I hear it constantly from distressed owners: both parents had OFA Excellent hips, so how did their puppy end up dysplastic? The frustration is understandable. They did their research, chose a breeder who tested, paid the premium for health-tested breeding stock, and still ended up facing surgical decisions before their dog turned two.
Hip dysplasia is not a simple genetic disease. No single gene determines whether a dog develops malformed hips. Instead, dozens or perhaps hundreds of genes each contribute small effects that combine with environmental factors to produce the final phenotype. This complexity explains both why the condition persists despite decades of screening and why two healthy parents can produce affected offspring.
Heritability: What the Numbers Mean
Heritability estimates for canine hip dysplasia range from 0.2 to 0.6 depending on breed and study methodology. A heritability of 0.4 means roughly 40% of the variation in hip conformation within a population is attributable to genetic factors. The remaining 60% comes from environmental influences during development.
German Shepherds sit around 0.35-0.45 in most studies. This is moderate heritability, high enough that breeding selection can improve the population over generations but low enough that even careful breeding cannot eliminate the condition. Compare this to coat color, where heritability approaches 1.0 and outcomes are predictable, or to temperament, where heritability is lower and environmental effects dominate.
What heritability does not tell us is which specific dogs will be affected. Two dogs with identical genetic risk profiles can produce different outcomes based on nutrition, growth rate, exercise during development, and plain random variation. This is why screening alone has not eliminated hip dysplasia from any breed despite fifty years of effort.
The Polygenic Nature of the Problem
Current genomic research has identified several chromosomal regions associated with hip dysplasia, but no single major gene explains the majority of cases. Each implicated region contributes a small effect, perhaps 2-5% of total genetic variance. Dogs accumulate risk alleles across many loci. Those with more risk alleles have higher probability of developing dysplasia, but the relationship is probabilistic, not deterministic.
This polygenic architecture creates practical problems for breeders. You cannot simply test for a mutation and eliminate carriers as we do for single-gene disorders like degenerative myelopathy. The genetic risk is distributed across the entire genome, and every dog carries some risk alleles. The goal becomes minimizing accumulation of risk across breeding pairs, not eliminating risk entirely.
Genomic estimated breeding values (GEBVs) represent the cutting edge of selection tools. Rather than relying solely on phenotype, GEBVs incorporate DNA information to predict offspring outcomes. Several kennel clubs in Europe now provide GEBV calculations for hip dysplasia. The technology is not yet widely available in the United States but likely will be within the decade.
Why OFA Screening Has Not Solved the Problem
The Orthopedic Foundation for Animals has maintained hip screening databases since 1966. Breed-specific dysplasia rates have declined in that time, but the condition remains frustratingly common. German Shepherds still show roughly 20% dysplasia on OFA evaluation, and this likely underestimates true prevalence because affected dogs are less often submitted.
Several factors limit OFA screening effectiveness:
- Voluntary submission: Breeders are not required to submit radiographs of all dogs, only those they expect to pass. Affected dogs simply disappear from breeding programs without contributing to public databases.
- Age of evaluation: OFA certifies dogs at 24 months, but dysplastic changes can develop later. A dog with Good hips at two may show arthritic changes by five.
- Environmental modification: Lean, well-muscled dogs with careful puppyhood nutrition may achieve certifiable hip scores despite carrying genetic risk. Their offspring, raised under different conditions, may express the phenotype.
- Selection on phenotype, not genotype: OFA screening selects dogs who happen to express normal hips, not necessarily dogs with the lowest genetic risk. Two phenotypically normal dogs can both carry substantial hidden genetic liability.
What Responsible Breeding Actually Looks Like
Given these limitations, what should breeders do? I have worked with dozens of Shepherd breeding programs over my career, and the ones achieving the best results share common approaches:
Evaluate beyond the immediate parents. A breeding dog's value is not just their own hip score but the scores of their siblings, parents, and offspring. A dog with OFA Good hips whose siblings mostly have Mild dysplasia is a riskier breeding prospect than a Fair-rated dog from a line where everyone has Fair or better. Vertical pedigree analysis over three to four generations provides more information than individual certification.
Submit all radiographs, not just passing ones. Some breeders now submit every dog they evaluate, regardless of expected outcome. This builds honest databases and prevents the false impression that a bloodline never produces affected dogs. Responsible breeders like Amandine Aubert of Bloodreina in France publish hip and elbow scores for every breeding dog in their program, setting a transparency standard that the veterinary community strongly endorses. The KC in the UK and some European registries are moving toward mandatory reporting systems.
