Palate Defect

Embryology

During embryogenesis the paired maxillary processes, the paired mandibular processes, and the median frontonasal process surround the primitive oral cavity. Medial and lateral nasal processes originate from the frontonasal process and extend on each side of the olfactory placodes. In contrast to humans, where the upper lip is formed by the maxillary and nasal processes, in dogs and cats the upper lip and the primary palate are both formed by the midline fusion of the maxillary processes [1].

At this stage of the development, the choanae open at the caudal end of the primary palate. Later, the lateral palatine processes move toward the midline and fuse with the downwardly growing nasal septum that originates from the nasal process. This constitutes the secondary palate which will ossify (hard palate), except in the caudal part where it will form the soft palate [2].

Anatomy

The upper lip and most rostral hard palate supported by the palatine processes of the incisive bones constitute the primary palate. The hard palate that is supported by the palatine processes of the maxillary bones and the horizontal laminae of the palatine bones together with the soft palate constitute the secondary palate [3]. The junction of the hard and soft palate is at the level of the first maxillary molar teeth. The incisive bones carry the incisor teeth. The maxillary bones carry the canine, premolar, and molar teeth. The palatine bones do not contain teeth.

Cornified stratified squamous epithelium covers the oral surface of the hard and soft palates. The oral mucosa covering the hard palate is developed into 6 to 10 transverse ridges and depressions (palatine rugae) [4]. The mucosa ends abruptly laterally at its junction with the short palatal free gingiva and has a thick tough connective tissue support, the mucoperiosteum, which is continuous with the periodontal ligaments of the maxillary teeth [5]. The incisive papilla is located on the midline rostral to the first transverse ridge and just caudal to the maxillary first incisor teeth. On either side of this papilla are the incisive ducts that extend caudodorsally through the palatine fissures into the floor of the nasal fossae. This duct communicates with the vomeronasal organ [3].

Unless stretched, the oral surface of the soft palate is thrown into many fine longitudinal folds and a few larger transverse ones, evidence of the mobility and slight elasticity of the soft palate. The oral mucosa of the soft palate is also richly endowed with palatine glands and lymphoid tissue. Dogs and cats possess several tonsil-like structures, but only the palatine tonsils are conspicuous as large, ovoid, discrete bodies, each partly concealed in its own tonsillar fossa by a tonsillar fold derived from the soft palate caudal to the palatoglossal folds [3]. Efferent lymphatics depart for the medial retropharyngeal lymph node.

The free edge of the soft palate curves laterally to form the left and right palatopharyngeal arches, which pass caudally and merge with the walls of the pharynx to create a large caudoventrally directed central hole - the intrapharyngeal ostium. The three parts of the pharynx (nasopharynx above, oropharynx below, and laryngopharynx behind) meet at this ostium, and a pair of palatopharyngeal muscles within the arches serves as its sphincter [3]. No uvula is present. There is no palatoglossal arch in the dog and cat comparable to that structure in humans, as they lack the palatoglossal muscle that forms the basis of the human arch. When the tongue is forcibly withdrawn from the mouth and moved to one side, a fold is developed on the opposite side, running from the body of the tongue to the initial part of the soft palate. Although this fold is not formed by muscle as in humans, is seems feasible to regard it as the palatoglossal fold, which distinguishes it from the palatoglossal arch of humans [3]. The minor palatine artery, infraorbital artery, and a common trunk that gives rise to the sphenopalatine and major palatine arteries are branches of the maxillary artery (Fig. 23.1) [3,6]. At its most caudal aspect the maxillary bone forms a small pointed spur, the pterygoid process. This process and the palatine bone form a notch or foramen, through which the minor palatine artery passes, which is the main blood supply to the soft palate.

Figure 23.1. Terminal branches of the maxillary artery. (From Evans H (ed): Miller’s Anatomy of the Dog, 3rd ed. Philadelphia: WB Saunders, 1993.)

The muscles of the soft palate consist of the paired intrinsic palatine muscles and the end ramifications of the paired tensor and levator veli palatini muscles [3,7]. The fibers of the palatine muscles are longitudinal and shorten the relatively long soft palate of the dog. Lateral radiographs in brachycephalic dogs reveal that their soft palate is thickened, suggesting that these animals have sustained contractions of their palatine muscles to maintain a patent airway. The tensor and levator veli palatini muscles stretch and lift the soft palate, respectively, with the aponeurosis of the tensor also serving as a structural support for the palate. The insertion of the tensor veli palatini muscle passes over the ventral edge of the hamular process of the pterygoid bone to reach rostrally in the soft palate. The main sensory supply to the soft palate is the minor palatine branch of the maxillary nerve (derived from the trigeminal nerve). The tensor veli palatini muscle is also supplied by a branch of the trigeminal nerve, while the levator veli palatini muscle is innervated by the facial nerve. Nerves from the pharyngeal plexus (derived from glossopharyngeal and vagus nerves) supply the palatopharyngeal muscles [3].

The lateral surface of the palatine bone forms the medial wall of the pterygopalatine fossa. There is one large opening, the maxillary foramen for the infraorbital artery, and two smaller openings, the sphenopalatine foramen for the sphenopalatine artery and the caudal palatine foramen for the major palatine artery. The infraorbital artery runs in the infraorbital canal and emerges at the infraorbital foramen. The sphenopalatine artery extends to the nasal cavity. The major palatine artery passes through the palatine canal with a delicate vein and relatively large satellite nerve and emerges again at the major palatine foramen that is located near the transverse palatine suture between the median palatine suture and the maxillary fourth premolar tooth, from where it runs rostrally in the palatine sulcus to the palatine fissures. This artery is the most important vascular structure of the palatal mucosa and needs to be preserved during surgical procedures. Within the palatine canal the nerve and artery divide so that one or more accessory palatine arteries and nerves emerge on the horizontal process of the palatine bone through minor palatine foramina situated caudal to the major palatine foramen [3].

