Canine Cleft Palate          


Cleft Palate-Drs.Foster & Smith,Inc
Cleft Palate
Cleft Palate-Why and When

 Cleft Palate

 Race Foster, DVM and Marty Smith, DVM
Drs. Foster & Smith, Inc.

This article will help you better understand cleft palate in puppies and kittens. If your pet is showing any symptoms or signs of disease, please contact your veterinarian. We want you and your pet to be happy andilldogcleft healthy.

Cleft palate is a skeletal disorder occasionally seen in puppies and kittens of all breeds. A cleft palate results when the bones forming the roof of the mouth do not grow normally. This results in an opening in the roof of the mouth that communicates into the nasal cavity.

What are the symptoms?
Puppies and kittens as young as one day old will often have milk come out their noses as they nurse. They may also inhale milk into their lungs, causing a difficulty in breathing or even pneumonia. When the pet's mouth is examined, a slit will be seen in the roof of the mouth.

What are the risks?

The milk tends to enter the nasal passages and lungs. Most patients will die at an early age from pneumonia and/or malnourishment.

What is the management?

Mild openings in the mouth roof can be surgically corrected. More severe instances cannot. Frequently if the cleft palate cannot be surgically closed, euthanasia is advised.

C 2009 Drs. Foster and Smith, Inc.Reprinted as a courtesy and with permission from ( On-line store at
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Cleft Palate
What is Cleft lip/palate?
This is an opening in the lip or the roof of the mouth that occurs due to failure of normal fusion processes during embryonic development. Cleft palate and cleft lip may result from either hereditary or environmental causes (such as the use of certain drugs during pregnancy).

How is cleft lip/palate inherited?
Cleft palate is believed to be an autosomal recessive trait in the Brittany spaniel.  In the English and French bulldog, pointer, and shih tzu, the trait may be autosomal dominant with incomplete penetrance.

What breeds are affected by cleft lip/palate?
English and French bulldog, pointer, shih tzu, Boston terrier, Brittany spaniel, cocker spaniel, dachshund, German shepherd, Labrador retriever, miniature schnauzer, and Pekingese.

For many breeds and many disorders, the studies to determine the mode of inheritance or the frequency in the breed have not been carried out, or are inconclusive. We have listed breeds for which there is a consensus among those investigating in this field and among veterinary practitioners, that the condition is significant in this breed.

What does cleft lip/palate mean to your dog & you?
Affected pups are born with the condition. A minor defect will cause little or no problem, while a more severe defect will cause signs such as a chronic nasal discharge (that may include food), poor growth, aspiration pneumonia (from inhalation of food), or even death.

How is cleft lip/palate diagnosed?
Your veterinarian will diagnose these conditions on physical examination.

How is cleft lip/palate treated?
Mild problems may not require any treatment, but more serious defects will require surgical repair to prevent complications such as aspiration pneumonia.

Breeding advice
Affected animals should not be used for breeding, and it is prudent to avoid breeding their parents and siblings as well.


Copyright © 1998 Canine Inherited Disorders Database. All rights reserved.
Revised: April 03, 2001.
This database is a joint initiative of the Sir James Dunn Animal Welfare Centre at the Atlantic Veterinary College, University of Prince Edward Island, and the Canadian Veterinary Medical Association.
reprinted with kind permission from:-
 Alice Crook, DVM,Coordinator, Sir James Dunn Animal Welfare Centre, Atlantic Veterinary College,University of Prince Edward Island, 550 University Ave.Charlottetown, PEI C1A 4P3

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 Fred Lanting
Hope that you never have a litter with cleft palates. But if you do, this may explain the cause of at least some cases.

