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Hip dysplasia in puppies--options and nutraceuticals (Proceedings)

Article

At birth most hips are normal. The femoral head and neck are cartilaginous and begin forming bone by endochondral ossification.

At birth most hips are normal.  The femoral head and neck are cartilaginous and begin forming bone by endochondral ossification.  Joint congruence and stability are dependent on periarticular soft tissues.  This congruency and stability is critical for normal joint development.  Disparity in the development can happen with any boney part of the joint or soft tissue including muscles, ligaments and the joint capsule.  The skeleton develops rapidly and small problems can rapidly lead to a chain reaction of disease.  If the hip joint is lax or unstable it leads to poor joint congruence which causes subluxation and further abnormal hip development.  A dog may have normal hips at birth but through genetics, nutritional or environmental factors, develops hip dysplasia (HD). 

Nutritional influences such as a high plane of nutrition or imbalance can lead to HD.  A high plane of nutrition affects growth rate and can lead to rapid bone growth and weight gain.  This can over-load the soft tissue support and has been shown to increase the frequency and severity of HD.  Studies have shown a faster than average weight gain may lead to HD, even with exercise restriction.  A dietary electrolyte imbalance may affect the synovial fluid.  A low dietary anion gap (sodium + potassium –chloride) results in less subluxation while excess may increase synovial fluid amount and joint laxity.  This may be due to surface tension and hydrostatic pressure. 

Paying special attention to “at risk” puppies during initial examination is a key component to managing these patients.  Asking pertinent questions about their normal activity, keeping them lean and on a balanced diet to avoid adverse nutritional influences are key.  In puppies that are large or giant breeds, or have known familial histories perform an Ortolani and Barden exam.  Also consider switching off puppy formulas at 6 months to slow the rate of growth.  You may also want to consider prophylactic management. 

A radiographic diagnosis of HD is more difficult in younger dogs but can be performed with various techniques.  The hip extended view is used by the Orthopedic Foundation for Animals (OFA), and the Norberg Angle.  Distraction radiography is used in the Penn HIP Program and Dorsolateral subluxation techniques.  The OFA scale does not require special equipment but identifies OA and is not a sensitive method to detect early or mild laxity. 

You can also not certify with OFA until they are 2 years of age making it a difficult screening test for puppies unless they are severely affected.  PennHIP requires certification to submit films as well as sedation or anesthesia of the patients.  You need three mandatory radiographs. The distraction index is calculated off the percent of the femoral head that is luxated out of the acetabulum.  A distraction index of greater than 0.3 is considered disease susceptible, but breed variation of measurements exist.  This modality has been shown to be statistically predictable at 16 weeks of age. 

Once you have a diagnosis or have decided for early prevention, time is one your side since you caught it early.  Medical management is 80% successful and is clinically more helpful the earlier you begin.  Weight control or reduction is the cornerstone to minimize the stress of the growing active joints.  A regulated exercise program should be utilized but not overdone.  OA disease modifying agents or nutraceuticals can be started early.  Physical rehabilitation can be tailored for a puppy and includes homework for owners that promote not only joint health but obedience and training.  NSAIDs can safely be used in puppies after 2 months if pain is an issue.  The key to conservative treatment or prevention of HD is the multimodal approach.  Controlled exercise programs should be designed for the active playful puppy. 

Consider postponing strict training until they are at least 6 months of age.  Excessive force even on normal joints can cause OA.  Agility, flyball, sporting and rescue training should be “walk through” training to get the idea and the motions without the force.  Exercise is good in moderation and will help reduce obesity as well as maintain a good range of motion.  Low impact exercise can be used liberally including swimming, walking, obedience class and leash training.  Studies have shown that even with radiographic evidence at a young age of HD, weight control and leash walking can dramatically increase the range of motion, exercise tolerance and long-term function for years. 

Nutraceuticals have been shown to be the most beneficial in offsetting OA when given before the inflammation starts, meaning preemptively when we suspect disease.  Since they have minimal if any side effects and the potential for a large impact, it is easy to prescribe them to owners who are willing.  Nutraceuticals have been called disease modifying agents, disease modifying osteoarthritic drugs, supplements, additive and vitamins.  The key to understanding the options are to realize the FDA does not regulate these products for efficacy or quality.  It is vital you find a company you like, believe in and has research to support their products and claims.  If you are using a product and not seeing results, then try a new source. 

