Plaque bacterienne

(Version Complète en Anglais)

 

Bacterial plaque or biofilm is characterized by a layer composed mainly of food residue, bacteria and their by-products that forms on the teeth and gums. It is the main cause of tooth decay and periodontal disease, which can lead to tooth loss.
Initially, this film assumes a soft consistency and, if it is not removed at this stage, it will mineralize, becoming hard (called tartar). To remove tartar, a set of clinical procedures (scaling and others) is required, performed by oral health professionals.

Bacterial plaque forms through a sequence of events that result in a structured and functionally organized microbial community of different species[i].
The distinct phases of plaque formation include:

1. Acquired film formation;
2. Reversible adhesion with weak physicochemical interactions between the cell surface and the pellicle, which can lead to increased adhesion via adhesion receptors (adhesins);
3. Co-adherence that leads to the adhesion of a new layer of secondary colonizers to the already adhered cells[ii];
4. Biofilm multiplication and formation (including exopolysaccharide synthesis) and occasionally, detachment.

The growing knowledge regarding bacterial adhesion and co-adhesion mechanisms can lead to strategies that control and influence the patterns of biofilm formation, since the properties of colonizing surfaces can be chemically modified and in turn make them less conducive to microbial colonization.
Despite this, cells can express multiple types of adhesin[iii], so that even if a large adhesin is blocked, other attachment mechanisms can be invoked, and although adhesion is necessary for colonization, the final proportions of a species within a mixed culture biofilm, such as dental plaque, will ultimately depend on an organism’s ability to grow and outperform neighboring cells.
Once formed, the global composition of the plaque community is diverse, with many species being detected at individual sites, and more than 600 different bacterial strains have been identified[iv].

The plaque species composition at any given site is characterized by the degree of stability or balance between the species that compose the community, despite minor environmental influences, e.g. ranging from diet, oral hygiene, host defenses, diurnal changes in saliva flow, etc. This stability (referred to as microbial homeostasis) is not due to any biological indifference between the resident organisms, but rather because of the balance imposed by numerous microbial interactions, including examples of both synergism and antagonism[v].
These interactions include conventional biochemical reactions, such as those necessary to catabolize complex host glycoproteins and to develop food chains. In addition, more subtle cellular signaling between cells can occur, which can lead to coordinated gene expression within the microbial community. These signaling strategies are currently being seen as potential targets for a new therapy[vi].

Dental Plaque Disorders

In any ecosystem, microbial homeostasis can decline when one of the critical parameters for ecological stability at the site suffers a substantial change. This results in the growth of previously smaller components of the community. And can then lead to pathological clinical consequences.
Significant parameters that regulate oral homeostasis include the integrity of host defenses (such as saliva flow) and diet composition[vii]. Individuals who regularly consume dietary components with a high content of fermented sugars have higher proportions of streptococci and lactobacilli in the plaque, while impaired neutrophil function is a risk factor for periodontal diseases.
Much less is known about how certain antimicrobial peptides regulate the microbiota that reside in different sites of the body, though it is clear that the reduction in some of their activities can increase the risk of caries. Certainly, antimicrobial peptides are being recognized as important components in the control of microbial populations in the mouth, although their role is complex because they are multifunctional and have more than mere antimicrobial action, for example, linking the innate and adaptive arms of the immune response[viii].

Dental Plaque and Pathology

Several studies have been carried out to determine the microbiota composition of the bacterial plaque, especially in areas of the mouth that present pathology, in order to identify the species directly involved in causing alterations. However, the interpretation of the data is hampered by the fact that the diseases caused by these microorganisms occur in locations that are naturally colonized by other species and also because the different characteristics associated with cariogenicity (acid production and tolerance, production of intra and extracellular polysaccharides) are not restricted to a single species.
In fact, the diverse evidence shows that the many strains of streptococci share several cariogenic characteristics and the fact that the different microorganisms of the bacterial plaque are in close physical contact to each other increases the probability of interactions between them, and hence also increases their pathogenic potential.
Despite these difficulties, it is now possible to associate an increase in caries with an increase in the proportion of acidogenic and aciduric bacteria, especially mutagenic streptococci (such S. mutans and S. sobrinus) and lactobacilli, which are able to demineralize dental enamel[ix]. These bacteria can quickly metabolize sugars into acids, resulting in a very low pH, which optimizes the growth of bacteria within the habitat, promoting proliferation and competition, and which in turn also prevents the development of bacteria that preserve tooth enamel, that thrive in more alkaline (base) environments (as they are sensitive to acidic environments).
In summary, dental plaque is a biofilm composed of a complex microbial community and is the etiologic agent of major dental diseases, such as dental caries and periodontal disease. The clinical picture of these dental diseases is the result of the cross-relationship between the pathogenic dental plaque biofilm and the host tissue response. In a healthy state, both the dental plaque biofilm and the adjacent tissues maintain a delicate balance, establishing a harmonious relationship between each other. However, changes occur during the disease process that transform this ‘healthy’ dental plaque into a ‘pathogenic’ biofilm.

