THE YOUNG AND THE OLD: NORMAL AND VARIATIONS FROM NORMAL Judy Rochette DVM, FAVD, Dipl AVDC The majority of notable findings in the oral cavity of the young pet are related to its formation and development, as well as the development and eruption of teeth, whereas senior pet variations reflect the gradual aging of the dental hard tissues and their supporting structures. The head, face, and oral cavity are some of the first structures to manifest in the developing embryo. The upper face forms from the neural tube while the lower face forms from branchial arches. The oral mucosa and upper alimentary tract form from the ectodermal layers. The mesenchymal layer provides the cells which will become subcutaneous tissues and the bone and supporting apparatus for the teeth. The teeth themselves are both ectodermal and mesodermal in origin. Any phenotypic variation from the "wild type" of head, or any genetic anomaly which affects the ectoderm or mesodermal tissues will likely have an effect on the oral cavity. Some of these anomalies have been intentionally introduced to create new "breeds". BRACHYCEPHALIC SYNDROME Brachycephalic syndrome is a set of dysfunctional anatomical airway variations familiar to veterinarians who deal with Bulldogs, Pugs and Boston Terriers but this syndrome is also a problem in Persian, Himalayan and Burmese cats. Stenotic nares, an elongated soft palate, hypoplastic trachea and everted laryngeal saccules can all inhibit respiration. Mouth breathing, stertor, exercise intolerance and collapse after exercise can be seen. Early surgical intervention to open the nares and shorten the palate will often arrest the development of everted saccules, lower respiratory tract inflammation and cardiac stress. Any animal with significant respiratory difficulty and/or that require corrective surgery should not be bred. (MAL)OCCLUSION A healthy occlusion resembles the "wild" phenotype with interdigitating cheek teeth that create a "pinking shears" affect, a mandibular canine tooth that occludes between the maxillary third incisor and canine tooth, and mandibular incisors that rest immediately distal to the maxillary incisor teeth. This model of occlusion is the most efficient and durable for a predator's diet. The skeletal architecture complements this oral arrangement by having strut reinforcement of the facial bones in the areas where maximum forces would occur. It can be detrimental for animals to have genotypic, and/or phenotypic variation from normal. What is considered acceptable as a breed standard may not be ideal for a pet's quality of life. The prevalence of malocclusion in domesticated cats has been poorly documented but one study in the United Kingdom reported the prevalence as 3.9% over all breeds of cats, with an increased prevalence (13%) in longhaired cats. It was not specified that the longhaired cats were brachycephalic breeds. The prevalence of malocclusion in the dog could not be found but Stockard's study proved that malocclusion in dogs or cats is primarily under genetic control, and most clinically significant malocclusions result from discrepant jaw lengths due to selection for specific breed standards. A Class 1 malocclusion which the American Veterinary Dental College has been defined as a "normal rostral-caudal relationship of the maxillary and mandibular dental arches with malposition of one or more individual teeth" can include rotation, tipping, and physical displacement. An example of a Class 1 malocclusion involves the maxillary canine tooth being facially tipped, and has been called a "lance" canine tooth. This tipping causes loss of the diastema where the mandibular canine tooth would normally occlude. The mandibular canine is forced to tip buccally and the tooth-on-tooth contact between the mandibular and maxillary canine teeth can also cause a concussive pulpitis with subsequent tooth death . Periodontal disease can also form around the crowded maxillary incisor and "lance" canine tooth. A Class 2 malocclusion occurs when the mandibular arch occludes caudal to its normal position relative to the maxillary arch. This occlusal abnormality is not as common in the cat as in the dog but does occur in all animals. In a growing animal a dental interlock of the mandibular canine teeth interfering with the distal surface of the maxillary canine teeth can act as an impediment to any corrective growth that may occur. Trauma to the soft tissues of the palate and maxillary alveolar ridge is common with this malocclusion. Periodontal disease secondary to damage to the attached gingiva of the maxillary canine tooth, oronasal fistula formation and dysmastication are all possible. Likely the most common occlusal problem is a Class 3 malocclusion, and symptomatic cases almost always accompany