Dr. Roshni Maurya, profile picture
Uploaded byDr. Roshni Maurya
43,116 views

Dental plaque

Dental plaque is a biofilm that forms on teeth. It is made up of bacteria, salivary components, and food debris embedded in an extracellular matrix. Plaque forms in stages - first, a protein pellicle forms on the tooth surface. Bacteria then attach to the pellicle and begin to colonize. As the bacteria multiply, they produce a matrix material between them made of carbohydrates, proteins, and lipids. Over time this leads to the development of a mature dental plaque biofilm.

Embed presentation

PRESENTED BY ROSHNI MAURYA 2ND YR PG STUDENT DENTAL PLAQUE
CONTENTS • Introduction • Definition • History • Composition • Classification/types of dental plaque • Formation/development • Growth dynamics of the dental plaque • Structural and physiological properties of dental plaque • Clinical significance of the plaque ( what makes plaque pathogenic?) • Conclusion
INTRODUCTION : • Dental plaque is the community of microorganisms found on a tooth surface as a biofilm, embedded in a matrix of polymers of host and bacterial origin • Plaque is derived from French word “PLAQUER” Which means “TO PLATE”
• WHO DEFINITION: plaque is a specific but highly variable structural entity resulting from colonization of microorganisms on tooth surfaces, restorations and other parts of oral cavity and consists of salivary components like mucin, desquamated epithelial cells, debris and microorgansims all embedded in a gelatinous extracellular matrix. • GLICKMAN: It is soft amorphous granular deposits which accumulate on surface of teeth, dental restoration and dental calculus. (Clinical periodontology 3rd ed.)
Definition • A highly variable entity resulting from the colonization and growth of m/o on the surfaces of the teeth and oral soft tissues and consisting of a number of microbial species and strains embedded in an extracellular matrix. American Dental Association • WH Boven, 1976. Dental plaque is defined clinically as a structured, resilient, yellow-grayish substance that adheres tenaciously to the intraoral hard surfaces, including removable and fixed restoration. (Carrnaza 10th ed.) • PD Marsh, 2004. Dental plaque can be defined as the diverse community of micro-organisms found on the tooth surface as a biofilm, embedded in an extracellular matrix of polymers of host and microbial origin.
• Dental plaque must be differentiated from other tooth deposits, like materia alba and calculus. • Materia Alba refers to soft accumulations of bacteria and tissue cells that lack the organized structure of dental plaque. • Calculus is hard deposits that form by mineralization of dental plaque and is generally covered by a layer of unmineralised plaque. 6
• Material alba • Calculus 7
Carranza 11th edition 8
CATE- GORY TOOTH DEPOSIT DESCRIPITION DERIVATION NON- MINER AL- IZED ACQUIRED PELLICLE Translucent, homogenous, thin, ultra structured film covering and adherent to the surfaces of the teeth, restorations, calculus, and other surfaces of the oral cavity Supra gingival :saliva Sub gingival :GCF MICRO- BIAL- PLAQUE Dense organized bacterial system embedded in an inter microbial matrix that adhere closely to the teeth, calculus, and other surfaces of the oral cavity Colonization of oral micro-organisms MATERIA ALBA Loosely adherent, ultra structured, white or grayish, white mass of oral debris and bacteria that lies over bacterial plaque Vigorous rinsing and water irrigation can remove materia alba Incidental accumulation FOOD DEBRIS Unstructured, loosely attached particulate matter self- cleansing activity of tongue and saliva and rinsing vigorously remove debris Food retention following eating MINE RAL- IZED SUPRA- GINGIVAL CALCULUS Calcified bacterial plaque: hard tenacious mass that forms on the clinical crown of the natural teeth & on dentures and other appliances Occurs coronal to the margin of gingiva ; is covered with bacterial plaque Plaque mineralization Source of minerals is saliva SUB- GINGIVAL CALCULUS Occurs apical to the margin of gingiva ; is covered with bacterial plaque Source of minerals is GCF
History
• The descriptive term gelatinous microbial plaque was first introduced by J.C William and G.V Black in 1898 to describe microbial colonies on tooth surfaces. • More recently, Black’s terminology has been shortened to the term ‘Plaque’ by Wild (1941) and its usage has been restricted to denote only those deposits that are predominantly microbial in nature.
Classification of Plaque
DENTAL PLAQUE SUPRA GINGIVAL PLAQUE SUB GINGIVAL PLAQUE TOOTH ATTACHED PLAQUE UN- ATTACHED PLAQUE PLAQUE ATTACHED TO EPITHELIUM CORONAL MARGINAL
SUPRAGINGIVAL PLAQUE SUBGINGIVAL PLAQUE
CHARACTE -RISTICS SUPRAGINGIVAL SUBGINGIVAL LOCATION Coronal MG Apical MG ORIGIN Salivary glycoprotein down growth bact from supra gingival plaque DISTRIBU- TION Starts proximal surface and other protected areas Heaviest collection on areas not cleaned daily by patient Cervical third , esp. facial and lingual Mandibular molars Proximal surfaces Pits and fissures plaque Shallow pocket Attached plaque covers calculus Unattached plaque extends to the periodontal attachment
ADHES- ION Firmly attached to acquired pellicle Surface bacteria (unattached ) loose: washed away by saliva Adhere to tooth surface subgingival pellicle  calculus RETEN- TION Rough surface teeth restoration , malpositioned or carious teeth Pocket hold plaque against tooth and overhanging margins SHAPE AND SIZE Friction of tongue lips cheeks , cervical area Thickness: thicker at the cervical end and on proximal surfaces Healthy gingival: thin plaque ,15 to 20 cells thick Chronic gingivitis: thick plaque,100 to 300 cells thick Molded by pocket wall, follows the form created by subgingival calculus
MICRO- ORGANISM Early plaque:formsGram+ve cocci Older plaque ( 3 to 4 days) increased number of filaments and fusiforms 4 to 9 days undistributed: more complex flora with rods, filamentous forms 7 to 12 days: vibrios, spirochetes, more gram org Anaerobic population Gram-neg , motile spirochete and rods SOURCE OF NOURISH- MENT Saliva ingested food Tissue fluid (sulcular fluid), exudates, leucocytes
STRUCTURE Densely packed three layers 1. tooth surface attached plaque: many gram positive rods and cocci 2. unattached plaque in middle: many gram neg, motile forms, spirochetes, leukocytes 3. epithelium attached plaque : gram neg, motile forms predominate, many leukocytes migrate through epithelium
Structure: • Early studies: plaque appears as a compacted consortium of microorganisms Confocal laser scanning microscopy has revealed Supra gingival plaque can have a • structured architecture polymer containing channel or pores have been observed that link the plaque/oral environment interface to the tooth surface ( Wood et al 2000,Auschillet al 2001,Zaura Arite et al 2001)
• the use of live /dead stains has indicated that bacterial vitality varies throughout the biofilm, with the most viable bacteria present in the central part of plaque , and lining the voids and channels (Auschill et al 2001) • this more open architecture should enable the molecule to readily move in and out of the plaque , but the presence of a matrix comprised of a diverge range of exo polymers creates a complex environment for accurately predicting the penetration and distribution of molecules with in plaque (Robinson et al 1997,Thurnheer et al 2003,Marcotte et al 2004).
Sub gingival plaque: Histological sections of human sub gingival plaque viewed by Conventional light microscopy suggested that: • a complex organization of attached microorganisms in which there can exist distinct tooth associated and epithelial associated biofilms, with the possibility of a less dense zone of organisms between the two (Socransky & Haffajee 2002)
• Between sub gingival plaque and the tooth an electron dense organic material is interposed , termed as cuticle. • This cuticle probably contains the remains of the epithelial attachment lamina originally connecting the junctional epithelium to the tooth , with the additional of material deposited from the gingival exudates (Frank & Cimasoni 1970, Lie & Selvig 1975, Eide et al 1983)
• It has been suggested that cuticle represents a secretory product of the adjacent epithelial cells. (Schroeder & Lisgarten 1977)
Composition of plaque
COMPOSITION OF PLAQUE: COMPOSED mainly of • Microorganisms , • Intermicrobial matrix (a) Bacterial portion: • 70 to 80 % of total solid plaque volume. • 1 g (WET WT)contains approx 1011 bacteria.
(B)Intermicrobial Matrix • the material present between the bacteria in the dental plaque is called the intermicrobial matrix. • accounts for approx 25% of plaque volume.
Three sources may contribute to the intermicrobial matrix: •the plaque microorganisms •the saliva •gingival exudates Degenerating or dead bacteria may also contribute to inter microbial matrix.
Organic and inorganic SOLIDS approx 20 % and water • WATER 70 to 80 % of solid matter, which higher in sub gingival plaque than supra gingival. INORGANIC: • Main Calcium and Phosphorus(mostly) magnesium, sodium fluoride(in small amount, higher than saliva) • CALCIUM AND PHOSPHATE more on lingual surface of anterior teeth. ORGANIC: • Surrounds microorganisms contains carbohydrates, proteins and lipids Inter bacterial matrix:
CARBOHYDRATES: Fructans (Levans) : • synthesized in plaque from dietary sucrose • provide a storage of energy which may be utilized by the microorganisms in time of low sugar supply Glucans: also synthesize from sucrose & of two types: • Dextran: serve as energy storage • Mutan: acts primarily as a skeleton in the matrix in much the same way as collagen stabilizes the intercellular substances of connective tissue.
• A fibrillar component is seen in the matrix between gram+ve cocci • In parts of the plaque with the presence of gram –ve organisms, the intermicrobial matrix is regularly characterized by the presence of small vesicles surrounded by trilaminar membrane, which is similar in structure to that of the outer envelope of the cell wall of gram -ve microorganisms. • Such vesicles may contain endotoxin and proteolytic enzymes, may also be involved in adherence between bacteria ( hofstad et al 1972, grenier and mayrand 1987) • In other regions it appears granular or homogenous Intermicrobial matrix in plaque varies considerably from region to region
Non bacterial microorganisms that are found in plaque include • mycoplasma species • yeast • protozoa, and • viruses The micro organisms exist with in a intracellular matrix that also contains • a few host cells, such as epithelial cells , • macrophages and • leukocytes
Selected Bacterial Species Found In Dental Plaque: Bacteria Facultative Anerobic Gram +ve Strep.mutans Strep.sanguis A.viscosus Gram -ve A.actinomycetemcomitans Capnocytophypa sp. Ekinella corrodens P.Gingivalis F.nucleatum P.intermedia B.forsythus C.rectus Spirochetes  T.denticola
PROTINES: • Supra gingival plaque contains proteins from saliva. • Sub gingival contains Albumin – cervical fluid and gingival exudates. LIPIDS: • lipopolysaccharides, endotoxins from gram negative bacteria.
