10 Signs of Hip Dysplasia in Dogs

You notice that over the last few months your dog, has been more reluctant to go out and play, and is having a more difficult time getting up, jumping, running, or climbing stairs.  This article will cover the 10 signs of hip dysplasia in dogs and the causes.

Dog Hip Joints and the Function of:

Your dog’s hip joints are under a lot of pressure as they run, jump, walk, and play.

It bears most of the load from their upper body weight when they launch themselves into motion and move about.

What Causes Dog Hip Dysplasia?

When the ball and socket of the hip joints haven’t grown in equal amounts, the joint wears prematurely and causes pain that can eventually make it difficult for them to move.

This is an inherited condition called hip dysplasia.

This is a chronic hip ailment that affects dogs of all ages.

Most pet owners think about hip problems, they imagine big, mature dogs struggling to get out of their beds.

This is not always the case—even young dogs full of energy can be diagnosed with the disease.

While dog hip dysplasia is most common in large-breed adult dogs, it can also affect small and medium breeds and puppies as young as five months old.

Canine or Dog Hip Dysplasia (CHD) is a condition that begins in dogs as they grow and results in instability or a loose fit (laxity) of the hip joint.

The hip joint laxity is responsible for potential clinical signs and symptoms of hip pain and limb dysfunction and progressive joint changes.

The hip joint is a ball and socket joint and continual abnormal movement of the femoral head (ball) deforms the acetabulum (socket).

The Long-Term Effect of Hip Dysplasia In Dogs

The long-term response to this joint laxity is the progressive loss of cartilage, the development of scar tissue around the joint, and the formation of osteophytes (bone spurs) around the ball and socket.

The cause of CHD is multifactorial (multiple causes); however, hereditary (genetics) is the biggest single risk factor.

Rapid weight gain and growth through excessive nutritional intake can complicate the development of CHD.

Joint changes characteristic of CHD are also associated with environmental factors such as nutrition,1–2 exercise,3 and the process of skeletal ossification.4,5

The condition affects essentially all breeds, with an estimated prevalence ranging from 1% to 80% according to the Orthopedic Foundation for Animals.

It appears to occur at a relatively high rate in large-bodied and brachycephalic (“short-headed.” Common examples of brachycephalic dog breeds include the English bulldog, French bulldog, Pug, Pekingese, and Boston terrier) dogs as well as those with high body length to height ratios.6,7

The periodic appearance of OA in joints other than the coxofemoral  (hip joint, which is a ball (femoral head) and socket (acetabulum)) joint8, 9 has led some to propose systemic contributions to CHD expression.10

These complexities, among others, complicate attempts to manage the CHD by selective breeding despite strict reporting and guidelines.

There are many theories to explain CHD joint degeneration, but joint laxity and irregular or delayed endochondral ( occurring within cartilage.) ossification are among the most popular.

The conditions are not mutually exclusive, and their phenotypic expression is variable within and among breeds.11 Partially ossified hip structures may become distorted during development due to mechanical stresses in joints with delayed endochondral ossification.12, 13

Joint components may be more vulnerable to deformation and damage from normal joint kinetics before they are fully ossified.12, 13, 14

Abnormal and delayed endochondral ossification in the coxofemoral joint has been identified in 15-day-old dogs that developed CHD by the time they were 12 months old,12,13 15 and in Great Danes with experimentally induced hip dysplasia.16

In contrast, comparably earlier joint ossification appears to occur in Greyhounds, a breed with one of the lowest incidences of CHD. While it is clear that variation in the process of endochondral ossification may play a role in the development of CHD, the exact relationships between ossification patterns, abnormal joint structure, and development of OA remain unclear.17

Affected joints usually develop varying degrees of synovial inflammation, articular cartilage damage  osteophytes,(bone spurs) and subchondral (the layer of bone just below the cartilage in a joint) bone sclerosis and remodeling.18-20

While there is no single, overarching description of the sequence of events in the process, there are changes that occur in many forms of dysplasia.

Recently, the dorsal acetabular rim angle (a measure of the dorsal slope [angle] of the subchondral articular acetabular surface relative to horizontal) was reported to be significantly larger (less femoral head coverage by the acetabulum) in dogs with coxofemoral joint laxity versus normal dogs as early as 1 week of age.14

Subluxation of the femoral head and delays in ossification of the craniodorsal acetabular margin are often visible by 8 weeks, and, in many cases, subluxation of the femoral head increases by around 12 weeks of age.15

Degeneration and microfractures of the articular cartilage, and thickening, inflammation, and deterioration of the joint capsule, tendinous insertions, and ligaments are often apparent by 5 months of age.15 Despite the presence of these degenerative traits in many dogs with degenerative coxofemoral joint changes, clinical signs are variable.15

