The Labrador Retriever is one of the world's most beloved breeds and one of the most well-documented in terms of joint health.

The OFA (Orthopedic Foundation for Animals) database contains over 234,000 hip radiographs for this breed alone, making it one of the largest corpora in all of cynology. This wealth of data allows for solid conclusions to be drawn, and not all of them are reassuring.

What studies clearly show: Labradors are predisposed to hip dysplasia, elbow dysplasia, cranial cruciate ligament rupture, and secondary osteoarthritis.

In addition, there is a genetic peculiarity specific to this breed: a mutation in the POMC gene associated, in about a quarter of Labradors, with less effective satiety and a tendency to gain weight (two factors that directly aggravate joint pathologies).

OFA, 1974-2015; Raffan et al., Cell Metab, 2016; Frontiers Vet Sci, systematic review

Hip and Elbow Dysplasia: Figures to Be Interpreted Correctly

The OFA database reports 11.5% hip dysplasia in Labradors among over 150,000 radiographs submitted between 1974 and 2015.

For the elbow, the rate is 10.2% over the same period.

These figures are likely underestimated due to selection bias: the OFA registry relies on voluntary submissions, and owners of affected dogs do not submit their X-rays in the same proportions as others.

The actual prevalence in the general population is therefore likely higher....

The good news: decades of selection based on these criteria have produced modest but real genetic improvement in hips.

The bad news: genetic improvement for elbows is almost nonexistent (contributing 1.1% of the phenotypic standard deviation, according to Lewis et al., Vet J, 2011).

Elbow dysplasia remains an unresolved problem in the breed.

What this means in practice:

A Labrador whose parents both have excellent hip and elbow scores has significantly less risk of developing dysplasia.

Requesting OFA or BVA/KC certificates for both parents is a serious minimum step before purchase!

It does not guarantee a healthy dog, but substantially reduces the risk...

CCL rupture: a breed-specific predisposition

The Labrador is among the breeds at highest risk for cranial cruciate ligament (CCL) rupture.

The reported prevalence in this breed is estimated at 5.79% (this is one of the highest recorded (Frontiers in Veterinary Science, 2025)).

Contrary to popular belief, CCL rupture in dogs is rarely an acute sports injury: in more than 75% of cases, it is a progressive degeneration of the ligament that eventually gives way.

Obesity multiplies the risk of CCL rupture by 3.8 (odds ratio).

In a Labrador predisposed to weight gain and ligament degeneration, the two factors combine.

It is this addition of risks that makes the breed particularly vulnerable.

The POMC gene: why your Labrador isn’t just “greedy”

In 2016, Eleanor Raffan's team (University of Cambridge, Cell Metabolism) identified a 14 base-pair deletion in the POMC (pro-opiomelanocortin) gene in Labradors.

This mutation disrupts the production of two neuropeptides: (β-MSH and β-endorphin) which play a key role in the feeling of satiety.

Result: carrier dogs tend to get hungry faster between meals and are more food-motivated.

Approximately 25% of Labradors carry at least one copy of this mutation.

For each copy present, body weight increases by an average of 1.9 kg.

This is not simply greed or a lack of training: it is a real biological predisposition, medically documented!

The POMC mutation is more frequent in guide dogs:

Raffan et al. observed that 76% of Labrador guide dogs carried the POMC mutation, compared to ~25% in the general population.

Explanation: highly food-motivated dogs are easier to train with positive reinforcement. Selection for work has therefore unintentionally favored the mutation. A genetic test is available.

The vicious cycle: obesity → joints → less exercise → obesity

In Labradors, the pathophysiology is particularly insidious. The POMC mutation promotes overweight.

Overweight exacerbates hip dysplasia and multiplies the risk of CCL rupture. The resulting joint pain reduces physical activity. Less activity further promotes weight gain.

And so on...

This mechanism is well-documented: excess weight increases mechanical load on weight-bearing joints, accelerates cartilage degradation, and leads to osteoarthritis earlier and more severely.

Maintaining a Labrador at an ideal weight throughout its life is one of the most effective preventive actions available (and one of the most impactful long-term measures).

Prevention: what is truly actionable

• Control weight from a young age: never let a Labrador become overweight. Excess weight is the most modifiable and impactful variable.

• Exclusively require OFA or BVA/KC radiographs of both parents before purchase.

• Prefer low-impact exercises (swimming, walking) over repeated jumping or sudden changes of direction.

• Monitor gait from 6 months: morning stiffness, lameness after exercise, or reluctance to climb stairs are early signs.

• Consider radiographic screening of hips and elbows between 12 and 18 months if parents are not certified.

• In case of a dysplasia diagnosis: early intervention (physiotherapy, weight management, appropriate pain relief) significantly delays progression to debilitating osteoarthritis.

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Sources

1. Raffan E. et al. (2016). A deletion in the canine POMC gene is associated with weight and appetite in obesity-prone Labrador Retrievers. Cell Metabolism, 23(5): 893–900. PubMed 27157046
2. OFA (Orthopedic Foundation for Animals): Breed statistics 1974–2015. ofa.org
3. Hou Y. et al. (2010). Retrospective analysis of genetic improvement of hip joints in a cohort of Labrador Retrievers in the USA: 1970-2007. PLoS ONE, 5(2): e9410
4. Lewis TW et al. (2011). Genetic evaluation of hip and elbow dysplasia scores in Labrador Retrievers in the UK. Veterinary Journal, 189: 227–233
5. UFAW: Labrador Retriever: Cranial cruciate ligament rupture. ufaw.org.uk
6. Frontiers in Veterinary Science (2025). Accuracy of cruciate ligament rupture risk prediction in Labrador Retrievers by genome-based polygenic risk score
7. Pettitt RA et al. (2020). Risk factors for canine osteoarthritis and predisposing arthropathies: a systematic review. Frontiers Vet Sci. PMC7198754