Domestic Feline Oral and Dental Diseases

20
Domestic Feline Oral and Dental Diseases


Alexander M. Reiter1, Norman Johnston2, Jamie G. Anderson3, Maria M. Soltero‐Rivera1, and Heidi B. Lobprise4


1 School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA


2 DentalVets, North Berwick, Scotland, UK


3 Sacramento Veterinary Dental Services, Rancho Cordova, CA, USA


4 Main Street Veterinary Dental Clinic, Flower Mound, TX, USA


20.1 Introduction


This chapter is a conglomeration of contributed topics: Tooth Resorption in Cats (Alexander M. Reiter and Maria M. Soltero‐Rivera), Feline Chronic Gingivostomatitis (Norman Johnston and Jamie Anderson), with directions to feline topics covered in other chapters and additional information on miscellaneous feline oral and dental diseases.


20.2 Tooth Resorption in Cats


20.2.1 Introduction


Tooth resorption (TR) is the most common disease affecting the dental hard tissues in domestic cats [1]. It is believed that at least one‐third of cats may develop TR during life, and the risk of developing TR increases with age [2]. Even though the condition may already have been present in cats living in the thirteenth century [3], it was not mentioned in the literature until 1930 and again anecdotally reported in the 1950s and 1960s [46]. Retrospective examinations of zoological and museum collections of feline skulls revealed a low prevalence of TR prior to the 1970s [1 79]. At some point the condition was thought to be caries [1012] until histological studies provided clear evidence of a resorptive process resulting from the destructive activity of odontoclasts [1315]. It is important to understand that TR can develop anywhere on the root surface and not just close to the cementoenamel junction (CEJ) [15]. In the absence of dental radiography, TR will first be noted clinically at the gingival margin often when it has already become an advanced lesion [16]. While attempts at repair can be noted by production of cementum and bone‐like hard tissue [1722], TR in cats is usually progressive and continues until the roots are completely resorbed or the crown breaks off, leaving an open wound and resorbing root remnants behind [1].


20.2.2 Etiology


The etiology of TR in domestic cats remains unknown. While there are many confirmed causes of TR for individual teeth in man, the etiology of TR affecting multiple, if not all, permanent teeth of cats is not known. Periodontal disease was considered to be a possible cause because TR near the gingival attachment often occurred together with periodontal disease [19, 23, 24]. However, a significant correlation between periodontitis and TR could not be demonstrated clinically, radiographically, or histologically in a necropsy study of cats [25]. Also, the very early TR usually originates at the root surface at some distance away from the gingiva [26]. Thus, the appearance of inflammatory cells may be a secondary, and not a primary, event during development of TR in cats [27]. One study apparently found a higher incidence of TR in feline immunodeficiency virus (FIV)‐positive cats; however, conclusions made in this study were vague due to the very small sample size and the lack of dental radiographs obtained [28]. Another study on an even smaller number of cats suggested a link between TR and feline herpesvirus‐1 (FHV‐1) [29]. Since the prevalence of TR is already high in the general cat population, it should not be surprising for cats with stomatitis to be affected at a similar or higher degree compared to cats without stomatitis [30, 31]. A more recent study demonstrated that there was no association between TR and feline calicivirus (FCV) [32].


Vasodentin (vascular tissue in circumpulpar dentin) and osteodentin (cellular inclusions/remnants of odontoblasts between dentinal tubules) were identified in feline permanent teeth, and TR apparently was observed in areas of the tooth in which osteodentin was most typically found [19, 33]. The layer of predentin was reported to be thin or not present in cats with TR [19]. Furcation, lateral and secondary canals connecting the pulp cavity with the periodontal ligament can be observed in permanent premolar and molar teeth in cats [3436]. Following experimental pulp injury, resorption of dental tissues and alveolar bone in the furcation area took place [36]. It was also speculated that the CEJ could be an area that favors the development of TR if the protective cementum layer fails to cover the dentin, thus attracting odontoclasts [37, 38]. A study on the elemental composition of teeth in cats revealed minimal differences in mineral content of enamel and cementum of normal and TR‐affected teeth [39].