PLAQUE AS A BIOFILM •As the bacteria attach to a surface and to each other, they cluster together to form sessile, mushroom-shaped microcolonies that are attached to the surface at a narrow base. •Each microcolony is a tiny, independent community containing thousands of compatible bacteria. •Different microcolonies may contain different combinations of bacterial species.
•Bacteria in the center of a microcolony may live in a strict anaerobic environment, while other bacteria at the edges of the fluid channels may live in an aerobic environment. •Thus, the biofilm structure provides a range of customized living environments (with differing pHs, nutrient availability, and oxygen concentrations) within which bacteria with different physiological needs can survive.
•The extracellular slime layer is a protective barrier that surrounds the mushroomshaped bacterial microcolonies. •The slime layer protects the bacterial microcolonies from antibiotics, antimicrobials, and host defense mechanisms. •A series of fluid channels penetrates the extracellular slime layer.
• These fluid channels provide nutrients and oxygen for the bacterial micro colonies and facilitate movement of bacterial metabolites, waste products, and enzymes within the biofilm structure. • Each bacterial microcolony uses chemical signals to create a primitive communication system used to communicate with other bacterial microcolonies
Quorum sensing Etiology and Pathogenesis of Periodontal Disease, 2010) • The regulation of bacterial gene expression in response to changes in cell density is known as quorum sensing. These bacteria then proliferate and communicate by signals to each other (Okuda et al. 2004). • In order to maintain the ecosystem, various anaerobes, anchor to each other by forming aggregated bacterial masses (Kigure et al. 1995; Okuda et al. 2004). • Quorum-sensing bacteria synthesize and secrete extracellular signaling molecules called autoinducers, which accumulate in the environment as the population increases (Okuda et al. 2004).
• Gram-positive bacteria generally communicate via small diffusible Peptides, while many gram-negative bacteria secrete Acyl Homoserine Lactones (AHLs) (Whitehead et al. 2001), which vary in structure depending on the species of bacteria that produce them. • Another system involves the synthesis of autoinducer- 2 is LuxS (Federle and Bassler 2003; Winzer et al. 2003). This system may be involved in cross-communication among both gram-positive and gram-negative bacteria. (Marsh 2004).
Plaque formation
stages of formation in dental plaque 1. Formation of pellicle 2. Attachment of bacteria to pellicle 3. Bacterial multiplication and colonization 4. Plaque growth and maturation 5. Matrix formation.
a) PELLICLE FORMATION: • formed by adsorption of proteins on tooth surface • composed of glycoprotein from saliva , adsorbed by hydroxyapatite • Have negative charged phosphate --interact +ve charge salivary crevicular macromolecules • This adsorbed material becomes highly insoluble coating over teeth, calculus, and restoration, complete and partial denture. DERIVATION: Supra gingival from saliva Sub gingival from gingival sulcus. It is translucent, homogenous, thin ultra structured film covering adherent tooth surface.
SIGNIFICANCE OF PELLICLE: • PROTECTIVE: provide barrier against acids thus may reduce dental caries attack. • LUBRICATION: keep surface moist prevent drying. • NIDUS FOR BACTERIA: Plaque formation by adherence of microorganisms. • ATTACHEMENT OF CALCULUS: A mode of calculus attachment in acquired pellicle.
b) BACTERIAL ATTACHEMENT TO PELLICLE: Initial attachment by selective adherence of specific bacteria from oral environment Small colonies Layers Microorganisms form in layer as grow and multiply When colony sizes increases it unite to form continuous plaque bacterial mass Organisms of first few hours are gram positive cocci, rods
c) MATRIX FORMATION: • Intermicrobial substances derived mainly from saliva for supra gingival plaque and • gingival sulcus fluid and exudates for sub gingival plaque • other product produced by certain bacteria, dietary source polysaccharide are sticky contribute to adhesion of plaque to teeth.
CHANGE IN PLAQUE MICROORGANISMS DAY 1 TO 2 gram +ve Cocci, Streptococci (dominate), Strepto mutans, Strepto sanguis DAY 2 TO 4 Cocci still dominate , increase gram+ve filamentous form, slender rods , gradually filamentous forms replaces cocci. DAY 4 TO 7 Filaments increases in numbers, and a more mixed flora begins to appear with rods, filamentous forms and Fusobacteria .  Plaque near margin thickens and develops a more mature flora with gram neg spirochetes and vibros .  As plaque spreads coronally, the new plaque has the characteristic coccal forms
DAY 7 TO 14 Vibros and spirochetes appear. No. of WBC increases , as plaque mature and thickens more,gram+ve anaerbic org appear “during this period sign of inflammation on gingiva occurs” DAY 14 TO 21 Vibros + spirochetes prevalent along with cocci and filamentous The densly packed filamentous organisms arrange themselves perpendicular to the tooth surface in a palisade “gingivitis evident clinically”.
Plaque formation at ultrastructual level 1. Formation of pellicle on the tooth surface 2. Initial adhesion and attachment of bacteria Phase 1: Transport to the surface Phase 2: Initial adhesion Phase 3: Attachment Phase 4: Colonization of surface and biofilm formation 3. Colonization and plaque maturation
Formation of pellicle • All surface of oral cavity (both hard and soft) are coated with a pellicle. • With in nanoseconds after a vigorously polishing the teeth, a thin layer, called acquired pellicle, covers the tooth surface. • Acquired pellicle term is misleading as it implies that bacteria can colonize only when pellicle is in place for few hours. • Bacteria can be part of early deposit, within seconds after prophylaxis. • Pellicle formation involves selective adsorption of macromolecules (eg glycoprotein) to apatite surface.
Forces involved in enamel pellicle formation: 1.Electrostatic forces (between hydorxyapatite surfaces which has negatively charged phosphate group, that interacts with opposite charged groups in the salivary macromolecules). 2.van der Waals force 3.Hydrostatic force (Detachment of adhering bacteria might occur through cohesive failure in conditioning film between bacteria and surface ,i.e. pellicle)
Initial Adhesion & Attachment of Bacteria Phase 1: Transport to the surface This include transport of bacteria to the tooth surface. Random contact occurs through: 1. Brownian motion (avg displacement of 40 µm/hr). 2. Through sedimentation of microorganisms. 3. Through liquid flow. 4. Through active bacterial movement (chemotactic movement).
PHASE 2: INITIAL ADHESION • The second stage results in an initial, reversible adhesion of bacterium, initiated by interaction between bacterium and the surface, from a certain distance (50 nm), through long range and short range forces, including van der Waals attractive and electrostatic repulsive forces.
Derjaguin, Landau, Verwey and Overbeek (DLVO) postulated that, • above a separation of 1 nm, the summation of vander wal (attaractive; GA) and electrostatic forces (repulsive; GE) describes total long range interaction. • If a particle reaches the primary minimum (<1nm from the surface), a group of short range forces (eg hydrogen bonding, ionic pair formation, steric interaction) dominates the strength of adhesion.
PHASE 3: ATTACHMENT • After initial adhesion, a firm anchorage will be established by specific interactions (covalent, ionic, or hydrogen bonding). • This follows direct contact or bridging true extra cellular filamentous appendages (with length up to 10nm). • On a rough surface, bacteria are better protected against shear forces so that a change from reversible to irreversible bonding occurs more easily and more frequently.
• Streptococci (mainly S. sanguis), bind to acidic proline-rich- proteins and other receptors in pellicle as α-amylase and sialic acid. • Actinomyces can also function as primary colonizers: eg A. viscosus possesses fimbrae that contain adhesins that specifically bind to proline-rich proteins of dental pellicle • A. viscosus reognises cryptic segments ( with lock &key mech.) of proline rich proteins, which are only available in adsorbed molecules. ( Mergenhagen et al 1987)
COLONIZATION & PLAQUE MATURATION • When the firmly attached microorganisms start growing and the newly formed bacterial clusters remain attached, micro colonies or a biofilm can develop. • From this stage Intrabacterial connections occur • at least 18 genera from the oral cavity have shown some form of co-aggregation (cell-to-cell recognition of genetically distinct partner cell types).
• All oral bacteria possess surface molecules that foster some type of cell to cell interaction. • This occurs primarily through the highly specific stereo chemical interaction of protein and carbohydrate molecules located on bacterial cell surfaces, in addition to the less specific interactions resulting from hydrophobic, electrostatic and van der waals forces. • Coaggregation is mediated by lectin-like adhesion and can be inhibited by lactose and other galactosides
Interactions of secondary colonizers with early colonizers include the coaggregation of a. Fusobacterium nucleatum with Streptococcus sanguis b. Prevotella loescheii with Actinomyces viscosus. c. Capnocytophaga ochraceus with A. viscosus. Coaggregation exist between a. Different gram positive species. b. Gram positive and gram negative species c. Different gram negative species (predominate in later stage) eg F. nucleatum with P. gingivalis or T. denticola. Special examples of coaggregations are a. “Corncob” formation b. “Test-tube brush” formation. c. Probiotics.
• “Corncob” formation have been observed between rod-shaped bacterial cells eg. Bacterionema matruchotii or Actinomyces sp. that forms inner core of the structure and coccal cells eg. Streptococci or P. gingivalis that attach along the surface of the rod shaped cells. • “Test-tube brush” composed of filamentous bacteria to which gram negative rods adhere. “Probiotics” : “literally meaning ‘for life” WHO defined it as live microorganisms which when administered in adequate amounts confer a health benefit on the host.
BENEFITS OF COMMUNITY LIFE STYLE to micro organisms: • A broad habitat range for growth. e,.g. oxygen consuming sp. create environmental conditions suitable for obligate anaerobes • A more efficient metabolism e.g. complex hast macromolecule can only be degraded by consortia of oral bacteria. • Increased resistance to stress and antimicrobial agents • Enhanced virulence ( pathogenic synergism) {Caldwell et al 1997, Shapiro ,1998, Marsh and Bowen,2000}
Relationship of Specific Microorganisms to Periodontal Diseases • Our understanding of the relationship between the microorganisms found in dental plaque and the common dental disease of periodontitis has undergone numerous phases historically • Early in the 19th century, it was felt that, like the situation with diseases such as tuberculosis, a specific bacterial species was responsible for the disease processes. • The criteria by which a given bacterial species was associated with disease historically has been through the application of Koch's Postulates.