 

Some options work better for certain cases, but generally speaking when added to a well balanced multimodal approach can make a big difference with regards to patient comfort and cartilage health.  Most contain glucosamine and chondroitin sulfate in various forms.  It is reported that they are absorbed by the GI tract, become incorporated into joint tissues, and provide the necessary precursors to maintain cartilage health and decrease inflammation.  Anecdotal reports, in vitro studies, and published clinical trials indicate that these agents are effective in treating OA.

Glucosamine is an amino-monosaccharide nutrient that has exhibited no toxicity even at high oral doses.  It is a precursor to the disaccharide unit of glycosaminoglycans, which comprise the proteoglycan ground substance of articular cartilage. Studies using radiolabeled compounds in man and animals have shown that 87% of orally administered glucosamine is absorbed.   Glucosamine acts by providing the regulatory stimulus and raw materials for synthesis of glycosaminoglycans.  Since chondrocytes obtain preformed glucosamine from the circulation (or synthesize it from glucose and amino acids), adequate glucosamine levels in the body are essential for synthesis of glycosaminoglycans in cartilage.  Glucosamine is also used directly for the production of hyaluronic acid by synoviocytes. 

In vitro biochemical and pharmacological studies indicate that the administration of glucosamine normalizes cartilage metabolism and stimulates the synthesis of proteoglycans.  In one study, glucosamine stimulated synthesis of glycosaminoglycans, proteoglycan and collagen, suggesting it not only provides raw material for their production, but may actually up-regulate synthesis.  The effects of glucosamine sulfate on human chondrocyte gene expression was also evaluated, assessing its effects on type II collagen, fibronectin and proteoglycans in normal adult chondrocytes.  Glucosamine modulated the expression of cartilage proteoglycans, decreased stromelysin mRNA levels in osteoarthritic chondrocytes, and preserved the constitutive expression of type II collagen and fibronectin in both normal and osteoarthritic chondrocytes.

Chondroitin Sulfate (CS) is a long chain polymer of a repeating disaccharide unit. It is the predominant glycosaminoglycan found in articular cartilage and can be purified from bovine, whale, and shark cartilage sources.  Bioavailability studies in rats, dogs and humans have shown 70% absorption of CS following oral administration.  Studies in rats and humans using radiolabeled CS have shown that CS does reach synovial fluid and articular cartilage.

When human articular chondrocytes were cultivated in clusters in the presence of CS, proteoglycan levels were significantly increased and collagenolytic activity was decreased. A similar study indicated that CS competitively inhibited degradative enzymes of proteoglycans in cartilage and synovium.  In a study of rabbits with chymopapain-induced stifle arthritis, proteoglycan depletion was reduced by the administration of CS.

Clinical trials in humans have also found CS to be effective in reducing the symptoms of OA. In a placebo-controlled, double-blinded study of 120 patients with OA of the knees and hips, treatment with CS resulted in significant improvements in pain-scale scores and pain-function index. In another study of 42 patients with knee OA, CS treatment significantly reduced pain and increased joint mobility. 

Bone and joint metabolism (as assessed by various biochemical markers) also stabilized in the patients treated with CS while remaining abnormal in patients receiving a placebo. Hyaluronate concentrations and viscosity were increased, and collagenolytic activity was decreased, in the synovial fluid of OA patients treated with CS for 10 days.  These clinical trials indicate that CS has a positive effect in controlling the symptoms associated with OA. Combinations of glucosamine and chondroitin sulfate are commonly used and it has been reported that these agents work synergistically. 

 

Dasuquin® (Nutramax Laboratories, Inc.) is a joint nutraceutical marketed for management of OA in dogs and cats.  It is a combination of glucosamine, chondroitin sulfate, decaffeinated tea polyphenols, and avocado/soybean unsaponifiables (ASU).  Tea polyphenols may have a positive effect on cartilage health and provide oxidative balance in the body.  ASU, which are biologically active lipids, have been shown to be more effective than chondroitin sulfate in inhibiting the expression of certain OA mediators responsible for cartilage breakdown. 

In in vitro studies, ASU has been shown to decrease the expression of COX-2 enzyme, TNF-α, IL-1β, and PGE2 in chondrocytes.  It was also shown to stimulate synthesis of cartilage matrix by increasing levels of TGF-ß.  A 2007 study found that dogs given ASU for 3 months had elevated levels of TGF-ß in their synovial fluid compared to control dogs.  The combination of ASU with glucosamine and chondroitin sulfate decreased the expression of numerous pro-inflammatory mediators, including TNF-α, IL-1β, and iNOS.  This decrease in pro-inflammatory mediators seen with Dasuquin® (Cosequin® with ASU) is greater than that seen with Cosequin® alone. In an in vivo study of the effects of Cosequin® on cartilage metabolism in dogs, serum samples were collected after treatment with Cosequin® and tested for circulating glycosaminoglycan content. 