Cats with TR in some studies were more likely to be older, female, taking medications, drinking city (versus well) water, and playing less often with toys [40, 41]. A history of abscesses, dental disease, gingivitis, feeding non‐commercial cat food and treats, consumption of cheese, butter and table foods, city residence, and being kept exclusively indoors were associated with an increased risk for TR [4143]. Also, cats diagnosed with FIV and feline leukemia virus (FeLV) were reported to have an increased risk of TR [41], although another study did not find an association between FIV or FeLV and TR [44]. Owners of cats with TR reported that their pets vomited more often compared to cats without TR [45]. Some studies reported that TR was found to be associated with excessive feeding of raw liver [21, 27, 45], but there were also cats fed predominantly with raw bovine liver that did not develop TR [46]. An increased prevalence of TR was significantly associated with a calcium‐deficient diet, decreased radiopacity of lamina dura and alveolar bone, and horizontal alveolar bone loss [46]. However, there is no evidence in the scientific literature that TR developed in cats with primary or secondary hyperparathyroidism [1]. A dry food diet was not found to be associated with less prevalence of TR in cats compared to feeding a soft food diet [1].


Coating the surface of dry kibbles with an acidic substance to preserve the food and enhance its palatability did not predispose teeth to TR [47]. A decreased risk for TR was found when cats were hunting prey or received a mixture of non‐commercial and commercial foods or treats [42]. Cats without TR were more likely to have owners who brushed their pets’ teeth and fed diets with higher magnesium, calcium, phosphorus, and potassium contents [40]. Consumption of commercial treats appeared to be protective against TR in cats [43]. Regular neutering of domestic cats was not found to be associated with TR [48, 49].


Because mechanical trauma from excessive occlusal force or traumatic occlusion can induce apical root resorption [6, 19], repeated compressive and tensile forces due to tooth flexure (e.g., from eating large dry kibbles) were suggested to cause TR in cats [23, 50, 51]. However, TR will develop on any teeth and any tooth surfaces, and not just on those exposed to occlusal or shearing forces. It was also suggested that local hypoxia [52] and local acidosis [53] could play a role in the pathogenesis of TR in cats after seeing an increase in osteoclast size and number in in vitro experiments.


The mRNA expression of interleukin (IL)‐1 beta and IL‐6 was higher in feline teeth with TR than in normal teeth [54]. Osteoprotegerin (OPG) mRNA expression was higher in gingival tissue associated with TR‐affected teeth than in normal gingival tissue, whereas the reverse was true of the receptor activator of nuclear factor‐kappa B ligand (RANKL) mRNA expression. The elevated expression of IL‐l beta and IL‐6 mRNA could play a role in the mediation of osteoclast activity in advanced TR. In contrast, OPG and RANKL might not appear to regulate osteoclasts in advanced disease. The results also suggested that OPG and RANKL mRNA play a role in mediating inflammatory responses in gingival cells and that OPG has an inhibiting effect on TR [54]. Another study found increased mRNA expression for inflammatory cytokines and the nuclear vitamin D receptor (nVDR), but not for RANKL and OPG, in tissue from TR‐affected cats compared with tissue from radiologically confirmed healthy controls [55]. The mRNA expression of nVDR was positively correlated with the mRNA expression of pro‐inflammatory (IL‐1beta, IL‐6, TNF‐alpha, and IFN‐gamma), anti‐inflammatory (IL‐10), pro‐resorptive (IL‐1beta, IL‐6, and TNF‐alpha), and anti‐resorptive (IFN‐gamma and IL‐10) cytokines in the course of TR. The results suggested that both inflammation and an overexpression of the nVDR were likely to be involved in TR in cats [55]. One study suggested that the high number of mast cells found in gingiva of feline teeth with TR is an indication for the role of these cells in the pathogenesis of TR in cats [56].