Integrative Approach

Health of the oral cavity is directly linked to the presence of several microorganisms that affect the development of gingivitis and periodontitis[x].
Regarding treatments with most substantiated evidence, the clear choice is the use of chlorhexidine mouthwash, in combination with mechanical treatments and adequate oral hygiene using a soft brush, use of dental floss and a tongue scraper to complete the oral hygiene[xi].
Over the last few decades, unconventional therapies have shown to be very useful and shed light on several ingredients/combinations that have real utility, with natural options being increasingly used with success as alternatives to pharmaceutical drugs, especially in mild or moderate situations and even as adjuncts in complex treatments[xii].
There are several complementary options, from essential oils from different plants such as Mentha arvensis, Aloé vera, xilitol, propólis, Tea tree, garlic, chitosan, sodium bicarbonate, activated carbon, nano-hydroxyapatite, hydrogen peroxide, pumice powder and /or hydrated silica[xiii]. But perhaps the most surprising option is the use of Ozone Therapy, which is promising, effective and safe in various dental conditions and procedures.
Ozonated water and oils have the ability to stabilize and release ozone in a balanced way, which makes them ideal ozone delivery systems. These forms of application are used alone or in combination in the treatment of dental disease, and there are several clinical applications in the fight against oral disease, especially in^[xiv]:

• Elimination of pathogens / Biofilm
• Periodontal/bone pocket disinfection
• Caries prevention
• Dental treatment
• Tooth extraction
• Tooth sensitivity
• Temporomandibular joint treatment
• Gingival recession
• Pain control/analgesic
• Acceleration of healing
• Tissue regeneration
• Halitosis control
• Remineralization of the tooth surface
• Teeth whitening

The use of toothpastes that use ozone oil are a good option to maintain/promote the health of the mouth, gums and teeth, especially in the prevention of bacterial plaque and in patients with periodontitis and/or other conditions and/or tendency towards dental disease.

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[i] Marsh PD. Dental plaque as a microbial biofilm. Caries Res. 2004 May-Jun;38(3):204-11. doi: 10.1159/000077756. PMID: 15153690.

[ii] Kolenbrander PE, Andersen RN, Kazmerak K, Palmer R, Allison D, Gibert P, Lappin-Scott H, Wilson M. Community structure and co-operation in biofilms. Cambridge University Press. 2000(59):65.

[iii] Zhang Y, Lei Y, Nobbs A, Khammanivong A, Herzberg MC. Inactivation of Streptococcus gordonii SspAB alters expression of multiple adhesin genes. Infect Immun. 2005 Jun;73(6):3351-7. doi: 10.1128/IAI.73.6.3351-3357.2005. PMID: 15908361; PMCID: PMC1111841.

Hasty DL, Ofek I, Courtney HS, Doyle RJ. Multiple adhesins of streptococci. Infect Immun. 1992 Jun;60(6):2147-52. doi: 10.1128/iai.60.6.2147-2152.1992. PMID: 1587582; PMCID: PMC257136.

[iv] Newman HN, Wilson M. Dental plaque revisited: oral biofilms in health and diseases. Bioline, Cardiff, United Kingdom. 1999 Nov 3.

[v] Marsh PD, Featherstone A, McKee AS, Hallsworth AS, Robinson C, Weatherell JA, Newman HN, Pitter AF. A microbiological study of early caries of approximal surfaces in schoolchildren. J Dent Res. 1989 Jul;68(7):1151-4. doi: 10.1177/00220345890680070301. PMID: 2632599.

[vi] Kolenbrander PE, Andersen RN, Blehert DS, Egland PG, Foster JS, Palmer RJ Jr. Communication among oral bacteria. Microbiol Mol Biol Rev. 2002 Sep;66(3):486-505, table of contents. doi: 10.1128/MMBR.66.3.486-505.2002. PMID: 12209001; PMCID: PMC120797.

Suntharalingam P, Cvitkovitch DG. Quorum sensing in streptococcal biofilm formation. Trends Microbiol. 2005 Jan;13(1):3-6. doi: 10.1016/j.tim.2004.11.009. PMID: 15639624.

