CHAPTER 2. Periodontal Diseases

DEFINITIONS Inflammation: A localized protective response elicited by injury or destruction of tissue, which serves to destroy, dilute, or wall off both the injurious agent and the injured tissue. A cellular and vascular reaction of tissues to injury. Gingivitis: Inflammation of the gingiva. Periodontitis: Inflammation of the supporting tissues of the teeth. Usually a progressively destructive change leading to loss of bone and periodontal ligament. An extension of inflammation from gingiva into the adjacent bone and ligament. Adult Periodontitis: A form of periodontitis that usually has an onset beyond age 35. Bone resorption usually progresses slowly and predominantly in the horizontal direction. Well-known local environmental factors are prominent and abnormalities in host defense have not been found. Juvenile Periodontitis: May be generalized or localized; onset during the circumpubertal period; familial distribution; relative paucity of microbial plaque; less acute signs of inflammation than would be expected based upon the severity of destruction; may be associated with abnormalities in leukocyte chemotaxis and bacteriocidal activity. Prepubertal Periodontitis: May be generalized or localized; onset between eruption of the primary dentition and puberty; may affect the primary and mixed dentition; characterized by severe gingival inflammation, rapid bone loss, tooth mobility, and tooth loss. Refractory Periodontitis: Includes patients who are unresponsive to any treatment provided—whateve r the thoroughness or frequency—a s well as patients with recurrent disease at single or multiple sites. The common forms of gingivitis and periodontitis are inflammatory processes initiated by bacterial plaque. Bacteria in the gingival crevice have been portrayed as an indigenous flora that trigger a self-destructive inflammatory response or as lethal pathogens which invade the host tissues to spark episodic bursts of disease activity. Current evidence suggests that bacterial products penetrate intact sulcular epithelium to initiate inflammation. Substantial evidence exists that bacteria can invade the host tissues as well. There are multiple defense mechanisms in the gingival sulcus: 1) the primary line of defense by polymorphonuclear leukocytes (PMNs) can form a wall between plaque and the epithelium; 2) the epithelial barrier is permeable and the site of ulceration, an early and important event in the development of gingivitis; 3) saliva, which contains secretory IgA, leukocytes, and lysozymes, aids host defense; 4) gingival fluid may flush substances from the pocket and contains PMNs and plasma factors, such as complement, non-specific opsonins, and immunoglobulins; and, 5) finally, the high rate of tissue turnover in the sulcus is protective (Page, 1986; Miyasaki, 1991).