It was hypothesized that the increase of TR recognized in the 1970s may be associated with aspects of domestication such as feeding commercial cat food [1, 6, 46]. Cats depend on dietary vitamin D intake because they are not able to produce vitamin D in the skin, but many commercial cat foods contain vitamin D concentrations in excess of current maximal allowances [5760]. One study found that cats with TR had significantly higher serum concentrations of 25‐hydroxyvitamin D (25OHD) compared to cats without TR, indicating that cats with TR must have ingested higher concentrations of dietary vitamin D. The cats with TR in that study also had significantly decreased urine specific gravity compared to cats without TR [44, 61]. It was proposed that dietary intake of excess vitamin D over several years could lead to periodontal ligament degeneration, hypercementosis, hyperosteoidosis, narrowing of the periodontal ligament space, dentoalveolar ankylosis, and replacement resorption. If such a process would occur close to the gingival attachment, an inflammatory component after lesion exposure to oral bacteria would join the disease [6]. Interestingly, when experimental animals were given excess vitamin D and vitamin D metabolites, the clinical, radiographic, and histologic changes induced resembled those found in teeth from cats with TR [6], including abnormal tooth extrusion and alveolar bone expansion [62, 63]. Other studies, however, could not demonstrate significantly higher serum concentrations of 25OHD in cats with TR compared to cats without TR [64, 65] and biochemical markers of bone turnover in the domestic cat were not different between cats with and without TR [66]. However, an increased mRNA expression of nVDR protein and the relative gene expression levels of 1‐alpha‐hydroxylase and the VDR‐target gene, 24‐hydroxylase, were indicative for the involvement of an active vitamin D signaling in the pathophysiology of TR in cats [64]. It was also suggested that more osteoclasts were formed in vitro from peripheral blood mononuclear cells (PBMCs) from cats with TR, compared to cats without TR, in the presence of M‐CSF/RANKL with 1,25(OH)(2)D possibly due to a higher expression of VDR in TR(+) osteoclast precursors [67].


20.2.3 Prevalence


About 25–75% of domestic cats are affected by TR, greatly depending on the population of animals investigated (general practice versus dental specialist practice) and the diagnostic methods applied (observation only, exploration with an instrument, and/or dental radiography) [1]. An apparent increase of TR was recognized after the 1960s [1] and thus TR in cats is thought to possibly be associated with aspects of domestication. The prevalence of TR is underestimated without dental radiography [68] or when missing teeth are not considered to have been lost due to TR [49]. TR was demonstrated in permanent teeth of stray and feral small domestic cats [4, 7, 17, 21, 69, 70] and captive and wild small and large cats [17 7177]. However, the prevalence of TR in these populations generally is considered to be low compared to that in domestic cats that are kept as pets.


It was reported that TR would occur more often on the labial and buccal aspects of premolar and molar teeth and less commonly on canine and incisor teeth [9, 40 7880]. The maxillary and mandibular third premolar, the maxillary fourth premolar, and the mandibular first molar teeth are most commonly affected [9, 49 8183]. The distribution pattern of affected teeth is symmetrical in most cats [84] and there is a high statistical correlation between TR of mandibular cheek teeth (in particular the mandibular third premolar tooth) and the TR status of the whole dentition [84, 85].


The condition is rarely seen in cats less than two years of age [80, 81]. There is an increasing prevalence of TR as cats get older, with the first teeth becoming affected usually at four to six years of age [9, 25, 40, 49 7880, 82 8688]. Pure‐bred cats appeared to be more commonly affected, but this finding was not statistically significant or was described for only small study samples [9, 80, 82, 89]. Persian and long‐haired cats were reported to have TR at a younger age as compared with other breeds [9, 89]. Gender, neutering, and age at neutering were not found to affect the prevalence of TR [48, 49].


20.2.4 History


Most affected cats will not show distinct clinical signs, in particular when teeth are affected by replacement resorption only (which is asymptomatic) and the TR is located apical to the gingival attachment (not yet exposed to oral bacteria) [1]. Pain associated with TR may result from exposure of sensitive nerve endings in the dentinal tubules (with possible pulpal irritation) or when a replacement resorption progresses coronally, becomes exposed to oral bacteria at the gingival margin, and an inflammatory component joins the initially non‐inflammatory process [6]. Cat owners may report halitosis, ptyalism, head shaking, dropping food while eating, reluctance to eat hard food, excessive tongue movements, repetitive lower jaw motions while eating, drinking, or grooming, sneezing, dysphagia, dehydration, anorexia, weight loss, and lethargy [81, 90, 91].


