The VOHC Seal: what does it mean?
An independent method has been developed that delivers an impartial assessment of the efficacy of products that claim to help reduce dental plaque or calculus in our pets, as Ana Nemec describes.
Published 30/03/2021
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The incidence and severity of many oral problems (e.g. periodontal disease) increase with age; however young animals can also suffer from oral or dental disorders. The timely diagnosis and treatment of these diseases is essential...
Oral examination should be a part of every clinical examination; timely detection and treatment of juvenile oral disease can often prevent subsequent problems.
A correct and definitive diagnosis of oral disease is often only possible with the help of intra-oral dental radiographs.
If teeth are clinically absent, radiography is essential in order to exclude the possibility of retained and impacted teeth.
Tooth fractures, even in milk teeth, always require treatment.
Persistent milk teeth should always be extracted as soon as the corresponding adult tooth erupts.
Number of teeth
Absence of all (anodontia) or almost all (oligodontia) teeth is rare; if present it is frequently related to a generalized disorder (e.g. ectodermal dysplasia). In contrast, one or a few missing teeth (hypodontia) is a more common finding (Figure 1). In particular, in brachycephalic, small and toy dog breeds the first premolars or last molars are often missing. Congenital aplasia of teeth is usually hereditary but trauma or infection during tooth development (< 4th month of life) can also lead to missing teeth. Hypodontia of permanent dentition is more common than with primary dentition. When a milk tooth is missing, in most (but not all) cases its adult successor is also missing. Radiography should always be used if teeth are absent in order to exclude the possibility of retained or impacted teeth. Hypodontia is mainly a cosmetic problem and requires no therapy, but depending on the breed standard some animals may be excluded from breeding 1 2. An excess of teeth (hyperdontia) can occur in both primary and adult dentition, and again this can be inherited or be related to problems during tooth development. Most frequently the incisors or premolars are involved (Figure 2). Again radiographs must be taken in order to differentiate supernumerary teeth from incompletely separated teeth (see below) and retained milk teeth. Supernumerary teeth can cause problems with eruption, crowding or deviation of adjacent teeth. Moreover, teeth that are crowded together accumulate more plaque, predisposing to periodontal disease. When this happens, the tooth which is most abnormal in terms of size, shape or position should be extracted. However if the hyperdontia causes no clinical problem, no therapy is needed 1 2.
Alteration in shape
Fusion is where two dental germs fuse together, and can involve the entire length of the tooth or just the root area, depending on the timepoint at which it occurs during tooth development. The pulp of both teeth can also be fused (Figure 4a and b). Both etiologies are unknown, although trauma and/or a genetic component have been suggested 1.
Concrescence is the fusion of two adjacent teeth by the root cementum; crowding of the roots or trauma are considered to be possible causes.
All three conditions typically require no treatment, unless changes lead to clinical problems such as periodontal or endodontic disease. Where treatment is advisable, pre-operative radiographs are essential to plan treatment, as roots are often abnormal in number or shape, and abnormal pulp conditions may be present 1.
Various developmental problems, with many different causes, can lead to structural defects (dysplasias) of the hard tissues (enamel and dentine) of the teeth. Typically these dysplasias are acquired (e.g. via trauma, infection) and may affect either the enamel or dentine in isolation, or the entire tooth (odontodysplasia) may be involved.
There are three types of enamel dysplasia: enamel hypoplasia, enamel hypomaturation and enamel hypomineralization. Enamel hypoplasia is characterized by an insufficient quantity of enamel. The defects can be focal or multifocal, and the crowns of affected teeth can show both dysplastic enamel and areas with normal enamel formation. In enamel hypomaturation and hypomineralization the enamel matrix development is disturbed, leading to the formation of soft enamel which is quickly eroded.
