Exploring Feline Oral Disease: The Fabulous Four
ACVIM 2008
John R. Lewis, VMD, FAVD, DAVDC
Philadelphia, PA, USA

Tooth Resorption--An Emerging Mystery?

Tooth resorption (TR) is common in cats. Most studies have found a prevalence rate of 20 to 70%, depending on the population of cats and the investigative methods employed.1 The lesions are usually appreciated clinically at the cervical portion of the tooth, which may be hidden by gingiva. However, recent histological studies have found that these lesions begin on the root surface, and radiographic changes can often be seen before a clinical lesion is obvious.2 When a lesion develops at the gingival margin, the adjacent gingiva often covers these lesions with a combination of hyperplastic gingiva and granulation tissue. A fine-tipped explorer (ODU #11/12 or Orban #17 explorers are good choices rather than the traditional Shepherd's hook #23) should be used to check for irregularities where the explorer catches on a rough defect with distinct borders. In the past, these lesions have been treated by restoration with glass ionomer cements, but follow-up studies have shown poor long-term results with restoration.3 Therefore, extraction is the treatment of choice. Dental radiographs of these teeth are a total necessity to evaluate the severity of resorption and to guide treatment.

Sometimes it is not possible to perform a complete tooth extraction due to severe root resorption where a portion of the root has been replaced by a reparative bone-cementum material. When this occurs, the tooth root becomes incorporated into the adjacent alveolar bone. Radiographs in this case suggest a non-inflammatory evidence of resorption, referred to as root replacement. Radiographic signs include loss of periodontal ligament space and decreased root density, approximating that of the surrounding bone density. When this radiographic appearance is seen, in the absence of: 1) periodontal pockets of affected tooth; 2) endodontic disease (no brainer); 3) stomatitis; or 4) immunosuppressive disease, it is possible to perform a crown amputation. Hard tissue with characteristics of tooth root is removed and resorbed root which has been replaced by bone is left in place. The tooth crown and coronal root segment are removed with a dental bur in a high-speed handpiece. The crestal alveolar bone is smoothed with a dental bur, and the gingiva is always closed with absorbable suture over the crown amputation site.4 Without dental radiographs, a determination cannot be made as to whether crown amputation is an acceptable technique.

Multiple etiologies have been proposed to explain TR, including extension of periodontal disease, genetic or anatomic anomalies, mechanical trauma, endocrine abnormalities, infectious disease, age-related changes, and dietary aspects. In a recent histological study, clinically and radiographically normal teeth of cats with TR on other teeth showed histological signs of periodontal ligament degeneration, hypercementosis, dentoalveolar ankylosis and resorption, suggesting that TR is a generalized disorder of all teeth rather than a focal disease of isolated teeth.2 It is generally accepted that the prevalence of TR has increased over the past four decades at a rate that cannot be explained entirely by increased awareness and improved diagnostics.5 Also, feral cats exhibited a much lower prevalence rate than that seen in domestic cats.6 It is difficult to explain the increased prevalence of TR by physiological degradation associated with aging. The cause of TR likely resides in an environmental change or aspect of domestication that (1) has increased in popularity since the 1960s; and (2) is capable of causing changes to the entire periodontium of multiple if not all permanent teeth.

Recent findings suggest that one aspect of domestication related to diet may possibly be associated with the development of TR. A statistically significant increase in serum 25-hydroxyvitamin D concentrations has been found to be present in cats with TR compared to cats with no clinical or radiographic evidence of TR.7 Experimental oversupplementation of vitamin D and its metabolites in dogs and rats has revealed marked periodontal ligament degeneration, hypercementosis, hyperosteoidosis and alveolar bone expansion, and several other histological changes that parallel those seen in cats with TR.8 Cats are unable to produce vitamin D in their skin.9 Nutritional research has shown that plasma concentrations of 25-hydroxyvitamin D in kittens is directly related to the dietary intake of vitamin D.10 Vitamin D must be obtained from food, although the requirement for cats appears to be low. Based upon mean plasma concentrations obtained after feeding a diet of known vitamin D level, a minimum vitamin D concentration of 250 IU/kg dry matter has been recommended for commercial diets.11 Marine fish, a common source of protein in dry and canned cat food, contains substantial levels of vitamin D. Mackerel flesh contains a mean of 9,500 IU/kg dry matter whereas mackerel viscera contains a mean of 144,000 IU/kg dry matter. Therefore, whole minced fish often contains 25,000 IU/kg dry matter.9 It has previously been determined that 36 of 49 (73%) canned cat foods tested had vitamin D concentrations greater than 1,500 IU/kg dry matter, and 15 of 49 (31%) foods tested were in excess of the Association of American Feed Control Officials' (AAFCO) recommended maximum level of 10,000 IU/kg dry matter.9 Though this is compelling evidence supporting a role of vitamin D in causing changes to the periodontium, a cause-and-effect relationship between chronic increased dietary intake of vitamin D and development of TR has not yet been proven.Experimental long-term feeding studies are imperative to definitively determine if vitamin D in the development of TR. There may be a connection between TR and other common feline oral pathology including alveolar bone expansion and tooth extrusion (supereruption), as cats with TR are significantly more likely to exhibit extrusion of their maxillary canine teeth.12