20.2.5 Clinical Findings


Dental deposits, hyperplastic gingiva, and granulation tissue often cover a clinically evident TR emerging at the gingival margin [17, 20, 81]. Thus, an accurate oral examination under general anesthesia must be performed for a proper diagnosis [92]. Because various degrees of oral inflammation may be present with TR [30, 93], the condition had previously been considered to be part of periodontal disease in cats [19, 87, 94]. A dental explorer can be used to detect any irregularities at the tooth surface near the gingival margin [15, 21]. Hyperplastic gingiva or granulation tissue covering a TR tends to bleed when touched [92]. The lower jaw was often reported to “chatter” or twitch when affected teeth were probed [21, 81, 93, 95]. Several studies on pain mechanisms in anesthetized cats demonstrated that reflex responses of the digastric and tongue muscles were elicited after dental stimulation, resulting in evoked licking movements of the tongue and jaw‐opening reflexes [1].


Canine teeth (in particular maxillary) often appear to extrude abnormally (abnormal tooth extrusion), leading to excessive exposure of the root surface [63, 92, 95]. The crowns of the teeth seem to be longer than they should be. Thickening of alveolar bone and local osteomyelitis (alveolar bone expansion) are often associated with this phenomenon [6, 62]. There is a bulbous expansion of the alveolar bone on the labial sides of the teeth. In advanced stages of TR, the crown can fracture off, leaving an open wound and root remnants behind [96]. A small sinus tract may occasionally be observed over the site of a retained root remnant [90, 97]. When the gingiva has grown over the root remnant, a bulge underneath the gingiva can be seen or palpated [1, 98].


20.2.6 Diagnostic Imaging Findings


Without dental radiography, TR below the gingival attachment (and thus the vast majority of TR) will not be detectable [9, 25, 68, 99, 100]. A clinically evident TR emerging at the gingival margin (inflammatory resorption) will generally be visible as a notched radiolucency in the tooth with sharp or scalloped margins (type 1 resorption). The periodontal ligament space may be of normal width apical to the TR, but there will be horizontal or vertical loss of alveolar bone adjacent to the TR. Lesions on mesial and distal tooth surfaces or in the furcation area usually are more obvious on radiographs than those on labial/buccal and lingual/palatal tooth surfaces [23, 96]. Apparent pulp involvement due to TR did not appear to be associated with radiographic evidence of periapical lucencies [101]. Fusion of the root and alveolar bone (dentoalveolar ankylosis) results in focalized or generalized disappearance of the periodontal ligament space and lamina dura on radiographs. Resorbed dental tissue will gradually be replaced by bone (replacement resorption). The root will take on a striated or moth‐eaten appearance (“ghost roots”) and the periodontal ligament space and lamina dura will disappear on radiographs (type 2 resorption). Unlike inflammatory resorption, adjacent bone usually is not resorbed [23, 96].


Teeth with abnormal extrusion and alveolar bone expansion may display regions of hypercementosis and infrabony pocketing. A radiographic study of periodontal disease in cats also identifies the expansile lesions, with 53% of cats showing alveolar bone expansion of at least one canine tooth [87]. Even in the 12 of 41 cats with normal alveolar bone height in that study, the teeth were already displaying some degree of expansion. Of the 11 (7%) cats with moderate to severe expansion, 10 of the 11 had severe vertical bone loss associated with the affected tissue [87].


Conventional computed tomography (CT) showed a fair to poor sensitivity but good to excellent specificity with regards to detection of TR in cats [102]. An earlier study using cone‐beam computed tomography (CBCT) reported that both periodontal disease and TR in cats could accurately be detected with this imaging modality [103].