These criteria were developed by Robert Koch in the late 1800's. The criteria are as follows: • A specific organism can always be found in association with a given disease. • The organism can be isolated and grown in pure culture in the laboratory. • The pure culture will produce the disease when inoculated into a susceptible animal. • It is possible to recover the organism in pure culture from the experimentally infected animal.
CURRENT HYPOTHESES ON THE ROLE OF PLAQUE BACTERIA IN THE ETIOLOGY OF DENTAL DISEASES • Non-specific plaque hypothesis • Specific plaque hypothesis • Ecological plaque hypothesis
• Both the Plaque and Non-plaque hypothesis were delineated in 1976 by Walter Loesche, a researcher at the University of Michigan. • According to non-specific plaque hypothesis periodontal disease results from the “elaboration of noxious products by the entire plaque flora”. • Specific plaque hypothesis states that “only certain plaque is pathogenic, and its pathogenicity depends on the presence of or increase in specific microrganisms”. For example role of Aactinobacillus actinomycetemcomitans in aggressive periodontitis. Thus plaque harboring specific pathogens results in a periodontal disease because these organisms produce substances that mediate the destruction of host tissues
Ecological plaque hypothesis: (By Marsh and Bradshaw; 1997) • Disease results from shifts in the balance of the resident plaque microflora. • A change in the nutrient status of a pocket or chemical and physical changes to the habitat are thus considered the primary cause for the overgrowth by pathogens • Disease could be controlled not only by targeting putative pathogens but also by interfering with the factors responsible for driving the deleterious shifts in the microflora as by reducing GCF rate , or the site could be made less anaerobic by use of redox agents
Growth dynamics of dental plaque
Ultra structural aspects: • Important changes in the plaque growth rate can be detected within first 24 hours. • During the first 2 to 8 hour, the adhering pioneering streptococci saturate the salivary pellicular binding sites and thus cover 3% to 30% of enamel surface. • Instead of steady growth during the next 20 hrs,a short period of rapid growth for 4 to 6 hr (Loesche suggested it as generation time) • After 1 day, the term biofilm is fully deserved -because organization takes place within it.
• As bacterial densities approach approximately 2- 6 million bacteria/mm2 on enamel surface, a marked increase in growth rate can be observed to 32 million bacteria/mm2 (doubling in 3 to 4 hrs.) • This occurs due to multiplication of already adhering microorganisms rather than by new colonizers. • Thickness of plaque increases slowly with time, increasing to 20 to 30 µm after 3 days
• During the first 24 hr, plaque growth is negligible from a clinical view point (<3% coverage of vestibular tooth surface, an amount that is clinically almost undetectable). • During the following 3 days, plaque growth increases at a rapid rate, then slows down from that point onward. • After 4 days, on average, 30 % of total tooth crown area will be covered with plaque. • There is ecologic shift within biofilm, with transition from early aerobic environment characterized by gram positive facultative species to a highly oxygen deprived environment in which gram-negative anaerobic microorganisms predominate. • During night, plaque growth rate is reduced by about 50%. This may be explained from the fact that supra gingival-plaque obtains its nutrients mainly from the saliva Clinical Aspects: Supra Gingival Plaque Formation:
Experimental gingivitis model • From day 0 on, when mechanical plaque control was stopped, plaque will slowly form on the teeth. • With time the plaque composition changes, with a shift to more gram negative species and more rods, filaments and from day 7 on spirals and spirochetes. • From day 3 on, the first symptoms of gingival inflammation become visible. • When proper plaque control is reestablished, the plaque composition returns to the initial situation and symptoms of gingivitis disappear
Topography of supragingival plaque Early plaque formation on teeth follows a typical topographic pattern, with initial growth along the gingival margin and from the inter dental spaces (areas protected against shear forces) to extend further in coronal direction. Early plaque formation on surface irregularities of teeth
Surface micro roughness Small plastic strip divided in half (a rough region, average roughness Ra 2.0µm, located mesially, and a smooth region Ra 0.1µm, located distally) was glued to the central upper incisors of a patient who refrained from oral hygiene for 3 days Disclosing agent used was : 0.5% neutral red
SMOOTH REGION ROUGH PART After removal, the strip was cut in small slices for microscopic evaluation Rough part contains a thicker plaque layer than smooth part . Arrow shows border between rough and smooth surface
Other factors determining supragingival plaque formation are: 1. Individual variables influencing plaque formation: “heavy or fast plaque” former and “light or slow plaque” former- this depends on various factors as • diet, chewing fibrous food, • smoking, • amalgam restorations, • tongue and palate brushing, • the colloidal stability in saliva, • antimicrobial factors of GCF and saliva • pellicle composition and • retention depth of dento-gingival area
2. Variation within the dentition In general early plaque formation occurs faster 1. In lower jaw compared to upper jaw 2. In molar areas 3. On buccal tooth surfaces compared to oral sites (especially in upper jaw) 4. In the interdental regions compared to the strict buccal or oral surfaces.
3. Impact of gingival inflammation • Plaque formation is more rapid on tooth surfaces facing inflamed gingival margins than on those adjacent to healthy gingiva. Substances from GCF as mineral, protein, carbohydrate favors both the initial adhesion and growth of early colonizing bacteria. 4. Impact of patient’s age • Subjects age does not influence de novo plaque formation. Developed plaque in older patient , resulted in more severe gingival inflammation, this indicate an increased susceptibility gingivitis with aging. 5. Spontaneous tooth cleaning • Only negligible differences in plaque extension (plaque retaining areas) areas is observed.
Changes in subgingival micro biota during 1st week after mechanical debridement reported only partial reduction from 108 to 105 followed by a fast regrowth to almost pretreatment level within 7 days. Smooth abutments (Ra<0.2 µm) were found to harbor 25 times less bacteria than rough ones, with a slight higher density of coccoid (ie non-pathogenic) cells Recent studies demonstrate that a complex subgingival microbiota, including most periopathogens, is established within 1 week after abutment (transmucosal implant) insertion De novo subgingival plaque formation Scanning electron microscope of bacteria invading dentinal tubules 15000x
PHYSIOLOGIC PROPERTIES OF DENTAL PLAQUE
Factor modifiers: • Oxidation Reduction potential (Saocransky et. at. 1964) • pH (Kleinbers and Hall 1969) • Temperature (Haffagee et al 1992) Factor antagonizes: • Bacteriocins (Rogers et. al. 1979, Hammond et. al. 1987, Steven et. al. 1987) • H2O2 (Holmberg and Hammond 1973, Hillman et. al. 1985 ) • Organic acids (Mashimo et. al. 1985)
•gingival sulcus and periodontal pocket provides the area for growth •mean temperature: Averages about 35ºC Ranges about 30ºC to 38ºC (Haffagee et al 1992) •pH : pH 7.0-8.5 ( Forscher et. at. 1954 , Kleinbers and Hall 1969, Cimasoni 1983) •Oxidation Reduction potential -300 to + 310mv at pH 7.0 (Onisi et. at. 1960, Kenney & Ash 1969)
• Early colonizers (e.g. Streptococci, Actinomyces) use oxygen and lower the redox potential of the environment, which then favours the growth of anaerobic species. Gram +ve sp. use • sugars as an energy source and • saliva as carbon source • The bacteria that predominate in mature plaque are ananerobic and use amino acid and small peptides as energy source.
• Lactate and Formate byproducts of metabolism of Streptococci and Actinomyces and may be used in metabolism of other plaque microorganisms The growth of P.gingivalis is enhanced by metabolic byproducts produced by other microorganisms, such as • succinate from Capnocytophaga ochraceus and • protoheme from Campylobacter rectus
Factor antagonizes For example: • S. sanguis produces H2O2 which inhibits growth of A.actinomycetemcomitans (Hillman et. al. 1985 ) • A.actinomycetemcomitans produces bacteriocins that inhibits S. sanguis (Hammond et. al. 1987, Steven et. al. 1987)
Sources of nutrients available: Mainly 3 sources: diet, host, and other sub gingival species Certain nutrients are: • Vit K analogues (Gibbons and Macdonald 1960) • Certain growth factors like hemin (Evans 1951, Gibbons and Macdonald 1960)
Host as source of nutrients: • Bacterial enzymes that degrade host proteins result in the release of ammonia, which may be used by bacteria as nitrogen source • Hemin iron from the breakdown of host Hb may be important in the metabolism of P.gingivalis • Increase in Steroid hormone are associated with significant increase in the proportions of P.intrmedia found in sub gingival plaque
Clinical significance of plaque
Suprgingival plaque • Microbial aggregations on the tooth surface if prevented from maturing may become compatible with gingival health. • Supragingival plaque if allowed to grow and mature, may induce gingivitis and can lead to the formation of a microenvironment that permits the development of subgingival plaque. • Therefore, supragingival plaque strongly influence the growth, accumulation and pathologic potential of sub gingival plaque, especially in the early stages of gingivitis and periodontitis.
Subgingival plaque • In association with the presence of supragingival plaque, there are inflammatory changes that modify the anatomic relationships of the gingival margin and tooth Surface. • This results in enlarged gingiva, which increases the space for bacterial colonization and also protects bacteria from normal cleansing mechanisms. They derive from GCF. • Many of these microorganisms lack the adherence ability and utilizes plaque bacteria as a means of colonization subgingival area.
conclusion • Dental plaque biofilm cannot be eliminated. However, the pathogenic nature of the dental plaque biofilm can be reduced by reducing the bioburden (total microbial load and different pathogenic isolates within that dental plaque biofilm) and maintaining a normal flora with appropriate oral hygiene methods that include daily brushing,flossing and rinsing with antimicrobial mouthrinses.This can result in the prevention or management of the associated sequelae, including the development of periodontal diseases and possibly the impact of periodontal diseases on specific systemic disorders. JADA, Vol. 137 November 2006.

