Cleft palate in dogs is frequently genetic, though not always. In many breeds, specific gene mutations passed from both parents cause the condition, following a recessive inheritance pattern. This means two dogs that appear completely normal can produce affected puppies if both carry the same faulty gene. Environmental factors during pregnancy, including certain medications and nutritional deficiencies, can also cause cleft palate independently or increase the risk in genetically susceptible dogs.
The Genetic Evidence
The strongest genetic link comes from research on Nova Scotia Duck Tolling Retrievers. Scientists identified a frameshift mutation in a gene called ADAMTS20 that causes a syndromic form of cleft lip, cleft palate, and fused toes. The condition follows a recessive inheritance pattern: when researchers tested unaffected parents and littermates, none of the 12 unaffected family members carried two copies of the mutation, while all parents were carriers with one copy. This means a puppy needs to inherit the defective gene from both its mother and father to be born with a cleft.
A second, separate mutation was also found in the same breed, a DNA insertion in the DLX6 gene that causes cleft palate along with jaw abnormalities. The fact that two independent genetic causes exist within a single breed hints at how genetically complex this condition can be. Multiple genes are involved in building the palate during fetal development, and a defect in any one of them can prevent the two halves of the roof of the mouth from fusing properly.
Breeds With the Highest Risk
A large study tracking orofacial clefts per 1,000 live births found stark differences between breeds. Boston Terriers had the highest incidence at roughly 143 per 1,000 births, meaning about 1 in 7 puppies was affected. French Bulldogs came next at about 98 per 1,000, followed by Cavalier King Charles Spaniels at roughly 75 per 1,000. Papillons and English Bulldogs also showed elevated rates of around 40 per 1,000. All of these breeds had significantly higher odds of cleft palate compared to Labrador Retrievers, which served as the baseline.
The pattern is telling. Brachycephalic breeds (those with shortened skulls and flat faces) dominate the high-risk list. Generations of selective breeding for a compressed facial structure appear to have concentrated the genetic variants that predispose dogs to palate defects. The more extreme the skull shape, the more likely the developmental process that fuses the palate will go wrong.
Environmental Causes During Pregnancy
Genetics isn’t the only pathway. Several environmental exposures during pregnancy can interfere with palate formation, even in breeds without a known genetic predisposition.
- Medications: Corticosteroids given during the first third of pregnancy can disrupt the growth and development of embryonic tissues, increasing the risk of cleft palate. Aspirin and certain antibiotics have also been implicated.
- Nutritional problems: Folic acid deficiency contributes to malformations of the palate and neural tube. On the flip side, excess vitamin A can overwhelm cell signaling pathways and cause underdevelopment of the palate shelves.
- Infections: Canine distemper virus during pregnancy can impair fetal tissue development and produce craniofacial abnormalities.
- Oxygen deprivation: Placental problems or circulatory issues in the mother can reduce oxygen supply to the embryo, compromising the cell migration needed for the two halves of the palate to meet and fuse.
- Chemical exposure: Pesticides and other chemical agents can interfere with cell movement during the critical window of palate formation.
In many real-world cases, it’s impossible to separate genetic and environmental contributions cleanly. A puppy with a mild genetic predisposition might develop normally under ideal conditions but be born with a cleft if the mother was exposed to a teratogen at the wrong moment.
Primary vs. Secondary Cleft Palate
Not all cleft palates look the same. A primary cleft affects the lip and nose, the structures at the front of the face. A secondary cleft affects the hard palate, the soft palate, or both, essentially leaving a gap in the roof of the mouth. Some puppies have both. The distinction matters because it affects how severe the feeding problems are, what kind of surgical repair is needed, and in some cases which genetic mutation is responsible.
What Cleft Palate Means for a Newborn Puppy
A puppy born with a cleft palate cannot nurse normally. The gap in the roof of the mouth prevents the suction needed to draw milk from the mother, and any milk that does enter the mouth can pass into the nasal cavity or be inhaled into the lungs. Without intervention, these puppies will not survive.
The standard rescue method is tube feeding. A soft, flexible catheter is measured from the puppy’s nose to its last rib, then gently inserted through the mouth and into the stomach. Warm formula is delivered by syringe, and the puppy is held upright and burped afterward. Newborns need feeding every two to three hours around the clock, with formula volume calculated by body weight. Healthy puppies should gain 5 to 10 percent of their body weight daily during the first week.
The first three days are the most critical: establishing safe feeding, maintaining body temperature, and preventing aspiration pneumonia. By weeks two and three, eyes and ears open and mobility improves. Cleft puppies often lag slightly behind their littermates early on but typically catch up. Around weeks three to four, caregivers can begin transitioning to softened solid food using elevated feeding positions to keep food from entering the nasal cavity. Environmental cleanliness matters more than usual, since food and formula particles that enter the nasal passage make these puppies more prone to infection.
Surgical Repair
Clefts involving the hard or soft palate can be surgically corrected. Most veterinary surgeons prefer to wait until the puppy is old enough to safely undergo anesthesia and has grown enough that the tissue can be successfully repositioned. The goal of surgery is to close the gap completely, creating a functional barrier between the mouth and nasal cavity. Some puppies need more than one procedure, particularly if the defect is large or if the first repair partially breaks down during healing.
Reducing the Risk in Breeding Dogs
If you’re breeding dogs, especially in high-risk breeds, the most effective step is to avoid repeating pairings that have produced affected puppies. Since the condition often follows a recessive pattern, both parents of an affected puppy are presumed carriers. Breeding either parent to a different carrier risks producing more affected offspring. In breeds where genetic tests exist, screening breeding stock before mating can identify carriers.
Folic acid supplementation offers an additional layer of protection. One study in Pugs and Chihuahuas found that giving folic acid from the onset of heat through day 40 of pregnancy decreased the occurrence of cleft lip and palate. This mirrors the well-established practice of folic acid supplementation in human pregnancies to prevent neural tube defects. Avoiding corticosteroids, unnecessary medications, and chemical exposures during the first trimester of canine pregnancy (roughly the first 20 days) also reduces risk, since this is the window when the palate is actively forming.