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THE PLAQUE-GINGIVITIS CONNECTION AND THE ROLE OF STANNOUS FLUORIDE

Stannous flouride
“This article is non-promotional in nature and intended for scientific educational learning”
INTRODUCTION

Based on a myriad of published research establishing clinical effectiveness, bioavailable SnF2 has a well-established history for several oral health benefits, including anti-plaque and anti-gingivitis efficacy. Along with its known bactericidal/bacteriostatic and acid suppression effects, research has discovered a new plaque virulence modulation mechanism. The research found that bioavailable SnF2 binds with gingival sulcus pathogenic endotoxins, to reduce the inflammatory cascade at its inception stage, and thus prevent or reduce the clinical manifestations of gingivitis irrespective of plaque quantity (1).

STANNOUS FLUORIDE IN TOOTHPASTE: THE BENEFITS

Poor plaque removal can lead to various oral diseases (e.g. caries, gingivitis) and conditions (e.g. tooth stain, calculus), so choosing the right toothpaste plays a critical role in protecting patients’ oral health and the appearance of their smile.Toothpaste is a convenient, cost-effective way to provide fluoride, anti-bacterial agents and other ingredients that provide benefits beyond brushing alone. Dental professionals are in a unique position to educate patients on the best toothpaste option to address their specific oral health needs.

There is a misconception that ‘all fluorides are the same.’ This is simply not true. Stannous Fluoride is unique among fluoride compounds offering gum health benefits not found with sodium fluoride or sodium monofluorophosphate. Whilst all three compounds provide anti-caries benefits, Stannous Fluoride, when effectively stabilized, has demonstrated broader and significantly greater protection than other fluorides against plaque, gum health issues and erosive tooth wear (1-5).

Stanous flouride
PLAQUE QUANTITY: DETERMINANT OF GINGIVITIS SEVERITY?

The cause-and-effect role of undisturbed plaque in initiating gingivitis is well-established, as is the correlation between plaque removal with an improvement in gingival bleeding and inflammation.6-9 Yet clinical research scientists observed a perplexing outcome: the magnitude of the overall gingivitis reduction benefit following regular SnF2 use was typically much larger than the magnitude of the mean plaque reduction benefit.1, 10, 11

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 SnF2 in reducing plaque toxicity below the gumline and heading off an inflammatory cascade. The reduction in subgingival plaque toxicity mechanisms appear to augment SnF2’s well-established sustained bactericidal/bacteriostatic and acid suppression actions to produce significant gingivitis improvements.

INFLAMMATION AND A NEW PATHWAY TO GINGIVITIS CONTROL

How Gingival Inflammation Develops

If plaque deposits are left undisturbed and allowed to mature, the subgingival microbiota composition shifts to predominately gram-negative anaerobic bacteria and becomes more virulent. If homeostasis is not restored by modulation or removal of the irritant, the inflammatory process is initiated, leading to visible local vasodilation, edema, and increased gingival crevicular fluid.12,13

A well-orchestrated intracellular signaling pathway governs the pathogen/host tissue interface. During the recognition phase, Toll-like receptors (TLR) in the periodontium, scan for bacterial pathogens like those residing in the biofilm of plaque, and then mount a complex defense reaction if provoked.13-18

TLRs bind and interact with plaque bacterial endotoxins, such as lipopolysaccharides (LPS) and lipoteichoic acid (LTA); which induces a series of events which includes the production of inflammatory-generating cytokines (e.g. interleukin-1beta, interleukin-6) and other effector molecules. Toxic metabolites produced by the invading pathogens further provoke and increase the TLR response and can result in reduced tissue repair, more inflammation, and greater permeability of the tissue (Figure 1). 13-18

Fig 1: In the gingival sulcus, the unique patterns of plaque bacteria are recognised by host “look out” cells (TLRs), spurring the interaction with them and their toxic metabolites and stimulating the recruitment of host inflammatory mediators to mount a defence. This leads to the classic clinical manifestations of gingivitis
IRA

Should the lesion progress to an established lesion with a proliferation of plasma cells, lymphocytes and macrophages, moderate- sever gingivitis will be apparent with clearly visible gingival contour colour and bleeding abnormalities (fig 2). Chronic inflammation results which may led to extracellular matrix tissue destruction and possible bone loss associated with periodontitis.

Figure 2:
Bleeding gums
Recognizable signs of established gingivitis include red, edematous, bleeding gums.
STANNOUS FLUORIDE AS A PLAQUE TOXICITY MODULATOR

To explore whether SnF2 could directly interact with bacterial endotoxins to affect pathogenicity, a series of laboratory and clinical investigations employing novel methodologies were conducted.15,16,19-23 This research revealed additional means by which bioavailable SnF2 apparently acts to control plaque while preventing and reducing gingivitis: SnF2 disrupts the gingival inflammation process by reducing plaque toxicity.