Congenital (genetically related) dysplasias are very rare and include amelogenesis imperfecta (enamel dysplasia) and dentinogenesis imperfecta (dentine dysplasia). Acquired enamel dysplasias are common in dogs but rather rare in cats. The defects are due to external influences during enamel formation (up to about the 4th month of life) and the extent of enamel damage depends on the intensity of the insult, the duration of its effect and the stage of enamel formation at the time of the damage. In principle, any systemic disease, such as distemper virus, as well as severe nutritional deficits at an early age, can lead to enamel dysplasia during tooth development in many or all teeth. Areas of normal enamel may be present as some enamel may have developed before the insult occurs (Figure 7).
Note that local effects such as trauma or inflammation (e.g. bite injuries, milk tooth fractures with pulp exposure and subsequent periapical inflammation, incorrect extraction of milk teeth) can also lead to enamel dysplasia, but these typically affect individual teeth (Figure 8).
Clinically, enamel dysplastic teeth show variable but extensive defects of the enamel. When the teeth erupt the defects are usually white in colour, although sometimes the enamel can be transparent. The defects quickly become yellow or brown due to deposition of food pigments, and the brittle enamel can easily flake off with chewing. Freshly exposed dentine is painful as the dentine tubules become exposed, but the pain subsides over time as a result of reparative dentine laid down by the odontoblasts of the dental pulp. However, in severe cases the irritation can lead to pulpitis or pulp necrosis, and teeth showing enamel dysplasia should be evaluated by radiography in order to rule out complications such as periapical lesions.
Affected teeth can have a very rough surface, leading to increased accumulation of plaque and tartar and thus a higher risk of periodontal disease. Treatment aims to seal the exposed dentine tubules; localized defects should be filled with composite, but for very extensive enamel defects the tooth can be crowned. These measures also restore a smooth surface to the tooth, reducing the risk of periodontal disease. Despite this, such teeth need good oral home care (daily tooth brushing) and the use of dental diets can be helpful to reduce the accumulation of plaque and the formation of tartar. Teeth that already show periapical lesions require endodontic therapy or should be extracted 1 2 4 5.
Fracture of immature permanent teeth
Whereas extraction is the treatment of choice for a broken milk tooth, the preferred treatment for a fractured permanent tooth is to preserve it, especially if the tooth is functionally important. Immature permanent teeth are characterized on radiography by thin dentine and an absence of root closure; conventional root canal treatment is not possible here. Uncomplicated fractures (where pulp is not exposed) should be treated by composite restoration; where a fracture is very near to the pulp, the site of the near-pulpal exposure is first sealed by indirect pulp capping (to preserve the pulp vitality) and then a composite restoration is applied to the entire fracture area (to seal any remaining exposed dentine tubules and mechanically protect the indirect pulp cap). If there is a complicated fracture (exposed pulp), the vitality of the pulp must be assessed. Where the pulp is vital, a partial pulpectomy performed under sterile conditions, followed by direct pulp capping and fracture site restoration, is necessary (Table 1). The prognosis for this sort of treatment depends primarily on the duration of pulp exposure, as the pulp starts to deteriorate after 48 hours (Figure 10).
Step 1 | Establish the vitality of the pulp; it should be red and bleed on careful probing. |
Step 2 | Perform dental radiography to rule out signs of pulp necrosis (periapical lucency, pulp diameter enlarged when compared to the opposite side). |
Step 3 | Isolate the tooth to be treated via a coffer dam and disinfect with chlorhexidine gluconate. |
Step 4 | Remove the inflamed portion of the pulp and, using sterile irrigation, create a sufficiently deep cavity for the filling. |
Step 5 | Control bleeding using moist sterile paper tips or cotton pellets. |
Step 6 | Direct capping with calcium hydroxide or mineral trioxide aggregate |
Step 7 | Apply an intermediate layer as base for the final restoration. |
Step 8 | Apply the final restoration. |
Step 9 | Post-operative radiography to evaluate. |
Step 10 | Repeat radiography after 6 months. |
In immature fractured teeth with a necrotic pulp, apexification (to obtain a hard tissue root closure) can be attempted (Table 2). The prognosis for this, however, is guarded. For all the treatment options described for fractured immature permanent teeth, periodic radiological follow-up is required for timely identification and treatment of any periapical pathological changes that may occur 2 3 46 7 8.
