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Dental plaque is a biofilm composed of aggregates of [[:Category:Bacteria|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.
Dental plaque is a biofilm composed of aggregates of [[:Category:Bacteria|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 [[:Category:Oral Cavity - Anatomy & Physiology|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 - Anatomy & Physiology|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 [[:Category:Anaerobic bacteria|anaerobic bacteria]].
As soon as a tooth becomes exposed to the [[:Category:Oral Cavity - Anatomy & Physiology|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|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 [[:Category:Anaerobic bacteria|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.
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. [[Oral Examination Under General Anaesthesia#Periodontal Probing Depth (PPD)|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. <font color ="red"> Pic4</font color>
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.
== Signalment ==
== Signalment ==
Diagnosis of periodontal disease :
Diagnosis of periodontal disease :