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DENTAL PLAQUE Contents Introduction Definition and structure Composition Classification Stages of plaque formation Plaque as a biofilm Human fetus →sterile oral cavity. Hours after birth→Facultative aerobic bacteria. Second day→anaerobic bacteria . Two weeks→nearly mature microbiota in the gut Oral cavity - >500 bacterial species, mostly commensal & beneficial Open growth system periodontal diseases unusual human infection. major reason anatomic feature of a mineralized structure, the tooth, partly exposed to the external environment and partly in the connective tissues Teeth & implants – hard non shedding surfaces, continually held in immediate proximity to the soft tissues of the periodontium Provide port of entry Dental Plaque - Definitions “ A soft deposit that form the biofilm adhering to the tooth surfaces in the oral cavity including removable and fixed restorations. Diverse community of microorganism found on tooth surface as biofilm embeded in an extracellular matrix of polymers of host and microbial origin (Marsh 2004) Clinically plaque is def as structured resilient, yellow grayish substance that adheres tenaciously to the intraoral hard surfaces including removable and fixed restorations Accumulates in the gingival third and in pits, cracks, fissures, overhanging restorations and around malaligned tooth Methods of detecting plaque Probing with a periodontal probe. Disclosing solution. Materia Alba - Soft accumulations of bacteria and tissue cells that lack the organised structure of dental plaque and are easily displaced by water spray. Calculus – Hard deposit that forms by mineralisation of dental plaque and is generally covered by a layer of unmineralised plaque Composition • • Water: 80-85% plaque mass ; • Cells: primarily bacteria, 1 gm (wet weight)= 1011 bacteria Non bacterial: Mycoplasma spp, yeasts, protozoa, viruses (conteras 2000) Host cells : epithelial cells, macrophages & leucocytes • Matrix: Organic • Inorganic Matrix : 20-30% plaque mass 1. Organic: Carbohydrates: Dextrans, levans, polysaccharides, galactose Lipids Proteins: Albumin, glycoproteins Misc: cxtracellular bacterial products, cell remnants, food 2. Inorganic: Calcium Phosphorus/ phosphate Na, Cl, F Classification SUPRAGINGIVAL PLAQUE Gram –positive cocci and short rods predominate at the tooth surface area, Gram –ve rods filaments as well as spirochaetes pedominate the outer surface of mature plaque mass. SUBGINGIVAL PLAQUE TOOTH ASSOCIATED ( Attached Plaque) Cervical part : densely arranged consists of gram +ve rods and cocci including Streptococcus mitis , Streptococcus sanguis, Actinobacillus Viscosus, A. naeslundi and Eubacterium species . Deeper parts filamentous forms are fewer Apical border of plaque mass is separated from junctional epithelium by a layer of host leukocytes. increased concentration of gram negative rods, spirochetes TISSUE / EPITHELIUM ASSOCIATED PLAQUE -Loosely arranged - Comprises of Gram-negative rods and cocci, large number of filaments, flagellated rods, spirochaetes. Presence of Porphyromonas gingivalis, Prevotella Intermedia, Tannerella Forsythia , Fusobacterium Nucleatum are predominant - Clinical signifance Marginal plaque→ gingivitis Supragingival and tooth associated subgingival plaque→calculus formation Tissue associated subgingival plaque→periodontal tissue destruction Subgingival tooth attached plaque→calculus formation and root caries Characteristic Supragingival plaque +/MOS Subgingival plaque Dominated by - Morph types Cocci, branching rods, filaments, spirochetes Dominated by rods and spirochetes Energy metabolism Facultative with some Dominated by anaerobes anaerobes Energy sources Generally ferment carbohydrates Many proteolytic forms Causes Can cause caries and gingivitis Can cause gingivitis and periodontitis Plaque formation 3 major phases of plaque formation MECHANISMS OF PLAQUE FORMATION Formation of pellicle Pellicle – Glycoprotein derived from components of saliva and GCF as well as bacterial and host tissue cell products and debris. Forms within nanoseconds after vigorous brushing Contains – glycoproteins (mucins), Phosphoproteins, Histidine rich proteins, enzymes (α- amylase) Forms by selective adsorption of the environmental macromolecules mechanisms involved in enamel pellicle formation include electrostatic, van der Waals, and hydrophobic forces . Can be removed by polishing . Recurs soon after removal. Fully