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Dental Biofilm
This document discusses biofilms and dental plaque. It begins by defining biofilms as self-produced extracellular matrices composed of biopolymers that allow microorganisms to stick to surfaces. Biofilms are found in various environments and contain diverse microbial communities embedded in a protective glycocalyx layer. As more microbes colonize the surface, mushroom-shaped structures called microcolonies form within the biofilm. Fluid channels also develop to transport nutrients and waste. Dental plaque is a specific oral biofilm that forms on teeth and other surfaces. It has both supragingival and subgingival components composed primarily of streptococci and other bacteria. Coaggregation and coadhesion between early and late colonizers aid in plaque maturation over time
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Dental Biofilm
- 3. What is biofilm..?? •The self-produced matrix of extracellular polymeric substance, which is also referred to as slime, is a polymeric conglomeration generally composed of extracellular biopolymers in various structural forms.
- 4. Where do wefind them..??
- 5. • One ormore communities of micro-organisms • Embedded in a glycocalyx that is attached to a solid surface. • Allows micro-organisms to stick to and multiply on surfaces
- 7. Bacterial Microcolonies • Mushroomshaped • Diversity – Microbes – Environment • O2 • pH • Temperature
- 8. Extra Cellular Layerof Mucous • Tight protective barrier that surrounds bacterial microcolonies • Protects bacterial microcolonies from antibiotics, antimicrobials, and the body's immune system
- 9. Fluid Forces • Saliva •Extensions from the main body of biofilms. • Can break free and to be swallowed, expectorated, or form new biofilm colonies in other areas of the mouth. • Cells clash to bacteria in biofilms. – Rapid spread of genes among bacteria – Leads to increased virulence of the bacteria and antimicrobial resistance – Means that the bacteria are in constant evolution
- 10. Fluid Channels • Directthe fluid in and around biofilms, – Nutrients and oxygen – Bacteria – Carry away bacterial waste • Liquids include everything from saliva that any drinks consumed.
- 11. COMPOSITION OF BIOFILM •Bacterial community- 20% • Glycocalyx membrane- 80%
- 12. Exopolysaccharides • Matrix madeup of water and aqueous solutes • Produced by bacteria • Function – Integrity of biofilm- Adhesiveness – Affect the hydrophilic or hydrophobic nature of the surface. – Aid in protecting microbial cells within the biofilm by preventing desiccation and attack by harmful agents – Binds essential nutrients like cations to create a locally rich environment favoring a specific microorganism
- 13. DENTAL PLAQUE • Dentalplaque can be defined as the soft deposits that form the biofilm adhering to the tooth surface or other hard surfaces in the oral cavity, including removable and fixed restorations Carranza 10th ed.
- 14. TYPES OF PLAQUE •SUPRA GINGIVAL • SUB GINGIVAL
- 15. SUPRA GINGIVAL PLAQUE •Originate from saliva • On the tooth surface: Gram + cocci and short rods predominate • On the outer surface of matured plaque: Gram –ve rods and filaments and spirochetes predominate.
- 16.
- 17. TOOTH ASSOCIATED PLAQUE •Predominated by gram +ve rods and cocci (S. mitis, A. viscosus, A. naslundi, Eubacterium) • At the cementum: filamentous micro- organisms predominate • At the apical border near junctional epithelium: Filamentous micro-oragnisms absent. More of gram –ve rods.