Let’s start at the beginning, with a short review of the birds and the bees. The sperm cell, with half the chromosomes needed for a new pup (and a little less than half the DNA it will get) penetrates the ovum (egg) and triggers cell division, with the multiplying cells having the right number of chromosomes, and characteristics from both families. After a while, these cells are seen to start segregating some in groups that will later form intestines, some groups that will become heart tissues, others destined to end up as reproductive organs, etc. It takes a while, so part of the way through the process, you might have a club whose members act alike for a time, but then, like Southern Baptists, split into splinter groups that become increasingly different from the cells whose division formed them. Some chromosomes in any one group go dormant, while others take over the job of activating the DNA and RNA that determine whether the cells are skin or hair cells, whether they express pigment, and a multitude of other inherited things. Chromosomes that deal with how a dog barks do not function in cells that make up the skin, even though all the chromosomes with their genes are in all the somatic body cells. After the first few divisions of the fertilized egg, the mass is called an embryo. Like a seed or acorn that contains all the leaves, bark, roots, growth patterns, disease resistance, and more, the animal embryo can be thought of as the grown dog and its descendants in future tense.

In some lower animals, the segregation of tissues in the embryonic urogenital tract never is completed, the way we understand it in mammals, where the genitals are near but distinct from the urinary organs. You can think of them as having an interrupted or halted development compared to the higher animals. However, the closer to the time of conception and early division, the less the differences in embryos of worms, frogs, Chihuahuas, water buffalos, and pterodactyls. The differences become apparent as the cell groups continue to specialize, which is an ongoing process up to and even after birth.

Sometimes something goes wrong during the embryonic development of structures on their way to completion. If development is halted or damaged, the part of the body that should be normal later, just isn’t. The example we are looking at here is the development of the central dorsal line of the body. Early embryos in that area look a little like flat worms or pancakes, and as they (we, too) grow, the edges curl or fold up and are supposed to unite along the top. Ever make raviolis or apple tarts? You fold the edges of the pastry so that the filling is enclosed, and you pinch the dough together in order to fuse it and keep the contents from falling or leaking out, until you can bake it. The spinal cord is the ravioli filling, and the finished vertebral column is the baked shell. If the phone rings before you pinch the dough, and your darling toddler daughter puts the half-completed job into the oven and cooks them before you get back, the contents are exposed. A similar thing can happen in the molding of the body if embryonic development is interrupted. Premature babies are at higher risk because some of them haven’t finished the process of closure before they are popped into the oven known as the world outside of the womb. Incomplete frontal skull bones, spina bifida, and hemivertebra are examples of the defects that can occur along the dorsal midline.

Midline closure defects are expressed in a variety of ways; in German Shepherd Dogs, I have seen incomplete closure to the midline of the scalp, incompletely formed tails, skull defects, spina bifida, and cleft palates. I believe them to be related in most cases. Sometimes other midline abnormalities are found; some would include umbilical hernias, and although they may be an embryo defect of another sort, I doubt those are related to the others. Cleft lip (harelip) is probably caused at a different time during gestation than cleft palate or the other disorders named above. As we say in good obedience training and many other things, Timing is everything.

Cleft palate is a condition in which, for genetic and/or environmental reasons, the hard surface of the roof of the mouth and the softer palate behind it fail to close completely. The first sign something is wrong (if you don't examine your pups immediately after delivery) is usually milk bubbling out the nose when the newborn attempts to nurse. In addition to strictly genetic cause, there are numerous other cases of environmentally-mediated cleft palate. It is a frequent defect found in offspring of diabetics. It has been produced experimentally by vitamin A imbalance whether too much or too little, and is often a result of poisons and steroids taken or produced by bitches in the first three weeks of gestation. Such corticosteroid production increase frequently can be associated with unsound character and/or a severe scare (fright). In canines, a deficiency of vitamin B-12 has also been identified as a cause. Antihistamines given early in pregnancy, at least in some doses, are also suspect. Viral infections at that stage, or certain other chemicals have also been determined to cause cleft palate. I believe natural or synthetic hormones and steroids are potentially very dangerous if given to bitches during pregnancy; most of the time, cleft palate is a steroid caused birth defect. Cortisone and similar steroids can also facilitate spontaneous bleeding, which is more perilous during whelping and surgical convalescence than at other times.

Possible Problems In The First Three Weeks

While some deaths and other difficulties are genetically controlled or otherwise out of the breeder's power to prevent, many are avoidable if the midwife/pediatrician is knowledgeable and careful. Generally speaking, if you pay heed to the subjects of genetics, nutrition, sanitation, disease prevention, and management, you'll increase your chances for a normal, healthy, successful litter growing to adulthood.

