Congenital Oronasal Fistulas (Cleft Palate and Cleft Lip) in Animals
Congenital oronasal fistulas result when the palatine shelves fail to fuse during gestation. This fusion typically occurs at 25–28 days of gestation in dogs and 47 days of gestation in horses. Clefts can be either of the primary palate (involving the lip and incisive bone), cleft lip (harelip); or of the secondary palate (involving the hard and soft palate), cleft palate. The conditions can occur singly or together. In dogs, CT studies have shown an association of cleft palate with other craniofacial abnormalities, including hypoplastic tympanic bullae, hypoplastic nasal turbinates, and maxillary malocclusions, mostly of the incisors. Affected animals should also be examined for neurologic signs because concurrent hydrocephalus has also been described.
Typically, animals are diagnosed with oronasal fistulas at birth or shortly after birth by oral examination, by observation of dysphagia or milk draining from the nares after nursing, and/or by clinical evaluation revealing respiratory compromise and signs of aspiration pneumonia. Many affected neonates are euthanized or die early in life. Although surgical repair has been undertaken in many species, success has varied, and complications such as surgical site dehiscence, continued nasal discharge, chronic ill thrift, and chronic pneumonia have been reported.
Courtesy of Dr. Lisa Pearson.
Cleft palate and cleft lip have been described in most domesticated animal species, including dogs, cats, ruminants, horses, and camelids. In dogs, brachycephalic breeds are overrepresented; other breeds with higher incidence include Beagles, Cocker Spaniels, Dachshunds, German Shepherd Dogs, Labrador Retrievers, Schnauzers, and Shetland Sheepdogs. The most commonly affected cat breed is the Siamese. Etiologies include genetic, teratogenic, and nutritional causes.
Modes of inheritance are monogenic autosomal recessive or incomplete dominant in several breeds. The mode is believed to be autosomal recessive in Brittanys, Pyrenean Shepherds, Beagles, and Boxers; in Bulldogs (French and English) and Shih Tzus, autosomal dominant inheritance with incomplete penetrance is suspected. Autosomal recessive inheritance patterns are evident in Angus cattle with congenital multiple arthrogryposis, in Charolais cattle with cleft palate and arthrogryposis, and in Texel sheep with cleft lip.
Teratogens and nutritional causes of cleft palate and cleft lip include high concentrations of vitamin A in the diet, administration of griseofulvin, folic acid deficiency, and ingestion of toxic plants during pregnancy. In cattle, ingestion of lupines during days 40–100 of gestation results in arthrogryposis and cleft palate due to the effects of anagyrine found in Lupinus sericeus and Lupinus caudatus. Ingestion of poison hemlock (Conium maculatum), which contains the toxic alkaloid coniine, produces similar clinical signs in both cattle and goats; ingestion of corn lily (Veratrum californicum) by sheep, goats, or cattle results in cleft lip and/or cleft palate in the fetus.
For puppies and kittens that are not euthanized, medical management is required until surgical options are explored. Patients are fed via orogastric tube until dry food can be tolerated. Water can be offered by overhead dispenser. In experimental settings, a custom-molded palate guard that enables adult dogs to eat and drink normally has been described. Aspiration pneumonia should be quickly identified and treated.
Patients should be at least 12 weeks old at the time of surgical correction, but some studies have shown higher success when surgery is performed at > 20 weeks of age or in adults. Surgical correction has a high failure rate because of the continued growth of puppies or kittens postoperatively, the small size of the patient, and irritation of the surgery site by the tongue and feed material. Surgical techniques depend on the location and size of the cleft defect. For secondary palate defects, sliding mucoperiosteal flaps or overlapping flaps are the most commonly used. Survival rates as high as 67% have been reported for horses undergoing either surgical or medical management of congenital cleft palate; however, there is great variation across case reports, and a wide range of complications may arise, depending on the severity of the defect.
Extensive involvement of the soft palate carries a poor prognosis, even with surgical intervention. Surgical repair should be attempted only after ethical questions have been addressed, and the affected animal should be surgically sterilized or removed from breeding stock to prevent reproduction of the anomaly in future offspring.
Occlusal Anomalies in Animals
Courtesy of Dr. Lisa Pearson.
Courtesy of Dr. Lisa Pearson.
Courtesy of Dr. Lisa Pearson.