20.2.7 Histological Findings


Numerous microscopic studies of the 1980s [20, 21, 45, 80, 104], 1990s [13 1719, 22, 105], and 2000s [26, 63, 106, 107] demonstrated that TR develops anywhere on the root surface and not just close to the CEJ [37, 38, 79], progressing through cementum into root dentin. This homogenous distribution of TR throughout the root surface has also been demonstrated radiographically [108]. Odontoclasts migrate from blood vessels in the periodontal ligament or alveolar bone toward the root surface where they resorb cementum and dentin, creating lacunae, lagoons, and canals in the dental hard tissues [13, 17, 19, 72].


One important histological study evaluated clinically and radiographically healthy teeth from cats with TR on other teeth [26]. Hyperemia, edema, and degeneration of the periodontal ligament with marked fiber disorientation, increased osteoid formation along alveolar bone surfaces, excessive formation of cellular cementum at apical and mid‐root surfaces, and of acellular cementum at cervical root surfaces, gradual narrowing of the periodontal ligament space, and areas of ankylotic fusion between the tooth and alveolar bone were found, demonstrating that a majority of TR in cats may be non‐inflammatory in origin [26]. Other studies confirmed that alterations in the periodontal ligament seen on histology may represent a pre‐clinical stage of TR in cats [109] and demonstrated that over half of clinically healthy teeth in cats exhibit TR on electron microscopy [79]. Significant associations were found between abnormal tooth extrusion and TR (four of four canine teeth with extrusion had resorption, compared to only 1 of 5 canine teeth without extrusion in one study)[63], as well as alveolar bone expansion and TR [62].


If the condition progresses into crown dentin, the enamel could become undermined and then either gets resorbed or loses its contact with originally intact dentin and breaks off [1]. Resorption of enamel as the initial event is only rarely observed [110]. TR that emerges at the gingival margin will be exposed to oral bacteria, which results in the formation of vascular and inflamed granulation tissue [18, 20, 82, 86, 105, 107, 111] and resorption of alveolar bone adjacent to the TR [1]. Many clinically evident TRs (i.e., lesions emerging at the gingival margin) appear histologically to be in both resorptive and reparative phases simultaneously [20]. During the reparative phase, cementoblast‐ or osteoblast‐like cells produce new hard tissue resembling cementum or bone‐like material [13 1722, 72]. Pulp involvement in the form of pulpitis is usually not seen until late in advanced stages of TR [17, 19, 21, 72].


In an evaluation of cats with and without TR, the distance between the alveolar margin (AM) and CEJ was significantly greater in teeth with TR [63]. Thickening of cementum, beyond that considered a normal physiological aging change, was identified, with the most notable changes in the cervical region of the roots. Hypercementosis was often associated with a decreased width of the periodontal ligament space, and cementicles (extensions of cementum into the periodontal ligament space) could be found [63]. Alveolar bone expansion manifested histologically as medullary fibrosis with mild to moderate pleocellular inflammation and modest proliferation of woven bone [62]. Teeth examined in that study had a distinct rim of peripheral sclerosis, consistent with an outward compression force of expansion. Changes could also occur in premolars and molars, but with more variability in the type of osseous changes and inflammation (including gingival changes), making this region more challenging to recognize clinical alveolar bone expansion than at the canine teeth [62].


20.2.8 Classification


TR can be internal or external. In cats, TR usually originates at the external surface of the tooth, i.e., the surface facing connective tissue of the periodontium (gingival connective tissue, periodontal ligament, and alveolar bone) [1]. Its classification in the human literature is made by type (surface, inflammatory, and replacement resorption) and area (cervical, lateral, and apical resorption) (Table 20.1).


Table 20.1 Classification of internal and external resorption by area and type.
















Internal External
Area Pulp chamber
Root canal
Cervical
Lateral
Apical
Type Inflammatory
Replacement
Surface
Inflammatory
Replacement

