Craniomandibular Osteopathy (Discovered in the Weimaraner; CMO)
Craniomandibular Osteopathy (Discovered in the Weimaraner; CMO). Autosomal dominant. Observed in 1 of 211 breeds tested in the Sniff Atlas, with measured at-risk genotype frequencies drawn from 12,296 dogs (Donner 2023). Because this is a dominant trait, a single copy places a dog at risk rather than making it a silent carrier; whether the phenotype appears still depends on penetrance, modifier genes, and environment.
Dominant trait. A single copy of this variant places a dog at risk; it does not make the dog a silent carrier. The breed frequencies below are therefore at-risk frequencies, and penetrance plus modifier genes determine whether the phenotype actually appears.
- OMIA identifier
- OMIA:000236-9615
- InheritanceInheritance patternWhat it isHow the condition is passed down: recessive (two copies needed), dominant (one copy), or more complex.For your dogRecessive means a single-copy carrier is usually healthy but can still pass it on.PreciselyThe documented mode of Mendelian transmission (autosomal recessive or dominant, X-linked, etc.) per OMIA.OMIA · documented
- Autosomal dominant
- Linked gene
- SLC35D1
- Human counterpart
- In humans, this gene is SLC35D1. In people, SLC35D1 appears tolerant of loss-of-function variation (gnomAD v4.1 constraint, LOEUF 0.98). Constraint measures intolerance to loss-of-function only and does not indicate importance; some tolerant genes cause disease through other mechanisms. In people, variants in the SLC35D1 gene have conflicting classifications in ClinVar, and none is expert-reviewed. The evidence is unsettled, not that variants here are benign.
- Source dataset
- Sniff Atlas v1.0.1 / DOI
Craniomandibular Osteopathy is a condition affecting the bones of the skull and jaw, causing abnormal bone growth that can lead to discomfort and difficulty with jaw movement.
How it is inherited. This condition is inherited in an autosomal dominant pattern, meaning that just one copy of the altered gene can cause the condition.
It has been discovered in Weimaraners, with about 16% carrying the gene variant linked to this condition.
Being a carrier is not the same as being affected; it’s worth asking your vet about testing if you have a Weimaraner or are concerned about this condition.
- Weimaraner · 16%
Educational carrier context from the Sniff disease layer (Donner 2023 (carrier) + substrate; educational, not diagnostic). Not a diagnosis and not a prediction about your dog. See the full carrier chart below for sample sizes and the Donner cohort when available.
Context source: Donner 2023 (carrier) + substrate; educational, not diagnostic · dataset doi:10.5281/zenodo.20566358 . We would rather give you a short plain summary with a receipt than invent comfort.
A model of human Caffey disease
Dogs with this condition carry a change in SLC35D1. In people, changes in the same gene cause Caffey disease. That makes affected dogs a naturally-occurring model of the human disease, and it is part of why studying dogs moves medicine forward for everyone. It does not mean your dog has the human disease. It means the two share an underlying biology.
In people, the disease is described as: Caffey disease is an osteosclerotic dysplasia characterized by acute inflammation with massive subperiosteal new bone formation usually involving the diaphyses of the long bones, as well as the ribs, mandible, scapulae, and clavicles. The disease is associated with fever, irritability pain and soft tissue swelling, with onset around the age of 2 months and resolving spontaneously by the age of 2 years. However, prenatal disease onset has also been described.
In humans it is also called: infantile cortical hyperostosis.
Mapped from OMIA via the human disease's OMIM entry to the Mondo Disease Ontology (Monarch Initiative, CC-BY 4.0). Sniff renders this as a model-of link; the canine disease remains the subject of this page.
From OMIA's curated record
Documented in OMIA (Online Mendelian Inheritance in Animals). This describes the disease as recorded in the published literature, not a prediction for any individual dog. As of 2026-06-03.
Summary
Molecular genetics
Inheritance
Human analog
OMIA links this condition to its human counterpart in OMIM (Mendelian Inheritance in Man), the place to read across to the deeper human literature for the same biology.
Source: OMIA (Nicholas, Tammen & the Sydney Informatics Hub), entry OMIA:000236-9615, doi:10.25910/2AMR-PV70 (CC-BY 4.0).
Published references
The peer-reviewed papers behind this disease, curated by OMIA. Starred entries are OMIA-designated landmark papers. Showing 6 of 21.