- 18. • Gram –verods and cocci • Filamentous bacteria • Flagellated rods • Spirochetes • Predominant are S. oralis, S. intermedius, Peptostreptococcus micros, P.g, P. intermedia, T. forsythia, F. nucleatum) • Host tissue cells TISSUE ASSOCIATED PLAQUE
- 19. COMPOSITION OF DENTALPLAQUE • 80% water • 20% solids, includes cells mainly bacteria making up 35% of the dry weight and extra cellular components making 65% of the dry weight • Other than bacteria, non bacterial organisms include: – Mycoplasma – Yeast – Protozoa – Viruses • Host cells – Epithelial Cells – Macrophages – Leukocytes
- 20. Intercellular Matrix ofDental Plaque Organic constituents Inorganic constituents Materials from Saliva, GCF and bacteria
- 21. ORGANIC CONSTITUENTS • Polysaccharides:Dextran 95% (adhesion), levan 5%, Sialic acid, fructose • Proteins: Albumin • Glycoproteins: Saliva • Lipid materials: Membrane remnants of bacteria and host cells
- 22. • Primarily: Calciumand Phosphates • Traces: Sodium, Potassium and Fluoride • Fluoride is derived from external sources like toothpaste, mouth washes INORGANIC CONSTITUENTS
- 23. For Formation of pellicle onthe tooth surface Initial adhesion and attachment of bacteria Colonization and plaque maturation
- 24. FORMATION OF PELLICLE •Within nanoseconds after vigorously polishing the teeth, a thin, saliva derived layer called the acquired pellicle covers the tooth surface. • Consists of more than 180 peptides, proteins, glycoproteins, including keratins, mucins, proline rich proteins and other molecules which function as adhesive sites for bacteria.
- 25. Ultrastructure of DentalPellicle • Thickness- 30-100nm • 2 hr pellicle: Granular structures which form globules, that connect to hydroxyapatite surface via stalk like structures • 24 hrs later: Globular structures get covered up by fibrillar particles: 500-900 nm thick • 36 hrs later: Pellicle becomes smooth and globular
- 26. • Studies ofearly (2 hr) enamel pellicle reveals that amino acid composition differs from that of saliva, indicating that the pellicle forms by selective adsorption of the environmental macromolecules. (Scannapieo FA et al, ‘Saliva and dental pellicles’ Complementary Periodontics, 1990 • Mechanisms involved are – Electrostatic forces – Van der Waals – Hydrophobic forces
- 27. Transport to surface Initial adhesion Attachment Colonization of the surfaceand biofilm formation Initial Adhesion and Attachment of Bacteria
- 28. Transport to thesurface • Random contacts occur through: – Brownian motion (40µm/hr) – Sedimentation of organisms – Liquid flow – Active bacterial movement (chemotactic activity) Transport to surface Initial adhesion Attachment Colonization of the surface and biofilm formation
- 29. Initial Adhesion • Reversibleadhesion of the bacterium and the surface • Initiated by interactions between bacterium and surface through long range and short range forces, including Van der Waals attractive forces and electrostatic repulsive forces Transport to surface Initial adhesion Attachment Colonization of the surface and biofilm formation
- 30. • First stepinvolves transportation of bacteria. Few are mobile and the majority of the organisms are transported by the bulk fluid. • Long range, between bacteria and pellicle coated enamel. The strength of this interaction is weak and span around 10-20 nm. Physical phase
- 31. • Next stepinvolves the closer movement of bacteria so that specific short range interaction occur. • This is to happen if water is removed between the two surfaces, brought about by bacterial cell components. This initial attachment of bacteria to surfaces is the initial part of adhesion, which makes the molecular or cellular phase of adhesion possible.
- 32. DLVO theory • Derjaguin,Landau,Verwey & Overbreak (DLVO) have postulated that above a separation distance of 1nm, the summation of previous two forces describes total range interaction also called as total Gibbs Energy (GTOT).
- 33. • The resultof summation (GTOT= GA+GE) is function of a separation distance between negatively charged particle and a negatively charged surface in a medium ionic strength suspension medium.