Surface resorption is confined to cementum and the outermost layer of dentin without inflammatory reaction in the periodontal ligament. It is asymptomatic and not visible on radiographs, often self‐limiting, and spontaneously repaired to establish the original root contour. Inflammatory resorption is resorption of cementum and dentin associated with inflammation in the adjacent gingival connective tissue and periodontal ligament with alveolar bone resorption usually located adjacent to root resorption. Replacement resorption is usually preceded by fusion of alveolar bone and the root surface (dentoalveolar ankylosis), resulting in focalized or generalized disappearance of the periodontal ligament space and lamina dura on radiographs, decreased physiological tooth mobility, and a high‐pitched sound upon tooth percussion. Resorbed root tissue is gradually replaced by bone, causing a moth‐eaten appearance of the root and disappearance of the periodontal ligament space and lamina dura on radiographs. Unlike inflammatory resorption, adjacent bone is not resorbed. Dentoalveolar ankylosis and replacement resorption are considered to be asymptomatic as long as the resorption remains below the gingival attachment. Cervical resorption is resorption of the cervical portion of the root. Lateral resorption is resorption of the mid‐portion of the root, and apical resorption is resorption of the apical portion of the root. Overlaps between resorption types and areas are common [1, 6].


Earlier reports used various numbers of stages and types to classify TR in cats [1, 112]. The American Veterinary Dental College currently suggests classification based on severity (stages 1–5) and radiographic appearance of the resorption (types 1–3) (www.avdc.org/Nomenclature/Nomen‐Teeth.html#resorption; accessed October 6, 2017). (Figure 20.1a–g). Stage 1 resorption is defined as mild dental hard tissue loss (cementum or cementum and enamel). Stage 2 resorption shows moderate dental hard tissue loss (cementum or cementum and enamel with loss of dentin that does not extend to the pulp cavity). Stage 3 resorption is defined as deep dental hard tissue loss (cementum or cementum and enamel with loss of dentin that extends to the pulp cavity) with most of the tooth still retaining its integrity. Stage 4 resorption shows extensive dental hard tissue loss (cementum or cementum and enamel with loss of dentin that extends to the pulp cavity) with most of the tooth having lost its integrity; there are substages 4a (crown and root equally affected), 4b (crown more severely affected than the root), and 4c (root more severely affected than the crown). Stage 5 resorption is defined as remnants of dental hard tissue visible only as irregular radiopacities with complete gingival covering (Table 20.2).

Diagram of the 5 stages of tooth resorption, illustrating mild dental hard tissue loss (stage 1), moderate hard tissue loss (stage 2), deep dental hard tissue loss with most of tooth retaining (stage 3), etc.

Figures 20.1 Tooth resorption – AVDC Classification of Clinical Stages.


Source: Copyright AVDC®, used with permission. www.avdc.org/Nomenclature/Nomen‐Teeth.html#resorption; accessed November 2017.


Table 20.2 Stages of tooth resorption (AVDC).


















Stage 1 Mild dental hard tissue loss (cementum or cementum and enamel)
Stage 2 Moderate dental hard tissue loss (cementum or cementum and enamel with loss of dentin that does not extend to the pulp cavity)
Stage 3 Deep dental hard tissue loss (cementum or cementum and enamel with loss of dentin that extends to the pulp cavity); most of the tooth retains its integrity
Stage 4 Extensive dental hard tissue loss (cementum or cementum and enamel with loss of dentin that extends to the pulp cavity); most of the tooth has lost its integrity
(a) Crown and root equally affected
(b) Crown more severely affected than the root
(c) Root more severely affected than the crown
Stage 5 Remnants of dental hard tissue visible only as irregular radiopacities; complete gingival covering

On a radiograph of a tooth with type 1 resorption, a focal or multifocal radiolucency is present in the tooth with otherwise normal radiopacity and normal periodontal ligament space (Figure 20.2a). On a radiograph of a tooth with type 2 resorption, there is narrowing or disappearance of the periodontal ligament space in at least some areas and decreased radiopacity of part of the tooth (Figure 20.2b). On a radiograph of a tooth with type 3 resorption, features of both type 1 and type 2 resorptions are present in the same tooth (Figure 20.2c). The affected tooth shows areas of normal and narrow or lost periodontal ligament space and there is focal or multifocal radiolucency in the tooth and decreased radiopacity in other areas of the tooth (Table 20.3). There is the consideration of possibly different etiologies for type 1 and type 2 resorptions [108].

Image described by caption and surrounding text.

Figures 20.2 Types of resorption based on radiographic appearance: (a) Type 1 (T1); (b) Type 2 (T2); (c) Type 3 (T3).