established pellicle – in 30 minutes. Initial Adhesion and Attachment of Bacteria Phase I: Transport to the surface Random contacts through brownian motion. Sedimentation of microorganisms Through liquid flow Active bacterial movement ( chemotactic activity). Phase 2 ; Initial adhesion Reversible adhesion of bacterium to the surface Through long and short range forces like van der Waals attractive and elecrostatic repulsive forces, hydrogen bonding Phase 3 : Attachment Firm anchorage→ specific interactions ( covalent, hydrogen bonding ) Direct contact or bridging through specific extracellular proteinecious components of organisms and complementory receptors ( proteins and glycoproteins or polysaccharides on the surface ) S. sanguis ( principle early coloniser )bind to proline rich proteins A. viscosus posses fimbriae →adhesins →proline rich proteins . . Colonisation and plaque maturation Plaque increases by two mechanisms. - Multiplication of bacteria already attached to the tooth surface. - Subsequent attachment and multiplication of new bacterial species to cells of bacteria already present in the plaque mass. Coaggregation Coaggregation - defined as the specific cell-to-cell recognition that occurs between genetically distinct cell types Occurs primarily through highly specific stereochemical interaction of protein and carbohydrate molecules located on the bacterial cell surface. Less specific interactions from hydrophobic, electrostatic and vanderWaals forces also occur. Early stages, coaggregation occurs among different gram positive species and between gram positive and gram negative species. Later stages between different gram negative species . Eg: E.nucleatum,P. gingivalis and T. denticola Primary colonizers are taught to prepare a favorable environment for secondary colonizers They are gram +ve aerobic micro organisms secondary colonizers do not initially colonize on to the clean tooth surface but adhere to bacteria already in the plaque mass They are gram -ve anaerobic micro organisms Secondary colonizers Gram negative species- Fusobacterium nucleatum, Prevotella intermedia , Porphyromonas gingivalis, Prevotella loeschii and capnocytophaga species. Adehere to the gram positive species already present in the plaque.. Tertiary colonisers After one week of plaque accumulation other gram negative species may also appear P gingivalis, C rectus., E corrodens A A Comitans and the oral spirochaetes( Treponema species) Spatiotemporal model of Oral bacterial colonization Kolenbrander et al Perio 2000 vol-42 Socransky etal →13000 plaque samples Used cluster analysis and community coordination techniques to demonstrate the presence of specific microbial groups. DNA hybridisation methodology defined “ complexes” of periodontal microorganisms Yellow complexes -streptococcus species. Purple complex consisting of Veillonella parvula and Actinomyces odontolyticus. Green Complex: E corrodens, A. actinomycetemcomitans serotype a, and Capnocytophaga species. Orange Complex : Fusobacterium , prevotela and Campylobacter species. Red Complex: P gingivalis, Tanerella forsythus and T denticola. They are aasociated with bleeding on probing. Actinomyces species V.parvula A.odontolyticus SUBJECTS - 185 PLAQUE SAMPLES- 13,261 40 subgingival microorganisms DNA-hybridization Socransky et al - 1998 P.intermedia P.nigrescens P.micros F.nucleatum C.rectus P.gingivalis T.forsythia T.denticola BOP Physiological properties of dental plaque Early colonisers use oxygen and reduce the redox potential which then favours anaerobic species. gram +ve species use sugars as energy source and saliva as carbon source. Mature plaque bacteria use aminoacids and small peptides as energy source Metabolic interactions among plaque bacteria Lactate and formate→by products of streptococci and actinomyecetes , used by other microbes. Growth of P gingivalis is enhanced by succinate from Capnocytophaga and protoheme by Campylobacter rectus. Hemin from breakdown of hemoglobin is important in the metabolism of P gingivalis. Steroid hormones→proportions of P intermedia in subgingival plaque. Microorganisms generally exhibit two distinct modes of behavior The first is the familiar free floating, or planktonic form in which single cells float or swim independently in some liquid medium. The second is an attached state in which cells are closely packed and firmly attached to each other in the form of a biofilm Plaque as a biofilm Defn: Matrix