Step 1 | Radiography to establish root length. |
Step 2 | Isolate the tooth to be treated using a coffer dam and disinfect with chlorhexidine gluconate. |
Step 3 | Remove necrotic pulp, carefully clean the root canal under sterile irrigation (avoid over-instrumentation) and dry with sterile paper tips. |
Step 4 | Completely fill the root canal with calcium hydroxide to promote formation of hard tissue at the apex. |
Step 5 | Apply temporary restoration. |
Step 6 | Replace the calcium hydroxide filling at regular (4-8 weeks) intervals after radiographic assessment to check for formation of a hard tissue root closure. |
Step 7 | Conventional root canal treatment (RCT). |
Step 8 | Post-operative radiography to evaluate. |
Step 9 | Repeat radiographic evaluation after 6 months. |
Alternative 7 | |
Step 1-3 | As steps 1-3 above. |
Step 4 | Seal the open apex with mineral trioxide aggregate (MTA), place an intermediate layer of glass ionomer cement over the MTA and immediately finish the RCT and restoration. |
Step 5 | Radiography to evaluate. |
Step 6 | Repeat radiography evaluation after 6 months. |
Persistent deciduous teeth
Prior to exfoliation the roots of each milk tooth are resorbed, so that it falls out to make space for the permanent tooth. Persistent milk teeth are teeth that, at the time of eruption of their permanent successors, are still present. They are frequently found in dogs of small and toy breeds but are rare in larger breeds and cats; a hereditary component is suspected. Persistent milk teeth frequently lead to displacement of the permanent teeth as the physiological position of the latter is blocked by the former. The permanent teeth mostly erupt lingually or palatally to the milk teeth; only the maxillary canine always erupts mesial to its milk tooth predecessor (Figure 11a and b). The crowding that results from persistent milk teeth predisposes to periodontal disease. For these reasons such teeth should always be extracted.
Pre-operative radiography usually facilitates identification of the correct tooth and also shows to what extent the milk tooth root has been resorbed. The milk teeth must be extracted carefully as they have long, thin roots that break easily; damage to the permanent dentition must be avoided. In difficult cases, and to remove fractured root remnants, an open (surgical) extraction technique is recommended 1 2 3 4 9.
Impacted and embedded teeth
Embedded and impacted teeth are teeth that have not erupted. With impacted teeth there is a physical barrier in the eruption path which prevents the tooth from erupting (e.g. other teeth, milk tooth remnants, very tough gums), whilst no such obstacle can be found with embedded teeth. Embedded and impacted teeth must be differentiated from missing teeth, and therefore radiography is mandatory whenever a tooth is clinically absent. Teeth that remain in the jaw can lead to formation of a dentigerous cyst, which can result in wide-spread bone absorption and damage to neighboring teeth (Figure 12).
With timely diagnosis of retained or impacted teeth before completion of root development, the obstacle in the eruption path can be removed and the crown can be freed to allow the tooth to erupt. If removal of the obstacle is not possible, the affected tooth should either be extracted or undergo regular radiological monitoring. If a cyst is present, the tooth and the entire cyst lining must be removed in order for the cyst to heal. With very widespread cysts, the defect can be filled with a bone graft 1 2 3.
Malocclusions are more common in the dog than in the cat. Treatment is indicated wherever the animal’s health is impaired, but is not required for purely cosmetic reasons. Abnormal tooth position with normal jaw length is known as dento-alveolar malocclusion; malocclusions due to a discrepancy in jaw length are known as baso-skeletal malocclusions. If there is no clear cause, or there are jaw abnormalities that cannot be explained by development or trauma, hereditary influences should be assumed. The malocclusion may already exist in the primary dentition or only occur in permanent dentition. Treatment options for malocclusions include extraction or crown reduction of the affected tooth, or orthodontic corrections.