- Whole genome sequencing indicates heterogeneity of hyperostotic disorders in dogs. · Genes (Basel) · 2020 · PMID 32033218
- Complex segregation analysis of craniomandibular osteopathy in Deutsch Drahthaar dogs. · Vet J · 2018 · PMID 29429484
- Idiopathic canine juvenile cranial hyperostosis in a Pit Bull Terrier. · N Z Vet J · 2011 · PMID 21660851
- Craniomandibular osteopathy with a unique neurological manifestation in a young Akita. · J Am Anim Hosp Assoc · 2010 · PMID 21189419
- Craniomandibular osteopathy in a bullmastiff. · Can Vet J · 2002 · PMID 12497967
- Breed susceptibility for developmental orthopedic diseases in dogs · J Am Anim Hosp Assoc · 2002 · PMID 12220032
References curated by OMIA (Nicholas, Tammen & the Sydney Informatics Hub), doi:10.25910/2AMR-PV70 (CC-BY 4.0). Full list at the OMIA entry.
Set each parent's status for Craniomandibular Osteopathy (Discovered in the Weimaraner; CMO) and see the odds for their puppies. Single dominant variant, exact Mendelian math.
These are the genetic odds for one known variant, not a promise: a real litter varies around them, and penetrance or other genes can change whether the condition ever appears. Use it to avoid pairing two carriers and to keep a line healthy, not to engineer a dog. Inheritance mode per OMIA.
See what Craniomandibular Osteopathy (Discovered in the Weimaraner; CMO) looks like in your dog's breed.
Observed only in small-sample breeds
Maximum at-risk frequency per breed across variants in the Donner 2023 cohort, with Wilson 95% confidence intervalsWilson 95% confidence intervalWhat it isThe range the true frequency is probably in. A wide range means we are less sure, usually because few dogs were tested.For your dogTrust tight ranges; treat wide ones as rough estimates.PreciselyA binomial-proportion confidence interval (Wilson score, 95%) that stays reliable at small sample sizes.Sniff Atlas methodology · statistical. The list below is split into well-sampled breeds (n ≥ 50 tested) and small-sample breeds (n < 50, where the Wilson CI typically spans more than 20 percentage points and frequencies should not be compared directly to the well-sampled entries). Frequencies are population-level, not per-litter or per-line.
▸ Also observed in 1 small-sample breed (n < 50)
Frequencies in this section are statistical estimates with wide Wilson 95% confidence intervals (typically >20 percentage points). Treat these as "at-risk dogs observed but the true population frequency is not yet measurable" rather than as comparable to the well-sampled entries above.
| Breed | Estimate | n tested |
|---|---|---|
| Weimaraner | 16.1% | 28 |
210 additional breeds in the Donner 2023 cohort were tested but showed no at-risk genotypes.
Scope
This record carries the breed-level carrier frequencies from the Donner 2023 cohort. Penetrance data (the fraction of at-risk dogs that develop the phenotype) is not yet quantified for this disease in the Sniff Atlas v1.0.1. The OMIA entry is the authoritative reference for the clinical phenotype, inheritance pattern, and gene assignment.
Predicted disease relevance at the per-dog level is UNPROVEN. The at-risk frequency is measured; phenotype outcome depends on penetrance, environment, and modifier loci. Consult a veterinarian for clinical interpretation.
Citations
If you use this record in published work, cite the Sniff Atlas (the published dataset that carries the breed-level carrier frequencies) and the upstream sources:
- Sniff Atlas v1.0.1 for the per-breed carrier frequencies:
Gehring, M. (2026). Sniff Atlas v1.0.1. Zenodo. https://doi.org/10.5281/zenodo.20566358. CC-BY 4.0.
- OMIA for the disease definition, inheritance, and gene assignment:
Nicholas, F. W., & Tammen, I. (2024). OMIA. Sydney Informatics Hub, The University of Sydney. https://doi.org/10.25910/2AMR-PV70. Entry: OMIA:000236-9615.
- Donner et al. 2023 for the breed × variant carrier-frequency cohort:
Donner, J., Freyer, J., Davison, S., Anderson, H., Blades, M., Honkanen, L., et al. (2023). Genetic prevalence and clinical relevance of canine Mendelian disease variants in over one million dogs. PLOS Genetics, 19(2), e1010651. https://doi.org/10.1371/journal.pgen.1010651.
Full citation formats (BibTeX, RIS, CITATION.cff) at sniff.world/cite.
Related
- Gene page: SLC35D1, cited identity, disease associations, and the human-gene bridge.
- Sniff Atlas v1.0.1, the source dataset for these frequencies.
- Browse breeds, per-breed Mendelian profiles, including this disease in context.
- OMIA entry OMIA:000236-9615, authoritative clinical reference.
- About OMIA, the catalogue this record comes from, and how Sniff uses it.