The Staffordshire Bull Terrier has consistently been among the most registered breeds in the French LOF (Book of French Origins).

It ranks 3rd in 2024 with 9,108 registrations and remains 3rd in 2025 with 8,694 registrations (Centrale Canine).

Its image as a compact, affectionate, and hardy dog has earned it lasting popularity.

This apparent robustness can mask pathologies for which veterinary literature now has solid data.

This article is not intended to discourage adoption. It aims to provide owners and future adopters with information that too few breeders spontaneously communicate (so that screening, monitoring, and prevention decisions can be made at the right time.)

Breed Profile

Table of Documented Risks

Elbow Dysplasia: The Most Documented Joint Risk in Staffies

Elbow dysplasia is the most well-established orthopedic predisposition in SBTs, with several independent studies converging on this finding.

What the studies say

Krotscheck et al. (2019) found an odds ratio of 3.08 for surgically treated elbow dysplasia in SBTs, ranking them 4th out of 12 breeds behind Labradors, Rottweilers, and German Shepherds.

O'Neill et al. (2020) confirm the signal in primary care: SBT accounts for 5.19% of elbow disease incidents in the UK, with a median diagnosis at 8.02 years. This is still later than the Labrador (6.42 years) and the German Shepherd (5.64 years).

Absolute prevalence estimates between 31 and 33% are cited in the literature (sources reported by Pegram et al., 2020), to be interpreted with caution depending on the methodologies.

What this changes in practice

A Staffie that limps on its foreleg, is stiff on leverage, or is reluctant to extend its elbow (especially between 4 and 18 months) deserves an evaluation with radiographs, or even a CT scan.

Point of vigilance: the clinical stoicism frequently observed in the breed (clearly mentioned by Pegram et al.) can mask a significant lesion behind a subtle sign.

This is not biological proof specific to the Staffie, but a widely shared clinical observation with real practical meaning!

Patellar luxation: what the science really says

Patellar luxation is documented in Staffordshire Bull Terriers, but the available data requires a nuanced reading: the breed is not considered to be classically predisposed to this pathology in large primary care studies.

In a large British study (Pegram et al., 2020, n=22,333 dogs), Staffordshire Bull Terriers had significantly fewer patellar luxations than other breeds. This result contradicts the preconceived notion of a predisposition of the Staffie in this criterion.

However, patellar luxation does exist in the breed and has been the subject of a specific morphological study.

Newman and Voss (2017) showed, on CT scans, that SBTs with patellar luxation presented specific conformational peculiarities (notably reduced femoral anteversion and external rotation of the femur) with direct implications for surgical planning.

Furthermore, a systematic review (Andrade et al., 2024) documents the co-occurrence of patellar luxation + cranial cruciate ligament rupture, which is more frequent in medium to large dogs.

If a Staffie presents with a hind limb lameness, a complete orthopedic evaluation is warranted.

L-2-Hydroxyglutaric Aciduria (L-2-HGA): the Staffie's specific genetic disease

L-2-HGA is the most specific pathology in Staffordshire Bull Terriers (SBT); (and the least known to the general public).

It is not an articular disease: it is a hereditary metabolic encephalopathy: (A brain disorder caused by the accumulation of toxic substances in the nervous system, due to an inherited metabolic defect.)

However, it produces locomotor signs that can be confused with musculoskeletal pathologies, particularly stiffness of all four limbs and gait disorders.

Disease mechanism

L-2-HGA is an inborn error of metabolism, inherited in an autosomal recessive manner, caused by mutations in the L2HGDH gene encoding L-2-hydroxyglutarate dehydrogenase.

When deficient, L-2-hydroxyglutaric acid accumulates in biological fluids (urine, blood, cerebrospinal fluid), causing progressive damage to the central nervous system.

Abramson et al. (Journal of Veterinary Internal Medicine, 2003; PubMed 12892307) were the first to describe the disease in 6 Staffies, characterizing clinical signs, biochemical abnormalities, and MRI findings.

This seminal study established the Staffie as the reference veterinary model for this disease, which has been known in humans since 1980.

Prevalence in the breed

Court et al. (Veterinary Record, 2010 — PubMed 20852250) identified exonic mutations of the L2HGDH gene in the Staffie.

In a cohort of 130 non-epileptic Staffies from the UK, 10.8% were carriers of the mutation.

A similar rate of 11.4% was found in a second independent cohort of 131 dogs.

This data is specifically related to non-epileptic dogs, which constitutes a selection bias to be considered when interpreting the frequency of carriers in the general population.

