Experimental gingivitis in man

Abstract

After 9–21 days without oral hygiene eleven experimental subjects with previously excellent oral hygiene and healthy gingivae developed heavy accumulations of plaque and generalized mild gingivitis. The individual rate of development of gingivitis was closely correlated with the rate of plaque accumulation. Characteristic bacteriological changes were revealed in the plaque along the gingival margin during this experiment. Initially, i.e. when the teeth were clean and the gingiva healthy, the extremely sparse plaque flora consisted almost exclusively of gram‐positive cocci and rods. The first phase of plaque development occurred during the first 2 days without oral hygiene and consisted of a proliferation of the gram‐positive cocci and rods and an addition of about 30 per cent gram‐negative cocci and rods. During the second phase (after 1–4 days) fusobacteria and filaments appeared and increased until they each made up about seven per cent of the flora. During the third phase (after 4–9 days) the flora was supplemented with spirilla and spirochetes, and at the end of the period without oral hygiene each of these two groups of organisms accounted for about two per cent of the plaque flora. In specific areas the gingival condition was correlated with the composition of the plaque and it was found that mild gingivitis could be diagnosed clinically at approximately the same time as the complex flora was established. However, sub‐clinical inflammation started much earlier, probably as a reaction to the first phases of plaque development. When oral hygiene was reinstituted, the plaque in most areas disappeared in 1–2 days and after 7–11 days the Plaque Index for each subject was as low as before the experiment. Correspondingly, after 1–2 days most tooth surfaces only harbored the original sparse flora of gram‐positive cocci and rods. The gingival inflammation in an area usually disappeared one day after the plaque had been removed.

Aggressive Periodontitis: microbes and host response, who to blame?

“…5 Hence, the emphasis was on a possible degenerative disease leading to bone resorption and tooth mobility. While the 1960s brought the evidence to confirm that dental plaque is the etiological factor of periodontal diseases, 6,7 crucial studies in the 1970s investigated a possible microbiological cause of what we now call AgP. As "non-specific" 8 and then "specific" 9 plaque hypotheses for periodontitis developed, it was now becoming clear that AgP was also a plaque-induced gingival disease.…”

Periodontitis is associated with a loss of colonization by Streptococcus sanguinis

“…Some of the members of the 'yellow' complex of oral streptococci are candidates for this position. Plaque samples from healthy gingival sulci normally contain a large number of oral streptococci (Theilade et al, 1966). Socransky et al (1998) previously showed that yellow complexes, as a total, were associated with shallow pockets (probing depth of ,3 mm).…”

Reparative Phase Events on Periodontal Disease Progression: Interpretation and Considerations

“…The bacterial plaque in proximity to the gingival margin seems to be the essential agent, which plays a role in inducing gingival inflammation [1][2][3][4][6][7][8][9][10]12]. The body of evidence is consistent and stems from epidemiologic data, microbiologic research, immunologic studies, and clinical observations [1][2][3][4][6][7][8][9][10]12,30,31]. The study of experimental gingivitis by the withdrawal of all forms of oral hygiene performed by Löe, et al [1] inflammation.…”

“…In periodontal disease, the risk factors may be defined as local environmental factors, behavioral factors in nature and systemic factors, which may be responsible in providing an ideal environment for bacterial colonization and/or fragility in a determinate tooth or teeth and adjacent periodontal tissues and/or interference in the inflammatory process [5,11,32,33]. Due to the association with risk factors, the opportunist endogenous bacteria, which are predominant in establishing gingival margin inflammation, also may induce destruction in the initial phase of periodontitis [1,2,8,10,17]. Periodontal disease could be considered as sequel of the inflammatory reaction, which must be always active, protecting individual against infection and possible septicemia, by bacteria present in the gingival sulcus, a critical area where junctional epithelium is an exclusive and fragile structure, separating connective tissue from an infected humid and warm oral environment.…”

“…The etiology of periodontal disease is multifactorial, in which bacterial plaque plays an essential role in the development of the disease [1][2][3][4][5][6][7][8][9][10][11][12]. Nevertheless, it has become clear that not all patients with periodontitis harbor the same subgingival microflora, and patients that harbor bacterial species recognized as indicators of periodontal disease may not develop periodontal breakdown all the time [3,6,7,10,[12][13][14][15].…”