Stomatitis

Diffuse inflammation of the entire oral cavity is seen commonly in cats. When inflammation is confined to the gingiva, it is referred to as gingivitis. When the inflammation extends beyond the mucogingival junction in cats, it is called stomatitis, or feline gingivostomatitis (FGS). Stomatitis may be due to a variety of causes, including ingestion of a caustic substance, uremia, viral exposure, plant foreign bodies, allergic response to drugs, or most commonly, immune-mediated causes. Cats are often affected by a type of stomatitis referred to as lymphocytic-plasmacytic stomatitis (LPS), which can involve gingiva, alveolar mucosa, buccal mucosa, sublingual mucosa, and even the mucosa of the caudal oral cavity lateral to the palatoglossal folds. Cats often present with decreased appetite or anorexia, halitosis, dehydration, and blood-tinged saliva. This can be further characterized based on location. Rostral stomatitis refers to inflammation adjacent to the teeth, and caudal stomatitis refers to inflammation in the caudal oral cavity lateral to and sometimes including the palatoglossal folds.

The cause of FGS is not clear, but it appears that cats develop inappropriate inflammation in the presence of even small amount of plaque accumulation. Many cats with FGS concurrently shed both herpesvirus and calicivirus.13 These viruses may have an effect on the immune system, resulting in an overzealous or deficient immune response to plaque. Therefore, plaque control in the form of frequent dental cleanings and home care is very important. Unfortunately, many FGS cats are so painful that home care is not feasible. Immunosuppressive agents such as corticosteroids and cyclosporine help in many cases, but when medical therapy fails or causes unacceptable side effects, full mouth extractions or nearly full-mouth extractions have been shown to provide clinical resolution of oral discomfort in approximately 80% of cases.14 A review of current knowledge of the disease was written by Lyons in VCNA, 2005.

There are some interesting questions that need to be answered regarding etiology and treatment of stomatitis. First, what is the role of Bartonella in the development of stomatitis? This is still unclear, though cats seropositive for Bartonella showed an increased incidence of stomatitis.15 It appears that azithromycin is not the magic bullet we had hoped it would be. If Bartonella does play a role, it may not be in every case, but rather in cases where proliferative mucosal disease is present. Proliferative vascular lesions of the oral cavity are seen in humans affected by bacillary angiomatosis, which is caused by B. henselae and/or B. quintana.16 A funded study is near completion looking at the effectiveness of cyclosporine in treatment of stomatitis. Also, CO2 laser as an adjunctive treatment of refractory stomatitis has helped to contribute to a cure in some cases, but this technology is not a panacea.17