- 34. Three stages 1. Secondaryminimum (reversible attraction) 2. Positive maximum (energy barrier) 3. Primary minimum (irreversible attraction)
- 35. • Extended DLVOtheory has been suggested in which the hydrophobic/hydrophilic interactions are included. So, the total adhesion energy can be expressed as: ΔG adh= ΔGvdW+ ΔGdE+ ΔGAB
- 36. • GEL iscalculated from Zeta potentials of interacting surfaces. • Calculation of G∆LW and G∆AB relies on contact angle measurements. • With various liquids on the interacting surfaces application of a thermodynamic approach becomes essential. • It considers free energy states of microorganisms in suspension and in an adhering state.
- 37. • ∆Gadh isnegative (nature tends to minimize free energy), adhesion is thermodynamically favoured and will proceed spontaneously.
- 38. ATTACHMENT • Firm anchorage betweenbacterium and surface established by specific interactions (ionic, covalent or hydrogen bonding) Transport to surface Initial adhesion Attachment Colonization of the surface and biofilm formation
- 39. • The bondingbetween bacteria and pellicle is mediated by specific extracellular protenaceous components (adhesions) of the organism and complementary receptors (proteins, glycoproteins, polysaccharides) on the surface (pellicle) and is species specific
- 40. These receptors arespecies specific . Eg. 1. Streptococci sangius ( early colonizer) binds to acidic proline rich proteins and other receptors such as α amylase and saliac acid. 2. Actinomyces species posses fimbriae that contains adhesins that specifically bind to proline rich proteins of dental pellicle.
- 41. • CRYPTITOPES - Theyare hidden receptors for bacterial adhesins. -Some molecules from the pellicle undergoes a conformational change when they adsorb to the tooth surface so that new receptors become available in adsorbed molecule . Eg. Proline rich proteins undergo conformational changes A.viscous recognizes cryptic segment of proline rich proteins.
- 42. Colonization of thesurface and biofilm formation Colonization of the surface and biofilm formation - Mainly by 2 mechanisms COAGREGGATION. COADHESION Transport to surface Initial adhesion Attachment Colonization of the surface and biofilm formation
- 43. • Co-aggregation isthe interaction between planktonic micro- organisms of a different strain or species • Co-adhesion is the interaction between a sessile, already adhering organism and planktonic micro-oganisms of a different strain or species
- 44. Co- Aggregation • Cellto cell recognition of a genetically distinct partner cell type
- 45. • Occurs primarilythrough 1. Highly specific interaction of protiens and carbohydrate molecules located on the bacterial cell surfaces. 2.Less specific interaction resulting from hydrophobic electrostatic & van der waals forces.
- 46. Primary Colonizers • Theyprovide new binding sites for adhesion by other oral bacteria • Metabolic activity of primary colonizers modifies the local micro environment which influences the ability of other bacteria to survive in the dental plaque biofilm.
- 48. Late colonizers • Theydo not initially colonize the clean tooth surface but adhere to the bacteria already in the plaque mass
- 50. • Co-aggregation -bylectin like adhesins. • Inhibition of co-aggregation- by lactose and galactosides. Eg. of co-aggregation between early colonizer & secondary colonizer: • F.Nucleatum with Actinomyces viscous. • Capnocytophaga Ochraceus with A.Viscous
- 51. • Early colonizerslike streptococci and actinomycetes are facultative anaerobes. • These 2 groups of primary colonizers prepare a favorable environment for later secondary colonizers like P.intermedia, P.Loeschilli, Capnocytophaga spp , F.nucleatum, Porphymonas gingivalis which have a more fastidious growth requirements. • During later stages of plaque formation co aggregation between different gram negative species is likely to predominate. Eg. Coaggregation of F. nucleatum with P. gingivalis or T. denticola
- 53. Specificity of strains •Streptococcal co-aggregation group 6 co- aggregates only with actinomyces co- aggregation group D.
- 54. Coaggregation Bridges: -A coaggregationbridge is formed when the common partner bears two or more types of coaggregation mediators. -Mediators can be various types of receptor polysaccharides, or various types of adhesins, or a mixture of the two. -Bridging is usually considered to be a cooperative event that brings three or more cell types into close proximity and fosters symbiotic relationships. -Bridging can also be an antagonistic event which brings together organisms that compete with each other for nutrient or other needs.
