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 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 , 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 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 that occludes between the maxillary third and , and mandibular 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 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 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 with subsequent tooth death . 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 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, amputation with immediate endodontic treatment to reseal the 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 formation and the latter to pericoronitis.

Retained 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 ). 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 most often missing. In people and dogs there is a strong genetic association. In localized populations of cats the maxillary second 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 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, supernumerary teeth can develop. These pathways are under genetic control, but environmental factors and/or metabolic disturbances can also disrupt formation. "Twinning" or "gemini" teeth arise when a tooth germ begins to produce a second tooth but does not complete the process.

Problems that can arise from supernumerary tooth formation include crowding/periodontal disease, concussive trauma with the apposing arcade, failure of eruption of either the extra tooth or an adjacent tooth, displacement of neighbouring teeth and pathology relating to dentigerous cyst formation.

Treatment involves extraction of any teeth which are compromised, or causing pathology to occur elsewhere in the oral cavity. Most situations require dental radiographs to accurately identify which tooth should be removed, and to confirm that the extra tooth hasn't fused with the original.

Enamel Folding Defects and Supernumerary Roots Formation of a tooth begins at the occlusal tip and progresses toward the root. In a multirooted tooth once the formative cells reach the area that will be the cementoenamel junction they converge towards each other, cease enamel production, and begin to create the roots. If the convergence of the cells becomes confused enamel folding defects occur. Extra deposits of enamel can be seen within the tooth crown and small clefts can be seen in the exterior of the tooth in the furcation area. These teeth tend to have open communication between the oral environment and the pulp chambers allowing bacterial ingress. These teeth tend to die, but not always. The mandibular first is the most often affected, and this is almost always bilateral. Disorganization of root formation may cause formation. This may predispose a tooth to periodontal disease. All roots need to be removed during an extraction. Extra roots may be of no consequence in other teeth.

Wear and Discolouration Odontoblasts produce , throughout a lifetime, without cessation. Early deposition is rapid but slows with age. If occurs slowly then reparative dentin can be made at an equivalent pace to maintain the integrity of the dental hard tissues protecting, and delineating, the pulp chamber. Exposed reparative dentin is slightly porous and will pick up stain, becoming cream-to-milk-chocolate in colour. This layer will be smooth, level with the walls of the tooth, and does not allow probing with an explorer. Affected teeth do not usually need treatment.

Other causes of abnormal tooth colour are extrinsic staining, and deposition of intrinsic pigments. Intrinsic staining tends to occur from deposition of pigments within the enamel and/or dentin matrix as the tooth is forming, or pigments may enter hematogenously to discolour dentinal layers which form later. Intrinsic staining therefore cannot be polished off. An example of this would be tetracycline (yellow/brown) staining from the antibiotic being given to the pregnant female, or to the neonate while the dentition is still forming. Porphyrins (pink fluorescence), bilirubin (green) and high iron content (brown/black) in water sources, are other sources of intrinsic staining. In human patients external and internal bleaching can lighten stains and veneers may provide further aesthetic camouflage. These measures are rarely taken in pets.

Extrinsic staining tends to be from contact with a pigmenting substance found in the environment. An example of this would include the brown discolouration hairless-breed kittens are reported to acquire from accumulation of skin oils/waxes on the teeth during nursing and grooming. (This extrinsic staining must be distinguished from .) Chlorhexidine mouth rinses used long-term can stain surface plaque brown. Food colouring and dyes from chew objects can also transfer colour to the oral cavity. Removal of the inciting agent may be sufficient to allow the pigmentation to fade. Polishing of the teeth with a medium grit pumice or polishing paste should resolve most cases.

