Common Oral Diseases

2. Common Oral Diseases

Prevalence of Feline Oral Diseases in Wild and Domesticated Populations

Whether wild or domesticated, a cat’s diet is dictated by its environment. In this respect, commercial food preparation is often considered to be an aggravating factor in the event of oral diseases. The analysis of the oral diseases of a population of wild cats provides an opportunity to study the potential link between a well-defined diet and the various diseases identified.

Four cats were introduced on Marion Island in the Indian Ocean in 1949 and the cat population grew rapidly. The diet of these cats is mostly seabirds (96%) associated with the ingestion of some pebbles. The postmortem analysis of a collection of 300 skulls from this cat population enabled the study of oral health. Despite the average age of the group being estimated at 2 - 3 years, the prevalence of periodontal disease in a moderate to severe form, was 48%. Taking account of missing teeth (probably due to periodontal disease), periodontal disease was prevalent in 61.8% of cats and 14.8% of the teeth observed. The prevalence of dental trauma and feline odontoclastic resorptive lesions (FORLs) was also high, statistically associated with the prevalence of periodontal disease. On the other hand, only 9% of cats in this study presented calculus, and then typically on the upper carnassials.

The highly specific diet of this wild cat population undoubtedly explains the high frequency of periodontal lesions and the low prevalence of dental calculus observed in such a young colony. When the cat tears apart the carcasses of seabirds, the sharp bone sections are probably responsible for gum trauma, which is assumed to favor the development of more severe periodontal inflammation (Verstraete et al, 1996).

In an Australian study, the analysis of oral diseases based on clinical and radiographic criteria in 29 wild cats and 20 domesticated cats (Clarke & Cameron, 1998) established that the prevalence of periodontal disease was not significantly different in cats fed with commercial foods and cats whose diet was mainly made up of small prey. A hunting-based diet does not provide natural protection from oral diseases for wild cats.

Veterinarian examination of 15,226 domesticated cats (Lund et al, 1998) showed that oral diseases are the most common of all diseases observed. Calculus is present in 24% of cats and 13% of them suffer from some form of gingivitis.

A more detailed analysis conducted by veterinarians specialized in dentistry confirms a strong prevalence of oral diseases. 73% of a population of 753 cats studied presented gingivitis; 67% presented dental calculus; 28% of them had missing teeth; 25% FORLs; 19% severe periodontitis; 12% stomatitis and 11% tooth fractures (Verhaerte & Van Wetter, 2004).

Periodontal disease is found in 32% of individuals presented to veterinarians specialized in dentistry. Out of a population of 152 cats, gingivitis and missing teeth were observed in 59% of cases, FORLs in 57% of cases, teeth fractures in 23% of cases and stomatitis in 2.6% of cases. The prevalence of dental calculus was estimated at 90% (Crossley, 1991).

The postmortem analysis of 81 cats whose death was unrelated to an established oral disease, based on pathological and clinical examination, reported a high prevalence of periodontal disease. 52% of cats older than 4 years of age presented a form of periodontal inflammation. More than 40% of animals aged over 9 years presented a severe form of the disease. Less than 3% of animals aged over 15 years presented any form of lesion due to periodontal disease (Gengler et al, 1995).

To summarize the studies above, the high prevalence of periodontal disease in cats cannot be ignored. There are no major differences between wild and domesticated populations and no apparent influence of commercial food. The presence of oral diseases is therefore not something that characterizes domesticated cats alone and is not necessarily associated with the feeding of commercial foods.

This information is unfortunately always underestimated. It does however shed light on the fact that the high prevalence of oral inflammation in cats is the most common cause of infectious disease in the species. The clinical impact turns out to be much greater than it appeared at first sight. It is especially clear in groups of wildcats whose health is generally related to interspecies competition and conditions the very survival of individuals. In the case of domesticated cats, the pain caused by oral disease is typically underestimated. Once they have been treated, these cats do show major behavioral modifications. Some owners describe this return to health as a "rebirth".