Start with the bitch, for a healthy female will make for a healthy litter in most instances. Some drugs or excessive vitamin A administered during pregnancy have been identified as causing cleft palate, reduced litter size, mummified fetuses, and nervous system disorders, as well as eye, ear, and heart defects in the pups. Exposure to too much carbaryl (Sevin is the most common tradename) insecticide may produce deformities in intestines and abdominal-thoracic fissures; other insecticides may cause skeletal deformities in pups if the pregnant bitch has been exposed to very high levels. Be sensible in your use of these, and your dam will likely be safe. A friend of mine tragically dosed his bitch with 10% Sevin dust (the concentration used for garden pests) instead of far less of the 5% dust used for fleas and ticks, when she was newly delivered of a litter of pups. It killed both her and all of the puppies. It was the wrong time to use it, and he used far too much.

During the first week, the combination of the dam's carelessness and failure to lactate account for the greatest losses in neonatal deaths, and the latter may be partly due to the breeder's carelessness in the area of sanitation and prevention of infection. Statistically speaking, the less common causes of death in that first week include cleft palates, which are probably found in less than 3 percent. Such pups either are euthanized on the second day or die soon after from aspiration pneumonia due to the milk they suck going through the nasal passages into the lungs.

Harelip is a split in the front portion of the palate, extending up the center of the front lip between where the middle incisors would later come in, and as far as the nose bulb in most cases. It is caused by a disruption in the embryo development at a slightly different time than cleft palate is. Sometimes, if the psycho-biochemical disruption has continued for a longer period of time than an instantaneous trauma, you may find both conditions in the same pups. You may have met people with both. Although it is surgically treatable in humans, it is not, or at least is not worth the effort, in dogs.

Brief Selections from Case Histories

Several years ago an Ohio dog club member had a small litter of puppies born with cleft palates. One puppy had the cleft palate alone, another had the malformed lip/mouth, and another puppy was born with all its internal organs outside its body. This is an instance of where midline closure defect is expressed on the ventral portion of the dog as well. All pups in the litter died.

She found out, through some detective work, that it was due to a chemical ingested or inhaled. Nothing in her house or yard would have caused this and she asked around the neighborhood if anyone sprayed any yard chemicals (pesticides, insecticides, herbicides). Nobody did, or at least in her neighborhood. She finally figured out that when she was visiting her son at a new neighborhood and park that her dog had been exposed to chemicals sprayed on the grass, and then found out that a neighbor of his across the street had in fact had the famous-name company spray their yard, but took the flags down as soon as they were finished. So her dog was exposed to the lawn chemicals by absorption through the very porous pads as well as possibly by inhaling for a day or two. This was at the critical point in her pregnancy and pups’ embryo development when this exposure would most likely cause this problem. The first trimester is the time of greatest risk.

I once bred a bitch who was hard as nails to a great show dog named Hein, noted for pigment and hips, and my litter had one somewhat flighty, spooky bitch pup whose temperament characteristics did not immediately show themselves. When that bitch grew up, the owners bred her. During the first trimester, this bitch had a sudden and traumatic fright. Even though it lasted only a few minutes, and her nervousness was at a peak for a few hours or more, the repercussions followed at parturition. Her litter all were born with cleft palates. A couple had harelip as well. All were euthanized. She never had any pups with cleft palate afterwards. The male that I bred my bitch to was of normal temperament, but produced more than his share of nervous offspring. One all-black son of his, bred by the owners and named Phantom, produced many spooky pups and a great deal more were produced by his offspring, in turn.

Such changes from the norm of midline closure are possible through that psychophysical route, such as a bitch in that stage of pregnancy being badly frightened or startled. Her own hormonal chemicals act the same way that administered steroids could. Of course, the always-flighty or nervous bitch is far more susceptible to such an unusual event than a stable bitch is.

