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PERIODONTAL DISEASE :
Periodontal disease is the result of the inflammatory response to dental plaque, i.e. oral bacteria, and is limited to the periodontium. It is probably the most common disease seen in small animal practice, with the great majority of dogs and cats over the age of 3 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. It is a unique infection in that it is not associated with a massive bacterial invasion of the tissues. 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. Infection of the periodontium may cause discomfort to the affected animal. There is also strong evidence that a focus of infection in the oral cavity has been associated with disease of distant organs. Consequently, prevention and treatment of periodontal diseases is, contrary to common belief, not a cosmetic issue, but a general health and welfare issue.
(pic PD1, PD2, PD3)
AETIOLOGY - The primary cause of gingivitis and periodontitis is accumulation of dental plaque on the tooth surfaces. Calculus (tartar) is only a secondary aetiological 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 subgingival region if left undisturbed. The formation of plaque involves two processes, namely the initial adherence of bacteria and then the continued accumulation of bacteria due to a combination of bacterial multiplication and further aggregation of bacteria to those cells that are already attached.
As soon as a tooth becomes exposed to the oral cavity, its surfaces are covered by the pellicle (an amorphous coating of salivary proteins and glycoproteins). The pellicle alters the charge and free energy of the tooth surfaces, which increases the efficiency of bacterial adhesion. Certain specific bacteria can adhere directly to the pellicle. These bacteria produce extracellular polysaccharides, which then aggregate other bacteria that are not otherwise able to adhere. The plaque associated with healthy gingiva is mainly comprised of aerobic and facultative anaerobic bacteria. As gingivitis develops, plaque extends subgingivally. Aerobes consume oxygen and a low redox potential is created, which makes the environment more suitable for the growth of anaerobic species. The aerobic population does not decrease, but with increasing numbers of anaerobes, the aerobic/anaerobic ratio decreases. The subgingival florae associated with periodontitis are predominantly anaerobic bacteria.
Dental calculus (tartar) is mineralized plaque. However, a layer of plaque always covers calculus. Both supragingival and subgingival plaque becomes mineralized. Supragingival 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. This is supported by well-controlled animal and clinical studies that have shown that the removal of subgingival plaque on top of subgingival calculus will result in healing of periodontal lesions and the maintenance of healthy periodontal tissues.
PATHOGENESIS
The pathogenic mechanisms involved in periodontal disease include:
• Direct injury by plaque microorganisms
• Indirect injury by plaque microorganisms via inflammation.
The microbiota in periodontal pockets is in a continual state of flux; periodontitis is a dynamic infection caused by a combination of bacterial vectors that change over time. As a result, the molecular events that trigger and sustain the inflammatory reactions constantly change. Many microbial products have little or no direct toxic effect on the host. However, they possess the potential to activate inflammatory reactions that cause the tissue damage. 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.
In gingivitis, the plaque-induced inflammation is limited to the soft tissue of the gingiva. As periodontitis occurs, the inflammatory destruction of the coronal part of the periodontal ligament allows apical migration of the epithelial attachment and the formation of a pathological periodontal pocket (i.e. periodontal probing depths around the tooth increase). If the inflammatory disease is permitted to progress, the crestal portion of the alveolar process begins to resorb. Alveolar bone destruction type and extent are diagnosed radiographically. Pic4
Disease progression is generally an episodic occurrence rather than a continuous process. Tissue destruction occurs as acute bursts of disease activity followed by relatively quiescent periods. The acute burst is clinically characterized by rapid deepening of the periodontal pocket as periodontal ligament fibres and alveolar bone are destroyed by the inflammatory reactions. The quiescent phase is not associated with clinical or radiographic evidence of disease progression. However, complete healing does not occur during this quiescent phase, because subgingival plaque remains on the root surfaces and inflammation persists in the connective tissue. The inactive phase can last for extended periods. 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.
Diagnosis of periodontal disease :
Periodontal disease is associated with loss of the attachment apparatus of the tooth. Clinically this is hard to detect and there is no correlation between the amount of calculus seen on the tooth and the degree of destruction. Loss of attachment usually involves the periodontal ligament, bone, root cementum and gingiva. Clinically, mobile teeth may be evident and some teeth may have evidence of gingival recession and root exposure indicating that there is periodontal disease but for a full assessment, an examination has to be performed under general anaesthesia. A periodontal probe is used to assess the depth of the gingival sulcus and whether there is loss of bone or periodontal ligament. A probing depth greater than 3mm in most dogs would be considered abnormal. This does vary based on the tooth and the size of the dog. Any depth over 0.5mm in cats would be considered abnormal. The periodontal probe is used to assess the degree of gingivitis, measure the pocket depth, check whether the tooth is mobile, whether there is bone loss between the roots (furcation exposure) and measure the amount of gingival recession. The whole circumference of the tooth needs to be evaluated. (pics PD5, PD6)
There are a number of methods that grade the severity of periodontal disease. It must be remembered though that different teeth in the mouth may be affected by different severities of the disease and even around each tooth, the degree of attachment loss may vary. Grading is based on the extent of attachment loss as this is indicative of periodontal destruction.
Grade 0 = Healthy Gingiva
Grade 1 = Established gingivitis
Grade 2 = Mild periodontitis (<25% attachment loss based on radiographs)
Grade 3 = Moderate periodontitis (25-50% attachment loss based on radiographs)
Grade 4 = Severe periodontitis (>50% attachment loss) (pic PD7)
Treatment of periodontitis is two stage – periodontal therapy performed under general anaesthesia, and the most important stage is then follow up home care following an oral hygiene program.
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[[Category:Teeth_-_Inflammatory_Pathology]] [[Category:Oral_Cavity_and_Gingiva_-_Pathology]] [[Category:Expert_Review - Small Animal]] [[Category:Dental_Diseases_-_Cat]] [[Category:Dental_Diseases_-_Dog]]
[[Category:Teeth_-_Inflammatory_Pathology]] [[Category:Oral_Cavity_and_Gingiva_-_Pathology]] [[Category:Expert_Review - Small Animal]] [[Category:Dental_Diseases_-_Cat]] [[Category:Dental_Diseases_-_Dog]]
[[Category:Dentistry]]
[[Category:Dentistry]][[Category:To Do - Dentistry]]