Autosomal recessive inheritance means that a dog must inherit two copies of the mutated gene to develop the disease.

A carrier of a single copy is clinically healthy but can transmit it.

Two mated carriers statistically produce 25% affected puppies, 50% healthy carriers, and 25% unaffected...

Clinical signs

Shea et al. (Veterinary Record, 2016 — PubMed 27729589) reported clinical data from 27 Staffies with confirmed L-2-HGA mutations:

The average age of onset of signs was 12 months (range: 2.5 to 60 months).

Gait disturbances were present in 26 out of 26 evaluated dogs, with stiffness of all four limbs being the earliest and most frequent sign (24/26).

19 out of 26 dogs presented with kyphosis and tremors.

18 dogs presented with paroxysmal episodes resembling epileptic seizures or dyskinetic episodes.

Behavioral changes were present in 24 out of 27 cases, including staring into space (21/24), signs suggestive of dementia (17/24), and loss of acquired learning (15/24).

These behavioral signs are often the first to alert owners, long before neurological deficits manifest.

Diagnosis and screening

Diagnosis relies on three pillars: brain MRI (symmetrical gray matter lesions), urinary organic acid analysis (elevated L-2-hydroxyglutaric acid), and DNA genetic testing targeting L2HGDH mutations.

Genetic testing is the most practical tool for screening breeding dogs: it identifies affected, carrier, or unaffected dogs at any age.

There is no curative treatment.

Prevention relies solely on screening breeding animals and eliminating carrier x carrier matings.

Warning signs to know

What you can concretely do

Before adoption:

• It is reasonable to require the L-2-HGA genetic status of both breeding dogs before purchase or adoption.

• Require elbow scores (OFA or equivalent) of both parents (the documented predisposition of the breed justifies this approach)...

• Avoid breeders who do not perform any genetic or orthopedic screening on their breeding dogs.

After adoption:

• Monitor gait from 4 to 18 months: any persistent forelimb lameness or stiffness after rest warrants veterinary evaluation.

• Do not interpret the absence of complaint as the absence of pain. Veterinarians frequently report that SBT-type dogs can mask their clinical signs (active vigilance remains necessary).

• Control weight throughout life: overweight exacerbates elbow dysplasia and accelerates progression to osteoarthritis.

• Implement an annual veterinary check-up from 3 years old, including orthopedic evaluation and elbow palpation.

• If neurological signs appear (tremors, stiffness of all four limbs, abnormal behaviors), request an L-2-HGA genetic test if not already done, or contact a veterinary neurologist.

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Sources

1. Krotscheck U. et al. (2019). Breed susceptibility to common surgically treated orthopedic diseases in 12 dog breeds. Acta Veterinaria Scandinavica, 61: 19. PubMed 31023333

2. O'Neill DG et al. (2020). Epidemiology and clinical management of elbow conditions in dogs under primary veterinary care in the UK. BMC Veterinary Research, 16: 240. PMC7371807

3. Pegram C. et al. (2020). Staffordshire Bull Terriers in the UK: predispositions and protections for disorders. Canine Genetics and Epidemiology, 7: 13. PMC7510130

4. Newman M., Voss K. (2017). CT evaluation of femoral and tibial conformation in English Staffordshire Bull Terriers, with or without congenital medial patellar luxation. Veterinary and Comparative Orthopaedics and Traumatology, 30(3): 191–199. PubMed 28331928

5. O'Neill DG et al. (2016). Epidemiology of patellar luxation in dogs under general veterinary care in England. Canine Genetics and Epidemiology, 3: 4. PMC4898461

6. Abramson CJ et al. (2003). L-2-hydroxyglutaric aciduria in Staffordshire Bull Terriers. Journal of Veterinary Internal Medicine, 17(4): 551–556. PubMed 12892307

7. Short AD et al. (2010). Exonic mutations of the L2HGDH gene in the Staffordshire bull terrier. Veterinary Record, 167(12): 455–457. PubMed 20852250

8. Shea A. et al. (2016). Clinical features and progression of L-2-hydroxyglutaric aciduria in 27 Staffordshire bull terriers. Veterinary Record, 179(21): 545. PubMed 27729589

9. Candela Andrade M., Slunsky P., Klass LG, Brunnberg L. (2022). Patellar luxation and concomitant cranial cruciate ligament rupture in dogs: a literature review. Veterinary Medicine-Czech, 67(4): 163–178. PMC11334444 / PubMed 39170807

10. Centrale Canine — LOF Statistics 2024 and 2025. centrale-canine.fr