Changes

==Pathogenesis==

==Pathogenesis==

 

The pathogenic mechanisms involved in periodontal disease include:

The pathogenic mechanisms involved in periodontal disease include:

*Direct injury by plaque microorganisms

*Direct injury by plaque microorganisms

*Indirect injury by plaque microorganisms via inflammation

*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. [[Dental Indices and Criteria#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>

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. [[Dental Indices and Criteria#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 [[Radiographic Interpretation of Periodontal Disease - Small Animal|diagnosed radiographically]].  

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.

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.