Denta Plaque Biofilms - [PDF Document] (2024)

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Dental Plaque Biofilms

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Dental Plaque Biofilms

By Jill S. Nield-Gehrig, RDH, MA*

Bacteria are the primary etiologic agents in periodontaldisease. More than 500 bacterialstrains may be found in dentalplaque.1 These bacteria have evolved to survive in theenvironmentof the tooth surface, gingival epithelium, and oral cavity. Recenttechnicaladvances have led to the recognition that dental plaque isa biofilm. Changes in thinkingabout the structure of dental plaquehave improved our understanding of why peri-odontitis is sodifficult to treat and will affect the strategies used to preventand controlperiodontitis in the future.

Bacterial LifestylesBacteria may be free-floating or attached toa surface. Recent advances in researchtechnology have allowedresearchers to study bacteria in their natural environment.

These studies have revealed that most bacteria live in complexcommunities calledbiofilms. A biofilm is a well-organized communityof bacteria that adheres to surfacesand is embedded in anextracellular slime layer. Once a bacterium attaches to asurface,it activates a whole different set of genes that gives thebacterium differentcharacteristics from those that it had as afree-floating organism. It has been estimatedthat more than 99% ofall bacteria on the earth live as attached bacteria.2 Biofilmscan

be found on medical and dentalimplants living in intravenousandurinary catheters, contactlenses, and prosthetic devices,such asheart valves, biliarystents, pacemakers, andartificial joints(Figure 1).Bacteria can also be life-threatening;Legionnaire'sdisease, which killed 29 peoplein 1976, was the resultof abacterial biofilm in the hotel'sair conditioning system.

The Structure of Biofilm

CommunitiesA biofilm community comprisesbacterial microcolonies,anextracellular slime layer, fluidchannels, and aprimitivecommunication system. Thebasic properties of thebiofilm

structure are summarized in the Table. As the bacteria attach toa surface and to each

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other, they cluster together to formsessile,mushroom-shapedmicrocolonies that are attached to thesurface at anarrow base (Figure 2).Each microcolony is a tiny,

independent community containingthousands of compatiblebacteria.Different microcolonies may containdifferent combinationsof bacterialspecies. Bacteria in the center of amicrocolony maylive in a strictanaerobic environment, while otherbacteriaat theedges of the fluid channels maylive in an aerobic environment(Figure3). Thus, the biofilm structure providesa range ofcustomized living envi-ronments (with differing pHs,nutrientavailability, and oxygen

concentrations) within which bacteria withdifferentphysiological needs can survive.

The extracellular slime layer is a protectivebarrier thatsurrounds the mushroom-shaped bacterial microcolonies. Theslimelayer protects the bacterial microcoloniesfrom antibiotics,antimicrobials, and hostdefense mechanisms. A series offluidchannels penetrates the extracellular slimelayer (Figure 4).These fluid channelsprovide nutrients and oxygen for thebacterialmicro colonies and facilitate

movement of bacterial metabolites, wasteproducts, and enzymeswithin the biofilmstructure. Each bacterial microcolonyuseschemical signals to create a primitivecommunication system usedtocommunicate with other bacterialmicrocolonies (Figure 5).

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Formation of Dental Plaque BiofilmsThe moment a baby passesthrough thebirth canal and takes its first breath,microbes begin toreside in its mouth.

Later, as the teeth erupt, additionalbacteria establish colonieson the toothsurfaces. Dental bacterial plaque is abiofilm thatadheres tenaciously to toothsurfaces, restorations, andprostheticappliances. Understanding the formation,composition, andcharacteristics of theplaque biofilm assists in its control(Figure6). The pattern of plaque biofilmdevelopment can be divided intothreephases:

1. Attachment of bacteria to a solidsurface;2. Formation ofmicrocolonies on thesurface; and3. Formation of the mature,subgingivalplaque biofilms (Figure 7).

The initial attachment of bacteria beginswith pellicleformation. The pellicle is a

thin coating of salivary proteins thatattach to the toothsurface within minutesafter a professional cleaning. Thepellicleacts like double-sided adhesive tape,adhering to the toothsurface on one sideand on the other side, providing a stickysurfacethat facilitates bacterialattachment to the tooth surface.Followingpellicle formation, bacteria begin to attachto the outersurface of the pellicle.

Bacteria connect to the pellicle and eachother with hundreds ofhairlike structurescalled fimbriae. Once they stick, thebacteriabegin producing substances thatstimulate other freefloatingbacteria to

join the community. Within the first 2days in which no furthercleaning isundertaken, the tooth's surface is

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colonized predominantly by gram-positive facultative cocci,which areprimarily streptococci species. It appearsthat the act ofattaching to a solidsurface stimulates the bacteria to

excrete an extracellular slime layer thathelps to anchor them tothe surface andprovides protection for the attachedbacteria.