a brachycephalic head. The mandibular arch occludes rostral to its normal position relative to the maxillary arch usually due to maxillary brachygnathia. Rotation of the maxillary cheek teeth to accommodate the smaller space results in crowding, which prevents an intact collar of attached gingiva around each tooth and allows periodontal disease to develop. The maxillary incisors may damage the lingual aspects of the mandibular canine teeth or the mandibular soft tissues. Under- eruption of teeth with subsequent pericoronitis is common. Treatment of a malocclusion should be directed towards removing the source of soft tissue trauma, relieving crowding, arresting tooth-on-tooth concussion, and restoring a functional occlusion. Orthodontic movement, crown amputation with immediate endodontic treatment to reseal the pulp chamber, or extraction of the offending tooth/teeth can all be utilized. What option is implemented depends on the operators skills, the temperament of the patient and the dedication, patience, and financial means of the owner. TEETH The formation, eruption, and shedding of the deciduous and permanent dentitions is a tightly choreographed series of events. Disruption anywhere along this pathway can result in visible oral pathology. Impaction During eruption the tooth moves from its position within the bone of the jaw to its functional position in occlusion, and the primary movement is coronal/axial. If the tooth is abnormal, or another dental structure interferes with the eruption pathway, eruption is impeded. An inability of the teeth to erupt through the gingiva can be resolved by operculectomy. If the gingival impediment is removed before apical closure of the successional tooth eruption potential still exists and the tooth may take its proper position within the dental arcade. If the impediment is not removed in time then the tooth may never erupt, or not erupt to its full height. The former situation can lead to dentigerous cyst formation and the latter to pericoronitis. Retained Deciduous Teeth Exfoliation of deciduous teeth is the result of progressive resorption of the tooth roots and the associated periodontal ligament. Resorption is triggered by pressure on the deciduous tooth from a successional tooth, from growth-related increases in forces of mastication that overwhelm the deciduous tooth support structures, and from apoptotic cell death. Missing successional teeth will delay shedding as will occlusal interference that removes mastication forces from a tooth. Apoptotic cell death is 80% genetically controlled so familial tendencies for retained deciduous teeth can be identified. If deciduous teeth are present when the adult tooth is erupting they must be removed to prevent displacement of the adult tooth, and avoids periodontal disease secondary to crowding. If the adult tooth is not present, if the patient is very small such that the size difference between the deciduous tooth and the adult tooth is minimal, if crowding is not present, if the roots are fully formed/not resorbing and if the owner is aware the deciduous tooth is more susceptible to fracture then deciduous teeth can be left in place to function - often for many years or even a lifetime. In cats early research appears to suggest that retained deciduous teeth may have a correlation with idiopathic patellar fracture, perhaps secondary to an underlying connective tissue disorder, but the pathophysiology is actually not known. Abnormalities in Tooth Number Failure of tooth formation results in the absence of a single tooth, or multiple teeth (oligodontia or partial anodontia). Global disruption of tooth formation results in absence of all teeth (anodontia). Reports of oligodontia or anodontia in cats are very sparse in the literature but is not rare in the dog with the first premolars most often missing. In people and dogs there is a strong genetic association. In localized populations of cats the maxillary second premolar was found to be missing in 3.4% of cats in the United Kingdom but the prevalence was 23.6% for a group in Mexico suggesting a genetic role for cats as well. Although alopecia, or hypotrichosis, has been associated with oligodontia in dogs and people, the feline breeds with known ectodermal defect syndromes (Sphinx, Devon Rex) do not seem to have this associated oligodontia, which suggests a different genetic modification for these phenotypes in the feline versus other species. Missing teeth must be confirmed radiographically to distinguish them from a failure of eruption, or fusion. Embedded teeth are at risk of dentigerous cyst formation and must be removed. Fused teeth usually do not need treatment. When the molecular signalling pathways involved in normal tooth development are overactive single, or multiple,