More Related Content

PPTX
Dental plaque
byDr. Mariyam Momin
 
ODP
Dental Plaque
byDr Sudeep Madhusudan Chaudhari
 
PPTX
Dental plaque formation
byGhadah Sidqi Qumsan
 
PPTX
Plaque
byGanesh Nair
 
PPT
Dental plaque
byParth Thakkar
 
PPTX
Plaque as a Biofilm
byPearl Bhardwaj
 
PPT
19.periodontal microbiology.ppt
byDrNavyadidla
 
PPTX
DENTAL PLAQUE - PART 2 (BIOFILM)
byDr.Malvika Thakur
 
Dental plaque
byDr. Mariyam Momin
 
Dental Plaque
byDr Sudeep Madhusudan Chaudhari
 
Dental plaque formation
byGhadah Sidqi Qumsan
 
Plaque
byGanesh Nair
 
Dental plaque
byParth Thakkar
 
Plaque as a Biofilm
byPearl Bhardwaj
 
19.periodontal microbiology.ppt
byDrNavyadidla
 
DENTAL PLAQUE - PART 2 (BIOFILM)
byDr.Malvika Thakur
 

What's hot

PPT
Dental Calculus
byAbhishek Gakhar
 
PPTX
Dental Plaque
byDr. Anuj S Parihar
 
PPTX
DENTAL PLAQUE - PART 1
byDr.Malvika Thakur
 
PPTX
Minimal Invasive Dentistry
byNabeela Basha
 
PPTX
Modifications of cavity preparations in pediatric dentistry
byKavya Kalapala
 
PPTX
Dentinal hypersensitivity
byNida Sumra
 
PPTX
Development of occlusion
byprincesoni3954
 
PPTX
Defence mechanism of gingiva
byAchi Joshi
 
PDF
Diseases of the Pulp
byDr. Nithin Mathew
 
PPTX
Caries diagnosis
byD Venkatesh Kumar
 
PPTX
Gingival inflammation and features
byNavneet Randhawa
 
PPTX
Clinical features of gingiva
byNadia Dhiman
 
PPTX
CASE HISTORY (1802).pptx
byDEATHRIDERS
 
PPTX
Trauma from occlusion
byNavneet Randhawa
 
PPTX
Periodontal probe
bydebasismitra
 
PPTX
Pulpotomy
bySumeet Vincent Tigga
 
PPTX
CARIES VACCINE
byDivya Gaur
 
PPTX
Pulpotomy
byDr. Roshni Maurya
 
PPTX
ANUG
byKingshuk Mazumder
 
PPTX
Host Modulation Therapy
byDr.Shraddha Kode
 
Dental Calculus
byAbhishek Gakhar
 
Dental Plaque
byDr. Anuj S Parihar
 
DENTAL PLAQUE - PART 1
byDr.Malvika Thakur
 
Minimal Invasive Dentistry
byNabeela Basha
 
Modifications of cavity preparations in pediatric dentistry
byKavya Kalapala
 
Dentinal hypersensitivity
byNida Sumra
 
Development of occlusion
byprincesoni3954
 
Defence mechanism of gingiva
byAchi Joshi
 
Diseases of the Pulp
byDr. Nithin Mathew
 
Caries diagnosis
byD Venkatesh Kumar
 
Gingival inflammation and features
byNavneet Randhawa
 
Clinical features of gingiva
byNadia Dhiman
 
CASE HISTORY (1802).pptx
byDEATHRIDERS
 
Trauma from occlusion
byNavneet Randhawa
 
Periodontal probe
bydebasismitra
 
Pulpotomy
bySumeet Vincent Tigga
 
CARIES VACCINE
byDivya Gaur
 
Pulpotomy
byDr. Roshni Maurya
 
ANUG
byKingshuk Mazumder
 
Host Modulation Therapy
byDr.Shraddha Kode
 

Viewers also liked

PPTX
Stainless steel crowns in Pediatric Dentistry
byRajesh Bariker
 
PPT
Gingival pigmentation
byNida Sumra
 
PPTX
Preventive Dentistry and Early Caries Detection
byghidalawand
 
PPTX
Odontoma (Doctor Faris Alabeedi MSc, MMedSc, PgDip, BDS.)
byDoctor Faris Alabeedi
 
PPT
1 enamel dentin pulp
byashish1801
 
PPTX
Dental plaque 1
byNitika Jain
 
PPTX
maxillary nerve block
byPriyanka Chowdhary
 
PDF
TMJ diagnosis
byIAU Dent
 
PPTX
Oral Surgery in Patients on Anticoagulant Therapy
byVarun Mittal
 
PPTX
Dental plaque part2
byDr. Roshni Maurya
 
PPTX
1.phonetics in cd
bydr zarir ruttonji
 
PPT
Retainers/ dental implant courses
byIndian dental academy
 
PPTX
Hepatitis B
byDrAmrita Rastogi
 
Stainless steel crowns in Pediatric Dentistry
byRajesh Bariker
 
Gingival pigmentation
byNida Sumra
 
Preventive Dentistry and Early Caries Detection
byghidalawand
 
Odontoma (Doctor Faris Alabeedi MSc, MMedSc, PgDip, BDS.)
byDoctor Faris Alabeedi
 