Periodontal Disease

Periodontal disease is the most common disease in cats. It is an inflammatory oral disease associated with the development of dental plaque. Periodontal disease is not a disease as such as much as a collection of periodontal inflammations with varied clinical characteristics chronic or aggressive, local or generalized. All stages are possible: from early-stage periodontal disease to moderate or severe forms. The way periodontal disease develops depends on the mechanical constraints that oppose the development of dental plaque, but also the local immune response of each individual.

In wild cat populations, oral inflammation could threaten the health and even the survival of individuals. (© Yves Lanceau - Bengale).

The incidence of periodontal disease on the general health of cats is widely underestimated. It is the source of chronic pain that owners are often unaware of and chronic bacterial diseases whose effects on the kidneys, lungs and heart are just starting to be better understood. Periodontal disease is the most common disease reported in cats, with a prevalence estimated at 30 - 70% of individuals according to studies and the evaluation criteria.

Description and Function of the Periodontium

The periodontium is the tissue that supports the teeth in the oral cavity. It connects the teeth, the bone structure of the jaws and the oral mucosa. Its development is associated with the eruption of the tooth and it disappears with its exfoliation. The periodontal tissue guarantees the integrity of dental structures and effectively protects the underlying anatomical structures from aggressions in the oral environment.

The periodontium is composed of the gum, the periodontal ligament, cement and the alveolar bone (Figure 9).

Figure 9. Composition of the periodontium.

The alveolar bone is a differentiated part of the jawbone. It is responsible for positioning the roots of the teeth in depressions known as dental alveoli.

The periodontal ligament is composed of collagen fibers, which connects the surface of the tooth root (cement) to the alveolar bone. Like a hydraulic shock absorber the periodontal ligament absorbs the pressures placed on the alveolar bone during prehension and the tearing of food. These specialized fibers improve the resistance to pressure of underlying bone tissue and generate a pain signal when the limit of its mechanical resistance is reached.

The cement covers the root of the tooth. It has a similar structure to bone, but without lacunas and channels.

The gum covers the underlying alveolar bone and tightly hugs the base of the crown of the tooth. The gum is composed of a squamous, keratinized epithelium, which is different from the loose, vascularized and non-keratinized alveolar mucosa. It is made up of two parts.
- The free gum is located at the level of the crown. It defines a space against the crown known as the gingival crevice, whose physiological depth is less than 0.5 mm in cats. The weak point of the tooth/gum junction is always the gingival crevice. The delimited space is fairly closed and is predisposed to accumulating dental plaque and various food debris. As its histological nature makes it more sensitive to the inflammatory process, the gingival crevice forms a gateway for periodontal disease. As a consequence, all attention must be focused on periodontal disease treatment and prevention programs.
- The gum attached to the tooth and the alveolar bone is an essential barrier against bacterial aggression. The seam of the gum is stuck against the bulge of the base of the crown and enhances this protective action.

Some 100 billion bacteria are discharged in the saliva every day. The oral cavity is therefore never sterile. There is always a minimal residual inflammation of the mucosa and the oral epithelium. A ‘healthy’ periodontium is therefore defined clinically. The criteria for evaluating a healthy periodontium in cats are the absence of visual evidence of inflammation and the depth of the gingival crevice less than 0.5 mm.

Healthy gum. (© N. Girard).

Pathogenesis of Periodontal Disease

The development of dental plaque in contact with all the surfaces of the tooth is a natural process resulting from the interaction between tooth and saliva. The anatomical sites predisposed to the deposition of dental plaque are the limit of the crown and the seams of the gum as well as the contacts between the teeth.

The adhesion and proliferation of bacteria on the surface of the enamel is not possible as such. The gradual colonization of the tooth surfaces by the bacteria is a succession of steps that steadily facilitate the adhesion and multiplication of bacteria:

- Physical adhesion of an organic film to the surface of the teeth.
- Secondary colonization by specific or pioneer bacteria.
- Bacterial proliferation from the colonized organic film.