enclosed bacterial populations adherent to each other and/or to surfaces and inter-surfaces Biofilm are organized structures composed of microcolonies of bacterial cells nonrandomly distributed in a shaped matrix or glycocalyx Nutrients penetrate by molecular diffusion Dental plaque →heterogenous structure fluid filled channels running across the plaque. Nutrients contact with sessile microcolonies by diffusion from water channels to the microcolony. Nature Of Biofilms Cooperating community of various types of microorganisms Microorganisms are arranged in microcolonies Microcolonies are surrounded by protective matrix Properties of biofilm Structure microcolonies of bacterial cells (15–20% by volume), non-randomly distributed in a shaped matrix or glycocalyx (75–80% volume) presence of voids or water channels Nutrients diffuse from the water channel to the microcolony rather than from the matrix. Microbial specificity of periodontal diseases Nonspecific Plaque Hypothesis Specific Plaque Hypothesis Ecological plaque hypothesis Nonspecific Plaque Hypothesis Non specific and specific hypotheses was proposed by Walter Loesche in 1976 Supported by epidemiologic studies that correlated pts age & amount of plaque with evidence of periodontitis (Russel 1967, lovadal 1958) Periodontal disease results from the “ Elaboration of noxious products by the entire plaque flora”. According to this hypothesis, when only small amounts of plaque are present, the noxious products are neutralized by the host. Similarly large amounts of plaque would produce large amounts of noxious products, which would essentially overwhelm the host defenses. According to this concept the control of periodontal disease depends on control of amount of plaque accumulation. Specific Plaque Hypothesis States that only certain plaque is pathogenic, and its pathogenicity depends on the presence of or increase in specific microorganisms Plaque harboring specific bacterial pathogens results in periodontal disease Recognition of A.a as pathogen in localized aggressive periodontitis Ecological shift hypothesis “Pathogenic bacteria is directly coupled to the changes in the environment.” Disease can be prevented not only by targeting the putative pathogens directly but also by interfering with their environment Factors affecting plaque formation Saliva Diet Oral Hygiene Habits Other local factors. Saliva. Non immune and immune ( secretary IgA) components of saliva provide an initial protective barrier against the invasion of foreign substances and pathogens in the oral cavity. Several studies have shown that bacterial attachment to the tooth surface is mediated by salivary glycoprotein that coat the tooth surface as part of the acquired enamel pellicle. DIET Consistency and texture: fibrous foods may be beneficial in periodontal health than soft, sticky foods. Chewing fibrous food exerts a natural cleaning action , particularly with respect to the removal of the plaque from gingival half of the tooth. Oral Hygiene Status In the absence of oral hygiene measures , plaque continues to accumulate until a balance is reached between the forces of plaque removal and those of plaque formation. Other local factors Margins of restorations: Overhanging margins of restorations changes the ecological balance of the gingival sulcus to an area that favours the growth of disease associated organisms Also inhibit the patients access to remove accumulated plaque. Subgingival margins are associated with large amounts of plaque accumulation , gingival inflammation and the rate of gingival fluid flow. Margins placed at the level of the gingival margin induce less severe inflammation. Supragingival margins →periodontal health. Contours Over contoured crowns and restorations→more plaque accumulation. ill fitting dentures Quantitative and qualitative changes in plaque Emergence of spirochaetal microrgnisms. Malocclusion Plaque control becomes more difficult. Orthodontic Therapy Retain plaque and food debris Increases P. melaninigenica , P intermedia, Actinimyces odontolyticus Direct injury to the gingiva as a result of overextented bands Exessive force → bone loss →increased mobility of teeth calculus Nidus for plaque formation Maintains and accentuates periodontal disease. Keeps plaque in close contact with the gingiva. Creates areas where plaque removal is impossible. Growth dynamics of plaque First 2-8 hours→pioneering streptococci , cover 3-30% OF ENAMEL SURFACE One