Periodontal disease is the result of the inflammatory response to dental plaque, i.e., oral bacteria, and is limited to the periodontium. It is the most common oral disease seen in dogs (1). It is also common in the cat (2). In fact, periodontal disease is probably the most common disease seen in small animal practice with the great majority of dogs and cats over the age of three years having a degree of disease that warrants intervention.
Periodontal disease is a collective term for a number of plaque-induced inflammatory lesions that affect the periodontium. Gingivitis is inflammation of the gingiva and is the earliest sign of disease. Individuals with untreated gingivitis may develop periodontitis. The inflammatory reactions in periodontitis result in destruction of the periodontal ligament and alveolar bone. The result of untreated periodontitis is ultimately exfoliation of the affected tooth. Thus, gingivitis is inflammation that is not associated with destruction (loss) of supporting tissue. It is reversible. In contrast, periodontitis is inflammation where the tooth has lost a variable degree of its support (attachment). It is irreversible.
Periodontal disease can cause discomfort to affected individuals. Moreover, there is strong circumstantial evidence that a focus of infection in the oral cavity may cause disease of distant organs (3). Consequently, prevention and treatment of periodontal disease is important for the general health of companion animals. It is not a cosmetic issue! This presentation details aetiology, pathogenesis, and outlines diagnostic methods and treatment options for individuals affected by periodontal disease.
The primary cause of gingivitis and periodontitis is accumulation of dental plaque on the tooth surfaces. Contrary to common belief, calculus (tartar) is only a secondary etiologic factor.
Dental plaque is a biofilm composed of aggregates of bacteria and their by-products, salivary components, oral debris and occasional epithelial and inflammatory cells. Plaque accumulation starts within minutes on a clean tooth surface. The initial accumulation of plaque occurs supragingivally but will extend into the sulcus and populate the sub-gingival region if left undisturbed.
Classic experiments have demonstrated that accumulation of plaque on the tooth surfaces reproducibly induces an inflammatory response in associated gingival tissues, and that removal of the plaque leads to disappearance of the clinical signs of this inflammation (4,5). Dental calculus is mineralised plaque. However, a layer of plaque always covers calculus. Both supra-gingival and subgingival plaque becomes mineralised. Supra-gingival calculus per se does not exert an irritant effect on the gingival tissues. The main importance of calculus in periodontal disease seems to be its role as a plaque retentive surface.
The pathogenic mechanisms involved in periodontal disease include:
Direct injury by plaque microorganisms and
Indirect injury by plaque microorganisms via inflammation.
It is now well accepted that it is the host's response to the plaque bacteria, rather than microbial virulence per se, that directly causes the tissue damage (6).
Other conditions, such as physical or psychological stress and malnutrition may impair protective responses, such as the production of antioxidants and acute phase proteins, and can aggravate periodontitis but do not actually cause destructive tissue inflammation. A genetic predisposition to destructive inflammation of the periodontium may be important in some individuals. In humans, a strong association has been observed between the severity of periodontitis and a specific genotype of the interleukin-1 (IL-1) gene cluster (7). Patients carrying this periodontitis-associated genotype (PAG) may demonstrate phenotypic differences, as indicated by elevated levels of IL-1ß in gingival sulcular (crevicular) fluid (8). No similar data are available for the dog or cat.
Undisturbed plaque accumulation results in gingivitis. While some individuals with untreated gingivitis will develop periodontitis, not all animals with untreated gingivitis do so. It cannot be predicted which individuals with gingivitis will develop periodontitis. However, animals in which clinically healthy gingivae are maintained will not develop periodontitis. Consequently, the aim in periodontal disease prevention and treatment is to establish and maintain clinically healthy gingivae to prevent periodontitis.
Gingivitis is defined as a reversible plaque-induced inflammation limited to the gingiva (i.e., no loss of periodontal attachment). It manifests clinically as swelling, reddening and often bleeding of the gingival margin.