A direct relationship between joint capsular collagen composition and mechanical properties was proposed over 30 years ago.21

Altered capsular collagen composition has been identified in children with congenitally dislocated hips22 and dogs with hip joint laxity.23

Joint capsular collagen fibrils were found to be more heterogeneous in 8-month-old Labrador Retriever puppies with severe coxofemoral (coxofemoral luxation is where the femoral head or ball is displaced)  joint laxity than those with normal joints.11

Abnormal collagen composition is thought to contribute to reduced joint capsule stiffness, which contributes to excess femoral head motion and abnormal mechanical stresses on the femoral greater trochanter (trochanter is a tubercle of the femur near its joint with the hip bone where the muscle attaches) and acetabular margins and cartilage.11

Over time, the abnormal forces are thought to result in deformation of the articulating structures and an incongruous joint.14.

10 Signs of Hip Dysplasia in Dogs

These symptoms may vary depending on the severity of the disease, the level of inflammation, the degree of looseness in the joint, and how long the dog has suffered from hip dysplasia.

Some dogs begin to show signs of hip dysplasia when they are as young as 8 weeks of age. Others develop it in conjunction with osteoarthritis as they age.

  • Decreased activity
  • Decreased range of motion
  • Difficulty or reluctance rising, jumping, running, or climbing stairs
  • Lameness in the hind end
  • Swaying, “bunny hopping” gait
  • Grating in the joint during movement
  • A decrease in thigh muscle mass
  • Noticeable enlargement of the shoulder muscles as they compensate for the hind end
  • Pain
  • Stiffness or limping

Treating Hip Dysplasia in Dogs

There are quite a few treatment options for hip dysplasia in dogs, ranging from lifestyle modifications to surgery.

If your dog’s hip dysplasia is not severe, or if your dog is not a candidate for surgery for medical or financial reasons, your veterinarian may recommend a nonsurgical approach. Depending on the severity of your dog’s hip dysplasia, the vet may suggest the following:

  • Weight reduction to take stress off of the hips
  • Exercise restriction, especially on hard surfaces
  • Physical therapy
  • Bone Broth
  • Anti-inflammatory medications (nonsteroidal anti-inflammatory drugs, corticosteroids)
  • Joint fluid modifiers, Type II Collagen Rich Bone broth, Glucosamine

If your dog is a good candidate for surgery, there are more options.

While there are  a few different surgical options, the most common surgeries veterinarians use to treat hip dysplasia in dogs are:

  • Double or triple pelvic osteotomy (DPO/TPO)
  • Femoral head ostectomy (FHO)
  • Total hip replacement (THR)

DPO/TPO

DPO/TPO surgery is usually performed in young dogs less than 10 months old. In this surgery, the function of the ball and socket joint is improved by selectively cutting the pelvic bone and rotating the segments.

Double or Triple Pelvic Osteotomy (DPO/TPO) is an option for young dogs (ideally less than 8–10 months old) with CHD but no visible radiographic arthritic changes. These surgical procedures involve cutting the pelvic bone in two (DPO) to three places (TPO) and rotating the segments to improve coverage of the ball by the socket and decrease hip laxity. 

TPO has been used successfully in dogsfor decades. Recent advancements in implant (locking plates and screws) technology now allow similar results with only two cuts made in the bone (DPO), thus a less invasive procedure.

The best time to recognize pathologic hip laxity is when the young dog is neutered (spayed or castrated) between 6–8 months old. 

This can often be done by the primary care veterinarian who does the sterilization procedure.

An x-ray must be taken and the hips can be palpated for joint laxity. Young dogs with lameness and early evidence of hip arthritis are not ideal candidates for DPO/TPO, nor are dogs with very severe hip laxity, as some puppies have no functional hip joint by 6 months of age.

THR

The most effective surgical treatment for hip dysplasia in dogs is a total hip replacement. The surgeon replaces the entire joint with metal and plastic implants. This returns hip function to a more normal range and eliminating most of the discomfort associated with hip dysplasia.

THR can be used in young dogs who cannot be successfully treated with JPS or DPO/TPO surgeries.

They must be managed medically until they are mature enough for THR, at least a year old. THR, based on evidence based medicine via multiple peer reviewed publications is the second surgical method that provides the most normal pain free function in dogs with CHD.

This surgical procedure eliminates hip pain by reproducing the mechanics of a normal hip joint with a more natural range of motion and limb function.

As with humans, canine THR involves replacement of both the ball and socket with metal and polyethylene (plastic) implants.

These components are fixated in place with bone cement, metal pegs, or “press fit” (bone ingrowth) methods.