Source: Copyright AVDC®, used with permission. www.avdc.org/Nomenclature/Nomen‐Teeth.html#resorption; accessed November 2017.


Table 20.3 Types of tooth resorption (AVDC).












Type 1 On a radiograph of a tooth with type 1 appearance, a focal or multifocal radiolucency is present in the tooth with otherwise normal radiopacity and normal periodontal ligament space.
Type 2 On a radiograph of a tooth with type 2 appearance, there is narrowing or disappearance of the periodontal ligament space in at least some areas and decreased radiopacity of part of the tooth.
Type 3 On a radiograph of a tooth with type 3 appearance, features of both type 1 and type 2 are present in the same tooth. A tooth with this appearance has areas of normal and narrow or lost periodontal ligament space, and there is focal or multifocal radiolucency in the tooth and decreased radiopacity in other areas of the tooth.

20.2.9 Treatment


Historically, a common approach for the treatment of TR included topical fluoride treatment of very early lesions, restoration with or without endodontic treatment of slightly to moderately advanced lesions, and extraction of teeth with severely advanced lesions [91 113117]. However, fluoride treatment remains controversial because it does not address the origin of TR (i.e., the disease apical to the gingival attachment). Furthermore, restorations with glass ionomer or composite were shown to fail in numerous studies of feline teeth with TR [82, 83, 95, 118].


One author recommended supportive homeopathic treatment without providing any proof of success [119]. Another reported a very high success rate when treating feline teeth with TR with an Nd:YAG laser, enameloplasty, and gingivoplasty [120]. Dental radiography and histopathological examination, however, were not performed to determine a true absence of TR progression in that study. Alendronate, a bisphosphonate compound that preferentially accumulates in the subgingival tooth surfaces, adjacent alveolar bone, and root canal system, effectively slowed or arrested the progression of TR [121]. However, only a very small number of cats were included in this proof‐of‐concept study.


The treatment of choice for many teeth with TR is complete extraction [24, 122, 123]. Multirooted teeth should be sectioned after removal of the alveolar bone on the labial and buccal aspects of the roots so that each single‐rooted crown–root segment can then be elevated and removed. A large mucoperiosteal flap is often made when multiple teeth or roots in one jaw quadrant need to be extracted [1, 92, 124]. Resorbing root remnants under non‐inflamed and intact gingiva and without periapical pathology on dental radiographs may be left where they are [125]. They often appear as a small gingival bulge in the area of a missing tooth (which should not be confused with neoplasia). However, root remnants underneath inflamed gingiva with sinus tracts must be extracted [1, 46, 126].


Teeth with dentoalveolar ankylosis and replacement (Type 2) resorption can be treated by means of crown amputation and intentional retention of resorbing root tissue [127, 128]. A flap is made, the crown is removed with a water‐cooled round bur to, or slightly below, the level of the alveolar mucosa, and the wound is rinsed and closed by suturing. Contraindications include periodontitis, endodontic, and periapical disease. Also, teeth of cats with stomatitis or that are FIV and/or FeLV‐positive should not be treated with crown amputation [84, 127, 128].


The so‐called “root pulverization/atomization” procedure [90, 92, 129] to crush very brittle or ankylosed root remnants into many particles with a water‐cooled round bur on a high‐speed dental handpiece is not recommended. Serious complications can occur with this technique, including incomplete root removal, trauma to sublingual soft tissues, alveolar bone, and neurovascular bundles, subcutaneous and sublingual emphysema, air embolus, and transportation of root remnants into the mandibular canal, infraorbital canal, or nasal cavity [95].