The adhesion of pioneer bacteria to the tooth surface is possible only after the development of an organic film (acquired pellicle) essentially formed from salivary components (glycoprotein, polypeptides, carbohydrate). Within a few hours of its development, specific bacteria (Streptococcus sanguis, Actynomyces viscosus) arrive to colonize the acquired pellicle, gradually saturating the entire surface (>6 million/sq. mm) and forming a biofilm, dental plaque (Figure 10). New bacterial appositions, which stimulate the phenomena of coaggregation and coadhesion, establish 90% of the dental plaque’s biomass within 24 hours.

Figure 10. Supragingival dental plaque on healthy teeth and gums. The phenomena of bacterial coaggregation and coadhesion facilitate the installation of 90% of the biomass of the dental plaque within 24 hours (the dental plaque is revealed using eosin-type vital staining). (© N. Girard).

Initially, dental plaque is essentially composed of aerobic Gram+ bacteria but this population develops rapidly. With the increase in the bacterial population comes the fall in oxygen in the air, from 12 - 14% in the mouth to 1 - 2% at the base of the gingival crevice. These new environmental conditions, which are associated with various sources of nutrients (diet, bacterial degradation, epithelial degradation), lead to the development of an anaerobic bacterial flora.

As the inflammatory process advances, so the proportion of Gram– bacteria (Porphyromonas sp, Prevotella sp, Peptostreptococcus sp), Fusobacterium and spirillians increases. The pathogenic role of these aggressive bacteria is much more pronounced and is exercised through various enzymes, toxins and degradation products (Haake et al, 2002).

To summarize, the dental plaque is a biofilm that forms on the tooth surface. It is composed of a community of bacterial species embedded inside an extracellular matrix of polymers produced by the hosts and the bacteria themselves (Marsh, 2004). Modification of its composition is closely associated with the development of periodontal inflammation. Its interrelation with the cat’s immune defense mechanisms conditions to some extent the scale of the periodontal inflammation.

Calculus is only a mineralized, fossilized form of dental plaque, consequential to the catalytic activity of some bacteria. It is deposited both above and under the gum (Figure 11). While calculus does not contain any pathogenic bacteria, its porous character favors the new accumulation of dental plaque. So while it does not cause the inflammation of the periodontium it is an aggravating factor.

Figure 11. Deposit of dental calculus in the cat. Accumulation of calculus on 100% of the upper PM4 associated with gum recession and exposure of the furcation. (© N. Girard).

The accumulation of dental plaque in the gingival crevice leads to inflammation of the gum seams (Figure 12). At this point, professional care together with the removal of the dental plaque will ensure full remission of the lesions. Without treatment, the dental plaque continues to accumulate and inflammation advances. The environmental conditions in the oral cavity become more favorable to an anaerobic bacterial population containing more and more Gram negative bacteria. Gingivitis, the reversible inflammatory stage, may stabilize or develop into periodontitis.

Figure 12. Generalized gingivitis. Pronounced gum edema from the canine to the carnassial; spontaneous bleeding around PM3. (© N. Girard).

The advancement of the inflammatory process inexorably leads to the collapse of the connecting tissues on the surface of the tooth. Dental plaque then colonizes the tooth root further down. The epithelium of the junction, which constitutes the lower limit of the gingival crevice, migrates to an apical region to heal in the "non-inflammatory" zone, creating a periodontal pocket. Periodontitis (Figure 13) is the irreversible stage of periodontal disease. The lesions are final and the main objective of treatment is to halt their advancement. The main cause of the development of periodontal disease is the disruption of the balance between the pathogenic bacterial flora of the dental plaque and the host’s immune response.

Figure 13. Severe local periodontitis of the upper left PM4. (© N. Girard).

