Patients with periodontal disease, the most common disease in dogs, suffer from progressive inflammation and destruction of
the tissues supporting the teeth. In addition to causing oral pain and tooth loss, periodontal infections can spread systemically
and may adversely affect various organs, including the heart, kidneys, and liver.1
Literally translated from Latin as "around the tooth," periodontium refers to the tissues that attach the teeth to the jaws. These structures include the gingiva, the alveolar bone, the cementum
(connective tissue that covers the tooth root), and the periodontal ligament (collagen fibers that attach the tooth to the
alveolar bone). The gingival sulcus is a shallow space around a tooth bounded by the tooth surface on one side and the marginal
epithelium lining the free gingival margin on the other.2 In periodontal disease, these tissues become progressively diseased and are destroyed while the tooth remains unaffected.
Therefore, we should not think of periodontal disease as tooth disease but rather as around-the-tooth disease.
The inflammation and destruction associated with periodontal disease is initiated by bacterial plaque accumulating on the
tooth surface. Hundreds of bacterial species inhabit the oral cavity, and probably many more have yet to be identified. However,
in people as well as in animals, certain bacteria are implicated as the primary cause of the disease and have been labeled
periodontopathogens. In people, Porphyromonas gingivalis, a black-pigmented, gram-negative anaerobe, has been identified as a periodontopathogen, and certain Porphyromonas species are also likely periodontopathogens in dogs.3,4 Additionally, it appears that complex interactions among the various microbe populations in the oral cavity influence the
disease's progression, so to think of periodontal disease as an infection with a single bacterial species would be an oversimplification.
However, when treating periodontal infection, specifically target the gram-negative anaerobes.
Many other factors, such as a patient's age, diet, chewing habits, occlusion, and size, can affect the severity of its periodontal
disease. A major factor appears to be a host's reaction to bacterial plaque. Bacterial endotoxins and other bacterial byproducts
primarily cause the tissue destruction, but the body's own inflammatory response—set into motion by the oral immune system—can
also influence the degree of tissue inflammation and destruction (i.e. a greater immune response can cause more tissue damage).
PERFORMING AN ORAL EXAMINATION
Ideally, oral examinations should be done in anesthetized patients because the diagnosis and staging of periodontal disease
require periodontal probing and radiographic examination. At least one problem is usually found in an awake patient that should
be addressed in an anesthetized patient, so always inform clients that complete dental diagnostic evaluation and treatment
DIAGNOSING PERIODONTAL DISEASE
The periodontal probe, an essential diagnostic tool, has calibrated markings for measuring the gingival sulcus depth (Figures 1A-1D). This depth, also known as pocket depth, is measured from the gingival margin to the apical extent of the pocket and should be checked on four sites around every
tooth. Normal pocket depth is 1 to 3 mm in dogs, but it can increase because of periodontal tissue destruction from disease
or because of pathologic overgrowth of the gingiva. Pockets caused solely by gingival overgrowth are termed pseudopockets. Exposure of the area where the roots join the crown in multirooted teeth is termed furcation exposure.