These studies showed that before the host TLRs in the gingival sulcus can mount the inflammatory response that would be expected when encountering plaque bacteria endotoxins, SnF2 present in the mouth (e.g. from toothbrushing) intervenes and binds the endotoxins, thus effectively blocking them from affixing with TLRs, and undermining the typical cytokine-driven series of events that leads to inflammation and bleeding (Figure3).
Figure 3:
Pathogen

With regular exposure to a properly formulated bioavailable SnF2 toothpaste, then, the customary deleterious effects of plaque endotoxins can be blunted, preventing gingivitis or reducing it to a level consistent with homeostasis, and lowering the potential for more advanced periodontal disease.15,16

Click on to view an animation illustrating this process.

Clinical Testing is Congruent with In Vitro Findings
A 4-week randomized controlled clinical trial of twice daily unsupervised brushing with a 0.454% bioavailable SnF2 dentifrice conducted by Klukowska et al (19), wherein subgingival plaque sampling in sites up to 4 mm in depth in both a low gingival bleeding cohort (‘healthy’) and a high bleeding cohort (‘diseased’) were evaluated. At Week 4, both cohorts saw significant (42% to 53%) mean reductions in gingival bleeding. The plaque sampling results in both the healthy and diseased groups provided evidence showed notably decreased LPS/LTA dye activity and TLR activity. This research provided insight into the depths of penetration of SnF2, its retention, and its ability to reduce subgingival plaque toxicity.

The effects of SnF2 to bind with endotoxins and thereby limit TRL4/TRL2 in initiating the inflammatory cascade, manifested both in the diseased, high bleeding sites and in the low bleeding sites with minimal measurable disease, suggesting a preventive as well as a treatment gingivitis strategy.

More confirmation of bioavailable SnF2’s ability to diminish the virulence of subgingival plaque – and thus the development of gingivitis – was demonstrated by recent clinical research evaluating gingival inflammation and bleeding in 99 adult subjects with gingivitis.23

After eight weeks of at-home 0.454% SnF2 toothpaste use, significant reductions in gingivitis and bleeding versus baseline were observed. These clinical observations were consistent with the results of subgingival plaque sampling, where TLR2 assay analyses of hTLR2 reporter gene activity showed significant (P=0.0004) mean reductions following two months of SnF2 brushing.
HOW CAN THIS BENEFIT YOUR PATIENTS?

To help patients choose a well-tested and effective product with the best likelihood of addressing their particular needs, evidence-based recommendations are paramount. In the case of bioavailable SnF2, there is a significant body of research supporting its use for a variety of indications, including plaque and gingivitis.

SnF2 formulations have been shown to act in the gingival sulcus, where disease begins by interfering with the inflammatory process itself via binding the toxins that would typically trigger a chain of events leading to the edema and bleeding that are characteristic of gingivitis.

In addition, for patient groups with existing gingivitis, Klukowska et al demonstrated minimally impacted (‘healthy’) participants still experienced statistically significant reductions in endotoxin and TLR activity with SnF2 usage;19 which is known to mitigate the inception of inflammation. Just as adults wear seatbelts when driving to protect against harm in a potential accident, antimicrobial SnF2 usage may provide a form of ‘insurance’ against the otherwise high statistical likelihood of developing gingivitis.

Conclusion

Stannous Fluoride is unique among fluoride compounds offering gum health benefits. In addition to its known bactericidal/bacteriostatic and acid suppression effects, recent research has discovered a new plaque virulence modulation mechanism in which bioavailable SnF2 binds with gingival sulcus pathogenic endotoxins to reduce the inflammatory cascade at its inception stage, and thus prevent or reduce the clinical manifestations of gingivitis irrespective of plaque quantity.

Regular toothbrushing with properly formulated SnF2 toothpaste provides an easy to implement strategy, not only for patients with existing gingivitis (treatment) but also for those with increased susceptibility or not yet manifesting symptoms (prevention).

Few other preventive measures are as cost-effective and easy to implement – and promise more in the way of meaningful plaque and gingivitis control.

