When we diagnose hip dysplasia owners want to know why their dog has it and what it means for their dog's future.
When we diagnose hip dysplasia owners want to know why their dog has it and what it means for their dog's future. Therapeutically, we need to explain both conservative and surgical options to our clients and help them decide which is best for them. Conservative therapy is multimodal and consists of dietary modification, provision of regular moderate exercise, chondroprotectants, and judicious use of nonsteroidal anti-inflammatory drugs (NSAIDS). One of the goals of multimodal therapy is to lower the dose of NSAID required to control joint pain. Surgical options include triple pelvic osteotomy, pubic symphysiodesis, femoral head and neck ostectomy and total hip replacement. The best time to diagnose hip dysplasia is when puppies are presented for examination and vaccination. The full range of surgical options are available when dogs are young and initiating conservative management at this phase may confer more benefit than when osteoarthritis is already well established. Hip dysplasia is diagnosed by evaluating the Ortolani sign followed by radiographs. A positive Ortolani sign indicates hip dysplasia even if there is not yet evidence of osteoarthritic change or obvious subluxation on pelvic radiographs. If dogs do not have an obvious lameness, owners may not be aware of a problem. The veterinarian can inquire about certain types of behavior that indicate joint pain. Common behaviors associated with joint pain are slowness to rise, difficulty with stairs or getting into a car, increased time of inactivity, abrupt cessation of play activity and difficulty posturing to void.
Hip dysplasia results from a combination of genetic predisposition and environmental triggers. We know that dogs that have the genetic basis for hip dysplasia and undergo rapid growth are at high risk for physical symptoms of hip dysplasia. The genetic profile for hip dysplasia is polygenic and therefore unpredictable. The heritability for hip dysplasia varies widely in that heritability scores range from a high of 0.6 to a low of 0.1. A heritability score of 1.0 signifies complete genetic control of disease expression whereas a score of 0.0 signifies complete lack of genetic contribution. Because of the heritability scores, environmental influences have a significant impact on the phenotypic expression of hip dysplasia. The influence of growth rate on bone development is an active area of study. Excess intake of energy alters bone development through changes in hormones that have a powerful impact on endochondral ossification. Specifically, increased energy alters levels of growth hormone (GH), insulin-like growth factor 1 (IGF-1) and thyroid hormones (T3 and T4). High levels of GH and IGF-1 alter the normal balance of vitamin D metabolites. There is an excess of 1,25(OH)2 D3 and a deficiency of 24,25(OH)2 D3. At the growth plate level this is thought to be responsible for retarded maturation of chondrocytes. There is evidence that endochondral ossification is abnormal in dogs with hip dysplasia. Onset of mineralization of the femoral head occurred significantly later in dysplastic than in normal Labrador retriever pups in one study. In another study, 100 % of German shepherd pups that did not have radiographic evidence of femoral head ossification by 15 days of age developed hip dysplasia by one year whereas less than half of those that did have femoral head ossification by this time developed hip dysplasia. The profound impact of limited energy consumption was demonstrated in a study comparing 2 groups of 8 week old Labrador retriever pups from a dysplastic breeding line. Starting at 8 weeks of age and continuing to 2 years of age, 1 group was fed ad lib and the second group was fed 25 % less. Radiographs at 2 years showed significantly less hip dysplasia in the limit-fed dogs. Continued restriction substantially reduced the prevalence and severity of hip dysplasia at 5 years of age.
Hip joint laxity is also an essential component to hip dysplasia. It is not yet clear exactly how abnormal endochondral ossification and hip joint laxity result in hip dysplasia. Dogs that develop hip dysplasia are born with apparently normal hip joints, but after they have reached a few weeks of age, joint laxity can be demonstrated. Joint laxity is thought to be heritable. Joint laxity may occur due to an accumulation of excessive joint fluid. When the hip is in a neutral position, it is primarily stabilized by a vacuum effect. Any increase in synovial fluid can disturb the vacuum effect and allow for subluxation of the joint. The early signs of hip dysplasia in dogs include effusive synovitis and accumulation of synovial effusion and there is a close association between the volume of synovial fluid and degree of hip laxity. Subluxation induces abnormal mechanical stress on the dorsal acetabular rim which contributes to degenerative change and conformational changes.
