation, hormonal release and muscle contraction. The three biological systems involved in controlling the amount of calcium in the blood are bones, kidneys and the intestine.
Calcium is contantly being recycled in and out of living bone. In the adult dog, under balanced conditions, both accretions (calcium uptake) and resorption (calcium loss from bone) values vary from 0.1 to 0.2 mmol per kilogram of body weight per day. [A millimole is a minute measure of molecular weight.] For the rapidly growing puppy these values are at least 100 times higher.10 Another difference between an adult dog and a puppy is their relative abilities to absorb calcium from the food they ingest. In the adult dog, the percentage of calcium assimilated from food varies from 0 to 90 percent, depending upon the composition of the food and its calcium content.11
A 1985 study, which examined the physical, biochemical and calcium metabolic changes in growing Great Danes, showed that young puppies do not have a mechanism to protect themselves against excessive calcium feeding. Under the influence of certain hormones, the calcium excess is routed to the bones. This results in severe pathological consequences for the patterning of the growing skeleton and the subsequent impairment of gait. Strongly correlated with high calcium intake is disturbed enchondral ossification (growth plate anomalies) causing the clinical appearance of radius curvus syndrome and osteochondrosis (a disturbance of bone formation within the cartilage, occurring during periods of maximum growth).12 Chronic, high calcium intake in large breed dogs has also been associated with hypercalcemia, elevation of the liver enzyme alkaline phosphatase, retardation of bone maturation, an increase in bone volume, a decrease in the number of bone resorption cells, and delayed maturation of cartilage.13 We can safely conclude that calcium plays a significant role in skeletal disease. The giant breed dogs, because of their rapid and intense growth, are sentinels for nutritionally influenced diseases. These changes, while exaggerated in the giant breeds, are just as real ‑ though they may be slower to surface and not as easily identified ‑ in the smaller breeds.
Vitamin C (L‑ascorbic acid) has frequently made it into the literature along with calcium. At one time or another vitamin C has been touted by somebody as a cureall for virtually any malady known to man and beast. This is not to discount the requirements for vitamin C, for it is absolutely necessary. Fortunately for dogs, they produce an enzyme called L‑gulonolactone oxidase, which allows them to synthesize vitamin C from glucose without having access to a dietary form of vitamin C. (A deficiency could only be the result of either a problem with absorption or an incrased need.) Interestingly, canines produce only 40 mg of ascorbate per kilogram of body weight, which is far less than other mammals with the ability to synthesize their own vitamin C. There is no established minimum daily requirement for vitamin C in canine nutrition. That said, let's look at the function of the vitamin C the dog manufactures.
Vitamin C figures prominently in the biosynthesis of collagen.14 Collagen is an important structural protein in the body. There are different types of collagen, but it is Type I collagen that appears most often in connective tissue, particularly in bone and ligaments. Vitamin C adds an ‑OH group to the two amino acids proline and lysine. Without this functional group there is a decrease in the number of cross‑links in collagen. Without this cross‑linking, the melting temperature of the protein is reduced from about 39 degrees to 23 degrees Centigrade. In other words, without the cross‑links this protein can be denatured at body temperatures.
There is experimental evidence that vitamin C may play a role in bone mineralization by stimulating bone resorption. What has been shown by one researcher to be efficacious in treating the physical manifestations of canine hip dysplasia (CHD) is a form of vitamin C called polyascorbate.15 Calcium ascorbate, used in conjunction with vitamin E, also is considered helpful in reducing the inflammatory processes that accompany the disease. In this form, vitamin C is taken up by the bone along with calcium, and this acts like a time release factor that keeps the blood plasma concentration high and the cells constantly "bathed" with vitamin C.
With all the continuing fuss about vitamin C in the fad literature, it was inevitable that it would be tried for treatment of hip dysplasia. Belfield (1976) conducted a somewhat anecdotal study on eight German Shepherd Dog litters of puppies from dysplastic parents or parents known to have produced dysplastic puppies.16 Megadoses of ascorbate were given to dams (2 to 4 grams of sodium ascorbate crystals per day) and to the pups (birth to 3 weeks‑calcium and vitamin E supplement; 3 weeks to 4 months‑500 grams ascorbate per day; 4 months to 1.5 to 2.0 years‑1 to 2 grams ascorbate per day.) Belfield claimed that none of the pups developed hip dysplasia, and breeders involved with the research were so convinced that they guaranteed dysplasia‑free puppies if the ascorbate therapy was followed by the new owner. It is significant to note that no follow‑up studies were published. While this is interesting, there is little accepted hard evidence to suggest that supplementation with ascorbate can prevent or ameliorate canine hip dysplasia. Readers are cautioned that large doses of vitamin C are not considered mainstream prophylaxis or therapy. The truth of the matter is that it is in the genes, not the diet, though diet may play a minor part.
