As a child, I was brought up in a family of dog breeders – German shepherds to be specific – so I grew up with canine hip dysplasia. During the 1970s, breeders keen to reduce the prevalence of hip dysplasia in their breed submitted radiographs to be read by a specialist panel in a pass/breeder’s letter/fail scheme.

In 1984, the BVA, in association with The Kennel Club (KC), instituted the BVA/KC hip dysplasia scoring scheme which is still going today (BVA, 2024).

My mother read a lot and thought she knew all about the condition. She believed  she was doing the best thing for her dogs by:

• Only buying-in and breeding from dogs with low hip scores.
• Providing puppies with reconstituted cow’s milk – because it was high in calcium, so good for bone development.
• Providing puppies with bone meal supplement – because it was high in calcium, so good for bone development.
• Feeding bitches with a complete food – came in frozen blocks of cereal and meat, analysis not known.
• Encouraging pups to play roughly and exercise vigorously from an early age.

Despite her best efforts, the puppies she raised had poor hip scores and some developed skeletal disease, including osteochondritis dissecans of the shoulder. We now know that high calcium intake during growth can result in impaired endochondral ossification and developmental skeletal diseases, including osteochondrosis and premature growth plate closure resulting in angular deformities (Hazewinkel et al, 1991; Schoenmakers et al, 2000).

We also know that vigorous exercise can stretch soft tissue structures supporting the hip, increasing the risk of joint laxity and subluxation of the femoral head.

Several early studies showed an improvement in hip scores by selective breeding using only animals with very low scores. For example, in one study of 584 German shepherds over a 3.5-year period (Riser et al, 1964) the incidence of hip dysplasia in a closed group was reduced from 39% to less than 17%.

However, after decades of screening, hip dysplasia remains a major problem in the UK canine population.

The success of UK and similar hip dysplasia breeding schemes at reducing hip scores has been shown to be very variable (Wilson, 2011) and, in my opinion, with few examples, disappointing, bordering on ineffective.

According to the BVA Canine Health Schemes website, the Hip Dysplasia Scheme Breed Specific Statistics 2022 show that German shepherds have 15-year mean/median scores of 14 and 11 respectively; and 5-year mean, minimum, maximum, and median scores of 11, 0, 104, and 11, so there has been no improvement in median score over that time period.

Unfortunately, we know that many vets and breeders do not submit radiographs from dogs with obvious poor hips on the radiographs, so the true mean and median scores are likely to be much higher.

Based on the data collected by the KC about dogs in the same pedigree line, they provide breeders with an “estimated breeding value (EBV)” to help decision-making about breeding from a specific dog. I have never seen a paper on the efficacy of this practice.

In recent decades, developments in managing hip dysplasia have centred on new, more invasive surgical procedures to correct the problem or relieve pain, including joint capsule denervation, pectineal myotomy, triple pelvic osteotomy, pubic fusion, dorsal acetabulum reinforcement and total hip replacement.

Some of these procedures are very expensive for owners and not without potentially serious consequences.

This is ironic as we know so much about the condition that we should really be focusing on prevention – not correction.

Back to basic principles

Embryological development of the hip joint

A comprehensive review of hip development has been described (Weber and Ritting, 2024). During embryological development cartilage, connective tissue, striated muscle and bone as well as blood vessels originate from the mesoderm. The bones that form the articulating hip joint start as a group of chondroblasts forming a cartilage model of the femoral diaphysis. At this stage, pre-cartilage at the future site of the femoral head is indistinguishable from the future acetabulum.

An interzone appears, with the acetabulum as a shallow depression proximally and distally, the femoral head and the overlying articular cartilage. Autolytic degeneration occurs by programmed cell death in this interzone to separate the two structures and form the actual joint space. This is the first time the hip joint could theoretically be “dislocated.”

The hip is well protected from dislocating in all directions, except for inferiorly, because the transverse acetabular ligament is poorly defined. The beginnings of synovial tissue and the ligamentum teres (round ligament) are found at this time in the middle layer of the interzone.

A snug fit between the spherical femoral head in the acetabulum is crucial for postnatal development of a congruent hip joint under Wolff’s Law. The primary disturbance in hip dysplasia is loss of femoral head congruency within the acetabulum, resulting in abnormal development of the femoral head and acetabular concavity.