Conservative treatment of hip dysplasia
Weight control is an important component of joint health. A dog's body condition score is judged by the ease of palpating the ribs and the presence of a waist seen from a dorsal view and an abdominal tuck from a lateral view. Clients are educated how to judge their pet's body weight. If a dog is as little as 10 to 12 % over their ideal body weight their lameness can be exacerbated. In one study on dogs with osteoarthritis, loss of 10% of their body weight over a 2 1/2 to 4 1/2 month period of time improved lameness scores significantly. Similar results were found in a weight control and walking exercise program. At the end of the study, dogs bore more weight on their affected legs as judged by force plate analysis. To induce weight loss, caloric intake is reduced by approximately 30 to 40 %. The goal is to achieve 1 to 2 % loss of body weight per week. The needed caloric intake can be calculated using the equation RER = 30 X BWkg + 70. The body weight is based on target weight. A fiber-enriched diet does improve a dog's satiety and has been shown to help reduce intake. Beagles fed a fiber-enriched diet voluntarily consumed less food than those fed a low fiber diet. Weight loss programs work best with scheduled rechecks so that volumes of food are adjusted as needed. Clients need to be advised on specific volumes of food, in terms of cups, cans, or both, that they need to feed. If necessary, therapeutic intervention (such as Slentrol) can be employed to induce weight loss.
The type of essential fatty acids (EFAs) in the diet impact joint physiology. Altering dietary EFAs can decrease the formation of arachidonic acid. Arachidonic acid is liberated from membrane phospholipids via the phospholipase enzyme, and by cycloxygenase enzymes, is converted to prostaglandins. Prostaglandins contribute to joint inflammation. Synovial fluid concentrations of PGE2 have been correlated with clinical pain in dogs. Sources of omega-3 EFAs include flaxseed oil (alpha-linoleic acid or ALA) and marine oils sources (EPA eicosapentaenoic acid, DHA docosahexanoic acid, DPA docosapentaenoic acid). Sources of omega-6 EFAs include dietary vegetable oil sources such as sunflower seed (LA linoleic acid) and animal fat sources (AA arachidonic acid). EPA can substitute in the chondrocyte cell membrane and compete with arachidonic acid for the same enzyme systems. The prostaglandins produced from EPA are less inflammatory than those synthesized from AA. It is important to use marine oils as the source of omega-3 fatty acids. There is improved incorporation into chondrocyte cell membranes with EPA. Additionally EPA was the only omega-3 fatty acid found to significantly decrease the loss of aggrecan in a canine cartilage molecule. Hills J/D and Purina J/M are both excellent commercial sources of an omega-3 enriched diet. Dogs with osteoarthritis fed Hills J/D for 90 days had improved weight bearing on force plate analysis.
Adequan is a polysulfated chondroitin administered to dogs by injection. Adequan is thought to modifiy the osteoarthritic process by preserving the matrix of joint cartilage. An important component of the matrix is aggrecan. Aggrecan consists of hyaluronic acid which forms the backbone. Proteoglycan molecules containing glycosaminoglycans (GAGs) attach to the hyaluronic acid backbone by link proteins. Aggrecan retains water and confers resiliency to joint cartilage. When Adequan was administered to puppies from a dysplastic line there was a reduced expression of hip dysplasia. When administered as a total of 8 dose to dogs with established arthritis there was a trend toward improvemet in lameness that did not reach significance. Adequan is approved by the FDA for intramuscular use but may be used off-label as a subcutaneous administration. Subcutaneous administration enables owners to be counseled how to administer the drug at home if they choose. One dosing regime is to give 4.4 mg/kg subcutaneously three times weekly for 4 weeks followed by once every 3 to 4 weeks for maintenance. Regular administration of polysulfated glycosaminoglycan along with weight control, dietary modulation and regular moderate exercise should decrease the amount of NSAID therapy required to achieve comfort.