1 enamel dentin pulp
byashish1801
 
Dental plaque 1
byNitika Jain
 
maxillary nerve block
byPriyanka Chowdhary
 
TMJ diagnosis
byIAU Dent
 
Oral Surgery in Patients on Anticoagulant Therapy
byVarun Mittal
 
Dental plaque part2
byDr. Roshni Maurya
 
1.phonetics in cd
bydr zarir ruttonji
 
Retainers/ dental implant courses
byIndian dental academy
 
Hepatitis B
byDrAmrita Rastogi
 

Similar to Dental plaque

PPTX
Dental plaque
bySucheta Prabhu Matondkar
 
PPTX
Dental Plaque by Dr. Ishu.pptx
byDr. ISHU SINGLA
 
PPTX
DENTAL PLAQUE PART 1 DR MANISHA CHOUBAY
byManisha Choubey
 
PPTX
dental_plaque.pptx
bymalti19
 
PPTX
Dental plaque.pptx
byDentalYoutube
 
PPTX
Dental plaque
byEnas Elgendy
 
PPTX
2 DENTAL PLAQUE.pptx
byDiptiPatil52
 
PPTX
Plaque in health and disease
byDr.SANDIP Bhattacharyya
 
PPTX
2. DENTAL PLAQUE.pptx
bySherinJames17
 
PPTX
Dental Plaque Biofilm byDr. Mohammed.pptx
byMohammed kareem
 
PPTX
plaque as a biofilm power point in periodontics
byTintumadonajoy
 
PPTX
PERIODONTAL MICROBIOLOGY.pptx
byIbrarHumayun
 
PPTX
DENTAL PLAQUE.pptx
byDivjotNarula
 
PPT
5 220224215404
byPhixonHastingsPv
 
PDF
38 Dental Plaque bbbbb. .pdf
bympanara32
 
PPTX
DENTAL PLAQUE AND ITS IMPORTANCE IN ORAL HEALTH
byiqradildar2
 
PPTX
chapter one copy.pptx
byNadiirMahamoud
 
PPTX
Dental-Plaque-1-202110221511350.pptx
byAnantaAggarwal1
 
PPTX
38.Dental Plaque Periodontology .pptx
bympanara32
 
PPT
5.11&amp; 12.11
byPhixonHastingsPv
 
Dental plaque
bySucheta Prabhu Matondkar
 
Dental Plaque by Dr. Ishu.pptx
byDr. ISHU SINGLA
 
DENTAL PLAQUE PART 1 DR MANISHA CHOUBAY
byManisha Choubey
 
dental_plaque.pptx
bymalti19
 
Dental plaque.pptx
byDentalYoutube
 
Dental plaque
byEnas Elgendy
 
2 DENTAL PLAQUE.pptx
byDiptiPatil52
 
Plaque in health and disease
byDr.SANDIP Bhattacharyya
 
2. DENTAL PLAQUE.pptx
bySherinJames17
 
Dental Plaque Biofilm byDr. Mohammed.pptx
byMohammed kareem
 
plaque as a biofilm power point in periodontics
byTintumadonajoy
 
PERIODONTAL MICROBIOLOGY.pptx
byIbrarHumayun
 
DENTAL PLAQUE.pptx
byDivjotNarula
 
5 220224215404
byPhixonHastingsPv
 
38 Dental Plaque bbbbb. .pdf
bympanara32
 
DENTAL PLAQUE AND ITS IMPORTANCE IN ORAL HEALTH
byiqradildar2
 
chapter one copy.pptx
byNadiirMahamoud
 
Dental-Plaque-1-202110221511350.pptx
byAnantaAggarwal1
 
38.Dental Plaque Periodontology .pptx
bympanara32
 
5.11&amp; 12.11
byPhixonHastingsPv
 

More from Dr. Roshni Maurya

PPTX
Apexification with mta
byDr. Roshni Maurya
 
PPTX
Fixed habit breaking appliance case 1 blue grass appliance
byDr. Roshni Maurya
 
PPTX
Cross bite correction
byDr. Roshni Maurya
 
PPTX
Surgical extraction of supernumerary tooth
byDr. Roshni Maurya
 
PPTX
Reatthachemnt of fractured central incisor
byDr. Roshni Maurya
 
PPTX
Pulpectomy case 2
byDr. Roshni Maurya
 
PPTX
Pulpectomy with ss crown case 3
byDr. Roshni Maurya
 
PPTX
Pulpectomy with ss crown case 2
byDr. Roshni Maurya
 
PPTX
Oligodontia
byDr. Roshni Maurya
 
PPTX
Pulpectomy case 1
byDr. Roshni Maurya
 
PPTX
Pulpectomy with ss crown case 1
byDr. Roshni Maurya
 
PPTX
Fracture of anterior teeth
byDr. Roshni Maurya
 
PPTX
Extra oral sinus
byDr. Roshni Maurya
 
PPTX
Orthodontic extrusion of impacted tooth
byDr. Roshni Maurya
 
PPTX
Reattachement of tooth
byDr. Roshni Maurya
 
PPTX
Surgical extraction of supernumerary tooth
byDr. Roshni Maurya
 
PPTX
Orthodontic extrusion
byDr. Roshni Maurya
 
PPTX
Impacted supernumerary teeth
byDr. Roshni Maurya
 
PPTX
Surgical extraction of dilacerated tooth
byDr. Roshni Maurya
 
PPTX
Biological crown
byDr. Roshni Maurya
 
Apexification with mta
byDr. Roshni Maurya
 
Fixed habit breaking appliance case 1 blue grass appliance
byDr. Roshni Maurya
 
Cross bite correction
byDr. Roshni Maurya
 
Surgical extraction of supernumerary tooth
byDr. Roshni Maurya
 
Reatthachemnt of fractured central incisor
byDr. Roshni Maurya
 
Pulpectomy case 2
byDr. Roshni Maurya
 
Pulpectomy with ss crown case 3
byDr. Roshni Maurya
 
Pulpectomy with ss crown case 2
byDr. Roshni Maurya
 
Oligodontia
byDr. Roshni Maurya
 
Pulpectomy case 1
byDr. Roshni Maurya
 
Pulpectomy with ss crown case 1
byDr. Roshni Maurya
 
Fracture of anterior teeth
byDr. Roshni Maurya
 
Extra oral sinus
byDr. Roshni Maurya
 
Orthodontic extrusion of impacted tooth
byDr. Roshni Maurya
 
Reattachement of tooth
byDr. Roshni Maurya
 
Surgical extraction of supernumerary tooth
byDr. Roshni Maurya
 
Orthodontic extrusion
byDr. Roshni Maurya
 
Impacted supernumerary teeth
byDr. Roshni Maurya
 
Surgical extraction of dilacerated tooth
byDr. Roshni Maurya
 
Biological crown
byDr. Roshni Maurya
 

Recently uploaded

PDF
Christmas Cooking Feast/Christmas Cooking Feast
byLahcen Idar
 
PPTX
Metformin safety during pregnancy in women with gestational diabetes mellitus
byDr. Om J Lakhani
 
PPT
Drinking water, also known as potable water, is water that is safe to drink o...
byDrShantikumarLaishra1
 
PPTX
Health Education: Meaning, Principles, Scope and Importance in Pharmacy
byBindu Nepal
 
PPTX
neoplasia prentation.pptx for pathology
bydrdaaha2
 
PPT
Introduction to Medicinal Chemistry and data therin
byChatgptgoa
 
PPTX
unit 02 urinary system.by zahid abbasi.pptx
byzahidali446434
 
PPTX
Feng_2023_Journal_Club_Presentation.pptx
byishitasingh0610
 
PPTX
NUT207 PPT ABOUT Patient or client dietition ethics
bynut2024uni
 
PPTX
Understanding Medication_Administration.pptx
bysofiasofi191980
 
PDF
SPA_L3 Core Glossary_2021.pdf healthcare
byaliciaquijanotorres1
 
PPTX
CGH RADIATION HAZARDS THE BASIC FACTS YOU SHOULD KNOW
byMuhammad Akhtar
 
PDF
3 Diabetes complications €& »?!!&&&&.pdf
byy2dyjdrrjk
 
PPTX
Liver - spleen - Pancreas- biliary surgery presentation for nurses
byShacharLaks1
 
PDF
Why Regular Blood Pressure, Cholesterol & Diabetes Monitoring Is Critical for...
byVighnahartaHeartCare
 
PPTX
Modular Operating Room Layout & Specifications
byGaddiel Industries
 
PPTX
IUGR_Management_Presentation-1.pptx for BSc students
byaddis18
 
PPTX
Congenital Adrenal Hyperplasia (CAH) and SIADH in Neonates
bylidulidiyasolomon
 
PDF
N8N Automation for Healthcare: Smarter Patient Intake & Scheduling in 2026.
byVirtual Nexgen Solutions
 
PDF
Common Eye Diseases and Symptoms - Dr. Chameen Sams Australia
byDr Chameen Samarawickrama
 
Christmas Cooking Feast/Christmas Cooking Feast
byLahcen Idar
 
Metformin safety during pregnancy in women with gestational diabetes mellitus
byDr. Om J Lakhani
 
Drinking water, also known as potable water, is water that is safe to drink o...
byDrShantikumarLaishra1
 
Health Education: Meaning, Principles, Scope and Importance in Pharmacy
byBindu Nepal
 
neoplasia prentation.pptx for pathology
bydrdaaha2
 
Introduction to Medicinal Chemistry and data therin
byChatgptgoa
 
unit 02 urinary system.by zahid abbasi.pptx
byzahidali446434
 
Feng_2023_Journal_Club_Presentation.pptx
byishitasingh0610
 
NUT207 PPT ABOUT Patient or client dietition ethics
bynut2024uni
 
Understanding Medication_Administration.pptx
bysofiasofi191980
 
SPA_L3 Core Glossary_2021.pdf healthcare
byaliciaquijanotorres1
 
CGH RADIATION HAZARDS THE BASIC FACTS YOU SHOULD KNOW
byMuhammad Akhtar
 
3 Diabetes complications €& »?!!&&&&.pdf
byy2dyjdrrjk
 
Liver - spleen - Pancreas- biliary surgery presentation for nurses
byShacharLaks1
 
Why Regular Blood Pressure, Cholesterol & Diabetes Monitoring Is Critical for...
byVighnahartaHeartCare
 
Modular Operating Room Layout & Specifications
byGaddiel Industries
 
IUGR_Management_Presentation-1.pptx for BSc students
byaddis18
 
Congenital Adrenal Hyperplasia (CAH) and SIADH in Neonates
bylidulidiyasolomon
 
N8N Automation for Healthcare: Smarter Patient Intake & Scheduling in 2026.
byVirtual Nexgen Solutions
 
Common Eye Diseases and Symptoms - Dr. Chameen Sams Australia
byDr Chameen Samarawickrama
 