[vii] Marsh PD. Host defenses and microbial homeostasis: role of microbial interactions. J Dent Res. 1989;68:1567-75.

[viii] Devine DA. Antimicrobial peptides in defence of the oral and respiratory tracts. Mol Immunol. 2003 Nov;40(7):431-43. doi: 10.1016/s0161-5890(03)00162-7. PMID: 14568389.

[ix] Bowden GH. Microbiology of root surface caries in humans. J Dent Res. 1990 May;69(5):1205-10. doi: 10.1177/00220345900690051701. PMID: 2186069.

Marsh PD. Microbiologic aspects of dental plaque and dental caries. Dent Clin North Am. 1999 Oct;43(4):599-614, v-vi. PMID: 10553246.

Becker MR, Paster BJ, Leys EJ, Moeschberger ML, Kenyon SG, Galvin JL, Boches SK, Dewhirst FE, Griffen AL. Molecular analysis of bacterial species associated with childhood caries. J Clin Microbiol. 2002 Mar;40(3):1001-9. doi: 10.1128/JCM.40.3.1001-1009.2002. PMID: 11880430; PMCID: PMC120252.

[x] Germano F, Bramanti E, Arcuri C, Cecchetti F, Cicciù M. Atomic force microscopy of bacteria from periodontal subgingival biofilm: Preliminary study results. Eur J Dent. 2013 Apr;7(2):152-158. doi: 10.4103/1305-7456.110155. PMID: 24883019; PMCID: PMC4023198.

Fiorillo L, Cervino G, Laino L, D’Amico C, Mauceri R, Tozum TF, Gaeta M, Cicciù M. Porphyromonas gingivalis, Periodontal and Systemic Implications: A Systematic Review. Dent J (Basel). 2019 Dec 11;7(4):114. doi: 10.3390/dj7040114. PMID: 31835888; PMCID: PMC6960968.

[xi] Ripari F, Cera A, Freda M, Zumbo G, Zara F, Vozza I. Tea Tree Oil versus Chlorhexidine Mouthwash in Treatment of Gingivitis: A Pilot Randomized, Double Blinded Clinical Trial. Eur J Dent. 2020 Feb;14(1):55-62. doi: 10.1055/s-0040-1703999. Epub 2020 Mar 13. PMID: 32168532; PMCID: PMC7069753.

[xii] Little JW. Complementary and alternative medicine: impact on dentistry. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004 Aug;98(2):137-45. doi: 10.1016/j.tripleo.2004.05.011. PMID: 15316539.

[xiii] Ercan N, Erdemir EO, Ozkan SY, Hendek MK. The comparative effect of propolis in two different vehicles; mouthwash and chewing-gum on plaque accumulation and gingival inflammation. Eur J Dent. 2015 Apr-Jun;9(2):272-276. doi: 10.4103/1305-7456.156851. PMID: 26038663; PMCID: PMC4439859.

Carvalho C, Fernandes WHC, Mouttinho TBF, Souza DM, Marcucci MC, D’Alpino PHP. Evidence-Based Studies and Perspectives of the Use of Brazilian Green and Red Propolis in Dentistry. Eur J Dent. 2019 Jul;13(3):459-465. doi: 10.1055/s-0039-1700598. Epub 2019 Dec 3. PMID: 31795009; PMCID: PMC6890504.

Gnatta JR, Pinto FM, Bruna CQ, Souza RQ, Graziano KU, Silva MJ. Comparison of hand hygiene antimicrobial efficacy: Melaleuca alternifolia essential oil versus triclosan. Rev Lat Am Enfermagem. 2013 Nov-Dec;21(6):1212-9. English, Portuguese, Spanish. doi: 10.1590/0104-1169.2957.2356. PMID: 24402336.

Budzyńska A, Wieckowska-Szakiel M, Sadowska B, Kalemba D, Rózalska B. Antibiofilm activity of selected plant essential oils and their major components. Pol J Microbiol. 2011;60(1):35-41. PMID: 21630572.

Groppo FC, Ramacciato JC, Simões RP, Flório FM, Sartoratto A. Antimicrobial activity of garlic, tea tree oil, and chlorhexidine against oral microorganisms. Int Dent J. 2002 Dec;52(6):433-7. doi: 10.1111/j.1875-595x.2002.tb00638.x. PMID: 12553397.

[xiv] Ozone therapy in dentistry: A strategic review. J Nat Sci Biol Med. 2011 Jul;2(2):151-3. doi: 10.4103/0976-9668.92318.

[xv] WebMd – Plaque and Your Teeth