Canine teeth exhibiting abnormal extrusion and alveolar bone expansion should have a complete evaluation, including radiographs (from different angles to “map” the extent of changes), periodontal probing to discover any advanced vertical bone loss, and tactile evaluation of mobility. Those with mild changes and without TR could be monitored with regular clinical examinations and dental radiographs, but progression should be expected. Those with moderate to severe changes should be considered candidates for extraction, although elevating labial flaps can be very challenging. While teeth with severe extrusion and increased mobility can often be removed by simple elevation, closure of the site can be difficult without surgical reduction of the thickened alveolar bone and careful release of the periosteum at the base of the mucoperiosteal flap. The pointed tips of opposing ipsilateral mandibular canine teeth can be gently rounded off with a white stone bur (odontoplasty) without entering the pulp chamber, followed by a dentinal conditioner and unfilled resin to seal the exposed dentinal tubules, in order to minimize the trauma they can cause to the maxillary extraction site and upper lip.


20.3 Feline Chronic Gingivostomatitis


20.3.1 Introduction


Feline chronic gingivostomatitis (FCGS) is a familiar problem in small animal practice. In reality, the term covers a wide range of manifestations from the most severe inflammation and ulceration of the whole oral cavity to more focal conditions where inflammation may be confined to specific tissues and locations. It can affect all oral and pharyngeal soft tissues commonly including gingiva, oral and pharyngeal mucosa, and the tongue. Inflammation can occasionally be confined to the tissues lateral to the palatoglossal folds, known as caudal mucositis (Figure 20.3). When inflammation affects the tissues overlying the teeth (premolars/molars/canines) it is termed alveolar mucositis. The term stomatitis is generally reserved for widespread oral inflammation that is beyond gingivitis and periodontal disease and may extend into submucosal tissues (www.avdc.org; accessed October 17, 2017, and www.avdc.org/Nomenclature/Nomen‐Oral_Pathology.html#inflammation).

Photo displaying an inflammation in the caudal mouth if cats with FCGS.

Figure 20.3 Evaluation of inflammation in the caudal mouth of cats with FCGS can be important in determining diagnosis, prognosis, and response to treatment.


This condition is reported to have prevalence of 0.7% in a study of nearly 5000 cats by 12 practices [130]. A second study [108] gave a prevalence of 5.5%. Anecdotally, the prevalence appears to be higher with lesions more intense and severe in North America and southern Europe.


20.3.2 Etiology


The actual etiology is not known but thought to be a complex result of reactions involving a number of disparate factors. It has previously been stated that environmental factors and bacterial infection (and the host response to it) acting in combination with viral infection all influence the disease process [131, 132].


One study [133] compared the oral bacterial flora in normal and FCGS diseased cats using traditional and culture independent methods (bacterial 16S rRNA gene sequencing) in order to identify novel pathogens and species that may be fastidious and challenging to cultivate. In diseased cats the oral flora was found to be less diverse, compared to normal cats, with Pasteurella multocida subsp. multocida representing more than half the identifiable flora of the oral cavity, lending credence to the theory that it may be an important factor in the etiology. Another study by the same group [134] discovered a group of novel and previously identified bacteria that have potential importance in the etiology that warrants further investigation using 16S rRNA gene sequencing. Subsequent studies have researched the oral microbiome of cats in more detail [135, 136].


The major difference between normal and diseased cats appears to be a hyperimmune response to the antigenic burden that is dental and oral plaque, though the relationship to plaque has not been definitively proven [137]. Low levels of plaque biofilm appear to initiate this abnormal response in susceptible individuals. A study of the innate immune response in both normal and FCGS cats [138] compared that response in the presence of putative pathogens previously identified. The study found a good correlation between the severity of clinical signs and the presence of several of these putative pathogens, including FCV and Tannerella forsythia. Complex interreactions occur in affected cats and bacteriology results suggest that opportunistic infections are likely to play a role in influencing the disease process.


The specific immunologic aberrations operating in this complex still need to be defined [139]. It is likely that immunologic mechanisms are intrinsic to the initiation and perpetuation of feline gingivitis stomatitis complex, just as they are in human idiopathic mucosal diseases such as oral lichen planus and recurrent aphthous ulceration. An early immunologic study proposed that increased immunoglobulin values in cats with chronic oral diseases were indicative of inadequate B cell function [140]

Only gold members can continue reading. Log In or Register to continue

Aug 15, 2020 | Posted by in GENERAL | Comments Off on Domestic Feline Oral and Dental Diseases
Premium Wordpress Themes by UFO Themes