Gingival hyperplasia may be the result of plaque-induced inflammation, i.e., hyperplastic gingivitis. It may also be of idiopathic or familial origin; and it can be induced by certain drugs, e.g., hydantoin, cyclosporins. Gingival hyperplasia is common in some breeds, e.g., Boxer, Springer Spaniel. There is an increase in periodontal probing depths due to the gingival overgrowth.
Uncomplicated gingivitis is generally not associated with discomfort or pain in humans. In fact, it is an insidious process and the patient may be unaware of its existence. The significance of gingivitis is that, if untreated, periodontitis may develop as described earlier.
Gingival hyperplasia does pose an additional concern. The hyperplastic gingiva alters the position of the gingival margin and results in a false or 'pseudo' pocket. It is called a pseudo pocket, as the increased periodontal probing depth is not due to destruction of periodontal ligament and alveolar bone with apical migration of the junctional epithelium as in periodontitis. Instead, the increased periodontal probing depth is due to the overgrowth of the gingiva. The presence of hyperplastic gingiva compromises tooth cleaning and may predispose to periodontitis. Radiography is mandatory for patients with gingival hyperplasia.
Individuals with untreated gingivitis may develop periodontitis. The inflammatory reactions in periodontitis result in destruction of the periodontal ligament and alveolar bone. The result of untreated periodontitis is eventually exfoliation of the affected tooth. It is important to remember that periodontitis is a site-specific disease, i.e., it may affect one or more sites of one or several teeth. Periodontitis can generally be considered irreversible. The aim of treatment is thus to prevent development of new lesions at other sites and to prevent further tissue destruction at sites, which are already affected.
Based on feedback from human patients, uncomplicated periodontitis is not associated with severe pain or discomfort. In contrast, complications such as the development of a lateral periodontal abscess or ulcers in the mucous membranes are very painful.
It has been shown that a severe infection in the oral cavity, as with extensive periodontitis will lead to a transient bacteraemia on chewing (9). In fact, an association has been demonstrated between periodontal disease and histopathologic changes in kidney, myocardium, and liver (2).
The treatment of periodontal disease is aimed at controlling the cause of the inflammation, i.e., dental plaque. Conservative or cause-related periodontal therapy consists of removal of plaque and calculus, and any other remedial procedures required, under general anaesthesia, in combination with daily maintenance of oral hygiene. The aim of treatment differs whether the patient has gingivitis only or if there is also periodontitis.
1. Hamp SE, et al (1984): A macroscopic and radiologic investigation of dental diseases in dogs. Veterinary Radiology 25, p86.
2. Reichart PA, et al (1984): Periodontal disease in the domestic cat: A histopathologic study. Journal of Periodontal Research 19, p67.
3. DeBowes LJ, et al (1996): Association of periodontal disease and histologic lesions in multiple organs from 45 dogs. Journal of Veterinary Dentistry 13, p57.
4. Löe H, et al (1965): Experimental gingivitis in man. Journal of Periodontology 36, p177.
5. Theilade E, et al (1966): Experimental gingivitis in man. II A longitudinal clinical and bacteriological investigation. Journal of Periodontal Research 1, p1.
6. Kinane DF, Lindhe J (1997): Pathogenesis of periodontitis. In: Lindhe J, Karring T, Lang NP (eds) Clinical Periodontology and Implant Dentistry. Munksgaard, Copenhagen, Denmark, p189-225.
7. Kornman KS, et al (1997): The interleukin 1 genotype as a severity factor in adult periodontal disease. Journal of Clinical Periodontology 24, p72.
8. Engebretson SP, et al (1999): The influence of interleukin gene polymorphism on expression of interleukin-1ß and tumour necrosis factor-a in periodontal tissue and gingival crevicular fluid. Journal of Periodontology 70, p567.
9. Thoden van Velzen SK, et al (1984): Plaque and systemic disease: a reappraisal of the focal infection concept. Journal of Clinical Periodontology 11, p209.