day , it can be called biofilm. After 4 days 30% of the tooth crown is covered by plaque. Variation within dentition Early plaque formation occurs faster in The lower jaw compared to upper jaw. In molar areas On buccal tooth surfaces compared to oral site Interdental regions Impact on gingival inflammation More rapid in tooth margins facing the inflamed gingival margins than adjacent healthy gingiva. Hence it is suggested that crevicular fluid enhances plaque accumulation. Impact on patient’s age Fransson etal detected no differences in amount or composition between a group of young( 20-25 years ) and older ( 65-68) plaque in older patients however resulted in more severe gingival inflammation. Microbial shift during disease Gram + to Gram – From cocci to rods to spirochetes Nonmotile to motile Facultative anaerobes to obligate anaerobes Fermenting to proteolytic Criteria for identification of periodontal pathogen Koch’s postulates Must be routinely isolated from diseased individuals Must be grown in pure culture in lab Must produce similar disease when inoculated into susceptible lab animal Must be recovered from lesions in a diseased lab animal In case of periodontitis, 3 specific problems are 1. Inability to culture all organisms 2. Difficulties in defining active sites 3. Lack of good animal model system Criteria for periodontal pathogen 1. Must be associated with disease 2. Decreased in sites that show clinical resolution of disease after treatment 3. Must demonstrate a host response 4. Capable of causing disease in experimental animal models 5. Must demonstrate virulence factors Virulence factors of bacteria associated with periodontal infection Virulence factors Mechanism of action Fimbriae, pilli Used as attachment , prevention of bacterial phagocytosis Protection from complement & immune system Activation of cytokine, ↑bone resorption capsule Lps Virulence factors Mechanism of action Peptidoglycan Induction of inflammatory mediators Breakdown of host c/t, Host tissue invasion Proteolytic enzymescollagenase, hyluronidase, hydrogen sulfides Microorganisms associated with specific periodontal diseases Periodontal health Actinomyeces(Viscosus and naeslundi) Streptococcus ( S.mitis and S sanguis Veillonella parvula, small amounts of gram negative species. Chronic gingivitis Gram positive ( 56%) , Gram negative ( 44%) Facultative -59% , Anaerobic-41% Gram positive are Actinomyeces(Viscosus and naeslundi) Streptococcus ( S.mitis and S sanguis) Gram negative –F nucleatum, P intermedia , V Parvula , Hemophilus, Capnocytophaga, Campylobacter species Chronic Periodontitis Anaerobic- 90% and Gram negative – 75% P gingivalis P intermedia C rectus E corrodens Viruses-EBV-1 F nucleatum Human cytomegalo A A comitans virus P streptococcus micros Treponema Eubacterium species Localised aggressive Periodontitis AA comitans P gingivalis E corrodens C rectus F nucleatum Bacteroides capillus Eubacterium brachy Capnocytophaga Herpes virus Generalised aggressive periodontoitis A A comitans P gingivalis P intermedia Capnocytophaga E corrodens Neisseria Key characteristics of Specific Periodontopathogens Actinobacillus actinomyecetemcomitans New name Aggregatibacter actinomyecetemcomitans Small ,straight or curved rod with rounded end Nonmotile and gram negative,capnophilic Forms ; five serotypes( a to e ) , based on differences in polysaccharide composition. Grows in white translucent ,smooth, nonhemolytic colony on blood agar. Possess virulence factors like lipopolysaccharide, leukotoxin,collagenase and protease. Tannerella forsythia Nonmotile,spindle shaped, highly pleomorphic rod, Gram negative obligate anaerobe Grows slowly only in anaerobic conditions and needs several growth factors from other species. Produce several proteolytic enzymes that are able to destroy immunoglobulns and factors of the complement system. Induces apoptotic cell death. Porphyromonas gingivalis Nonmotile , pleomorphic rod, gram negative obligate anaerobe Different forms are present based on their genotype. Grows in anerobic medium with dark pigmentation ( brown, dark green or black ) on blood agar. Has strong proteolytic activity. Aggressive periodontal pathogen- fimbriae mediate adhesion and capsule defend against phagocytosis. Produces proteases , collagenases , hemolysins Potential to invade soft tissues. Prevotella intermedia, Prevotella nigrescens Short rounded gram negative rods, Grow anaerobically with dark pigmentation. Campylobacter