Dental plaque

  • 1.
    PRESENTED BY ROSHNI MAURYA 2NDYR PG STUDENT DENTAL PLAQUE
  • 2.
    CONTENTS • Introduction • Definition •History • Composition • Classification/types of dental plaque • Formation/development • Growth dynamics of the dental plaque • Structural and physiological properties of dental plaque • Clinical significance of the plaque ( what makes plaque pathogenic?) • Conclusion
  • 3.
    INTRODUCTION : • Dentalplaque is the community of microorganisms found on a tooth surface as a biofilm, embedded in a matrix of polymers of host and bacterial origin • Plaque is derived from French word “PLAQUER” Which means “TO PLATE”
  • 4.
    • WHO DEFINITION:plaque is a specific but highly variable structural entity resulting from colonization of microorganisms on tooth surfaces, restorations and other parts of oral cavity and consists of salivary components like mucin, desquamated epithelial cells, debris and microorgansims all embedded in a gelatinous extracellular matrix. • GLICKMAN: It is soft amorphous granular deposits which accumulate on surface of teeth, dental restoration and dental calculus. (Clinical periodontology 3rd ed.)
  • 5.
    Definition • A highlyvariable entity resulting from the colonization and growth of m/o on the surfaces of the teeth and oral soft tissues and consisting of a number of microbial species and strains embedded in an extracellular matrix. American Dental Association • WH Boven, 1976. Dental plaque is defined clinically as a structured, resilient, yellow-grayish substance that adheres tenaciously to the intraoral hard surfaces, including removable and fixed restoration. (Carrnaza 10th ed.) • PD Marsh, 2004. Dental plaque can be defined as the diverse community of micro-organisms found on the tooth surface as a biofilm, embedded in an extracellular matrix of polymers of host and microbial origin.
  • 6.
    • Dental plaquemust be differentiated from other tooth deposits, like materia alba and calculus. • Materia Alba refers to soft accumulations of bacteria and tissue cells that lack the organized structure of dental plaque. • Calculus is hard deposits that form by mineralization of dental plaque and is generally covered by a layer of unmineralised plaque. 6
  • 7.
    • Material alba• Calculus 7
  • 8.
  • 9.
    CATE- GORY TOOTH DEPOSIT DESCRIPITION DERIVATION NON- MINER AL- IZED ACQUIRED PELLICLE Translucent, homogenous,thin, ultra structured film covering and adherent to the surfaces of the teeth, restorations, calculus, and other surfaces of the oral cavity Supra gingival :saliva Sub gingival :GCF MICRO- BIAL- PLAQUE Dense organized bacterial system embedded in an inter microbial matrix that adhere closely to the teeth, calculus, and other surfaces of the oral cavity Colonization of oral micro-organisms MATERIA ALBA Loosely adherent, ultra structured, white or grayish, white mass of oral debris and bacteria that lies over bacterial plaque Vigorous rinsing and water irrigation can remove materia alba Incidental accumulation FOOD DEBRIS Unstructured, loosely attached particulate matter self- cleansing activity of tongue and saliva and rinsing vigorously remove debris Food retention following eating MINE RAL- IZED SUPRA- GINGIVAL CALCULUS Calcified bacterial plaque: hard tenacious mass that forms on the clinical crown of the natural teeth & on dentures and other appliances Occurs coronal to the margin of gingiva ; is covered with bacterial plaque Plaque mineralization Source of minerals is saliva SUB- GINGIVAL CALCULUS Occurs apical to the margin of gingiva ; is covered with bacterial plaque Source of minerals is GCF
  • 10.
  • 11.
    • The descriptiveterm gelatinous microbial plaque was first introduced by J.C William and G.V Black in 1898 to describe microbial colonies on tooth surfaces. • More recently, Black’s terminology has been shortened to the term ‘Plaque’ by Wild (1941) and its usage has been restricted to denote only those deposits that are predominantly microbial in nature.
  • 12.
  • 13.
    DENTAL PLAQUE SUPRA GINGIVAL PLAQUE SUBGINGIVAL PLAQUE TOOTH ATTACHED PLAQUE UN- ATTACHED PLAQUE PLAQUE ATTACHED TO EPITHELIUM CORONAL MARGINAL
  • 14.
  • 15.
    CHARACTE -RISTICS SUPRAGINGIVAL SUBGINGIVAL LOCATION CoronalMG Apical MG ORIGIN Salivary glycoprotein down growth bact from supra gingival plaque DISTRIBU- TION Starts proximal surface and other protected areas Heaviest collection on areas not cleaned daily by patient Cervical third , esp. facial and lingual Mandibular molars Proximal surfaces Pits and fissures plaque Shallow pocket Attached plaque covers calculus Unattached plaque extends to the periodontal attachment
  • 16.
    ADHES- ION Firmly attached toacquired pellicle Surface bacteria (unattached ) loose: washed away by saliva Adhere to tooth surface subgingival pellicle  calculus RETEN- TION Rough surface teeth restoration , malpositioned or carious teeth Pocket hold plaque against tooth and overhanging margins SHAPE AND SIZE Friction of tongue lips cheeks , cervical area Thickness: thicker at the cervical end and on proximal surfaces Healthy gingival: thin plaque ,15 to 20 cells thick Chronic gingivitis: thick plaque,100 to 300 cells thick Molded by pocket wall, follows the form created by subgingival calculus
  • 17.
    MICRO- ORGANISM Early plaque:formsGram+ve cocci Older plaque( 3 to 4 days) increased number of filaments and fusiforms 4 to 9 days undistributed: more complex flora with rods, filamentous forms 7 to 12 days: vibrios, spirochetes, more gram org Anaerobic population Gram-neg , motile spirochete and rods SOURCE OF NOURISH- MENT Saliva ingested food Tissue fluid (sulcular fluid), exudates, leucocytes
  • 18.
    STRUCTURE Densely packedthree layers 1. tooth surface attached plaque: many gram positive rods and cocci 2. unattached plaque in middle: many gram neg, motile forms, spirochetes, leukocytes 3. epithelium attached plaque : gram neg, motile forms predominate, many leukocytes migrate through epithelium
  • 19.
    Structure: • Early studies:plaque appears as a compacted consortium of microorganisms Confocal laser scanning microscopy has revealed Supra gingival plaque can have a • structured architecture polymer containing channel or pores have been observed that link the plaque/oral environment interface to the tooth surface ( Wood et al 2000,Auschillet al 2001,Zaura Arite et al 2001)
  • 20.
    • the useof live /dead stains has indicated that bacterial vitality varies throughout the biofilm, with the most viable bacteria present in the central part of plaque , and lining the voids and channels (Auschill et al 2001) • this more open architecture should enable the molecule to readily move in and out of the plaque , but the presence of a matrix comprised of a diverge range of exo polymers creates a complex environment for accurately predicting the penetration and distribution of molecules with in plaque (Robinson et al 1997,Thurnheer et al 2003,Marcotte et al 2004).
  • 21.
    Sub gingival plaque: Histologicalsections of human sub gingival plaque viewed by Conventional light microscopy suggested that: • a complex organization of attached microorganisms in which there can exist distinct tooth associated and epithelial associated biofilms, with the possibility of a less dense zone of organisms between the two (Socransky & Haffajee 2002)
  • 22.
    • Between subgingival plaque and the tooth an electron dense organic material is interposed , termed as cuticle. • This cuticle probably contains the remains of the epithelial attachment lamina originally connecting the junctional epithelium to the tooth , with the additional of material deposited from the gingival exudates (Frank & Cimasoni 1970, Lie & Selvig 1975, Eide et al 1983)
  • 23.
    • It hasbeen suggested that cuticle represents a secretory product of the adjacent epithelial cells. (Schroeder & Lisgarten 1977)
  • 24.
  • 25.
    COMPOSITION OF PLAQUE: COMPOSEDmainly of • Microorganisms , • Intermicrobial matrix (a) Bacterial portion: • 70 to 80 % of total solid plaque volume. • 1 g (WET WT)contains approx 1011 bacteria.
  • 26.
    (B)Intermicrobial Matrix • thematerial present between the bacteria in the dental plaque is called the intermicrobial matrix. • accounts for approx 25% of plaque volume.
  • 27.
    Three sources maycontribute to the intermicrobial matrix: •the plaque microorganisms •the saliva •gingival exudates Degenerating or dead bacteria may also contribute to inter microbial matrix.
  • 28.
    Organic and inorganicSOLIDS approx 20 % and water • WATER 70 to 80 % of solid matter, which higher in sub gingival plaque than supra gingival. INORGANIC: • Main Calcium and Phosphorus(mostly) magnesium, sodium fluoride(in small amount, higher than saliva) • CALCIUM AND PHOSPHATE more on lingual surface of anterior teeth. ORGANIC: • Surrounds microorganisms contains carbohydrates, proteins and lipids Inter bacterial matrix:
  • 29.
    CARBOHYDRATES: Fructans (Levans) : •synthesized in plaque from dietary sucrose • provide a storage of energy which may be utilized by the microorganisms in time of low sugar supply Glucans: also synthesize from sucrose & of two types: • Dextran: serve as energy storage • Mutan: acts primarily as a skeleton in the matrix in much the same way as collagen stabilizes the intercellular substances of connective tissue.
  • 30.
    • A fibrillarcomponent is seen in the matrix between gram+ve cocci • In parts of the plaque with the presence of gram –ve organisms, the intermicrobial matrix is regularly characterized by the presence of small vesicles surrounded by trilaminar membrane, which is similar in structure to that of the outer envelope of the cell wall of gram -ve microorganisms. • Such vesicles may contain endotoxin and proteolytic enzymes, may also be involved in adherence between bacteria ( hofstad et al 1972, grenier and mayrand 1987) • In other regions it appears granular or homogenous Intermicrobial matrix in plaque varies considerably from region to region
  • 31.
    Non bacterial microorganismsthat are found in plaque include • mycoplasma species • yeast • protozoa, and • viruses The micro organisms exist with in a intracellular matrix that also contains • a few host cells, such as epithelial cells , • macrophages and • leukocytes