In humans, as many as 95% of cases of subluxation or frank hip dislocation can be successfully treated with conservative abduction devices such as the Pavlik harness. However, intra-articular pathology like acetabular cartilage hypertrophy or accessory centres of ossification may develop concurrently.

In young puppies, the earliest dysplastic joint changes are oedema of the round ligament attached to the femoral head  with torn fibres and capillary haemorrhage at the tearing sites (Smith et al, 2024), increased ligament volume and synovial fluid volume. In one study, ligament volume was significantly greater in puppies displaying overt osteoarthritis and in puppies at high risk for osteoarthritis based on parental phenotype. Another study showed that Labrador retrievers at high risk for osteoarthritis (as determined by a high distraction index) had oedema of the ligament and cartilage in the femoral head.

In the first two weeks of life the round ligament seems primarily responsible for maintaining hip joint stability as, if forced to luxate, the femoral head fractures at the fovea (attachment of the ligament). After two weeks of age, the ligament begins to lengthen, and in dysplastic dogs excessive lengthening permits lateral subluxation of the hip joint.

So, the round ligament is an important stabiliser of the hip, and with the capsular ligaments prevent subluxation of the femoral head at the extremes of motion (O’Donnell et al, 2018).

Radiographic signs of canine hip dysplasia, femoral head subluxation and under-development of the cranial acetabular rim are present by seven weeks. From 60 to 90 days of age, the degree of subluxation increases and significant radiographic changes are evident. Articular cartilage is worn and roughened on the dorsal surface of the femoral head at its point of contact with the acetabular rim. Evidence of palpable or radiographic laxity appears prior to degenerative structural changes.

Osteophyte development

Osteophyte formation occurs at locations where forces elevate the periosteum. Excessive biomechanical forces do this, such as jarring during movement due to soft tissue laxity in the joint.

Ligaments should be flexible enough to move, but firm enough to provide support. Signs of ligament laxity are sometimes indistinguishable from those associated with osteoarthritis:

• Pain, numbness or tingling.
• Muscle spasms.
• Frequent injuries -strains/sprains.
• Joint dislocation.
• Increased range of motion (hypermobility)
• Joints that click or crack (crepitus)

More research is required to determine the relationships between nutrition, ligament laxity and hip dysplasia.

As mentioned, copper is important for normal soft tissue development and we know that deficiency is associated with hyperextension of the phalanges in puppies, also we see magnesium deficiency-related hyperextension of carpal joints. The role of these in hip instability has yet to be investigated.

Degenerative joint disease

The intra-articular inflammation and degeneration that results from the osteoarthritis secondary to dysplasia are progressive, destroy articular cartilage resulting in crepitus, reduced range of movement and pain.

Canine hip dysplasia

Hip dysplasia is a multifactorial, moderately heritable disease in certain dog breeds. Gene expression can result in increased prevalence because of influence on conformation that encourages inappropriate biomechanical forces through the hips, abnormal endochondral ossification or increased laxity of soft tissues surrounding the hip. In large breed dogs, rapid growth, increased size and weight gain may cause excessive biomechanical forces on the joint and surrounding soft tissues.

If we consider what we know about hip dysplasia we can surmise that we should be able to prevent it – even in breeds predisposed to develop the condition. So, what do we know?

• Hip dysplasia can be defined as: a condition affecting the hip joint where the femoral head is not fully covered by the acetabulum, or subluxation of femoral head.
• Puppies are not born with hip dysplasia – they have a cartilaginous skeleton, and the dysplasia develops subsequently due to hip malformation and increased joint laxity.
• If there is not a tight fit of the femoral head within the acetabulum, excessive movement and subluxation will, under Wolff’s Law, result in the development of a shallow acetabulum and malformed femoral head.
• Important in this process is laxity of the soft tissues supporting the hip joint, such as the round ligament, joint capsule and muscle mass.
• In large breeds the trend to select for rapidly growing larger frames may alter biomechanical forces around the hip joints.
• There are some situations in which genetic inheritance obviously plays a primary role. The most obvious is the German shepherd, in which breeding lines have been selected to exacerbate the slope of the back, so that when standing the crouched stance is putting abnormal biomechanical forces on the hip joint, which is extended when standing, and the dog has an abnormal gait.
• This increases force on the cranial acetabular edge, the main weight-bearing section, which becomes more bone dense and appears white on radiographs (Figure 2).
• Vigorous exercise can stretch peri-articular structures, so controlled exercise in growing puppies is important.
• Diet restriction (25% less food intake) can prevent the occurrence of hip dysplasia in high risk breeds.