FHO

FHO surgery can be performed on young and mature dogs. The surgery involves cutting off the femoral head, or “ball,” of the hip joint.

This results in the body creating a “false” joint that reduces the discomfort associated with hip dysplasia. While FHO does not recreate normal hip function, it can be a successful pain management strategy.

The last surgical option to alleviate the pain secondary to severe hip laxity/dysplasia is femoral head ostectomy (FHO) surgery.

This surgical procedure can be done at any age and can provide enough comfort in a dog weighing less than 60–70 lbs to avoid the daily use of anti-inflammatory pain medication, thus avoiding costs and side effects that limit or negate its use. 

Young dogs that do not meet the criteria for DPO/TPO or JPS procedures, or dogs who do not respond satisfactorily to medical treatment alone may benefit from FHO. 

This technique involves removing the femoral portion of the hip joint (i.e., the ball) to reduce the pain produced by abnormal hip joint contact that wears away the joint cartilage, and the stretching of the soft tissues around the joint due to laxity.

Following an FHO, a “false joint” develops with the muscles around the hip now transferring the forces from the leg to the pelvis during limb movement.

The goal of an FHO is to relieve the pain associated with CHD, not to maintain/recreate normal hip function. 

Two weeks following FHO surgery the puppy/adult dog is encouraged to exercise, often receiving anti-inflammatory drugs daily during the initial 1–2 months post-op. Then these drugs may only be necessary intermittently.

FHO dogs must remain slim throughout their lives and follow a limited exercise program i.e. leash walks and confinement to the yard and house. 

They cannot be athletic dogs who hunt, do agility, high level obedience, run with their owners, etc. If those activities are what the owner wishes to do with their dog, then a THR would be necessary.

Medical Management of Hip Dysplasia

    • Maintenance of minimal body weight.
    • Limited exercise routine i.e. leash walks of a length the dog tolerates comfortably. 
    • Daily or intermittent (a better option if it can be done effectively) use of non-steroidal anti-inflammatory drugs (NSAIDs).
        • These drugs can be very effective in relieving pain. However, NSAIDs can have significant side effects that if used daily must be monitored with blood tests to avoid kidney and liver damage.
        • The monitoring interval depends on the age of the dog and the dosage level of the drug. Ideally the lowest daily dose that provides obvious comfort should be used for long term therapy.
        • If the maximum daily dose is required, the risk of side effects is greater and the cost of the drug and monitoring can exceed the cost of surgical intervention if the dog is young or middle aged. 
        • Cartilage protective supplements are often recommended, Type II Collagen or Native (undenatured) type II collagen works via an immune-mediated process, known as oral tolerance.
          • Through this mode of action native type II collagen is recognized by the immune system as an endogenous substance, i.e. naturally occurring in the body, and deactivates the body ’s immune response against its own collagen.
            • Native (undenatured) type II collagen form is required at doses
              Type II Undenatured collagen and treating hip dysplasia in dogs
              as low as 10 mg/day for dogs. Clinical studies show that supplementing native (undenatured) type II collagen can help to modulate the immune response against endogenous type II collagen, therefore, reducing joint inflammation and cartilage degradation.
            • Even at the smaller dosages, undenatured Type II Collagen has also been reported to be more effective than the glucosamine and chondroitin sulfate supplements.
            • Thanks to this specific mechanism of action, it takes just a small amount of native type II collagen to support joint health.
            • The enriched Active Dawg chicken bone broth has had positive results in several clinical studies, which include reducing COX-2, (without impacting COX-1) and reducing protein kinase A (PKA) inflammation markers, as well as increasing probiotic organisms like Lactobacillus. This special enriched chicken bone broth has more chondroitin and collagen than other bone broths and is naturally rich in electrolytes.
              • Cox-1 inhibitors can reduce inflammation, but they may also decrease the natural protective mucus lining of the stomach.

          Mechanism of Action of Type II Undenatured Collagen

            • Native (undenatured) type II collagen passes through the stomach and reaches the intestine.
            • It interacts with the Peyer’s patches in the intestine, which are lymphoid nodules responsible for immune surveillance of the intestinal tract.
            • It turns off the immune response against endogenous type II collagen
            • It reduces joint inflammation and cartilage degradation, supporting joint health
          • Physical therapy can be helpful in dogs who lead a very sedentary life style because the owners work long hours. The dog, like ourselves, become stiff if they do not move around frequently. Joint movement and muscle strength help keep them comfortable and more mobile. Physical therapy is also used for dogs undergoing surgery for CHD. This helps strengthen the muscles and increases the speed of recovery.

