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may be reduced or eliminated by proper plaque and calculus removal. However, periodontal bone loss is irreversible (without regenerative surgery). Although bone loss is irreversible, it is possible to arrest its progression. However, it is more difficult to maintain periodontally diseased teeth in comparison to healthy teeth. Additionally, periodontal attachment loss may be present with or without active inflammation.
Periodontal disease is initiated by oral bacteria which adhere to the teeth in a substance called plaque. Plaque is a biofilm, which is made up almost entirely of oral bacteria, contained in a matrix composed of salivary glycoproteins and extracellular polysaccharides. Calculus (or tartar) is basically plaque which has secondarily become calcified by the minerals in saliva.
It is important to note that rough tooth surfaces will greatly increase the speed of plaque and calculus formation. Therefore any condition which detracts
from the smooth tooth surface should be addressed. This can be as simple as a bonded sealant or in some cases can be better treated by a composite restoration. Another condition which commonly hastens the onset of periodontal disease is crowding. This will impair the not only homecare efforts, but also the natural cleaning ability of the patient.
Plaque and calculus may contain up to 100,000,000,000 bacteria per gram. More importantly, bacteria become must more resistant to antiseptics
and antibiotics than their free living or “planktonic” counterparts. In fact, they are 1,000 to 1,500 times more resistant to antibiotics and antiseptic concentrations need to be up to 500,000 times that which would kill singular bacteria.
Plaque on the tooth surface is known as supragingival plaque. Once it extends under the free gingival margin and into the area known as the gingival sulcus (between the gingiva and the teeth or alveolar bone), it is called subgingival plaque. Supragingival plaque likely affects the pathogenicity of the subgingival plaque in the early stages of periodontal disease. However, once the periodontal pocket forms, the effect of the supragingival plaque and calculus is minimal. Therefore, control of supragingival plaque alone is ineffective in controlling the progression of periodontal disease.
Initial plaque bacteria consists of predominately non- motile, gram-positive, aerobic facultative rods and cocci. Gingivitis is initiated by an increase in the overall number of bacteria, which are primarily motile gram negative rods and anaerobes. The specific plaque hypothesis
is based on the fact that these few species are seen in virtually all cases of chronic periodontal disease.
The bacteria in the subgingival plaque secrete toxins as well as metabolic products. Also produced are cytotoxins and bacterial endotoxins which can invade
tissues on their own, and in turn cause inflammation to the gingival and periodontal tissues. This inflammation causes damage to the gingival tissues and initially results in gingivitis. Eventually, the inflammation can lead to periodontitis, i.e. the destruction of the attachment between the periodontal tissues and the teeth.
In addition to directly stimulating inflammation, the bacterial metabolic byproducts also elicit an inflammatory response from the animal. White blood cells and other inflammatory mediators migrate out of the periodontal soft tissues and into the periodontal space due to increased vascular permeability and increased space between the crevecular epithelial cells. White blood cells fight the infection by phagocytizing bacteria, but may also release enzymes to destroy the bacterial invaders either by design or after their death. When released into the sulcus, these enzymes will cause further inflammation of the delicate gingival and periodontal tissues. In fact, the progression of periodontal disease is determined by the virulence of the bacteria combined with the host response. It is the host response that often damages
the periodontal tissues. However, patients with deficient immune systems typically have more severe periodontal disease than those individuals in good health.
The inflammation produced by the combination of the subgingival bacteria and the host response damages the soft tissue attachment of the tooth, and decreases the bony support via osteoclastic activity. This causes the periodontal attachment of the tooth to move apically. The end stage of periodontal disease is tooth loss; however the disease has created significant problems prior to tooth exfoliation.
Clinical Features:
It is important to be familiar with normal features in order to identify abnormal findings. Normal gingival tissues are coral pink in color (allowing for normal pigmentation), and have a thin, knife-like edge, with a smooth and regular texture. In addition, there should be no demonstrable plaque or calculus on the dentition.
The first obvious clinical sign of gingivitis is erythema followed by edema of the gingiva. However, it is now known that the FIRST evidence of gingivitis is bleeding during brushing, probing, or after chewing hard/rough toys. Therefore it is important to realize that normal appearing teeth/gums can actually be infected. If the first stages of gingivitis are not treated, it will progress into edema, spontaneous bleeding, and halitosis.
The development of halitosis in pets is almost always due to periodontal disease. As previously stated, periodontal disease is caused by an increase in anaerobic bacteria. Certain strains of these bacteria will digest protein as their energy source (generally provided by the host). Some amino acids contain sulfur and this digestion creates products called volatile
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