Description of Periodontal Disease in Cats

First and foremost, it should be noted that few publications deal with periodontal disease in cats, contrary to a large quantity of publications on the disease in dogs. We would also observe that the expression of periodontal disease in cats is generally described on the model of the dog or human, without taking account of any feline particularities.

- A clinical radiographic and histological study has helped outline the development of periodontal disease in 15 cats (Reichart et al, 1984). A loss of attachment appeared in 25% of premolars and molars, essentially localized to the buccal surface. A pronounced to severe gingivitis was shown in 56% of premolars and molars (buccal surface) and 25% of canines and incisors (buccal surface). After radiographic analysis, alveolar bone loss appeared to be significant in 77% of premolars and molars. Bone loss was also observed on the buccal surface of 82% and on the oral surface of 75% of incisors and canines. The general distribution of observed lesions in cats (gingivitis, alveolar bone loss, inflammatory FORL) was more pronounced in the premolars and molars.

Bearing in mind the high percentage of bone loss shown in the canines and incisors, however, together with the high percentage of missing incisors, it would appear that these teeth are highly susceptible to periodontal disease (Reichart et al, 1984).

A form of periodontitis was shown using dental radiography in 69% of cats presented to the specialist veterinary dentistry department of the University of California, Davis. The results of this study confirm that generalized horizontal bone loss (Figure 14) is the most common form of bone loss in cats (38%). In total, the height of the alveolar bone was normal in just 28% of cases (Lommer & Verstraete, 2001).
Figure 14. Generalized horizontal bone loss during periodontal disease in the cat with respect to the right lower carnassial. (© N. Girard).

A clinical and radiographic study based on the oral examination of 109 healthy cats fed with dry food confirms these results. The presence of moderate to severe gingivitis associated with the presence of bleeding during periodontal probing was 13%. The average loss of periodontal attachment observed was 0.49 mm (c=1.28) with higher average values in the canines: 1.2 mm in the upper canine and 0.8 mm in the lower canine. Loss of attachment greater or equal to 2 mm was observed in 3.4% of examinations of the vestibular surface, 3% of the distal surface, 2.3% of the mesial surface and 2.2% of the lingual part. Gum recession (Figure 15) was observed in 10% of teeth. Absent teeth were most often upper premolars and incisors (21.1% and 11.4% respectively). Furcation (Figure 16) was observed in 18% of multi-root teeth and on average in two teeth of every cat examined. The radiographical analysis revealed a high prevalence of bone loss with respect to the dental arches: 21% of upper teeth and 42% of lower teeth. Horizontal and/or vertical bone loss was revealed in 52% and 14% of lower teeth respectively. The simplified analysis of premolars and molars underlines the importance of the inflammatory process: bone loss was observed in 66.5% of teeth (Girard et al, 2008).

Periodontal disease in cats is characterized by a low proportion of periodontal pockets (Figure 17), the strong prevalence of osteolysis in its horizontal form, a high proportion of gum recession and the early appearance of furcation.

Figure 15. Severe gum recession around a canine tooth in the cat. Pronounced gum recession and alveolar bone loss around the upper and lower canines. (© N. Girard).

Figure 16. Furcation around the upper pm3 in the cat. (© N. Girard).

Figure 17. Periodontal pocket in the cat. (© N. Girard).

Predisposing Factors

Many factors have an influence on the development of periodontal disease:
- Excessive accumulation of dental plaque in the junction between the tooth and gum (absence of oral hygiene, low fiber diet)
- Inflammation promoted by a probable insufficiency of the local immune system or in the presence of systemic diseases such as diabetes mellitus, thyroid, liver or kidney insufficiency
- A familial and/or genetic effect is often evoked but never proven
- Facial conformation, malocclusion, occlusion trauma.

Tooth Resorptions

Definition

Tooth resorptions are lesions by which the gradual loss of tooth substance is observed (Figure 18). In cats, they are commonly known as feline odontoclastic resorptive lesions (FORLs), as the process of tooth resorption is controlled by multinuclear odontoclastic cells (odontoclasts) (Gautier et al, 2001). These lesions affect the interior and/or exterior of the tooth and their clinical diagnosis is often delicate. Tooth resorptions are also observed in humans and dogs. They are generally due to periodontal inflammation or mechanical constraints with respect to the periodontal ligament (orthodontic treatment, tooth trauma).