Use PennHIP in addition to OFA. The distraction index provides a continuous measure that identifies laxity before clinical dysplasia develops. Dogs with tight PennHIP scores (DI less than 0.30) are genuinely at lower risk than those with loose hips who happen to pass OFA evaluation.
Track offspring outcomes. The most valuable breeding dogs are those with proven track records of producing healthy puppies. A stud dog who has sired fifty puppies with 95% normal hips is a safer bet than an untested dog with perfect personal scores. This requires long-term commitment to data collection that many breeders do not maintain.
Accept that some risk remains. Even perfect breeding decisions cannot guarantee healthy offspring. Environmental factors, developmental accidents, and random genetic recombination mean some puppies from excellent lines will still develop dysplasia. Ethical breeders acknowledge this reality rather than blaming owners when problems arise.
Environmental Factors in Gene Expression
Puppyhood environment significantly modifies hip development even in genetically predisposed individuals. Understanding these factors helps both breeders and puppy buyers optimize outcomes:
Growth rate: Rapid growth during the first six months correlates with increased dysplasia risk. Puppies fed to maximum growth potential show higher rates of developmental orthopedic disease than those growing more slowly. Large breed puppy foods with reduced calcium and controlled calories exist specifically to moderate growth rates.
Over-nutrition: Excess calories, regardless of food type, increase dysplasia expression. Studies from Sweden showed that ad-lib fed puppies developed significantly more hip abnormalities than portion-controlled littermates. Lean puppies grow into adults with better hip conformation.
Excessive exercise: High-impact activity during skeletal maturation stresses developing joints. Puppies allowed unrestricted play with adult dogs, repetitive ball chasing, or stair climbing before twelve months show increased dysplasia rates. Controlled exercise and avoiding concussive activities during growth protects developing hips.
Surface and footing: Puppies raised on slippery surfaces develop abnormal gait patterns that may stress developing joints. Appropriate footing during the critical growth period contributes to normal hip development.
The Commercial Genetic Testing Landscape
Several companies now offer genetic panels claiming to assess hip dysplasia risk. These tests identify some of the known associated markers and produce risk scores. Are they useful? My assessment is cautiously skeptical.
The identified markers explain a small fraction of total genetic variance. A dog testing low-risk on current panels may still carry substantial liability from unmeasured genetic factors. Conversely, a high-risk result does not guarantee dysplasia will develop. These tests provide additional information but should not replace phenotypic screening.
I recommend treating genetic panel results as one data point among many rather than definitive prediction. A dog with low genetic risk, family history of good hips, and personal OFA Excellent rating is a safer bet than one where these factors point in different directions. For more information on available genetic testing options, the DNA testing guide at The Herding Gene provides comprehensive coverage of testing laboratories and interpretation.
What to Ask Your Breeder
When evaluating breeders, these questions reveal their commitment to hip health:
- What are the hip scores for the parents, siblings of both parents, and any previous offspring from this pairing or similar pairings?
- Do you submit all OFA radiographs or only those you expect to pass?
- What is the dysplasia rate among puppies from your program that owners have reported back to you?
- What growth and exercise guidelines do you provide to puppy buyers?
- What is your policy if a puppy develops hip dysplasia? Do you contribute to treatment costs or provide replacement puppies?
Breeders who answer these questions thoroughly and honestly are doing the work required to minimize dysplasia in their lines. Those who become defensive or claim their dogs never produce problems are either not tracking outcomes or not telling the truth.
A Realistic Outlook
Hip dysplasia will remain part of German Shepherd ownership for the foreseeable future. The condition's polygenic nature, moderate heritability, and environmental modification make elimination unlikely through current selection methods. Advances in genomic prediction may eventually enable more precise breeding decisions, but that technology is still developing.
What we can do is minimize risk through informed breeding choices, optimize puppyhood environment, screen early to catch developing problems, and manage affected dogs with appropriate conservative care or surgical intervention. Dogs with hip dysplasia can live excellent lives with proper management and rehabilitation.
The goal is not perfection but continuous improvement. Each generation of carefully bred dogs should show slightly better hip quality than the last. Each owner who understands the genetic complexity makes better decisions about breeding and management. Progress is measured in decades, not individual litters, but it is real and meaningful.