rectus. Rare motile organism Gram negative, short rod, curved or helical Motility→polar flagellum Grows anaerobically with dark pigmentationwhen sulphide is added. Gets transformed in to greyish FeS Produces leukotoxin Less virulent and less proteolytic Fusobacterium nucleatum Gram negative, cigar shaped bacilli with pointed ends. Several subspecies are present Grows anaerobically in blood agar. Can trigger the release of cytokines.,elastase and oxygen radicals from leukocytes Coaggregates with most of the oral microorganisms. Bridging organism between primary and secondary colonisers. Spatiotemporal model of Oral bacterial colonization Kolenbrander et al Perio 2000 vol-42 Peptostreptococcus micros Rare cocci in periodontitis Gram positive and grows obligate anaerobically. Eubacterium species. Gram positive , obligate anaerobic , small pleomorphic rod Several forms are classified including E nodatum, E timidum, E brachy. Grow anaerobically but with difficulty in standard blood agar. Spirochaetes Diverse group of spiral and motile organisms Helical rods 5-15µm long , diameter 0.5µm Have 3 to 8 irregular spirals Cell wall is gram negative , but they stain poorly. Forms: T denticola, T. Vincenti , T socranski, T pallidum Able to travel through viscous enviroment like GCF and penetrate epithelium and connective tissue Some have the capacity to degrade collagen and even dentin T denticola produces proteolytic enzymes that can destroy immunoglobulins( IgA, IgM, IgG) or complement factors Antiplaque agents Depending on efficacy and substantivity , they are classified as. First generation agents- reduce plaque score by 20- 50 percent, efficacy is limited because of poor substantivity.eg- antibiotics, , quarterinary ammonium compunds, sanguinarine. Should be used 4 to 6 times daily. Second generation agents- retained longer in the tissues, slow release property provides overall reduction in plaque score by 70 to 90 percent ( should be used twice daily)eg- chlorhexidiene, triclosan with either copolymer or zinc citrate. Third generation agents: Should be effective against specific periodontopathic organisms. The most promising agent is Delmopinol which is a surface active agent .Weak antimicrobial agent , can exert its effect by binding to salivary proteins and thereby alters the cohesive and adhesive properties of the film formed. QUARTERNARY AMMONIUM COMPOUNDS Cetylpyridinium chloride (0.05%) Cationic and rapidly binds to oral tissues Rapidly released , hence not as effective as chlorhexidiene. Rupture of cell wall and alteration of cytoplasmic contents. Side effects are similar to that of chlorhexidiene. SANGUINARINE Used as both mouth rinse and tooth paste. Alkaloid extract from blood root plant (Sangiunaria Canadensis) Contain the extract at 0.03% and 0.2 % Zinc chloride Plaque reduction of 17-42 %, reduction in gingivitis is 1742% Burning sensation BISGUANIDES: Chlorhexidiene gluconate→most widely used 0.12% or 0.2% Rupture of bacterial cell walls and precipitation of the cytoplasmic content. Reduces plaque by 50-55% and gingivitis by 45%. Should be used twice daily. Brown staining of teeth, taste alteration, oral desquamation, increase in calculus formation ESSENTIAL OILS Listerine→Neutral in electric charge. Combination of phenol related essential oils , thymol and eucalyptol , mixed with menthol and methyl salicylate. Cell wall destruction, inhibition of bacterial enzymes Plaque reduction of 20 -34 % was noticed. Initial burning sensation TRICLOSAN Available as mouthrinses and dentrifices. Bisphenol and nonionic germicide with low toxicity and broad spectrum antibacterial activity. Widely used in soaps, antiperspirants and cosmetic toiletries. Various formulations enhance their ability to bind to plaque and teeth. Zinc citrate →antiplaque affect Copolymer of methoxyethylene and maleic acid→increase retention time. Pyrophosphates →enhance anticalculus properties. Conclusion Bacterial plaque is regarded as one of the main aetiological factors in the initiation and promotion of periodontal disease ie gingivitis and periodontitis . The knowledge of the fact has been derived from epidmological studies as well as clinical experiments . Several clinical studies established the direct cause and effect relationship between plaque and inflammation. Thus it is of paramount importance to understand the complex structure of plaque and its inter relation and influence on the development of oral diseases.