When I had mentioned that observation in a magazine article, someone wrote to me, How could that theory account for the marked association of facial cleft with brachycephaly? Short-faced bitches are more nervous and flighty perhaps? Or could it be genetic, I wonder! No, as I had written, there are more causes than this one. Nervous temperament can be and usually is very strongly genetic, as would be any unusual or "touchy" reaction to steroidal imbalance. Plus, brachycephalic dogs, however lovely in the eyes of owners, are short-faced because of abnormal pituitary/hypophysis glands. This "master gland" affects all other endocrine glands and all hormones, directly or indirectly. Including those that affect cleft palate. Perhaps the defect that causes a Bulldog face with pushed-in nose and undershot jaw is side-by-side with the defect that directly or indirectly interferes with normal midline closure in the embryo just before birth or earlier in gestation.

Although kennel-blind fanciers of Lhasa Apsos and other short-faced breeds have claimed that this opinion is not supported by anything we know about endocrinology or genetics, I have studied enough biology and genetics to disagree. It is generally assumed that the growth patterns such as shape of head (some breeds such as Saints, Newfies, etc. retaining "juvenile" looks) are related to the function of the pituitary/hypophysis, and growth hormones interacting with other hormones. I learned a long time ago that the pituitary/hypophysis of breeds with Pug/Peke/Bulldog-type faces are physically different than those in breeds with "ancestral" type heads (GSDs, wolves, Malamutes, Spitz, etc.) I leave it up to the naysayers to come up with a better explanation as to why these brachycephalic breeds have the look of a dog that ran 35 mph into a brick wall.

A Westie breeder wrote to me: We also one time had a whole litter of clefts. There was no history of clefts in either the line of the dog or the bitch. In fact, we had bred both sire and dam previously with no clefts at all. We spoke to various veterinarians about this. And they determined it was from a viral infection that I had when the puppies were in the critical period of gestation. Could be. Environmental irregularities can make for somatic irregularities. That same correspondent later wrote, Thank you! This explains the cleft palate puppy we had last year after our two bitches got into a fight. Dusty was at the critical time for palate development. And my other bitch lost her whole litter! Hormones! Ugh!

To avoid midline closure defects, there are several steps you should take. Naturally, the first is to be careful about your choice of breeding pairs. After insuring the genetic component as much as feasible, make sure that the environment is one that promotes good health and avoids toxins and psychological traumas. Don’t let your bitch roam, especially during the first 3 weeks of pregnancy. Make sure you do everything to favor full-term gestation. If you have brachycephalic (especially toy) breeds such as Pekes, Pugs, Bulldogs, Bostons, and the like, research the ancestors and siblings for any problems before you breed your own dog.

And, since it is not all that common, Don’t worry; be happy.

Copyright  Fred Lanting,  All rights reserved, but reprinting allowed after permission.  Please read his other articles on , for example, or e-mail him at: or for specific articles.

Editor’s Note:  A well-respected and frequent GSD specialty and all-breed judge for many clubs around the world, with KC and other-country credentials, Mr. Lanting since 1966 has lectured on Gait-and-Structure, Canine Orthopedic Disorders, and other topics, and has judged in about 30 countries. He has been described by a former OFA director as the world’s leading non-veterinarian authority on hip dysplasia. He has lectured at numerous veterinary schools in the USA and abroad, and is the author of the following “must read” books for the dog owner (E-mail for curriculum vitae). “Canine HD and Other Orthopedics Disorders” : This expanded revision is a comprehensive (nearly 600-page), amply illustrated, annotated, monumental work that is suitable as a coffee-table book, a reference work for breeders and veterinarians, and a study adjunct for veterinary students. It is equally valuable for the owner of any breed. It covers every aspect of HD and other orthopedic, bone, or spinal disorders, and includes genetics, diagnostic methods, treatment options, and the role of environment. Your autographed copy will be mailed from the USA as soon as the appropriate amount is received and is processed. Pricing: US $68 in the U.S., or ask about mail overseas. Combine orders with “The Total German Shepherd Dog” by the same author ($50 plus $4 postage). 17 of the 20 chapters are suitable for owners of any breed. Order both at once direct from the author, and the postage will be waived.

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