Figure 18. Feline odontoclastic resorptive lesion.

Prevalence

A high prevalence of FORL has been shown in various cat populations and especially in domestic cats. According to the populations studied and/or the methodology used, the results were between 28% and 67% (Coles, 1990; Van Messum et al, 1992). Such a variation is connected with the choice of population studied (specialist dental department, general dental department, healthy population) or the diagnostic methods used (clinical examination +/- radiological examination). Two studies of healthy cat populations reporting both a clinical and radiological examination revealed an average prevalence of 30% (Ingham et al, 2002a; Girard et al, 2008).

Pathogenesis

FORLs in cats are mostly external tooth lesions. The resorbed tooth tissue is gradually replaced by newly formed cement or bone tissue. FORLs are initiated in the radicular cement and then develop through the dentine and/or the crown. The alveolar bone and the adjacent periodontal ligament are also included locally in the tooth resorption process.

The tooth canal is only affected at the end of the process, signaling an internal tooth resorptive lesion. Inflammation of the tooth pulp is rare except at the end, when a degenerative state is described. The enamel of the crown may resorb itself in time, but more commonly it fractures due to the absence of underlying support, leading to the clinical appearance of a tooth cavity (Okuda & Harvey, 1992).

FORLs mainly appear in the buccal part of the crown. Sixty-nine percent of the FORLs revealed are associated with an inflammatory phenomenon and 30% display signs of repair (Reichart et al, 1984).

Etiologies of FORLs

External FORLs may have one or more origins. In human dentistry, the disease may be associated with:

- A chronic inflammatory process adjacent to a cyst, benign or malignant tumor,

or
- Be the consequence of dental trauma (mechanical/occlusal) or orthodontic tooth displacement. Lesions are qualified differently depending on whether an inflammatory process is present. Surface FORLs, dentoalveolar ankylosis and replacement lesions are considered to be the consequence of tooth traumas and qualified as non-inflammatory. On the other hand, apical FORLs and periradicular periodontitis are the consequence of lesions of the tooth pulp and are qualified as inflammatory lesions (radicular inflammatory tooth resorptions).

FORLs of the neck of the tooth are often confused with radicular inflammatory tooth resorptions. They are considered to be inflammatory because they are associated with inflammatory damage to the epithelial attachment (in the event of periodontal disease for example) (Andreasen, 1985; Trope et al, 2002).

The precise etiology of FORLs remains unknown and is still the subject of discussion and research. The suspected role of masticatory mechanical constraints and chronic inflammation due to periodontal disease is underlined in various histological (Gorrel & Larsson, 2002; Roux et al, 2002) and radiographic (DuPont & DeBowes, 2002) studies as well as one clinical study (Girard et al, 2008). Excessive vitamin D intake through the diet (Reiter et al, 2005) is proposed as a cofactor, although this continues to be debated. The precise role of specific histological dental structures in cats (vasodentine, osteodentine) has not been fully explained. Any interactions in the calcium regulation process associated with resorptions have been proposed (Okuda & Harvey, 1992).

Current veterinary recommendations propose the differentiation of FORLs based on the results of the radiographic evaluation:
- Type 1 FORL: observation of a physiological periodontal ligament space (lamina dura) and radio density of the affected root similar to that of healthy adjacent roots (Figure 19)
- Type 2 FORL: disappearance of the lamina dura in the radiographic examination and radio density of the affected root similar to that of the adjacent alveolar bone (bone remodeling) (Figure 20).

Figure 19. Type 1 FORL of the lower M1. (© N. Girard).

Figure 20. Type 2 FORL of the lower left PM3.