A small rostral septal branch of the major palatine artery passes through the palatine fissure dorsomedially and anastomoses with a branch of the sphenopalatine artery, which supplies the mucosa on the nasal side of the hard palate and the nasal septum. A small artery extends rostrolaterally and passes through the interdental space between the canine and third incisor teeth, anastomosing with the lateral nasal artery. The most rostral aspect of the major palatine artery branches profusely and anastomoses with its fellow. At the anastomosis a small vessel runs dorsally through the incisive foramen near the interincisive suture in the incisive canal, joining the right and left lateral nasal arteries. The main channel draining the area of the hard palate runs caudally in the soft tissue of the hard palate as a spongy, poorly developed venous plexus. The plexus continues in the soft palate, where it lies dorsal to the palatine glands and lateral to the palatine muscles. It empties into the maxillary vein caudal to the temporomandibular joint, ventrolateral to the tympanic bulla. The lymphatics go to the medial retropharyngeal lymph nodes [3].

Etiology

Congenital defects of formation of the lip and palatal structures have been reported in both dogs and cats and may be inherited or result from an insult during fetal development.5 A wide variety of dog and cat breeds have been affected. Brachycephalic dog breeds have been reported to be at higher risk. Growth of the palatine portions of facial bones must compete successfully with growth of the skull width to achieve midline closure of the palate. Broad-headed fetuses have a greater tendency to develop a cleft palate. The sporadic nature of these conditions and the wide range of dog and cat breeds that are affected suggest that in many cases the cause is an intrauterine insult rather than inheritance,5 although all types of clefts, from partial unilateral to complete bilateral, have been produced in dogs in mating trials. As in children, unilateral harelips in dogs are almost always on the left side, and cleft lips may be associated with abnormalities of the secondary palate. According to the stage of development and the severity of the cause, other physical or neurologic abnormalities may be present. Clefts can occur if the intrauterine insult (trauma, stress, corticosteroids, antimitotic drugs, nutritional, hormonal, viral, and toxic factors) occurs at a specific time in fetal development (25th to 28th day in dogs) [2].

Acquired palate defects result from chronic infections (severe periodontal disease), trauma (e.g., high-rise syndrome, electric cord and gunshot injury, dog bites and foreign body penetration, and pressure wounds secondary to malocclusion), neoplasia, and surgical and radiation therapy (Table 23.1) [5]. In all cases, the cause of the defect must be removed prior to repair. The most common cause of oronasal fistula is loss of incisive and/or maxillary bone associated with severe periodontal disease or tooth extraction. Traumatic cleft palate is commonly seen in cats after high-rise trauma. The defect that develops from electric cord injury is due to thermal necrosis of the soft and hard tissues of the palate.

Pathophysiology

Whereas the hard palate forms a rigid partition between the oral and nasal cavities, the soft palate forms a valve. When elevated during swallowing, it closes off the nasopharynx, and when depressed during nose breathing, it closes off the oropharynx [3]. During swallowing, it works with the epiglottis, which closes off the distal airway, to allow a bolus of ingesta to cross the respiratory tract. Thus, the palate allows independent functioning of the respiratory and digestive systems and is especially important during the neonatal period, when sucking requires an airtight oral cavity [5].

Congenital palate defects manifest either as cleft lip or cleft palate. Defects of the primary palate are obvious at birth as an abnormal fissure in the upper lip (harelip) and/or a cleft of the most rostral hard palate (Fig. 23.2A). Affected animals must be examined for coexisting clefts of the secondary palate. Except for being externally visible, clefts of the primary palate rarely result in clinical signs beyond local rhinitis, and repair may be performed for esthetic reasons. Clefts of the secondary palate (cleft hard and/or soft palate) are more common and more serious, although they are rarely visible externally. They are almost always along the midline and are usually associated with a midline soft palate abnormality (Fig. 23.2B). Soft palate defects without hard palate defects may occur in the midline or may be unilateral [8]. The prognosis for congenital absence of the soft palate, as opposed to cleft soft palate, is poor because restoration of a palatopharyngeal sphincteric ring and normal swallowing function may not be achieved despite careful planning and meticulous surgical technique [9,10]. Clefts of the secondary palate frequently go unnoticed until a neonate demonstrates clinical signs, including failure to create negative pressure for nursing, nasal discharge (drainage of milk from the nares during or after nursing), coughing, gagging, sneezing, nasal reflux, tonsillitis, rhinitis, laryngotracheitis, aspiration pneumonia, poor weight gain, and general unthriftiness. Early diagnosis is important so that these secondary problems can be avoided. The prognosis without surgical repair is guarded because of the risk of aspiration.

Figure 23.2A. Defect of the primary palate presenting as harelip in a Bull Terrier.

Figure 23.2B. Defect of the secondary palate presenting as cleft of the hard and soft palates in a German shepherd dog.

An acute oronasal fistula following tooth extraction is diagnosed by direct visualization of the nasal cavity and hemorrhage at the nostril. Clinical signs of a chronic oronasal fistula include sneezing and ipsilateral nasal discharge. A defect in the area of a missing tooth that communicates with the nasal cavity may be noted on oral examination [5]. Patients with large acquired palate defects may show similar clinical signs as those with congenital defects of the secondary palate (Fig. 23.3). The further caudal and the larger a defect, the more severe become the clinical signs.

Figure 23.3. Acquired hard palate defect after gunshot trauma.