Genetic inheritance as a main factor

Gene expression plays a role in conformation, growth rate and other factors that predispose to the development of hip dysplasia. Nevertheless, in a pivotal lifetime study of 48 predisposed Labrador retrievers (Kealy et al, 2002), littermates were split into two groups, one fed according to a feeding guide, and the other group fed 25% less food. There were some very important findings:

• The group fed 25% less food lived on average 18 months longer.
• In the group fed 25% less food the onset of age-related diseases was delayed by two years.
• The hip joints were radiographed every year for 12 years. Remarkably, there was a 6-year delay in the appearance of osteophytes around the hip joints. These first appeared at 3 years of age in the control group and at 9 years of age in the diet-restricted group.
• None of the diet-restricted dogs developed clinical signs of hip osteoarthritis during their lifetime

Many authors have interpreted these differences as being due to one group being obese, but this is not true. The body condition scores (BCS – on a 1-9 point scale) from 6 to 12 years of age, were higher (P < 0.01) for dogs in the controlled-feeding group (6.7 ± 0.19) than for dogs in the restricted-feeding group (4.6 ± 0.19). So, the control group dogs were overweight, not obese, and the diet-restricted group were slightly underweight. This difference does not seem to explain why hip dysplasia-related osteoarthritis did not occur in the diet-restricted individuals (see Table 1).

Further attention should be paid to the reduced intake of nutrients in this study, which may have influenced hip development, notably minerals and trace elements, but possibly others such as vitamins A and D and amino acids.

It is critically important to feed a complete and balanced ration during growth, but this is easier said than done. In a study we conducted at the University of Nottingham (Davies et al, 2017), only 6% of wet and 38% of dry UK foods claiming to be complete were compliant with FEDIAF nutritional guidelines. For example, 29% of wet and 20% of dry complete pet foods contained a Ca:P ratio outside the recommended reference range. Two foods had Ca:P ≤ 0.25 whereas three had a Ca:P ratio of ≥ 2.5. If fed exclusively these diets would result in skeletal disease.

The levels of other minerals involved in normal endochondral ossification were also often incorrect. For example, copper is important for connective tissue formation (collagen and elastin), as well-bone formation, and 20% of wet foods tested did not meet FEDIAF guidelines.

Many breeders these days like to feed niche foods such as raw meat-based foods, vegetarian/vegan foods or homemade recipes. All of these can be imbalanced and non-compliant with FEDIAF standards, and it is virtually impossible to make a homemade ration that is complete and balanced every time (Davies, 2014).

Steps that can be taken by breeders now to reduce risk of hip dysplasia

• Continue to participate in hip scoring schemes and only breed from dogs with low scores.
• Stop breeding from lines of dogs with high scores, or resulting in dogs with high scores.
• Ensure pregnant bitches and growing puppies are fed a complete ration without excess, insufficient or inappropriate balance of minerals and trace elements. Most complete foods do not comply, so only use products from companies that:
  • Analyse every batch after production to ensure compliance.
  • Conduct feeding trials to ensure efficacy in growing puppies.
  • Use a product manufactured to a fixed formula for each batch. This minimises batch-to-batch differences.
• Avoid feeding nutritional supplements – especially minerals such as calcium.
• Maintain a lean body mass.
• Avoid vigorous exercise until growth plates have fused, so between 9 and 12 months of age.

Further research needed

Further research is needed to:

• Re-visit the lifetime study of Labrador retrievers to determine what reduced nutrient intakes could be linked to hip stability, other than body weight/condition score.
• Investigate factors that can affect the strength of joint capsule, round ligament and other structures that support the congruity of the canine hip.
• Determine specific gene expression involved in ligament structure and strength linked to development of hip dysplasia

Summary

Hip dysplasia has been prevented in high-risk breed puppies by reducing food intake (by 25% compared to a control group), maintaining a lean appearance with a body condition score of 4.6 (+/- 0.19)/9. This, in combination with avoidance of vigorous exercise during growth, should prevent progression to the more serious manifestations of hip dysplasia and avoid the need for long-term medications or surgical interventions.

Further studies are needed to determine the specific nutritional factors involved in the development of hip dysplasia.

• • Appeared in Vet Times (2025), Volume 55, Issue 7, Pages 10-13