Occlusal abnormalities due to abnormal lengths of the maxilla and mandible are common in animals. Brachygnathism, also called overbite, overshot, overjet, short lower jaw, or parrot mouth in horses, is manifest when the mandible is shorter than the maxilla. The condition can be found, with varying severity and incidence, in all species of animals.
Recessive traits and disorders associated with brachygnathism have been identified in Red Angus and Simmental cattle, as well as in Merino sheep. Congenital brachygnathism in cattle may also be due to bovine viral diarrhea virus. Brachygnathism is common in horses—the result of either a lengthened maxilla or a shortened mandible. Modes of inheritance are unknown. The condition may develop in utero as a result of treatment of the mare with griseofulvin.
Most horses do not experience dysphagia; however, cheek teeth malocclusions are common, and regular dental care is required. Correction can be attempted in foals via surgical placement of tension band wires around the maxillary incisors to inhibit maxillary growth so that the occlusal surfaces can align better as the mandible continues to grow.
In small animals, mild forms of brachygnathism may be of no clinical importance; however, more severe forms may result in trauma to the hard palate or restriction of normal mandibular growth secondary to erupting adult mandibular canine teeth. Treatment varies from none to various orthodontic or endodontic procedures, depending on the severity of the condition. Often, the mandibular canine teeth are removed, or crown reduction is performed, with concurrent pulpotomy or root canal. Intervention early in life is recommended and improves both short- and longterm outcomes.
Courtesy of Dr. Lisa Pearson.
Courtesy of Dr. Ben Colmery III.
Prognathism, also called undershot, underjet, or, in horses, monkey mouth or sow mouth, is identified when the mandible is longer than the maxilla. In brachycephalic dogs and Persian cats, prognathism is considered a normal breed characteristic. In horses, it occurs more commonly in miniature and Arabian breeds. The severity varies, and the condition may not require treatment. In severe cases in foals, surgical placement of tension band wires can allow for continued maxillary growth while restricting the mandibular growth. The most severe consequences of prognathism result from malocclusions. Affected foals may have difficulty nursing, and older animals may experience difficulty grazing. Cheek teeth malocclusions should be addressed with regular dental care.
Chondrodysplasia, a simple dominant trait of Dexter cattle, is a lethal defect that can result in “bulldog calves,” which are characterized by severe skeletal malformation and craniofacial dysplasia that has the appearance of prognathism.
Tongue Anomalies in Animals
Ankyloglossia, also called tongue-tie, is a disorder of Anatolian Shepherd Dogs characterized by a short, thickened lingual frenulum that inhibits normal movements of the tongue. By an unknown mechanism, the normal fetal apoptosis of the cranial two-thirds of the frenulum does not occur. Clinically, the tongue appears notched or W-shaped. Animals may experience dysphagia; difficulty suckling, drinking, or licking; trouble vocalizing; and impedence of panting and therefore thermoregulation. Frenoplasty is corrective. Breeding of affected animals is not recommended.
Microglossia is a congenital defect characterized by missing or underdeveloped lateral and rostral thin portions of the tongue that result in prehensile and motility disturbances. It is often referred to as “bird tongue” in dogs and may be a component of fading puppy syndrome, because affected puppies have difficulty nursing and swallowing and can aspirate or quickly become dehydrated. In cattle, excessive salivation has been observed. Even with supportive dietary measures, the prognosis is poor.
Macroglossia, or large tongue, has been described in association with nasopharyngeal dysgenesis in Dachshunds. It also occurs in double-muscled cattle breeds, such as the Belgian Blue, and it can inhibit nursing in calves.
Epitheliogenesis imperfecta is a disorder of the skin in which the epithelium is absent, revealing the dermis. Commonly affected areas include the limbs, back, and oral mucosa and tongue. The disorder is inherited in a simple recessive manner and is well described in sheep, cattle, and horses, particularly Saddlebreds. Euthanasia is typically elected, but surgical repair may be attempted in select cases.
Tight-lip Syndrome of Chinese Shar-Pei
Tight-lip syndrome, a small or absent lower lip vestibule, is a congenital defect of some Chinese Shar-Pei dogs. The lower lip covers the mandibular incisors and canines, disrupting normal occlusion, inhibiting mandibular growth, and leading the dog to bite on the lip, thus presenting welfare issues. In extreme cases, the mandibular incisors become lingually directed. Surgical correction by cheiloplasty using several different mucosal flap techniques has been described. Any animals that have undergone surgical correction should not be presented for conformation showing and should not be bred.