- 56. COAGGREGATION COMPETITION: Competition occurswhen multiple cell types recognize the same coaggregation mediator on the common coaggregation partner. Model depicting competition for binding sites on Streptococcus oralis .
- 57. Morphological types • Corncobformation: – Feature of plaque present on teeth associated with gingivitis . – A central gram negative filamentous core supports the outer coccal cells, which are firmly attached by interbacterial adherence or coaggregation. – Detected between streptococcus and actinomyces Described by Gibbsons and Nygaard
- 58. • Test tubebrush: – Composed of a central axis of a filamentous bacterium with perpendicularly associated short filaments. – Commonly seen in the subgingival plaque of teeth associated with periodontitis – Detected between filaments of bacteria to which gram – ve rods adhere.
- 59. Socransky et al(1998)
- 60. • Most periodontalsites either all or none of the species belonging to the same complex • Red complex seldom detected in the absence of orange complex; higher the orange complex higher the red complex. • Yellow and green cluster show similar preference for each other; weaker relation with orange and red complex. • Purple complex, loose relation with all the other complexes. • Yellow and green associated with sites with PD< 3mm and red orange complexes with sites having PD > 4mm
- 61. Distribution of differentcomplexes in subgingival plaque sample Kigure et al (1995)
- 62. CO-ADHESION • Some bacteriaare unable to bind directly to the conditioning film, but are able to interact with molecules on bacteria that are already attached (co-adhesion), also by adhesin-receptor interactions. • One bacterium, Fusobacterium nucleatum, can co-adhere with almost all other bacteria found in dental plaque, and is considered to be a key bridging organism between early and later colonisers.
- 63. • Adhesins canbe subdivided into two main classes: – Fimbrial adhesins • Fimbriae • Pili • Curli • Type IV pili – Non fimbrial adhesins • Autotransporter • Outer membrane • Secreted adhesins – Those attached with biofilm formation Perio 2000, Vol 52, 2010, 12-37 Adhesins
- 64. • Fimbrial adhesinsof gram negative are classified into 5 major classes based on the biosynthetic pathway. 1. Chaperone –Usher(CU )pili 2. Curli 3. Type IV pili 4. Type III secretion pili 5. Type IV secretion pili
- 65. Importance of foodchains • Provide metabolites which serve as energy source for other members. (eg) lactate utilization by Veillonella produced by streptococci • Formation of symbiotic relationship • Making the environment favorable (eg) generation of ammonia by F.nucleatum elevating pH favorable for the growth of P.gingivalis
- 66. • Stimulation ofgrowth of other bacteria (eg) stimulation of growth of T.denticola by butyric acid produced by P.gingivalis • Increasing the virulence of organisms (eg) more virulent strains of P.gingivalis in the presence of S.gordonii. • Removal of toxic metabolites (eg) protection from hydrogen peroxide by A.neaslundii • Utilization of metabolic products for maintaining structural integrity (eg) succinic acid produced by T.denticola integrated onto the cell wall of P.gingivalis
- 67. Bacterial competitive interactions •Both synergistic and antagonistic interactions seen • Antagonism can be mediated by metabolites or through bacteriocins • Can influence localization of residents in the film
- 68. Bacterial competitive interactions Bacterialsynergism Bacterial antagonism
- 69. Metabolic products • Streptococciproduce hydrogen per oxide which are toxic to many bacteria • S.oligofermentus lactic acid hydrogen peroxide toxic to S.mutans • Short chain fatty acids like lactic acid lowers pH, having a disadvantageous effect and less aciduric bacteria.