Contemporary NSAIDs are cyclooxygenase-1 (COX-1) sparing and show proven efficacy and safety. Any NSAID may induce gastrointestinal, renal or hepatic toxicity, particularly if given outside of dosing recommendations or along with aspirin or steroids. Carprofen, deracoxib, meloxicam, firocoxib and tepoxalin have induced positive responses with regard to lameness as judged by subjective evaluation and carprofen, deracoxib and firocoxib have shown positive responses by force plate analysis. Owners should be apprised of the danger of giving aspirin, especially when treating with a COX-1 sparing NSAID, and should know to stop the medication and contact a veterinarian if they notice vomiting, diarrhea or lethargy while on the medication. If a dog is clinically lame, the NSAID is prescribed at a full dose for approximately 2 weeks and is then tapered to the lowest effective dose. An example would be to treat for 2 weeks at a full dose, 2 weeks at a half dose, then reduce to a quarter daily dose. Some dogs with mild joint discomfort only need intermittent administration after the first 4 weeks; often corresponding to days when they have the most intense exercise. After the first 4 to 6 weeks, the other therapeutic modalities should begin to exert an effect and permit a decrease in NSAID dosage. It is ineffective to prescribe a short duration of NSAID and provide no further follow up. Owners are made aware that arthritis follows a course of exacerbations and remissions. During a flare-up the NSAID should be reloaded at the full dose for 1 to 2 weeks and then tapered again. Other modes of treatment such as icing the region can also be helpful during a flare-up.
Surgical options include juvenile pubic symphysiodesis (JPS), triple pelvic osteotomy (TPO), femoral head and neck ostectomy (FHO), and total hip replacement (THR). JPS and TPO are the most desirable procedures, given appropriate case selection, because these 2 procedures allow the dog to retain their hip joint. These surgeries must be done within a limited window of time. FHO can yield satisfactory and comfortable function with postoperative rehabilitation. Total hip replacement can produce a nearly normal gait in a short period of time following surgery. There are more potential postoperative concerns with a total hip replacement than with an FHO and there is considerably more expense with THR. A benefit of THR is that even with bilateral hip dysplasia 85 % of cases become clinically sound with a THR on one side. This advantage does not occur with an FHO.
JPS is a procedure designed to arrest pubic growth and thereby promote relative overgrowth of the dorsal acetabular rim to obtain improve coverage of the femoral head. JPS is performed by approaching the pubis and removing the cranial half of the pubic symphysis with rongeurs. JPS must be performed in very young dogs, ages 15 to 20 weeks. Since dogs are rarely symptomatic for hip dysplasia at this age, the procedure is more of a prophylactic one in an at-risk dog. The Penn Hip distraction technique is an excellent diagnostic tool for case selection. Dogs with a distraction index (DI) greater than 0.3 are susceptible to development of degenerative joint disease (djd) from hip dysplasia. In one study of dysplastic dogs, only 25 % of those treated with JPS at 15 to 20 weeks of age developed DJD whereas 83 % of control dogs did. JPS is most successful when performed close to 15 weeks of age. JPS is much less invasive than TPO.
Triple pelvic osteotomy is accomplished by performing pubic, ischial and ilial osteotomies in order to rotate the acetabulum. The acetabulum is generally rotated 20, 30 or 40 degrees. Reported results with TPO are good. One study on 21 dogs showed that all dogs had improved weightbearing by force plate analysis. Degenerative joint disease did progress in all hip joints. Improvement in weight bearing occurs by 5 to 10 weeks after surgery. Another study showed that there was no correlation between the degree of preoperative DJD and postoperative DJD. Mild preoperative DJD is not a reason to exclude a dog from TPO surgery. There is a strong correlation between age and postoperative DJD. Dogs that had a TPO at 12 months of age were 7 times more likely to develop postoperative DJD than those having surgery at 6 months of age. It is ideal to diagnose hip dysplasia when puppies are 4 to 6 months old so that the best surgical outcome can be obtained. Although mild DJD is not an exclusion criteria, the quality of the Ortolani may be. In my experience, patients with a good "capture" on their Ortolani are better candidates for surgery than those with a weak shifting Ortolani.