  • 32.
    Selected Bacterial SpeciesFound In Dental Plaque: Bacteria Facultative Anerobic Gram +ve Strep.mutans Strep.sanguis A.viscosus Gram -ve A.actinomycetemcomitans Capnocytophypa sp. Ekinella corrodens P.Gingivalis F.nucleatum P.intermedia B.forsythus C.rectus Spirochetes  T.denticola
  • 33.
    PROTINES: • Supra gingivalplaque contains proteins from saliva. • Sub gingival contains Albumin – cervical fluid and gingival exudates. LIPIDS: • lipopolysaccharides, endotoxins from gram negative bacteria.
  • 34.
    PLAQUE AS ABIOFILM •As the bacteria attach to a surface and to each other, they cluster together to form sessile, mushroom-shaped microcolonies that are attached to the surface at a narrow base. •Each microcolony is a tiny, independent community containing thousands of compatible bacteria. •Different microcolonies may contain different combinations of bacterial species.
  • 35.
    •Bacteria in thecenter of a microcolony may live in a strict anaerobic environment, while other bacteria at the edges of the fluid channels may live in an aerobic environment. •Thus, the biofilm structure provides a range of customized living environments (with differing pHs, nutrient availability, and oxygen concentrations) within which bacteria with different physiological needs can survive.
  • 36.
    •The extracellular slimelayer is a protective barrier that surrounds the mushroomshaped bacterial microcolonies. •The slime layer protects the bacterial microcolonies from antibiotics, antimicrobials, and host defense mechanisms. •A series of fluid channels penetrates the extracellular slime layer.
  • 37.
    • These fluidchannels provide nutrients and oxygen for the bacterial micro colonies and facilitate movement of bacterial metabolites, waste products, and enzymes within the biofilm structure. • Each bacterial microcolony uses chemical signals to create a primitive communication system used to communicate with other bacterial microcolonies
  • 38.
    Quorum sensing Etiology andPathogenesis of Periodontal Disease, 2010) • The regulation of bacterial gene expression in response to changes in cell density is known as quorum sensing. These bacteria then proliferate and communicate by signals to each other (Okuda et al. 2004). • In order to maintain the ecosystem, various anaerobes, anchor to each other by forming aggregated bacterial masses (Kigure et al. 1995; Okuda et al. 2004). • Quorum-sensing bacteria synthesize and secrete extracellular signaling molecules called autoinducers, which accumulate in the environment as the population increases (Okuda et al. 2004).
  • 39.
    • Gram-positive bacteriagenerally communicate via small diffusible Peptides, while many gram-negative bacteria secrete Acyl Homoserine Lactones (AHLs) (Whitehead et al. 2001), which vary in structure depending on the species of bacteria that produce them. • Another system involves the synthesis of autoinducer- 2 is LuxS (Federle and Bassler 2003; Winzer et al. 2003). This system may be involved in cross-communication among both gram-positive and gram-negative bacteria. (Marsh 2004).
  • 40.
  • 43.
    stages of formationin dental plaque 1. Formation of pellicle 2. Attachment of bacteria to pellicle 3. Bacterial multiplication and colonization 4. Plaque growth and maturation 5. Matrix formation.
  • 44.
    a) PELLICLE FORMATION: •formed by adsorption of proteins on tooth surface • composed of glycoprotein from saliva , adsorbed by hydroxyapatite • Have negative charged phosphate --interact +ve charge salivary crevicular macromolecules • This adsorbed material becomes highly insoluble coating over teeth, calculus, and restoration, complete and partial denture. DERIVATION: Supra gingival from saliva Sub gingival from gingival sulcus. It is translucent, homogenous, thin ultra structured film covering adherent tooth surface.
  • 45.
    SIGNIFICANCE OF PELLICLE: •PROTECTIVE: provide barrier against acids thus may reduce dental caries attack. • LUBRICATION: keep surface moist prevent drying. • NIDUS FOR BACTERIA: Plaque formation by adherence of microorganisms. • ATTACHEMENT OF CALCULUS: A mode of calculus attachment in acquired pellicle.
  • 46.
    b) BACTERIAL ATTACHEMENT TOPELLICLE: Initial attachment by selective adherence of specific bacteria from oral environment Small colonies Layers Microorganisms form in layer as grow and multiply When colony sizes increases it unite to form continuous plaque bacterial mass Organisms of first few hours are gram positive cocci, rods
  • 47.
    c) MATRIX FORMATION: •Intermicrobial substances derived mainly from saliva for supra gingival plaque and • gingival sulcus fluid and exudates for sub gingival plaque • other product produced by certain bacteria, dietary source polysaccharide are sticky contribute to adhesion of plaque to teeth.
  • 48.
    CHANGE IN PLAQUEMICROORGANISMS DAY 1 TO 2 gram +ve Cocci, Streptococci (dominate), Strepto mutans, Strepto sanguis DAY 2 TO 4 Cocci still dominate , increase gram+ve filamentous form, slender rods , gradually filamentous forms replaces cocci. DAY 4 TO 7 Filaments increases in numbers, and a more mixed flora begins to appear with rods, filamentous forms and Fusobacteria .  Plaque near margin thickens and develops a more mature flora with gram neg spirochetes and vibros .  As plaque spreads coronally, the new plaque has the characteristic coccal forms
  • 49.
    DAY 7 TO14 Vibros and spirochetes appear. No. of WBC increases , as plaque mature and thickens more,gram+ve anaerbic org appear “during this period sign of inflammation on gingiva occurs” DAY 14 TO 21 Vibros + spirochetes prevalent along with cocci and filamentous The densly packed filamentous organisms arrange themselves perpendicular to the tooth surface in a palisade “gingivitis evident clinically”.
  • 50.
    Plaque formation atultrastructual level 1. Formation of pellicle on the tooth surface 2. Initial adhesion and attachment of bacteria Phase 1: Transport to the surface Phase 2: Initial adhesion Phase 3: Attachment Phase 4: Colonization of surface and biofilm formation 3. Colonization and plaque maturation
  • 51.
    Formation of pellicle •All surface of oral cavity (both hard and soft) are coated with a pellicle. • With in nanoseconds after a vigorously polishing the teeth, a thin layer, called acquired pellicle, covers the tooth surface. • Acquired pellicle term is misleading as it implies that bacteria can colonize only when pellicle is in place for few hours. • Bacteria can be part of early deposit, within seconds after prophylaxis. • Pellicle formation involves selective adsorption of macromolecules (eg glycoprotein) to apatite surface.
  • 52.
    Forces involved inenamel pellicle formation: 1.Electrostatic forces (between hydorxyapatite surfaces which has negatively charged phosphate group, that interacts with opposite charged groups in the salivary macromolecules). 2.van der Waals force 3.Hydrostatic force (Detachment of adhering bacteria might occur through cohesive failure in conditioning film between bacteria and surface ,i.e. pellicle)
  • 53.
    Initial Adhesion &Attachment of Bacteria Phase 1: Transport to the surface This include transport of bacteria to the tooth surface. Random contact occurs through: 1. Brownian motion (avg displacement of 40 µm/hr). 2. Through sedimentation of microorganisms. 3. Through liquid flow. 4. Through active bacterial movement (chemotactic movement).
  • 54.
    PHASE 2: INITIALADHESION • The second stage results in an initial, reversible adhesion of bacterium, initiated by interaction between bacterium and the surface, from a certain distance (50 nm), through long range and short range forces, including van der Waals attractive and electrostatic repulsive forces.
  • 55.
    Derjaguin, Landau, Verweyand Overbeek (DLVO) postulated that, • above a separation of 1 nm, the summation of vander wal (attaractive; GA) and electrostatic forces (repulsive; GE) describes total long range interaction. • If a particle reaches the primary minimum (<1nm from the surface), a group of short range forces (eg hydrogen bonding, ionic pair formation, steric interaction) dominates the strength of adhesion.
  • 56.
    PHASE 3: ATTACHMENT •After initial adhesion, a firm anchorage will be established by specific interactions (covalent, ionic, or hydrogen bonding). • This follows direct contact or bridging true extra cellular filamentous appendages (with length up to 10nm). • On a rough surface, bacteria are better protected against shear forces so that a change from reversible to irreversible bonding occurs more easily and more frequently.
  • 57.
    • Streptococci (mainlyS. sanguis), bind to acidic proline-rich- proteins and other receptors in pellicle as α-amylase and sialic acid. • Actinomyces can also function as primary colonizers: eg A. viscosus possesses fimbrae that contain adhesins that specifically bind to proline-rich proteins of dental pellicle • A. viscosus reognises cryptic segments ( with lock &key mech.) of proline rich proteins, which are only available in adsorbed molecules. ( Mergenhagen et al 1987)
  • 58.
    COLONIZATION & PLAQUEMATURATION • When the firmly attached microorganisms start growing and the newly formed bacterial clusters remain attached, micro colonies or a biofilm can develop. • From this stage Intrabacterial connections occur • at least 18 genera from the oral cavity have shown some form of co-aggregation (cell-to-cell recognition of genetically distinct partner cell types).
  • 59.
    • All oralbacteria possess surface molecules that foster some type of cell to cell interaction. • This occurs primarily through the highly specific stereo chemical interaction of protein and carbohydrate molecules located on bacterial cell surfaces, in addition to the less specific interactions resulting from hydrophobic, electrostatic and van der waals forces. • Coaggregation is mediated by lectin-like adhesion and can be inhibited by lactose and other galactosides
  • 60.