Microcolony formation begins once thesurface of the tooth hasbeen coveredwith attached bacteria. The biofilmgrows primarilythrough cell division ofthe adherent bacteria, rather thanthroughthe attachment of new bacteria.Next, the proliferating bacteriabegin togrow away from the tooth. Plaquedoubling times are rapid inearlydevelopment and slower in more maturebiofilms. Bacterialblooms are periodswhen specific species or groups ofspecies grow atrapidly acceleratedrates. A second wave of bacterialcolonizersadheres to bacteria that arealready attached to the pellicle.

Coaggregation is the ability of newbacterial colonizers toadhere to thepreviously attached cells. The bacteriaclustertogether to form sessile,mushroom-shaped micro colonies thatareattached to the tooth surface at anarrow base. The resultofcoaggregation is the formation of acomplex array of differentbacterialinked to one another.

Following a few days of undisturbedplaque formation, thegingival margin becomes inflamed and swollen. Theseinflammatorychanges result in the creation of a deepened gingival sulcus. Thebiofilmextends into this subgingival region and flourishes in thisprotected environment,resulting in the formation of a maturesubgingival plaque biofilm. Gingival inflammationdoes not appearuntil the biofilm changes from one composed largely ofgram-positivebacteria to one containing gram-negative anaerobes. Asubgingival bacterial

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microcolony, predominantly composed of gram-negative anaerobicbacteria, becomesestablished in the gingival sulcus between 3 and12 weeks after the beginning ofsupragingival plaque formation. Mostbacterial species currently suspected of beingperiodontal pathogensare anaerobic, gram-negative bacteria.

Control and Removal of DentalPlaque BiofilmsThe recentrecognition thatsubgingival plaque is a biofilm helpsconsiderablyin understanding itspersistence and resistance to thehost's defensesystem. The formationof biofilms by subgingival bacteriaprovidesthe bacteria with anadvantage that permits long-termsurvival withinthe sulcus or pocketenvironment.

Bacterial microcolonies are protectedby one another and bytheextracellular slime layer and areunusually resistant toantibiotics(administered systemically),antimicrobials (administeredlocally),and the body's defense system.

Antibiotic doses that kill free-floating

bacteria, for example, need to beincreased as much as 1,500times tokill biofilm bacteria (and at these high

doses, the antibiotic would kill the patient before the biofilmbacteria).2,3 It is likely thatseveral mechanisms are responsiblefor biofilm resistance to antibiotics andantimicrobial agents. Theslime layer may prevent the drugs from penetrating fully intothedepth of the biofilm. Bacteria can develop resistance toantimicrobial drugs byproducing a thicker protective slime layer.The slime layer may protect the bacteriaagainst leukocytes(defensive cells of the body's immune system). Antibioticorantimicrobial therapy usually will not kill the biofilm; thebiofilm can be destroyed, how-ever, by simply wiping them off(disrupting their attachment to a surface).

Due to the structure of biofilms, physical removal of bacterialplaque biofilms is themost effective means of control. Subgingivalplaque within pockets cannot be reachedby brushes, floss, or oralrinses. Therefore, frequent periodontal debridement ofsubgingivalroot surfaces by a dental hygienist or dentist is an essentialcomponent inthe treatment of periodontitis.

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ConclusionMore than 500 bacterial strains havebeen identified indental biofilm. Expertsagree that most forms of periodontaldiseaseare caused by specific

pathogens, particularly gram-negativebacteria. The recognitionthat dentalplaque is a biofilm helps to explain whyperiodontaldiseases have been sodifficult to prevent and to treat.Periodontalpathogens within a biofilmenvironment behave very differentlyfromfree-floating bacteria. The

protective extracellular slime matrix makes bacteria extremelyresistant to antibiotics,antimicrobial agents, and host defensemechanisms. Mechanical removal is the mosteffective treatmentcurrently available for the control of dental plaque biofilms.

References 1. Kroes I, Lepp PW, Reiman DA Bacterial diversitywithin the human subgingivalcrevice. Proc Natl Acad SciUSA1999;96(25):14547-14552.2. Coghlan A Slime City. NewScientist1996;2045:32-36.3. Elder MJ, Stapelton F, Evans E, DartJK.Biofilm-related infections in ophthalmologyEye1995;9(Pt.1):102-109.4. Nield-Gehrig JS and Willmann DE. Foundations ofPeriodontics for the DentalHygienist. Philadelphia: LippincottWilliams & Wilkins 2003:67-73.

*Textbook author, international speaker, and dental hygieneconsultant, Asheville,North Carolina. She can be reached at[emailprotected].

Portions of this presentation have been adapted with permissionfrom Nield-Gehrig JSand Willmann DE. Foundations of Periodonticsfor the Dental Hygienist; @ 2003Lippincott Williams & Wilkins(http://www.lww.com/).