SUPERERUPTION Supereruption can be an age-related manifestation of normal post-eruption physiologic processes that maintain the tooth position within the alveolar bone, or it may be associated with pathology. The normal eruptive tension within the periodontal ligaments continues throughout life, and is usually offset by occlusal intrusive forces. An imbalance between eruptive and intrusive forces, combined with cemental hypertrophy (see ) and senile atrophy of the alveolar processes with gingival recession may increase the length of the clinical crown. Close examination of these teeth will reveal the cementoenamel junction is coronal to the alveolar ridge. Prolonged supereruption results in a tooth which becomes so extruded that anchorage is compromised and the tooth may become loose, and lost, from normal mastication forces. Affected cats may show some sensitivity from root exposure. Treatment to reduce this sensitivity may include the professional application of unfilled resins and/or fluoride products.

Pathologic extrusion can occur in association with . Radiographic and histologic assessment of teeth, affected with replacement resorption and/or extrusion showed a statistical association between extrusion and root resorption. For this reason any extruded tooth should be assessed for resorption. However, because loss of the periodontal ligament space in early replacement resorption can be difficult to differentiate from hypercementosis on radiographs clinical judgement must be employed when making extraction decisions for these patients.

HYPERCEMENTOSIS Hypercementosis is a normal, age-related infilling phenomenon which is secondary to axial movement typically seen in older cats. Radiographs show increased density and thickening of the periapical area secondary to the benign deposition of layers of , and increased deposition of periapical alveolar bone. In many cases the periodontal ligament space is no longer clearly discernible and the tooth may appear to be fused with the bone. This condition must be distinguished from ankylosis associated with root resorption because these roots are not undergoing pathologic change and should never be crown amputated. If the tooth requires extraction the tooth must be extracted in total.

CHRONIC ALVEOLITIS/OSTEITIS Feline chronic alveolitis is a species-specific manifestation of chronic periodontal disease. Alveolitis/osteitis is characterized by inflammation and outward expansion of the bone around a canine tooth, and in some cases, loss of supporting periodontal structures. Treatment involves treatment of the periodontal disease, alveoplasty to return the bone to more anatomically normal contours and remove infrabony pockets, and in the case of extraction, and will facilitate a tension-free closure of the surgery site.

SYMPHYSEAL BONE LOSS and OPEN MOUTH JAW LOCKING In the majority of mammals the symphysis is a fibrous union joining the two together. With age that joint may become lax. Radiographic examination may show a widened symphysis that may be mistaken for traumatic separation. Irregularities in density can also be seen in aging pets, often exacerbated by severe periodontal disease of the mandibular incisor or canine teeth. The significance of a mobile symphysis is controversial. If the patient is asymptomatic treatment is not needed. If mobility is affecting the ability to eat, or is causing pain, dental acrylic can be used to stabilize the fibrous union. Figure eight wiring around the canine teeth is not a recommended long-term solution because the wire can cause inward rotation of the mandibles which will stress the temperomandibular joints. Additionally the wires may contribute to gingival trauma. Circumferential wiring around the mandibles leaves exposed wire that bacteria can utilize to gain access to the subcutaneous tissues. This is not an acceptable long-term stabilization technique either.

In a small number of patients symphyseal laxity, likely combined with mildly deformed temperomandibular fossas, may allow the mandibular body to rotate buccally and the coronoid process to interfere with the zygomatic process with open-mouth jaw locking as the presenting complaint. Open-mouth jaw locking with lateral displacement of the coronoid process has been reported in several head types including dolicocephalics and bracycephalics with Boxers over- represented. Patients present in acute distress, unable to close their mouths, with a palpable bump lateral to the zygomatic arch on the affected side. Skull radiographs will confirm the displacement. Analgesics combined with sedation or anesthesia may allow the to be opened maximally so the coronoid can be manipulated and the dislocation reduced. Recurrence is common. Some cats and dogs learn to unlock their jaws themselves. The permanent solution to this problem is to remove a portion of the zygomatic arch and/or the coronoid process but may be controlled with intermandibular arthrodesis.

SUMMARY In the majority of cases of oral variation, early detection via thorough oral examination and dental radiographs, and treatment by astute veterinary practitioners, will limit the comorbidity of the conditions described. To date the veterinary literature has sparse information about many of the conditions listed above, but as genetic information becomes available and we become more consistent at detecting and documenting these problems, we should get better data on their frequency and causes.