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Re-examining the Plaque-Gingivitis Connection and the Role of Stannous Fluoride

Course Number: 579

Plaque Quantity: Determinant of Gingivitis Severity?

The cause-and-effect role of undisturbed, proliferating pathogenic plaque in initiating the classic signs of gingivitis is well-established, as is the correlation between plaque removal and a corresponding improvement in gingival bleeding and inflammation.1-4 Yet clinical research scientists observed a perplexing outcome in review of investigations of a bioavailable stannous fluoride (SnF(2) ) dentifrice: the magnitude of the overall gingivitis reduction benefit following regular SnF(2) use was typically much larger than the magnitude of the mean plaque reduction benefit.5-7 Table 1 shows results from three 6-month clinical studies comparing bioavailable SnF(2)  dentifrice with a negative control. Six-month data revealed that SnF(2)  users averaged 17-22% less gingivitis and 33-57% less gingival bleeding, but only 3-8% less plaque compared with the negative control.

Table 1. Comparison of Gingivitis and Plaque Quantity Reduction Benefits with Bioavailable Stannous Fluoride Reference.

Gingivitis Reduction BenefitBleeding Reduction BenefitPlaque Reduction Benefit
McClanahan et al., J Clin Dent, 1997520.5%33.4%3.1%*
Mankodi et al., J Clin Periodontol, 2005621.7%57.1%6.9%
Mallatt et al. J Clin Periodontol, 2007716.9%40.8%8.5%

*p>0.05. All other values p<0.05.

What might explain this disproportionate gingivitis-to-plaque reduction benefit ratio? If lowered plaque mass did not appear to align with the reduction in gingivitis on a parallel basis, what accounted for the strikingly greater relative decrease in gingival inflammation and bleeding? These intriguing results spurred new inquiry and research and led to recent findings revealing the actions of SnF(2)  in reducing plaque toxicity below the gumline and heading off an inflammatory cascade. Brushing with bioavailable SnF(2)  dentifrice provides gingivitis-fighting efficacy that goes beyond plaque quantity reduction; the reduction in subgingival plaque toxicity mechanisms appear to augment SnF(2)’s well-established sustained bactericidal/bacteriostatic and acid suppression actions to produce significant gingivitis improvements.

In considering Emily and Daniel, it is now known that the quantity of undisturbed plaque is not necessarily always a clear predictor of the gingival health status and degree of bleeding for any given patient. Instead, while some patients like Daniel can seemingly maintain relative gingival health (at least initially) despite subpar oral hygiene, another subset of patients like Emily may struggle to stave off gingivitis even when oral hygiene is good.

A new body of evidence around gingivitis/periodontitis causality has emerged in recent years that suggests certain individuals seem to have an increased susceptibility to developing gingivitis irrespective of their plaque removal efforts, and/or are more likely to see their gingivitis evolve into the early stages of periodontal disease than others with comparable plaque levels and plaque bacterial composition.8,9

Multiple published reports on this population variability suggest that the influence of an individual’s genetic factors and host response play a significant role in the gingival inflammatory response to plaque pathogenicity and the development and progression of disease for some.8-12 In-office patient profiling of genetic gingivitis susceptibility is not currently a reality, but the knowledge that a subset of patients may have an exaggerated response to even small quantities of plaque has important implications for prevention and treatment that go beyond routine mechanical oral hygiene, especially in light of very notable new findings about the anti-inflammatory properties of a mainstay in oral antimicrobials: stannous fluoride.