A recent study (1993) observed that synovial fluid volume as related to osmolality correlated highly with the incidence of hip dysplasia.17 This suggested that the swelling of the joint capsule from excess fluid pressure might be forcing the femoral head out of position in the acetabulum.
Before any radiographic indications appear, there are structural changes at the tissue level of muscles, ligaments and cartilage. Cellular changes and molecular changes occur both in the joint capsule and in the synovial fluid. One study suggested that one of the first observable changes of the disease process is hypertrophy or swelling of the pectineus muscle fibers.18 This hypertrophy is thought to be a compensatory adaptation to extreme contractile tensions and may be the result of the muscle mass trying to hold the acetabulum and the femoral head in proper position.
Another study showed that the composition of the pectineus muscle was significantly different between 2‑month‑old puppes that eventually developed normal hips, and those that were dysplastic by 24 months.19 The two groups differed by the size of the muscle fibers, but this time, the dysplastic animals had smaller than normal muscle fibers (hypotrophy) and the ratio between contractile tissue and non‑contractile tissue was lower. Thus, not only did the affected animals have diminished capacity to contract their muscles, their muscles were also less elastic. This study begs the question of joint laxity: Once stretched, would the muscles tend to remain stretched, thus resulting in a looser hip joint? Unfortunately, it cannot be said with any certainty whether these differences are causal or correlative.
It is certain, however, that hip dysplasia is characterized by joint laxity.20,21,22,23,24 Whether such laxity is the result of the pathological processes involved in the disease, or whether the laxity is the cause of the disease, connot be determined. Remember, however, that loose joints and hip dysplasia are found together. We will be coming back to this point in later articles. There is a little twist to what we find: All dogs that have hip dysplasia have loose hips, but not all dogs with loose hips have hip dysplasia. It is not known which comes first: remodeling of the bony surfaces leading to abnormal wear of articular surfaces and joint instability or visa versa. It may very well be that both processes are concurrent and/or iterative processes.
Other changes that can precede either clinical signs, like pain and gait abnormalities, or radiographic evidence of hip dysplasia include thickening of the joint capsule and selling of the round ligament. Subtle and early changes in articular cartilage structure also precede clinical signs. Specifically, in affected animals, the ratio between Type A cells and Type B cells differs from the norm. Type A cells are macrophages, i.e., large mononuclear cells produced by the immune system which ingest damaged cells and blood tissue. Type B cells are fibroblasts which are precursors of connective tissue. In one study, the population of type A cells increased.25 Conceptually this makes sense, as the function of macrophages is to scavenge damaged cells, which would be the case if articular cartilage is being damaged. Note that these changes can only be observed after dissection and examination under an electron microscope. While diagnostic and predictive, such examination is without use to the clinician who is trying to diagnose the disorder. What is important to remember is that these changes are found in dogs whose X-rays showed them to be perfectly normal at the time of radiographic study. As a concerned breeder or fancier of dogs, this should alarm you. Do not be too alarmed, however, because there is hope for predictive techniques. These will be covered in later articles in this series.
The major study demonstrating the polygenic and multifactorial aspects of canine hip dysplasia is probably the 1991 German study on German Shepherd Dogs.26 Unfortunately, the article is in German and we know of no translations available. While this poses no problem for co-author Thorpe-Vargas, as she used to be at the Max Planck Institute in Germany, it is a real problem for co-author Cargill, as he has to take her word for it, supported only by Medline abstracts in English! The importance of this study is that it covered 10,595 dogs. Furthermore, this study attempted to quantify both environmental influences and genetic influences on the frequency of hip dysplasia. Models were developed using the following variables - independent random variables: age at X-raying, sex, birth year, season, litter size, percent of X-rayed dogs in each litter and sex ratio of litter; independent fixed variables: sire and dam.
Through multiple linear and non-linear regression methods it was shown that sire, dam, sex and age at X-raying all showed statistically significant influence on the occurrence of hip dysplasia. The heritability indices (H2) were - Relationship: full siblings, H2 - 0.30; maternal half-siblings, H2 = 0.48; and paternal half-siblings, H2 = 0.11.
The researchers’ caveat at the end of the study was that only the paternal half siblings’ heritability index should be accepted because kennel and breeder effects are confounded with the dam effect. Their overall conclusion was that the frequency of hip dysplasia could be reduced if selection for breeding based upon the estimation of breeding values (H2) with respect to the frequency of hip dysplasia in all relatives was implemented.