This is an abridged version of Re-examining the Plaque-Gingivitis Connection and the Role of Stannous Fluoride

REFERENCES
1 Mallatt M, Mankodi S, Bauroth K et al. (2007) A controlled 6-month clinical trial to study the effects of a Stannous Fluoride dentifrice on gingivitis. Journal of Clinical Periodontology 34:762–767.
2 Sharma NC, Qaqish J, He T, et al. (2013) Superior plaque reduction efficacy of a Stannous Fluoride dentifrice. The Journal of Clinical Dentistry 24:31-36.
3 Archila L, Bartizek RD, Winston JL, et al. (2004) The comparative efficacy of stabilised Stannous Fluoride/sodium hexametaphosphate dentifrice and sodium fluoride/triclosan/copolymer dentifrice for the control of gingivitis: a 6-month randomized clinical study. Journal of Periodontology 75(12):1592-1599.
4 Hooper SM, Newcombe RG, Faller R, et al. (2007) The protective effects of toothpaste against erosion by orange juice in situ and in vitro. Journal of Dentistry 35:476-481.
5 West NX, He T, Macdonald EL, et al. (2017) Erosion protection benefits of stabilized SnF2 dentifrice versus an arginine-sodium monofluorophosphate dentifrice: results from in vitro and in situ clinical studies. Clinical Oral Investigations 21(2):533-540.
6 Löe H, Theilade E, Jensen SB. Experimental gingivitis in man. J Periodontol. 1965 May-Jun;36:177-87. doi: 10.1902/jop.1965.36.3.177.
7 Theilade E, Wright WH, Jensen SB, et al. Experimental gingivitis in man II. A longitudinal and bacteriological investigation. J Periodontal Res. 1966;1:1-13
8 Page RC. The etiology and pathogenesis of periodontitis. Compend Contin Educ Dent. 2002 May;23(5 Suppl):11-4.
9 Lang NP. Commentary: bacteria play a critical role in the etiology of periodontal disease. J Periodontol. 2014 Feb;85(2):211-3. doi: 10.1902/jop.2013.130699.
10 McClanahan SF, Beiswanger BB, Bartizek RD, et al. A comparison of stabilized stannous fluoride dentifrice and triclosan/copolymer dentifrice for efficacy in the reduction of gingivitis and gingival bleeding: Six-month clinical results. J Clin Dent. 1997;8(2 Spec No):39-45.
11 Mankodi S, Bartizek RD, Winston JL, et al. Anti-gingivitis efficacy of a stabilized 0.454% stannous fluoride/sodium hexametaphosphate dentifrice: a controlled six-month clinical trial. J Clin Periodontol. 2005 Jan;32(1):75-80. doi: 10.1111/j.1600-051X.2004.00639.x.
12 Page RC, Schroeder HE. Pathogenesis of inflammatory periodontal disease. A summary of current work. Lab Invest. 1976 Mar;34(3):235-49.
13 Cekici A, Kantarci A, Hasturk H, et al. Inflammatory and immune pathways in the pathogenesis of periodontal disease. Periodontol 2000. 2014 Feb;64(1):57-80. doi: 10.1111/prd.12002.
14 White DJ. Advantages of using antimicrobial toothpastes. New understandings regarding their effects on dental plaque virulence in gum disease. Catapult Education. 2017 Sep 14.
15 Haught C, Xie S, Circello B, et al. Lipopolysaccharide and lipoteichoic acid virulence deactivation by stannous fluoride. J Clin Dent. 2016 Sep;27(3):84-89.
16 Haught JC, Xie S, Circello B, et al. Lipopolysaccharide and lipoteichoic acid binding by antimicrobials used in oral care formulations. Am J Dent. 2016 Dec;29(6):328-332.
17 Huggins T, Haught JC, Xie S, et al. Quantitation of endotoxin and lipoteichoic acid virulence using toll receptor report gene. Am J Dent. 2016 Dec;29(6):321-327.
18 Hans M, Hans VM. Toll-like receptors and their dual role in periodontitis: a review. J Oral Sci. 2011 Sep;53(3):263-71.
19 Klukowska M, Haught JC, Xie S, et al. Clinical effect of stabilized stannous fluoride dentifrice in reducing plaque microbial virulence I: Microbiological and receptor cell findings. J Clin Dent. 2017 Jun;28(2):16-26.
20 Cannon M, Khambe, Klukowska M, et al. Clinical effects of stabilized stannous fluoride dentifrice in reducing plaque microbial virulence II: Metabonomic changes. J Clin Dent. 2018 Mar;29(1):1-12.
21 Klukowska M, Goyal CR, Khambe D, et al. Response of chronic gingivitis to hygiene therapy and experimental gingivitis. Clinical, microbiological and metabonomic changes. Am J Dent. 2015 Oct;28(5):273-84.
22 Klukowska M, Ramji N, Combs C, et al. Subgingival uptake and retention of stannous fluoride from dentifrice: Gingival crevicular fluid concentration in sulci post-brushing. Am J Dent. 2018 Aug;31(4):184-188.
23 Klukowska MA, Goyal C, Qaqish JG, et al. The effect of SnF2 dentifrice on virulence of subgingival plaque. J Dent Res 2018;97(Spec Iss A):Abstract 755.
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