- 70. Bacteriocins • Proteinaceous bactericidalsubstances produced by bacteria to inhibit the growth of closely related bacterial species or strains (Hojo et al 2009) • Regulated by genetic and environmental factors • Enable bacteria to select their neighbours, promote the establishment of a community with specific bacterial species. • Usually narrow spectrum with few exceptions like antibiotics
- 71. • Streptococcus producesmutacins (mutacin I – V) active against S.sanguinis • Inhibition of growth of P.gingivalis, T.forsythia, S.salivarius, S.sanguinis by bacteriocin produced by L.paracaesi • Nigrescin, produced by P.nigrescens display bactericidal effect against P.gingivalis, P.intermedia, T.forsythia, Actinomyces spp. • Bacteriocin production also reported by P.intermedia, A.a, C.ochracea, F.nucleatum, E.corrodens, H.influenzae
- 72. Clinical significance • Bacteriadetermine their neighbours • Prevention of pathogenic biofilm formation bacteriocins produced by S.pyogenes and S.salivarius are structurally similar, antagonize each other when colonise at the same time, inhibit the growth of other via antagonizing growth dependent signaling, prevent the biofilm formation of the former by the latter. • Maintain ecological balance
- 73. CHANGING VIEWS OFPLAQUE
- 74. • Specific plaquehypothesis– of the diverse organisms in the microflora, only a very limited number are actively involved in the disease (Loesche 1976) . • Non specific plaque hypothesis– many organisms play a role, and the disease is a result of overall interaction of plaque and the host (Theilade 1986) . • Ecologic plaque hypothesis– change in the key environmental factor(s) will trigger a shift in the balance of resident flora, and this might predispose to the disease (Marsh 1991) • Microbial shift hypothesis - due to decrease in the no: of beneficial symbionts and/or increase in the number of pathogen (dysbiosis)
- 75. De Novo SupragingivalPlaque Formation: Clinical Aspects • During 1st 24 hrs, starting from a clean tooth surface, plaque growth is negligible from clinical view point • Following 3 days, plaque growth increases at a rapid rat, then slows down • After 4 days, on average 30% of total crown area will be covered with plaque. Plaque does not seem to increase substantially after 4th day
- 76. Topography of SupragingivalPlaque • Initial along gingival margin and interdental space, then coronally • Grooves, cracks, perikymata or pits
- 77. Surface micro-roughness • Threshold:0.2 micrometers
- 78. Variation within dentition •Lowers • Buccal • Molars • Interdental
- 79. Impact of gingivalinflammation • Increased GCF- favours initial adhesion and colonization
- 80. Impact of Ptsage • No influence
- 81. De Novo SubgingivalPlaque Formation • Early studies, using culturing techniques examined changes in subgingival microbiota during 1st week after mechanical debridement, partial reduction followed by fast regrowth to almost pre treatment levels within 7 days. • This reveals that a high proportion of treated tooth surfaces still harbored plaque & calculus after scaling, these remaining bacteria were considered primary source for subgingival recolonization.
- 82. Ageing & Microflora •Following tooth eruption the isolation frequency of spirochetes & black pigmented anaerobes increases. • Increased prevalence of spirochetes & black pigmented anaerobes is found in teenagers, this is due to hormones entering gingival crevice & acting as a novel nutrient source. • Rise in P. intermedia in plaque during 2nd trimester of pregnancy has been ascribed due to elevated levels of oestradiol & progesterone which supplies napthoquinone for growth of this microorganism.
- 83.
- 84. Definition • It isdefined as the cell density dependent regulation of gene expression in response to soluble signals called autoinducers (Bassler 1999) • Quorum sensing can occur within a single bacterial species as well as between diverse species, and can regulate a host of different processes, essentially serving as a simple communication network.
- 85. Why the namequorum?? • Accumulation of a stimulatory concentration of an extra-cellular autoinducer can only occur when a minimum number of cells i,e critical cell density called a “quorum,” is present.
