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Periodontal disease is a broad term for inflammation and/or infection of the tissues that support and surround the teeth. Gingivitis refers to inflammation of the gingiva. It is a normal response to plaque antigen that affects nearly all adult dogs and cats. Periodontitis is a more severe disease that involves inflammation of the periodontal ligament and alveolar bone. Periodontitis is much more common in certain breeds but can affect any individual.
Etiology and Pathogenesis
The oral cavity normally supports a rich bacterial microflora, much of which thrives in plaque on tooth surfaces. Bacterial plaque constantly presents antigen to the marginal gingiva, stimulating the normal inflammatory response and resulting in gingivitis. The bacteria in plaque are predominantly nonmotile gram-positive aerobes, including Staphylococcus spp and Streptococcus spp, but many others are also present. While this microbiota does stimulate an immune response, the bacteria in a healthy mouth exist in relative commensal harmony with the host. They may even be beneficial by helping to limit the numbers of more pathogenic bacteria. If the plaque becomes very thick because of poor oral hygiene, the bacterial population can become more pathogenic, with a higher percentage of nonmotile anaerobic rods. The bacteria found in the presence of inflammation include Bacteroides fragilis, Peptostreptococcus, Porphyromonas gulae, Porphyromonas salivosa, Porphyromonas denticanis, Prevotella intermedia, Treponema spp, Bacteroides splanchnicus, (Odoribacter denticanis proposed), and many others. Interestingly, some of the common human periodontopathogens such as Aggregatibacter (Actinobacillus) actinomycetemcomitans are notably absent in animals. Subgingival plaque (plaque on the root surface under the gingival margin) is also commonly inhabited by these more pathogenic species of bacteria. Periodontitis is caused by the host response to subgingival plaque. Inflammatory mediators produced by the host directly result in bone and tissue damage around the root. The bacteria themselves and their metabolic products also contribute to the bone damage. Development of periodontitis is also affected by other intrinsic (eg, genetics, tooth crowding, thin alveolar bone, age) and extrinsic (eg, diet, stress, concurrent disease, oral hygiene) factors.
Clinical Findings and Lesions
Mild (grade 1) gingivitis is characterized by hyperemia of the marginal gingival blood vessels. In moderate (grade 2) gingivitis, there is edema of the gingival margins that appears as “rolled margins,” thickening of the tissues adjacent to the teeth. In grade 3 (severe) gingivitis, there is ulceration of the surface epithelium. Gingivitis is not painful, and the only outward sign is redness and halitosis. A form of juvenile-onset gingivitis is seen in some cats at 6–8 mo of age. These cats often have moderate to severe gingivitis that is unusual in young animals.
Mild (grade 1) periodontitis is characterized by early periodontal pocket formation as the supportive tissues are damaged. The pocket may extend up to one-third the length of the root. In moderate (grade 2) periodontitis, the loss of root attachment affects more than one-third and up to two-thirds of the root length. Loss of attachment over two-thirds of the root length is considered severe (grade 3) and is often accompanied by tooth mobility and discomfort. Unless mobility or a periodontal abscess develops, periodontitis does not cause discomfort. Gingival recession, furcation exposure, and alveolar bone loss can also occur. Oral radiographs provide valuable information about the severity and pattern of alveolar bone loss.
Treatment
Removal of the bacterial plaque that causes gingivitis resolves the inflammation, quickly returning the tissue to health. Professional dental cleaning, scaling, and polishing are performed under general anesthesia. Tooth cleaning on an awake patient improves the appearance of the tooth crowns but does not improve the periodontal health. If the gingivitis does not resolve, further examination should be performed to identify additional complicating conditions such as persistent subgingival plaque and calculus or the presence of predisposing factor(s). Some less common causes of gingivitis, including systemic disease (eg, uremic stomatitis), autoimmune disease, juvenile gingivitis, etc, may require more than only plaque removal.
Periodontitis requires more aggressive treatment. Root scaling (removing calculus) and planing (smoothing the root and removing diseased cementum) are performed. Shallow pockets are treated closed, but pockets that are >6 mm deep require surgery to expose the root surface for adequate treatment. Placement of locally active antibiotics into the pocket may be helpful. Extraction is often the best treatment for teeth with increased mobility that have a guarded to poor prognosis. Periodontitis is not as readily reversible as gingivitis, requiring osseous surgery and placement of osseous implants and barrier membranes to achieve guided tissue and guided bone regeneration. This is not a good option for pockets on the palatal side of maxillary canine teeth that have already progressed to form an oronasal fistula; treatment requires extraction of the canine tooth and surgical fistula repair. Deep infrabony defects with bone loss that undermines a furcation can infect the pulp through a lateral or furcal canal, resulting in secondary endodontic disease. Saving these teeth would also require endodontic therapy (see below), and the prognosis is determined by the periodontal disease.
Teeth that have become mobile because of loss of attachment and bony support should be extracted. They can sometimes be saved through bone grafts, open periodontal surgery, and support splints, but the disease will recur without drastic changes in home oral hygiene. Extraction allows the tissues to heal. A dog or cat can function much better and with more comfort without a tooth than with an infected and mobile tooth.
Prevention
Prevention of gingivitis is the same as its treatment; plaque removal and control. Plaque is a typical biofilm, composed of many microorganisms that differ from their planktonic forms. In a biofilm, microorganisms are more resistant to antibiotics, disinfectants, and antibacterial agents. However, biofilms are easily and effectively removed mechanically with a toothbrush. Even large accumulations of supragingival plaque are easily removed by toothbrushing. The teeth should be brushed daily to remove plaque and prevent calculus (tartar) accumulation. Cats rarely allow regular toothbrushing, so the plaque should be removed by wiping with a gauze pad at least every second or third day. Only the outside (buccal/labial) surfaces of the maxillary teeth need to be brushed in most dogs and cats. Plaque that remains on the tooth surface for >3 days mineralizes to form calculus that cannot be removed by brushing. While calculus gives the appearance of unhealthy teeth, its contribution to periodontal disease is minor.
Texture of the diet, toys, and treats can affect the self-cleaning mechanisms of the teeth. Firm fibrous items that allow tooth penetration can wipe plaque from the tooth surfaces during chewing. In addition to texture, some diets are formulated to include ingredients that help decrease oral bacteria or slow plaque mineralization.
Products that slow or prevent the attachment of pellicle or the adhesion of pioneering plaque bacteria may provide some benefit.
Prevention of periodontitis is more complicated. Regular oral hygiene to remove supragingival plaque provides some protection to help prevent the development of subgingival plaque and to minimize the numbers of periodontopathogens. More importantly, predisposing factors should be identified and removed. Severe crowding can be relieved through selective extractions, predisposing anatomy can be modified, diabetes or renal failure can be treated and controlled, and inappropriate behaviors or parafunctional habits that damage the tissues can be addressed.
Last full review/revision March 2012 by Jack Easley, DVM, MS, DABVP (Equine); Gregg A. DuPont, DVM, Fellow AVD, DAVDC
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