Note for Pet Owners:
This information is provided by Provet for educational purposes only.

You should seek the advice of your veterinarian if your pet is ill as only he or she can correctly advise on the diagnosis and recommend the treatment that is most appropriate for your pet.

Because there may be an hereditary basis for this condition affected animals should not be used for breeding

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Provet is conducting an investigation into the possible link between excessive dietary vitamin A intake and the occurrence of congenital cleft palate. If you see a case please submit the case history with full details of the food given and any nutritional supplements administered to . If we get sufficient cases submitted we shall publish the results on this website.

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Cleft palate is commonly seen by veterinarians in dogs, cats and other species. Unfortunately many neonates with this disorder die early or are destroyed by the breeder so accurate statistics on the true incidence of the disease are not available. 

Defects (clefts) in the hard palate that forms the roof of the mouth, or the soft palate which lies caudally  and separates the oropharynx from the nasopharynx may be congenital or acquired. The cleft can involve the soft palate alone, the hard palate alone or both. The defect can be bilateral (ie involve tissues lying both sides of the midline) or unilateral. The latter are usually seen in the soft palate.

A newborn puppy with severe cleft palate

Congenital cleft palate is an abnormality which is thought to occur during fusion of the maxillary process with the medial nasal process, when the mesodermal fusion develops across the fused epithelial surfaces. If the epithelial barrier does not degenerate or if the mesodermal connective tissue is deficient cleft palate results. 

Acquired clefts are due to trauma - usually road traffic accidents or falls from a height.

A cat with acquired cleft hard palate and soft palate following trauma


There are several possible causes for congenital cleft palate:

a) Genetic cause

An hereditary basis for the disease is suspected for congenital clefts but the mechanism has not yet been determined. Any such genetic trait  is thought to be multifactorial recessive, polygenic and dominant with partial penetration.

b) Excess vitamin A intake during pregnancy

In 1967 Wiersig and Swenson reported that 125,000 IU of Vitamin A per kilogram body weight given to Beagle bitches on days 17-22 of gestation resulted in cleft palate developing in their puppies.

Vitamin A is an essential nutrient for normal growth and defects in bone growth are seen with insufficient as well as excessive dietary intake.  Vitamin A has a controlling influence over both the osteoblasts and osteoclasts in epithelial cartilage and so there is a rational explanation as to why excessive vitamin A intake might result in cleft palate.

In addition, commercially prepared complete pet foods contain more than sufficient available vitamin A yet breeders and owners frequently supplement their pet's ration with vitamin supplements. High vitamin A content is also a feature of many natural food sources including liver and fish oils. Cod liver oil is a very popular nutritional supplement with pet owners and it contains 18000mg per 100ml (4000 IU per gram). Some vitamin injections contain as much as 500,000 IU of vitamin A per ml.

c) Cortisone 

Administration of cortisone during pregnancy can lead to the development of cleft palate in the fetus

d) Hydroxyurea

Administration of the cytotoxic drug hydroxyurea (hydroxycarbamide) is reported to cause cleft palate.

Acquired cleft palate is common following falls from a height, and less commonly following road traffic accidents.

Breed Occurrence
The following breeds of dog have been reported to have cleft palates : mixed and small terrier breeds, Beagle,  Bernese Mountain Dog, Boston Terrier, Bullmastiff, Bull Terrier, Chihuahua, Cocker Spaniel, Collie, Dachshund, English Bulldog, German Shepherd Dog, Golden Retriever, Miniature Schnauzer, Norwegian Elkhound, Pekingese, Shih Tzu, Staffordshire Bull Terrier, Toy Poodle Wire-haired Fox Terrier, 

Brachycephalic breeds are reported to have about 30% risk, whereas German Shepherd Dogs have the lowest risk.

In cats cleft palates have been reported in mixed breeds, Siamese, Manx and Abyssinians - with Abyssinians having the highest risk.

There is a visible split in the roof of the mouth or the soft palate. This results in food material (particularly fluids) passing into the nasal cavity and the following signs :

  • Fluids eg milk pass down the nose during feeding
  • Sneezing
  • Coughing/gagging
  • Snuffling
  • Rhinitis
  • Pneumonia (due aspiration of foods)
  • Poor weight gain
  • Stunted growth
  • Inability to feed properly 

Bronchopneumonia accounts for 30% of deaths due to cleft palate.

Cleft palate is sometimes associated with congenital deformities in other body systems.

Inhalation of foods leading to aspiration pneumonia - and death

Diagnosis is based on the clinical signs and careful visual examination of the oral cavity. Fine-line fissures sometimes occur in the hard palate in the midline of the roof of the mouth following trauma such as road traffic accidents or falls from a height. These can be difficult to detect unless a careful examination is made.

Consider excess dietary vitamin A intake as a possible cause for congenital cleft palate when it occurs and review the mothers nutritional history.



For the prevention of congenital cleft palate Provet makes the following  recommendations :

  • Excessive dietary vitamin A intake must be avoided during pregnancy, so
    • Avoid unregulated multivitamin or vitamin A supplementation during pregnancy
    • Avoid unregulated liver intake during pregnancy
    • Avoid unregulated fish oil supplementation during pregnancy
    • Great care is needed when administering parenteral vitamin supplements to pregnant animals
  • Feed a complete pet food formulated for pregnancy without supplements


Surgical repair of acquired lesions, and closure of congenital defects is recommended. In all cases surgery should be performed as soon as possible before secondary complications occur.  

Severe defects may be very difficult or even impossible to repair and in severely affected neonates euthanasia should be considered.

If both the hard palate and soft palate are involved the hard palate should be closed first, followed by the soft palate. If necessary two separate procedures should be performed.

Most techniques involve the use of a flap taken by undermining the tissue on one or both sides of the defect and suturing them together. Techniques using artificial prostheses to close large defects have also been described in the literature, but these are not readily available and rejection is a common problem.

It is important to :

Good for minor defects. Guarded to poor for severe defects. Poor once secondary complication of inhalation pneumonia has developed.

Long term problems
Respiratory infections.


Updated January 2016