- 86. Quorum sensing isdependent on cell density Low level of signalling molecules Increased level of molecules Activation of gene expression Lesscelldensity
- 87. HOW BACTERIA TALKTO EACH OTHER: Bacteria Inducer Receptor AI Transcription of genes
- 88. • Quorum sensing-controlledbehaviors are those that only occur when bacteria are at high cell population densities. • These behaviors are ones that are unproductive when undertaken by an individual bacterium but become effective by the simultaneous action of a group of cells.
- 89. ROLE OF QS Thereis an increase in • Virulence and pathogenicity • Secondary metabolite production • Motility • Conjugation • Biofilm formation • Growth inhibition
- 90. Key players inquorum sensing Autoinducers • AHL • Autoinducer 2 • Cyclic dipeptides • Bradyoxetin • Other types Autoinducer synthases • AHL synthases • AI2 synthases • Synthases of other types of autoinducers Quorum sensing Regulators • Lux R type • Lux P/Q type
- 91. Types of Quorumsensing molecules Autoinducer 1 1st detected in Vibrio fisheri - by Chemically – N – Acyl Homoserine Lactone(AHL) Proteins involved are designated as Lux I & Lux R Lux I - Catalyses the synthesis of AHL Lux R - transcriptional regulator Autoinducer 1 is not common in oral biofilm. It usually regulates gene expression in genetically identical cells.
- 92. Autoinducer 2 First observedby Schauder et al 2001 • Collection of molecules formed from spontaneous rearrangement of 4,5 dihydroxy-2-3 pentanedione (DPP) • Produced by both gran +ve & -ve organism • Gene responsible for it production - lux S - protein - LuxS
- 93. • In theabsence of two component response circuit (receptor protein) auto inducer does not function in cell-cell communication but functions in basic metabolism - catalyses methyl cycle. Autoinducer 2 mediate gene expression in mixed communities. It is also density dependent Commensal bacteria respond to low levels and pathogenic bacteria respond to high levels of autoinducer 2
- 94. Other functions ofautoinducer 2 1. Regulate iron uptake in Aa 2. Regulate hemin (iron source) acquisition in Pg. 3. Regulate enzymes involved in stress related function. 4. Control the formation of multi species biofilm. 5. Induces expression of leukotoxon in Aa and modulate protease activities in Pg.
- 95. • Transposons –elements capable of excision from the chromosome of the donor genome, transfer to recipient cell and get integrates its genome. • Integron – gene cassette system – mechanism that allows bacteria to accumulate diverse genes at a common locus, useful in acquiring antibiotic resistance, are site specific recombinase of Intl family . • Genomic islands – regions of genome acquired horizontally. • Combination of these. Mobile genetic elements
- 96. • Plasmid -It is an extra chromosomal genetic element consisting of DNA situated in the cytoplasm in free state and reproducing independently. • They are grouped into incompatibility groups (inc groups) based on their inability to co-exist in the same cell.
- 97. • Bacteriophage -viruses that parasitize bacteria and consist of nucleic acid core and a protein coat.
- 98. Genetic exchange Conjugation Bacterium Bacterium Transduction Bacterium Bacterium Transformation DNA outsidethe cell is fragmented and combined with bacterial DNA plasmid bacteriophage
- 99. Detachment Can be Movementof Individual cells or Biofilm en masse
- 100. Individual Cell Transfer •The detachment of cells from biofilm is essential to allow colonization of new habitats by bacteria. • Cells detach in different fashions. Erosion - detachment of single cells in a continuous predictable fashion the Sloughing - sporadic detachment of large groups of cells or Intermediate process whereby large pieces of biofilm are shed from the biofilm in a predictable manner, resulting in detached clusters consisting of about 104 cells.
- 101. • The detachmentrate was shown to be about six clusters per mm2 of surface per hour. • Can be within the oral cavity and from subject to subject (bacterial translocation) • Microbes show centers of spread called bacterial reservoir. • Both horizontal (spouse to spouse for P.gingivalis) and vertical transmission (parent to child for A.a) has been demonstrated.