        Prognosis For Dogs With Hip Dysplasia

        Dogs with hip dysplasia often lead long, full lives, especially with treatment. If you think that your dog may be affected, talk to your veterinarian. Treatment options and lifestyle changes you can make to keep your dog comfortable well into old age.

         

        References:

        1. Impellizeri JA, Tetrick MA, Muir P. Effect of weight reduction on clinical signs of lameness in dogs with hip osteoarthritis. J Am Vet Med Assoc. 2001;216:1089–109

        2. Kealy RD, Lawler DF, Ballam JM, et al. Evaluation of the effect of limited food consumption on radiographic evidence of osteoarthritis in dogs. J Am Vet Med Assoc. 2000;217:1678–1680.

        3. Greene LM, Marcellin-Little DJ, Lascelles BD. Associations among exercise duration, lameness severity, and hip joint range of motion in Labrador retrievers with hip dysplasia. J Am Vet Med Assoc. 2013;242: 1528–1533.

        4. Madsen JS, Reimann I, Svalastoga E. Delayed ossification of the femoral head in dogs with hip dysplasia. J Small Anim Pract. 1991;32: 351–354.

        5. Todhunter RJ, Zachos TA, Gilbert RO, et al. Onset of epiphyseal mineralization and growth plate closure in radiographically normal and dysplastic Labrador retrievers. J Am Vet Med Assoc. 1997;210: 1458–1462.

        6. The Orthopedic Foundation for Animals [webpage on the Internet]. The OFA’s Hip Radiograph Procedures. Available from: http://www.offa.org/hd_procedures.html. Accessed January 10, 2015.

        7. Roberts T, McGreevy PD. Selection for breed-specific long-bodied phenotypes is associated with increased expression of canine hip dysplasia. Vet J. 2010;183:266–272.

        8. Farquhar T, Bertram J, Todhunter RJ, Burton-Warster N, Lust G. Variations in composition of cartilage from shoulder joints of young dogs at risk for developing canine hip dysplasia. J Am Vet Med Assoc. 1997;210:1483–1485.

        9. Olsewski JM, Lust G, Rendano VT, Summers BA. Degenerative joint disease: multiple joint involvement in young and mature dogs. Am J Vet Res. 1983;44:1300–1308.

        10. Lust G. An overview of the pathogenesis of canine hip dysplasia. J Am Vet Med Assoc. 1997;210:1443–1445.

        11. Todhunter RJ, Lust G. Hip dysplasia: pathogenesis. In: Slatter ED, editor. Textbook of Small Animal Surgery. Philadelphia, PA, USA: Saunders; 2003.

        12. Madsen JS, Reimann I, Svalastoga E. Delayed ossification of the femoral head in dogs with hip dysplasia. J Small Anim Pract. 1991;32: 351–354.

        13. Vanden Berg-Foels WS, Todhunter RJ, Schwager SJ, Reeves AP. Effect of early postnatal body weight on femoral head ossification onset and hip osteoarthritis in a canine model of developmental dysplasia of the hip. Pediatr Res. 2006;60:549–554.

        14. Fujiki M, Kurima Y, Yamanokuchi K, Misumi K, Sakamoto H. Computed tomographic evaluation of growth-related changes in the hip joints of young dogs. Am J Vet Res. 2007;68:730–734

        15. Riser WH. The dysplastic hip joint: radiologic and histologic development. Vet Pathol. 1975;12:279–305.

        16. Wu FM, Hedhammar å, Krook L. Overnutrition and skeletal disease. An experimental study in growing Great Dane dogs. IX. The long bones. Cornell Vet. 1974;64:83–114.

        17. Chalmers HJ, Dykes NL, Lust G, et al. Assessment of bone mineral density of the femoral head in dogs with early osteoarthritis. Am J Vet Res. 2006;67:796–800.

        18. Barr ARS, Benny HR, Gibbs C. Clinical hip dysplasia in growing dogs: the long-term results of conservative management. J Small Anim Pract. 1987;28:243–252.

        19. Bijlsma JW, Berenbaum F, Lafeber FP. Osteoarthritis: an update with relevance for clinical practice. Lancet. 2011;377:2115–2126

        20. Buckwalter JA, Martin JA. Osteoarthritis. Adv Drug Deliv Rev. 2006;58: 150–167

        21. Grant ME, Prockop DJ. The biosynthesis of collagen. N Engl J Med. 1972;286:194–199

        22. Skirving AP, Sims TJ, Bailey AJ. Congenital dislocation of the hip: a possible inborn error of collagen metabolism. J Inherit Metab Dis. 1984;7:27–31.

        23, Madsen JS. The joint capsule and joint laxity in dogs with hip dysplasia. J Am Vet Med Assoc. 1997;210:1463–1465

         

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