Median serum glycosaminoglycan levels were significantly increased in treated dogs.  When normal calf cartilage segments were exposed to the serum from the treated dogs, the biosynthetic activity of chondrocytes was significantly increased and proteolytic degradation of the cartilage segments cultured in serum was reduced. In vitro studies at the Nutramax laboratories also demonstrated the beneficial effect of Dasuquin® on chondrocytes from different species incluing  equine, camelid, canine, feline and bovine.  Dasuquin®I inhibited the production of inflammatory mediators and signaling molecules in the inflammatory cascade.

Omega acid supplementation was discovered when dermatologic patients were experiencing relief from their OA.  Maintaining a high content of the long chain omega-3 fatty acids EPA, and DHA is the key with this nutraceutical.  Short chain omega-3s compete with omega-6s for conversion to long chain fatty acids and then for uptake into cell membranes.  Omega-3s and omega-6s have different effects on the inflammatory response.  Omega-6 arachidonic acid is the precursor to more pro-inflammatory mediators.  While omega-3 EPA is a precursor to less potent inflammatory mediators. 

Omega-3s are readily available from several companies for veterinary as well as human products.  Pet foods that contain them must be kept in a sealed bag for less than 30 days or they dry out.  Fish oils will also help lubricate the skin and shine the coat.  For large breed dogs I follow the human label recommendation for full grown dogs or half the dose for puppies.  If you overdose the oils, they can have soft stool or diarrhea and should decrease the dose. 

Some other options that are developing for easy oral administration include green-lipped mussel, methyl-sulfonyl-methane, duralactin and S-adenyl-L-methionine.  Less research or anecdotal evidence exists for these but is continually being developed. 

The use of joint nutraceuticals in dogs prior to the development of OA is controversial.  No controlled studies have been reported that document the efficacy of nutraceuticals in preventing the development of OA.  However, because of their reported effects on improving cartilage matrix and reducing levels of inflammatory mediators within the joint, many clinicians have advocated the prophylactic use of joint nutraceuticals, particularly in athletic and large dogs that might be susceptible to joint injury.  Additional research is needed to confirm the value of prophylactic use of joint nutraceuticals.

 

here are also surgical options to diminish the signs of OA in puppies that have HD.  The two surgical options are Juvenile Pubic Symphysiodesis (JPS) and Triple Pelvic Osteotomy (TPO).  JPS is a simple procedure performed on puppies 12 to 20 weeks of age.  But the optimal results are achieved on puppies less than 16 weeks old.  Please note that this age is before the PennHIP certification age.  The procedure fuses the pubic symphysis with electrocautery via a ventral midline incision.  There are no implants and, with proper protection of the urethra and depth to avoid the colon, very few potential side effects.  Electrocautery is used every 2-3 mm along the symphysis to cause thermal necrosis and premature closure.  The pelvis continues to grow in all other planes while being static at the pubis, resulting in ventroversion of the acetabulum. 

This procedure is not readily detectable on OFA and PennHIP films and should therefore only be performed on animals that will be sterilized to avoid certifying or breeding falsely represented hip conformation. The TPO is typically performed on dogs less than 10-12 months of age without radiographic signs of OA.  It is used to correct hip laxity.  Three osteotomies are made on the pubis, ischium and ilium to allow reorientation of the acetabulum.  Then an angled plate is placed on the ilium to secure the weight bearing axis for boney healing.  The forced manual ventroversion increases dorsal coverage of the femoral head and reduces the formation of OA by improving joint stability and congruence.  However bilateral surgery is not performed due to high complication rates and surgeries should be staged at least 4 weeks apart.  

Potential complications include a narrowed pelvic canal, sciatic neuropraxia, implant failure and an abnormal gait.  Lameness improves in 92% of dogs and the progression of OA appears to be slowed with this procedure.  The JPS and TPO procedures have similar effects on hip conformation, although neither eliminate laxity or completely cure HD.  They can arrest or limit the progression of HD in mild to moderate cases.  Both of these preventative surgeries require early puppy screening and counseling of owners about potential benefits and expected outcomes. 

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