- 102. En masse transfer •This possibility has been demonstrated in vitro studies of mixed biofilm that showed movement of intact biofilm structures across solid surfaces while remaining attached to them. • Advantage in that formation of the biofilm is not reliant on planktonic cells, which are known to be more susceptible to antimicrobial agents . Stoodley 1991
- 104. Negative regulators ofQS Anti- activator proteins • AHL degradation enzymes • RNA dependant regulation Interference of QS e • Furanones • L-canavanine • Human hormones Bacterial components • Transgenic plants • Synthetic analogues
- 105. Mechanism of smallQuorum quenching inhibitors synthetic AIPs Interferes with the signal or decreases the receptor concentration Triclosan and closantel Inhibits enoyl-ACP reductase an intermediate in AHLbiosynthesis Structural mimics of QS inhibitors Enzyme inhibitors Inhibitor of histidine kinase sensor
- 106. PERIODONTAL HEALTH 102to 103 bacteria. Certain bacterial species have been proposed to be beneficial to the host, including S. sanguis, Veilonella parvula, and C. ochraceus(Carranza 10th) Bacteria associated with periodontal diseases are often found in the subgingival microflora at healthy sites, although they are normally present in small proportions(Rose & Maeley, 6th) Nonmotile nature.
- 107. GINGIVITIS 104 to106 bacteria. Gram-negative bacteria. Compared with healthy sites, noticeable increase also occur in the numbers of motile bacteria, including cultivable and uncultivable Treponemas (spirochetes). Pregnancy associated gingivitis is accompanied by dramatic increases in levels of P. intermedia, which uses the steroid as growth factors(Carranza,10th )
- 108. CHRONIC PERIODONTITIS C.rectus, P. gingivalis, P. intermedia, F. nucleatum and T. forsythia were found to be elevated in the active sites(Carranza,10th ) Sites with chronic periodontitis will be populated with greater proportions of gram-negative organisms and motile bacteria. Certain gram-negative bacteria with pronounced virulence properties have been strongly implicated as etiologic agents e.g. P. gingivalis and Tannerella forsythus.
- 109. LOCALIZED AGGRESSIVE PERIODONTITIS Gram -ve, and anaerobic rods. The most numerous isolates are several species from the genera Eubacterium, A. naeslundii, F. nucleatum, C. rectus, and Veillonella parvula. In some populations, a strong case can be made for Aa playing a causative role in LAP, especially in cases in which patients harbor highly leukotoxic strains of the organism. However, some populations of patients with LAP do not harbor Aa, and in still others P. gingivalis may be etiologically more important.
- 110. GENERALIZED AGGRESSIVE PERIODONTITIS Thesub-gingival flora in patients with generalized aggressive peri- odontitis resembles that in other forms of periodontitis. The predominant subgingival bacteria in patients with generalized aggressive periodontitis are P. gingivalis, T. forsythis A. actinomycetemcomitans, and Campylobacter species.
- 111. REFRACTORY CHRONIC PERIODONTITIS Unusuallydiverse and may contain enteric rods, staphylococci, and Candida. Persistently high levels are found of one or more of P. gingivalis, T. forsythis, S. inter-medius, P. intermedia, Peptostreptococcus micros, and Eikenella corrodens. Persistence of Streptococcus constellatus has also been reported.
- 112. NECROTIZING ULCERATIVE GINGIVITIS/PERIODONTITIS Morethan 50% of the isolated species were strict anaerobes with P. gingivalis and F. nucleatum accounting for 7-8% and 3.4%, respectively.
- 113. PERIODONTAL ABSCESSES Thebacteria isolated from abscesses are similar to those associated with chronic and aggressive forms of periodontitis. An average of approximately 70% of the cultivable flora in exudates from periodontal abscesses are gram-negative and about 50% are anaerobic rods. Periodontal abscesses revealed a high prevalence of the following putative pathogens: F. nucleatum (70.8%), P. micros (70.6%), P. intermedia (62.5%), P. gingivalis (50.0%), and T. forsythis (47.1%). Enteric bacteria, coagulase-negative staphylococci, and Candida albicans have also been detected.