The combined study of the location of FORLs depending on their radiographic type shows significant differences (Girard et al, 2008). Among house cats, the greater prevalence of type 1 lesions is observed in the lower carnassial and type 2 lesions in PM3. Among purebred cats a significant difference is observed for incisors (Type 2 FORL) and the lower carnassial (Type 1 FORL). The distribution of FORLs in the mouth is not uniform according to the type of lesion observed radiographically. This information corroborates the hypothesis that different etiologies cause feline resorptive lesions.

The analysis of FORLs in a population of cats treated at the dentistry department of the University of California, Davis, reveal a significant association between FORL and the presence of severe localized vertical alveolar bone loss (Lommer & Verstraete, 2001).

The high prevalence of FORLs in the wild cat population on Marion Island (see above) fed almost exclusively with seabirds reduces the role some authors feel commercial food plays in the appearance of these tooth lesions. The author rather sees a consequence of feline oral inflammatory pathologies like periodontal disease and feline stomatitis (Verstraete et al, 1996).

An in-depth statistical analysis of the distribution of FORLs and 14 clinical and radiographic criteria associated with periodontal disease underlines a strong association (Girard et al, 2008). The global prevalence of FORLs may be significantly correlated to 6 of these periodontal parameters as well as age. Type 1 and 2 resorptions appear as two different phenomena without any association criteria. Type 1 FORL is significantly associated with 8 of the periodontal variables and so is strongly associated with periodontal disease. Type 2 FORL is correlated with just 2 periodontal parameters so the correlation to periodontal disease is low.

Age appears to be a factor strongly associated with the presence of type 2 FORL and weakly associated with type 1 FORL. All of these observations suggest that type 1 FORL is less sensitive to age with regard to its supposed link to the development of periodontal disease.

Stomatitis

The term feline stomatitis covers all the oral diseases characterized by a pronounced inflammation of the oral mucosa (Figure 21). Their prevalence appears to be low, although few statistical studies have been published on the subject (2.6% according to Crossley, 1991; 12% according to Verhaert & Van Wetter, 2004). Studies of large human populations show a prevalence of 5 - 15% of aggressive forms of periodontal inflammation, supposedly associated with ethnic predisposition (Wolf et al, 2005).

Figure 21. Stomatitis lesions in a cat. Jugal buccal stomatitis. (© N. Girard).

The analysis of tooth diseases in a population of 109 cats reveals 5.5% cases of stomatitis (3.7% buccal stomatitis, 1.8% caudal stomatitis) and 12.8% aggressive periodontitis (Girard et al, 2008). All these aggressive inflammatory diseases affected purebred cats, none of them housecats. The real impact of breed is still undergoing evaluation with respect to the probable familial effect.

The different types of stomatitis are known and dreaded, because they are generally a real therapeutic challenge. They are so painful that they disrupt the appetite and even the very survival of affected animals. The veterinarians’ feeling of helplessness is amplified by the many uncertainties related to the etiology of these diseases.

The clinical management of feline stomatitis demands great diagnostic and therapeutic rigor. Recent studies confirm the role of the Calicivirus in the development of caudal stomatitis (Addie et al, 2003). The most descriptive clinical examination is needed to advance the etiological analysis of feline stomatitis. Few published studies use an appropriate terminology to correctly evaluate a given type of medication, complementary examination or viral etiology. More precise information on the therapeutic benefits of selected substances, the role of selected viruses (FCV, HV1, FIV, FeLV) and the best histopathological (especially immunohistological) knowledge in this disease is expected to be found in the years to come.

Conclusion

Feline oral diseases are varied and in the majority of cases they include an inflammatory component. While the prevalence of periodontal disease is not really different from its occurrence in other species, the cat does suffer from relatively aggressive forms: inflammatory extension with respect to the oral mucosa (stomatitis) and FORLs that may render the clinical diagnosis more delicate when associated with chronic periodontitis. The local immune system is often perceived as one of the key factors of aggressive oral inflammation.