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Professional Version

Periodontal Disease in Small Animals


Alexander M. Reiter

, Dipl. Tzt., DEVDC, DAVDC, Department of Clinical Sciences & Advanced Medicine, School of Veterinary Medicine, University of Pennsylvania

Reviewed/Revised Dec 2013 | Modified Oct 2022
Topic Resources

Periodontal disease is infection and inflammation of the periodontium (the tissues that surround and support the teeth) due to plaque bacteria and the host’s response to the bacterial insult. Gingivitis is common in dogs and cats and refers to inflammation of the gingiva in response to plaque antigen. Periodontitis is a more severe disease that involves inflammation of the periodontal ligament and alveolar bone, eventually causing loss of attachment (periodontal pocketing, gingival recession, bone resorption). Periodontitis is much more common in certain dog and cat breeds, but it can affect any individual.

Etiology and Pathogenesis:

The oral cavity supports a rich bacterial microflora, much of which thrives in plaque on tooth surfaces. Bacterial plaque on the crown surface of a tooth constantly presents antigen to the marginal gingiva, stimulating an 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. Although this microbiota does stimulate an immune response, the bacteria in an otherwise healthy mouth exist in relative commensal harmony with the host. They may even be beneficial by helping to limit the numbers of periodontopathogenic bacteria. If the plaque becomes very thick because of poor oral hygiene and oxygen within the plaque is depleted, the bacterial population can become more pathogenic, with a higher percentage of nonmotile, gram-negative anaerobic rods. The bacteria found in the presence of teeth with periodontal disease include Bacteroides fragilis, Peptostreptococcus, Porphyromonas gulae, Porphyromonas salivosa, Porphyromonas denticanis, Prevotella intermedia, Treponema spp, Bacteroides splanchnicus, and many others. Interestingly, some of the common human periodontopathogens such as Haemophilus (formerly Actinobacillus) actinomycetemcomitans are notably absent in animals. Subgingival plaque (plaque on the tooth surface below the gingival margin) is also commonly inhabited by these more periodontopathogenic species of bacteria. Periodontitis is caused by the host's 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:

Periodontal disease is classified in stages. In teeth with healthy periodontal tissues, no gingivitis or periodontitis is evident.

Stage 1: There is gingivitis only, without attachment loss; the height and architecture of the alveolar margin are normal.

Stage 2: There is early periodontitis with < 25% of attachment loss or, at most, there is a stage 1 furcation involvement in multirooted teeth (see below). There are early radiographic signs of periodontitis. The loss of periodontal attachment is < 25% as measured by probing of the clinical attachment level or by radiographic determination of the distance of the alveolar margin from the cementoenamel junction relative to the length of the root.

Stage 3: There is moderate periodontitis, with 25%–50% of attachment loss as measured by probing of the clinical attachment level or by radiographic determination of the distance of the alveolar margin from the cementoenamel junction relative to the length of the root, or there is a stage 2 furcation involvement in multirooted teeth (see below).

Stage 4: There is advanced periodontitis, with >50% of attachment loss as measured by probing of the clinical attachment level or by radiographic determination of the distance of the alveolar margin from the cementoenamel junction relative to the length of the root, or there is a stage 3 furcation involvement in multirooted teeth (see below).

A stage 1 furcation involvement exists when a periodontal probe extends less than halfway under the crown in any direction of a multirooted tooth with attachment loss. A stage 2 furcation involvement exists when a periodontal probe extends greater than halfway under the crown of a multirooted tooth with attachment loss but not through and through. A stage 3 furcation involvement exists when a periodontal probe extends under the crown of a multirooted tooth, through and through from one side of the furcation out the other.

A stage 0 mobility up to 0.2 mm is physiologic. A stage 1 mobility is present when tooth mobility is increased in any direction other than axial over a distance of >0.2 mm and up to 0.5 mm. A stage 2 mobility is present when tooth mobility is increased in any direction other than axial over a distance of >0.5 mm and up to 1 mm. A stage 3 mobility is present when tooth mobility is increased in any direction other than axial over a distance >1 mm or any axial movement.


Removal of the bacterial plaque on the tooth surfaces is of utmost importance. This can reverse gingivitis, returning the gingiva to a healthy, uninflamed state. This is achieved through professional dental cleaning (scaling and polishing) with power and hand instruments under general anesthesia. Dental cleaning on an awake animal improves the cosmetic appearance of the tooth crowns but does not improve periodontal health. The owner might falsely believe the condition has been treated, while periodontal disease continues to thrive. 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 periodontal treatment. Root scaling (removing plaque and calculus on exposed root surfaces) and planing (smoothing the root surfaces by removing textural irregularities and diseased cementum) are performed, followed by gingival curettage that removes the infected and inflamed inside layer of a periodontal pocket. Shallow periodontal pockets are treated in a closed fashion, but pockets >6 mm deep require open surgery (creation of a periodontal flap) to expose the root surface and alveolar bone for adequate treatment (root scaling/planing and alveoloplasty). The connective tissue side of the flap needs to be debrided before wound closure to avoid contact of infected and inflamed granulation tissue with the planed root surfaces. Local placement of a gel containing antibiotics (eg, doxycycline) into cleaned periodontal pockets 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. Lost bone may be augmented by use of bone grafts or bone graft substitutes. Barrier membranes should be placed between the bone defect and gingival tissues to achieve guided tissue regeneration. Maxillary canine teeth with pockets on their palatal side that have already progressed to form an oronasal fistula require extraction and oronasal fistula repair. Deep infrabony defects in multirooted teeth with bone loss that undermines a furcation can infect the pulp through a furcation canal, resulting in secondary endodontic disease. Similarly, if periodontitis has progressed apically and reached the apex of the root of a tooth, secondary endodontic disease will develop. Saving such teeth also requires endodontic therapy (see below), and the prognosis is determined by the extent of periodontal disease.

Teeth that have become mobile because of loss of attachment should be extracted. They can sometimes be saved through major periodontal surgery procedures, but disease will recur without drastic changes in home oral hygiene. Extraction allows the tissues to heal. A pet dog or cat can function perfectly fine without teeth.


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. Some dogs and cats may not 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 (labial and buccal) surfaces of the teeth may be approachable for brushing 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. Although 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-cleansing 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. The Veterinary Oral Health Council website ( ) provides further information about products that meet certain requirements for plaque and/or calculus control.

Prevention of periodontitis is more complicated. Regular oral hygiene to remove supragingival plaque provides some protection to help prevent development of subgingival plaque and to minimize the number of periodontopathogens in the mouth. 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.

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