- 114. PERIIMPLANTITIS High proportionof anaerobic gram negative rods, motile organisms, and spirochetes). Species such as Aa, Pg, Tf, P. micros, C. rectus, Fusobacterium, and Capnocytophaga are often isolated from failing sites. Other species such as Pseudomonas aeruginosa, enterobacteriaceae, Candida albicans and staphylococci, are also frequently detected around implants.
- 115. FIGHTING ORAL BIOFILMS- ADJUNCTIVETREATMENTS • Scaling and root planing is the primary therapy of choice for most clinicians, and it is widely considered the gold standard for treating periodontitis. • However,scaling and root planing alone often does not produce the clinical outcomes desired in severe cases. OTHER ADJUNCTIVE THERAPY ARE: 1. Antibiotics 2. Antiseptics 3. Host modulation therapy. 4. Photodynamic therapy.
- 116. Antibiotic resistance - characteristicfeature of biofilm • BIC of chlorhexidine and amine fluoride was 300 and 75 times greater respectively, when S.sobrinus was grown in biofilm compared to planktonic cells • Biofilms of P.gingivalis tolerated 160 times the MIC of metronidazole than planktonic cells Scaling and root planing cornerstone of periodontal therapy
- 117.
- 118. . • Thebiofilm matrix may restrict the penetration of a charged antimicrobial agent (diffusion-reaction theory) • Agent may also bind to, and inhibit, the organisms at the surface of the biofilm, leaving cells in the depths of the biofilm relatively unaffected. • The novel phenotype expressed in a biofilm may result in the drug target being modified or not expressed, or the organism may use alternative metabolic strategies
- 119. • Bacteria replicateonly slowly in an established biofilm and, as a consequence, are inherently less susceptible than faster dividing cells.• In addition, samples of gingival crevicular fluid (GCF) can contain sufficient ß lactamase to inactivate the concentrations of antibiotic delivered to the site • A susceptible pathogen can be rendered resistant if neighbouring, non-pathogenic cells produce a neutralising or drug-degrading enzyme.
- 120. Can viruses formbiofilms? • The recent finding that the human T-cell leukemia virus type 1 (HTLV-1) encases itself in a carbohydrate-rich adhesive extracellular ‘cocoon’, which enables its efficient and protected transfer between cells, unveiled a new infectious entity and a novel mechanism of viral transmission. • These HTLV-1 structures are observed at the surface of T cells from HTLV-1-infected patients and are reminiscent of bacterial biofilms. • The virus controls the synthesis of the matrix, which surrounds the virions and attaches them to the T cell surface. • Similar to bacterial biofilms, viral biofilms could represent ‘viral communities’ with enhanced infectious capacity and improved spread compared with ‘free’ viral particles, and might constitute a key reservoir for chronic infections. Maria-Isabel Thoulouze, Andrés Alcover
- 121. Bacteriophage and Biofilms •Phages along with other viruses can become trapped non-specifically within biofilm extracellular polymeric substances (EPS). • Can degrade these polymers • Can infect bacteria that can go on to making up biofilms
- 122. Conclusion In order toadjust a complex microbial ecosystem to one that is compatible to health, it is essential to define the range of species that colonize the area, recognize their relationship with each other and the host, and develop effective strategies to guide these ecosystems to those compatible with long-term oral health.
- 123. REFERENCES -Clinical Peridontology 10thedition: Carranza, Neuman& Takei. -Peridontology 2000 Vol 38 2005. -Peridontology 2000 Vol 42 2006. -Peridontology 2000 Vol 52 2010. -Peridontology 2000 Vol 55 2011.