Linguoversion, or lingual displacement of the lower canine teeth in dogs, is a common malocclusion that always requires treatment. Full details are outwith the scope of this article but some brief notes are appropriate. If the lower deciduous canine teeth are lingually displaced and impinge on the palate, this may lead to interlocking of the maxilla and mandible which can affect jaw growth. Frequently, dogs with this problem already have a retrognathic mandible (Figure 13) and here the lower canines should be extracted as early as possible; this immediately eliminates pain caused by the teeth impinging on the palate and allows the proper genetic development of the lower jaw.
The approach to the problem in the adult patient should, on the contrary, involve retention of the affected teeth; options include orthodontic correction of the malocclusion or shortening of the lower canine teeth. Orthodontic correction involves the use of expansion screws or inclined planes which move the teeth into a position that avoids trauma to the palate (Figure 14a and b). Shortening the lower canine teeth immediately eliminates the pain experienced when the teeth impinge on the maxilla; however, endodontic treatment is required with this option as in almost all cases the pulp is opened when the tooth is shortened. In addition a partial pulpotomy and direct pulp capping should be carried out, as the roots of the teeth concerned are generally not yet mature (Table 1). For full details on orthodontic correction, the clinician is referred to the relevant literature 1 2 3 10 11.
A cleft palate is formed by missing or incomplete fusion of the palatine shelves during fetal development, and presents clinically as a longitudinal defect of the primary (incisive bone) and/or secondary palate (maxillary and palatine bone and soft palate) (Figure 15). This results in the affected animal being unable to suckle; food is frequently inhaled into the respiratory tract, leading to pneumonia. Clinically an affected animal demonstrates coughing and sneezing, with milk noted at the nostrils when suckling. Such animals are often retarded in their physical development and are frequently euthanized. Should a surgical closure of the defect be planned, the animal must be fed several times a day by tube until attaining a reasonable size; surgery can usually be attempted at 2-4 months of age when the animal is big enough to allow the extensive mobilization of the oral tissues necessary to permit closure of the cleft palate. The surgical intervention must be carefully planned as the first attempt offers the best chance of success; despite this, in many cases follow-up operations are needed to completely close the defect.
The two methods most often employed to close the cleft palate are the bi-pedicle advancement technique and the overlapping flap technique. For the first, the medial edges of the palate in the area of the cleft palate are incised and the mucosa of the palate undermined. Lateral releasing incisions ensure the necessary mobility of the resulting mucoperiosteal flaps (Figure 15). Blood supply to the area from the major palatine artery must be preserved and the flaps must be mobilized as much as possible to allow tension-free closure of the defect; the lateral release incisions heal by secondary granulation. The disadvantage of this method is that sutures are positioned over the defect and have no bony support. For the overlapping flap technique, a flap from the palatine mucosa is prepared on one side of the cleft palate, with the incision made parallel to the teeth and the base of the flap located at the cleft. The flap is folded over the defect, drawn to the opposite side of the cleft and sutured in position, so that the former oral epithelium forms the floor of the nose and the connective tissue side faces the oral cavity. Here too preservation of the blood supply from the major palatine artery is vital. The advantage of this method is that the sutures are supported by bone on one side of the defect; the disadvantage is that the technique is more difficult, requiring extensive preparation and leaving a large area of exposed bone to granulate 1 2 3 4 12 13.
Verhaert L. Developmental oral and dental conditions. In: Tutt C, Deeprose J, Crossley D. (eds) BSAVA Manual of Canine and Feline Dentistry 3rd ed. Gloucester: BSAVA 2007;77-95.
Jan Schreyer
Jan Schreyer, Tierärztliche Gemeinschaftspraxis, Chemnitz, Germany Read more
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