Abstract
T H E R E IS A B U N D A N T evidence to implicate microorga nisms as the primary etiologic agents of various forms of periodontal disease (for reviews see 1 6 ) . Particularly convincing were the demonstrations by Loe and co workers that removal of dental plaque by rigorous plaque control procedures 7 , 8 or antiseptic agents 9 , 1 0 could prevent or reverse clinical gingivitis in human volunteers. More recently, Lindhe and Nyman 1 1 and Rosling et a l . 1 2 demonstrated that progress of destruc tive periodontitis could be halted and partially reversed by surgical procedures when accompanied by twice monthly professional tooth cleaning. These studies in dicated that suppression of the total microbiota could be effective in controlling both gingivitis and destruc tive periodontitis in humans. What the studies did not and could not indicate is whether all or only segments of the microbiota were responsible for the observed clinical response. The success of antibiotic therapy in controlling the acute phase of acute necrotizing ulcera tive gingivit is 1 3 1 7 indicates the etiologic role of micro organisms in this form of human periodontal disease. Since only some of the species resident in bacterial plaque are sensitive to a given antibiotic, it is clear that only a finite segment of the microbiota is responsible for this disease. It would seem that there is sufficient evidence that microorganisms play a primary role in the etiology of most forms of human periodontal disease. The question is no longer whether organisms cause periodontal dis eases but rather are specific organisms responsible for specific disease forms?
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