Many of the world’s militaries are good sources of information on German Shepherd Dogs. The goals of such organizations have been to improve behavioral traits and to reduce the frequency of CHD. One of the more interesting studies in the literature is the one based upon information provided by the U.S. Army’s Division of Biosensor Research on the German Shepherd Dogs bred between 1968 and 1976.27 Detailed records were available for 575 animals representing 4 years, 18 sires, 71 dams and 48 human handlers. Variance component estimates were made, which allowed estimates of the heritabilities for both temperament and CHD scores to be made. The heritability index (H2) for temperament was 0.51 and for CHS was 0.26. Interestingly, in this population the genetic correlation between good temperament and bad hips was -0.33. Given the selection process of the U.S. Army, it was not surprising to find that dogs with good temperaments also had good hips. Because of the extremely high heritability index for temperament, records of the animal being evaluated can be used for repeat breeding selection rather than the records of the progeny.
A 1993 Autrian dissertation looked at a population of 10,750 Hovawarts from 1962 to 1988, out of which CHD findings were available for 4,387 dogs.28 The goal of the idssertation was to statistically calculate two parameters. The first was a prediction coefficient based upon the CHD findings of all the ancestors of a specific animal. The second was a “taint” coefficient calculated on the basis of the CHD findings of all ancestors as well as of the individual CHD finding as well as those of any offspring already checked for CHD. The conlusions of the dissertation were that both the “rediction” and “tain” coefficients were useful in calculating the relative CHD rish of the prospective offspring when selecting breeding partners. A connection was found between the CHD findings and the inbreeding level of an animal as calculated from the “ancestor loss coefficient” and Malecot’s “coefficient de parente.” Thus, increasing levels of inbreeding increase the rish of CHD. There was no difference between males and females for risk of CHD. Detailed coverage of the various genetic coefficents is beyond the scope of this article. Readers are directed to modern comprehensive texts, idssertation abstracts and the like in genetics should more than a passing familiarity withh the intricacies of these coefficients be required.
Conclusions: While environmental effects, to include nutrition and excersise, may play a part in mitigating or delaying the onset of clinical signs and clinical symptoms, hip dysplasia remains a genetically transmitted disease. Only by rigorous genetci selection will the incidence rate be reduced. In the meantime, it makes snse to have lean puppies that are exercised regularly and to avoid breeding any animals from litters that showed signs of hip dysplasia. It is probable that even normal exercise levels may increase the phenotypic expression of CHD of a genetically predisposed dog. Stay away from calcium supplementation of any kind; all it can do is hurt. There is no conclusive evidence that vitamim C can prevent hip dysplasia, but there is some evidence that vitamin C may be useful in reducing pain and inflammation in the dysplastic dog. Let your conscience and your veterinarian be your guides in supplementing with vitamin C. Fortunately, large doses of vitamin C are readily excreted, but it is still possible to cause untoward side effects with megadoses.
The next article in the series will address the abnormal hip, to include differential diagnosis, observation, palpation, fluid sampling and sedated and unsedated radiographic studies.
1. Hanssen I. “Hip dysplasia in dogs in relation to their month of birth.” Vet Rec. 1991 May 4; 128(18):425-6.
2. Kealy R.D., Olsson S.E., Monti K.L., Lawler D.F., Biery D.N., Helms R.W., Lust G., Smith G.K. “Effects of limited food consumption on the incidence of hip dysplasia in growing dogs.” J Am Vet Med Assoc. 1992 September 15;201(6):857-63.
3. Kealy R.D., Lawler D.Fl., Monti K.L., Biery D.N., Helms R.W., Lust G., Olsson S.E., Smith G.D. “Effects of dietary electrolyte balance on subluxation of the femoral head in growing dogs.” Am J Vet Res. 1993 April:54(4):555-62.
4. Cargill J.C. “Feed That Dog! Part II.” DOG WORLD. 1993 August/75(8):12.
8. “Effects of dietary electrolyte balance” pp.555-62.
9. Smith G.K., Gregor T.P., Rhodes W.H., Biery D.N. “Coxofemoral joint laxity from distration radiography and its contemporaneous and prospective correlation with laxity, subjective score, and evidence of degenerative joint disease from conventional hip-extended radiography in dogs.” Am J Vet Res. 1993 July;54(7):1023.
10. Hedhammer A., Wu F.M., Krook L., Schryver H.F., de Lahunta A., Wahlen J.P., Kallfelz F.A., Nunez E.A., Hintz H.F., Sheffy B.E., Ryan G.D. “Overnutrition and skeletal disease. An experimental study in growing Great Dane dogs.” Cornell Veterinarian. 1974:65 suppl5:11-160.
11. Hedhammer, A., Drook L., Schryver H.F., Kallfelz F. “Calcium balance in the dog.” In “Nutrition of the Dog and Cat,” ed. Anderson R.S.; Pergamom Press, Oxford 1980:119-27.
12. Hazewinkel H.A.W. “Influence of different calcium intakes on calcium metabolism and skeletal development in young Great Danes.” PhD Thesis Utrecht State Univ. 1985.