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

At birth the 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 congruence 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).

A presumptive diagnosis of HD can often be made based on clinical signs or physical examination. Palpating for crepitus, a luxated hip or performing the Ortolani and Barden maneuvers can all help make a correct diagnosis of HD. A radiographic diagnosis of HD is more easily made in older dogs. 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 yet is not a sensitive method to detect early or mild laxity. 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.

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 diseased joints. A regulated exercise program should be utilized but not overdone. OA disease modifying agents or nutraceuticals can be started early. The key to conservative treatment of HD is the multimodal approach. Excessive force even on normal joints can cause OA. Exercise is good in moderation and will help reduce obesity as well as maintain a good range of motion and comfort.

Weight loss is the easiest and perhaps most beneficial part of a multimodal approach to OA. Minimizing the work the diseased joints have to contend with should be paramount to any regime. Dogs with OA should be kept on the thin side of normal. With proper weight management, many dogs are able to stop taking pain medications until much later in the disease process. Commercially available diets are geared towards weight loss as well as joint comfort. Diets should be low calorie and low in protein while providing an otherwise balanced nutritional plane. Having truthful conversations about treats and table scraps should be geared to reveal honest habits. Caloric responsibility should be encouraged and adjustments made to account for the dogs’ favorite treats or foods.

Exercise is also important to maintain a good range of motion and weight level. Minimizing concussive forces like stairs, jumping, climbing, running, and horse play should be minimized while still maintaining a good quality of life. Encourage leash walks, swimming and pay close attention to what activities make them sorer afterwards. While we don’t want to lock our patients in a box or take away their quality of life, easing their burden is important for their joints. If they love to play fetch on the weekends, make their owners aware that that will be a painful time and they should premedicate or otherwise adjust the protocol for their pet. Having thick warm bedding should also be encouraged to help aching joints. If an overweight animal prefers the hard, cold floor, suggest placing a fan near the orthopedic bed to encourage usage.

NSAIDs are readily available and widely used for OA in dogs. The important thing is to find a drug that works well for each patient and to make the owners aware of potential side effects. If one stops working for a patient, try switching to a different one. When switching NSAIDs, a wash out period of at least two half lives is recommended. NSAIDs can be used for painful flair ups, around times of increased activity, or later in the disease, for daily maintenance pain relief. For patients with NSAID sensitivities or for patients needing additional pain medication there are other options as well.

Tramadol is a synthetic mu opiod with a wide safety margin. It can be given several times a day which make it ideal for use around exercise or physical rehabilitation periods. I typically use 5 mg/kg up to 4 times daily. Gabapentin is a GABA analogue design to treat epilepsy but is widely used for neuropathic pain and OA in people. The most common side effect appears to be sedation. An accepted canine dose is 5-10 mg/kg 2-3 times daily. Acetaminophen with codeine is an additional option for OA management. Due to the limited pill size it is often times easier to dose than tramadol in larger patients. Since it is not considered a COX1 or COX2 drug, side effects should be minimal when used concurrently with NSAIDs, but should still be considered. This drug is dosed off the codeine at 1-2 mg/kg three times daily.

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, additives 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 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 including equine, camelid, canine, feline and bovine. Dasuquin® 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 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.

Adequan (Luitpold Pharmaceuticals) is a polysulfated glycosaminoglycan (PSGAG). This agent has been used to treat OA for many years and is approved for use in horses and dogs. Studies have shown that injected Adequan® does reach therapeutic levels in serum, synovial fluid, cartilage and tendons. Though experimental evidence of Adequan®’s positive anabolic effect on cartilage is conflicting, its ability to decrease cartilage catabolism has been shown in numerous studies on both horses and dogs. These findings suggest Adequan® may be useful if administered early in the disease process.

Other studies evaluating the effect of PSGAGs on joint health after transection of the cranial cruciate ligament in dogs have been equivocal. Treatment did not preserve cartilage biochemical and biomechanical properties in one study, but did improve joint health in another. In dogs, a dosage of 5mg/kg IM twice weekly is commonly recommended.

HA (hyaluronic acid, sodium hyaluronate) is a non-sulfated GAG that is a major component of synovial fluid. HA is thought to enhance joint health by increasing the viscosity of the joint fluid, reducing inflammation, and scavenging free radicals. In a research study of HA used to treat dogs with transected cranial cruciate ligaments, a positive effect on cartilage biochemical parameters was noted. Based on experience and scientific evidence from its use in humans and in horses, HA may be beneficial in treating OA in dogs.

If medical management is not a option or is not working for your patient, there are two salvage procedures; Total Hip Arthroplasty (THA) and Femoral head and neck ostectomy (FHO). THA is indicated for large and giant breed dogs but is available in sizes for small dogs and cats. Unilateral replacement is adequate for 80% of dogs. The procedure is technically challenging and expensive. There are cemented and cementless systems with templates and modular designs for a custom fit. The prognosis for a pain-free function is 95% having a good to excellent outcome.

Potential complications include infection, luxation, fracture, sciatic neuropraxia or implant loosening. FHO is used to preserve limb function in severe OA when medical management is ineffective or when a THA has unrepairable complications. It is typically performed in small dogs and cats but can be used for larger dogs when THA is not feasible. It is less expensive and easier to perform than a THA. The prognosis is good in smaller patients but much better if muscle atrophy is not severe. Postoperative physical therapy is important to achieve a flexible pseudoarthrosis.


By Jennifer L. Wardlaw, DVM, MS, DACVS