Total hip replacement can yield excellent postoperative results. Implants are secured either with cement or by a biologic "press fit" where bony ingrowth occurs in beads on the implant. Although there is currently no comparative study on long term loosening of cemented versus press fit hips, the assumption is that very young dogs (those 12 to 18 months of age) are likelier to avoid loosening problems long term with a press fit hip. Many surgeons still have a greater degree of experience with cemented hips and newer cementing techniques produce very good results. In a recent study of cemented total hip replacement, the overall complication rate was 12 %. Luxation occurred in 7 % of cases and aseptic loosening in 2 %. Clients need to be aware of potential complications. Luxation between the femoral head and acetabular components can occur and is at highest risk within the first 40 days after surgery. If this complication occurs it is generally resolved by replacing the cup at a different angle. Infection is the worst complication to occur because it requires removal of implants. The risk of infection is extremely low. Dogs must be scrutinized for any pre-existing infection prior to surgery. Skin, ear, dental or urinary tract infections are diagnosed and treated prior to surgery.
Femoral head and neck ostectomy is a salvage procedure for hip pain. Dogs can do very well with an FHO. Good results require postoperative rehabilitation. Range of motion exercises to maintain joint extension are very important. Postoperative walking, swimming or underwater treadmill are also advised. NSAID therapy is recommended for approximately 6 weeks after FHO. In my experience it can take 6 months to have very good walking on the operated leg whereas a THR yields a faster return of function. Larger breed dogs can also do well with an FHO with postoperative rehabilitation.
Guest editorial. Food for thought on canine developmental orthopedic disease. Vet Surg 35:211-13, 2006.
Todhunter RJ et al. Onset of epiphyseal mineralization and growth plate closure in radiographically normal and dysplastic Labrador retrievers. JAVMA 210:1458-62,1997.
Madsen JS. The joint capsule and joint laxity in dogs with hip dysplasia. JAVMA 210:1463-65,1997.
Kealy RD et al. Effects of limited food consumption on the incidence of hip dysplasia in growing dogs. JAVMA 201:857-63, 1992.
Impellizeri J et al. Effect of weight reduction on clinical signs of lameness in dogs with hip osteoarthritis. JAVMA 216:1089-91, 2000.
Lust G et al. Effects of intramuscular administration of glycosaminoglycan polysulfates on signs of incipient hip dysplasia in growing pups. AJVR 53:1836-43, 1992.
Clegg DO et al. The efficacy of glucosamine and chondroitin sulfate in patients with painful knee osteoarthritis: the glucosamine/chondroitin arthritis intervention trial (GAIT). In proceedings, American College of Rheumatology Annual Scientific Meeting 2005.
Bauer JE. Responses of dogs to dietary omega-3 fatty acids. JAVMA 231:1657-61,2007.
Patricelli AJ et al. Juvenile pubic symphysiodesis in dysplastic puppies at 15 and 20 weeks of age. Vet Surg 31:435-44, 2002.
Johnson AJ et al. Triple pelvic osteotomy: Effect on limb function and progression of degenerative joint disease. JAAHA 34:260-64, 1998.
Rasmussen LM et al. Preoperative variables affecting long term outcome of triple pelvic osteotomy for treatment of naturally developing hip dysplasia in dogs. JAVMA 213:80-85, 1998.
Ota J et al. Short term loosening of the femoral component in canine total hip replacement: effects of cementing technique on cement mantle grade. Vet Surg 34:345-52,2005.