Periodontal Disease

Periodontal disease (PD) is the most common disease occurring in dogs and cats.18 The periodontium is composed of four supporting structures of the tooth: 1) peridontal ligament; 2) gingival connective tissue; 3) alveolar bone forming the tooth socket; and 4) cementum covering the surface of the root. Healthy gingiva has a sharp, tapered edge (margin) that lies closely against the crown of the tooth. The free gingiva forms a moat around the tooth called the gingival sulcus. The epithelial attachment to the tooth crown forms the bottom of the gingival sulcus. Periodontitis is caused by accumulation of subgingival plaque and the body's response to it. Plaque is a white/tan film that collects around and within the gingival sulcus of the tooth. It is composed of bacteria, food debris, exfoliated cells, and salivary glycoproteins. Within as quickly as 24 hours if left undisturbed, plaque will mineralize on the teeth to form dental calculus (sometimes referred to by the term "tartar"), a light brown or yellow raised irregular deposit adherent to the tooth and root surfaces. This irregular, plaque retentive surface of calculus allows for further plaque accumulation. As the plaque accumulates within the gingival sulcus, it damages the gingival tissues by releasing bacterial by-products which can damage the periodontium. The patient's immune response may also cause tissue damage through the release of inflammatory cytokines from white blood cells as they attempt to destroy the bacteria. In the early stages, the gingiva becomes inflamed and bleeds easily. As the disease progresses periodontitis results in attachment loss. Attachment loss is clinically detectable in its earliest stages by measuring pocket depths with a periodontal probe in the anesthetized patient. The depth of this sulcus is less than 1 mm in the cat. If the depth is greater than this, it is due to either pocket or pseudopocket formation. A pocket forms when there is loss of attachment of the junctional epithelium which allows the probe to extend deeper than normal. A pseudopocket is caused by overgrowth of the gingiva, called gingival hyperplasia (histological diagnosis) or gingival enlargement (clinical diagnosis). Probing depths may be increased in these cases even though there is no loss of attachment of the junctional epithelium. Gingival enlargement is uncommon in cats compared to dogs. Removal of excess gingiva is necessary in cases where pseudopockets are present to prevent accumulation of plaque and hair in the pseudopockets. In contrast, treatment of true pockets is accomplished by use of curettes to perform subgingival curettage and root planing. The difficulty in performing advanced peridontal procedures in cats is that a gingival collar must be present in order to preserve a tooth, and any degree of gingival recession may make it difficult to fulfill this criterion. In cases of advanced periodontal disease, extraction of the affected tooth may be the most appropriate treatment, especially if home care is not feasible. Studies are ongoing to evaluate the degree of inflammatory mediators in cats detectable in serum before and after dental disease is treated.

Oral Neoplasia

Oral tumors account for approximately 10% of all feline neoplasia. These tumors are often aggressive and prognosis depends on early detection. The most common oral tumor in cats is squamous cell carcinoma (SCC), which accounts for approximately 70% of all oral tumors in cats.19 To be able to provide a cure for SCC, early detection is particularly important in cats due to the patient's smaller size and need to obtain clean surgical margins while still maintaining adequate function. Cats that undergo radical maxillectomy or mandibulectomy for removal of an oral tumor generally function well postoperatively, and the majority of clients are pleased with long term quality of life and appearance. Cats do recover more slowly from maxillectomy and mandibulectomy than dogs and often require placement of a feeding tube (usually an esophagostomy tube) during the recovery period, whereas dogs usually eat and drink within 24 hours after surgery. One study found that 12% of cats undergoing mandibulectomy never regained the ability to eat.20

A number of "take home points" for cats with suspected SCC follow. First, it is important to obtain a biopsy in suspected cases, because SCC lesions can look similar to other lesions such as feline stomatitis or eosinophilic granulomas. Use of advanced diagnostics such as dental radiographs or CT scan is very important in determining which patients may be cured with surgery. Although SCC in cats is historically considered unlikely to metastasize, aspiration of mandibular lymph nodes is warranted prior to mandibulectomy or maxillectomy, since the author has seen a number of cases which have metastasized to the mandibular nodes. Finally, the possibility of a surgical cure is not always possible depending on location and size of the tumor. Sublingual and caudal maxillary masses are unlikely to be cured surgically. However, rostral and mid-body mandibular masses may be amenable to radical resection by an experienced oral surgeon.

One study which looked at risk factors for development of feline SCC showed an increased risk in cats who wore flea collars. Other risk factors included intake of tuna and a diet consisting of predominantly canned foods.21 Studies looking at use of chemotherapeutic polyamine inhibitors for non-resectable tumors are ongoing at two universities.

References

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8.  Reiter AM, et al. Vet Clin Small Anim 2005;35:913-942.

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10. Morris JG, et al. J Nutr 1999;129:909-912.

11. Morris JG, Earle KE. J Clin Nutrition 1996;3:93-96.

12. Lewis JR, et al. J Vet Dent (in print).

13. Lommer M, Verstraete FJM. Oral Microbiol Immunol 2003;18(2)131-134.

14. Hennet P. J Vet Dent 1997;14(1):15-21.

15. Glaus T, et al. J Clin Microbiol. 1997;35(11):2883-2885.

16. Lopez de Blanc S, et al. Oral Pathol Med 2000;29:91-96.

17. Lewis JR, et al. J Vet Dent 2007;24(4).

18. Harvey, CE. Vet Clin Small Anim 2005;31:819-836.

19. Harvey, CE, Emily PP. Small Animal Dentistry 1993.

20. Northrup NC, etal. J Am Anim Hosp Assoc 2006;42(5):350-60.

21. Bertone ER, et al. J Vet Intern Med 2003;17(4):557-62.

Speaker Information
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John Lewis, VMD, FAVD, DAVDC
University of Pennsylvania
Philadelphia, PA


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