    Interactions of secondarycolonizers with early colonizers include the coaggregation of a. Fusobacterium nucleatum with Streptococcus sanguis b. Prevotella loescheii with Actinomyces viscosus. c. Capnocytophaga ochraceus with A. viscosus. Coaggregation exist between a. Different gram positive species. b. Gram positive and gram negative species c. Different gram negative species (predominate in later stage) eg F. nucleatum with P. gingivalis or T. denticola. Special examples of coaggregations are a. “Corncob” formation b. “Test-tube brush” formation. c. Probiotics.
  • 61.
    • “Corncob” formationhave been observed between rod-shaped bacterial cells eg. Bacterionema matruchotii or Actinomyces sp. that forms inner core of the structure and coccal cells eg. Streptococci or P. gingivalis that attach along the surface of the rod shaped cells. • “Test-tube brush” composed of filamentous bacteria to which gram negative rods adhere. “Probiotics” : “literally meaning ‘for life” WHO defined it as live microorganisms which when administered in adequate amounts confer a health benefit on the host.
  • 62.
    BENEFITS OF COMMUNITYLIFE STYLE to micro organisms: • A broad habitat range for growth. e,.g. oxygen consuming sp. create environmental conditions suitable for obligate anaerobes • A more efficient metabolism e.g. complex hast macromolecule can only be degraded by consortia of oral bacteria. • Increased resistance to stress and antimicrobial agents • Enhanced virulence ( pathogenic synergism) {Caldwell et al 1997, Shapiro ,1998, Marsh and Bowen,2000}
  • 63.
    Relationship of SpecificMicroorganisms to Periodontal Diseases • Our understanding of the relationship between the microorganisms found in dental plaque and the common dental disease of periodontitis has undergone numerous phases historically • Early in the 19th century, it was felt that, like the situation with diseases such as tuberculosis, a specific bacterial species was responsible for the disease processes. • The criteria by which a given bacterial species was associated with disease historically has been through the application of Koch's Postulates.
  • 64.
    These criteria weredeveloped by Robert Koch in the late 1800's. The criteria are as follows: • A specific organism can always be found in association with a given disease. • The organism can be isolated and grown in pure culture in the laboratory. • The pure culture will produce the disease when inoculated into a susceptible animal. • It is possible to recover the organism in pure culture from the experimentally infected animal.
  • 65.
    CURRENT HYPOTHESES ONTHE ROLE OF PLAQUE BACTERIA IN THE ETIOLOGY OF DENTAL DISEASES • Non-specific plaque hypothesis • Specific plaque hypothesis • Ecological plaque hypothesis
  • 66.
    • Both thePlaque and Non-plaque hypothesis were delineated in 1976 by Walter Loesche, a researcher at the University of Michigan. • According to non-specific plaque hypothesis periodontal disease results from the “elaboration of noxious products by the entire plaque flora”. • Specific plaque hypothesis states that “only certain plaque is pathogenic, and its pathogenicity depends on the presence of or increase in specific microrganisms”. For example role of Aactinobacillus actinomycetemcomitans in aggressive periodontitis. Thus plaque harboring specific pathogens results in a periodontal disease because these organisms produce substances that mediate the destruction of host tissues
  • 67.
    Ecological plaque hypothesis: (ByMarsh and Bradshaw; 1997) • Disease results from shifts in the balance of the resident plaque microflora. • A change in the nutrient status of a pocket or chemical and physical changes to the habitat are thus considered the primary cause for the overgrowth by pathogens • Disease could be controlled not only by targeting putative pathogens but also by interfering with the factors responsible for driving the deleterious shifts in the microflora as by reducing GCF rate , or the site could be made less anaerobic by use of redox agents
  • 69.
    Growth dynamics ofdental plaque
  • 70.
    Ultra structural aspects: •Important changes in the plaque growth rate can be detected within first 24 hours. • During the first 2 to 8 hour, the adhering pioneering streptococci saturate the salivary pellicular binding sites and thus cover 3% to 30% of enamel surface. • Instead of steady growth during the next 20 hrs,a short period of rapid growth for 4 to 6 hr (Loesche suggested it as generation time) • After 1 day, the term biofilm is fully deserved -because organization takes place within it.
  • 71.
    • As bacterialdensities approach approximately 2- 6 million bacteria/mm2 on enamel surface, a marked increase in growth rate can be observed to 32 million bacteria/mm2 (doubling in 3 to 4 hrs.) • This occurs due to multiplication of already adhering microorganisms rather than by new colonizers. • Thickness of plaque increases slowly with time, increasing to 20 to 30 µm after 3 days
  • 72.
    • During thefirst 24 hr, plaque growth is negligible from a clinical view point (<3% coverage of vestibular tooth surface, an amount that is clinically almost undetectable). • During the following 3 days, plaque growth increases at a rapid rate, then slows down from that point onward. • After 4 days, on average, 30 % of total tooth crown area will be covered with plaque. • There is ecologic shift within biofilm, with transition from early aerobic environment characterized by gram positive facultative species to a highly oxygen deprived environment in which gram-negative anaerobic microorganisms predominate. • During night, plaque growth rate is reduced by about 50%. This may be explained from the fact that supra gingival-plaque obtains its nutrients mainly from the saliva Clinical Aspects: Supra Gingival Plaque Formation:
  • 73.
    Experimental gingivitis model •From day 0 on, when mechanical plaque control was stopped, plaque will slowly form on the teeth. • With time the plaque composition changes, with a shift to more gram negative species and more rods, filaments and from day 7 on spirals and spirochetes. • From day 3 on, the first symptoms of gingival inflammation become visible. • When proper plaque control is reestablished, the plaque composition returns to the initial situation and symptoms of gingivitis disappear
  • 74.
    Topography of supragingivalplaque Early plaque formation on teeth follows a typical topographic pattern, with initial growth along the gingival margin and from the inter dental spaces (areas protected against shear forces) to extend further in coronal direction. Early plaque formation on surface irregularities of teeth
  • 75.
    Surface micro roughness Smallplastic strip divided in half (a rough region, average roughness Ra 2.0µm, located mesially, and a smooth region Ra 0.1µm, located distally) was glued to the central upper incisors of a patient who refrained from oral hygiene for 3 days Disclosing agent used was : 0.5% neutral red
  • 76.
    SMOOTH REGION ROUGH PART Afterremoval, the strip was cut in small slices for microscopic evaluation Rough part contains a thicker plaque layer than smooth part . Arrow shows border between rough and smooth surface
  • 77.
    Other factors determiningsupragingival plaque formation are: 1. Individual variables influencing plaque formation: “heavy or fast plaque” former and “light or slow plaque” former- this depends on various factors as • diet, chewing fibrous food, • smoking, • amalgam restorations, • tongue and palate brushing, • the colloidal stability in saliva, • antimicrobial factors of GCF and saliva • pellicle composition and • retention depth of dento-gingival area
  • 78.
    2. Variation withinthe dentition In general early plaque formation occurs faster 1. In lower jaw compared to upper jaw 2. In molar areas 3. On buccal tooth surfaces compared to oral sites (especially in upper jaw) 4. In the interdental regions compared to the strict buccal or oral surfaces.
  • 79.
    3. Impact ofgingival inflammation • Plaque formation is more rapid on tooth surfaces facing inflamed gingival margins than on those adjacent to healthy gingiva. Substances from GCF as mineral, protein, carbohydrate favors both the initial adhesion and growth of early colonizing bacteria. 4. Impact of patient’s age • Subjects age does not influence de novo plaque formation. Developed plaque in older patient , resulted in more severe gingival inflammation, this indicate an increased susceptibility gingivitis with aging. 5. Spontaneous tooth cleaning • Only negligible differences in plaque extension (plaque retaining areas) areas is observed.
  • 80.
    Changes in subgingivalmicro biota during 1st week after mechanical debridement reported only partial reduction from 108 to 105 followed by a fast regrowth to almost pretreatment level within 7 days. Smooth abutments (Ra<0.2 µm) were found to harbor 25 times less bacteria than rough ones, with a slight higher density of coccoid (ie non-pathogenic) cells Recent studies demonstrate that a complex subgingival microbiota, including most periopathogens, is established within 1 week after abutment (transmucosal implant) insertion De novo subgingival plaque formation Scanning electron microscope of bacteria invading dentinal tubules 15000x
  • 81.
  • 82.
    Factor modifiers: • OxidationReduction potential (Saocransky et. at. 1964) • pH (Kleinbers and Hall 1969) • Temperature (Haffagee et al 1992) Factor antagonizes: • Bacteriocins (Rogers et. al. 1979, Hammond et. al. 1987, Steven et. al. 1987) • H2O2 (Holmberg and Hammond 1973, Hillman et. al. 1985 ) • Organic acids (Mashimo et. al. 1985)
  • 83.
    •gingival sulcus andperiodontal pocket provides the area for growth •mean temperature: Averages about 35ºC Ranges about 30ºC to 38ºC (Haffagee et al 1992) •pH : pH 7.0-8.5 ( Forscher et. at. 1954 , Kleinbers and Hall 1969, Cimasoni 1983) •Oxidation Reduction potential -300 to + 310mv at pH 7.0 (Onisi et. at. 1960, Kenney & Ash 1969)
  • 84.
    • Early colonizers(e.g. Streptococci, Actinomyces) use oxygen and lower the redox potential of the environment, which then favours the growth of anaerobic species. Gram +ve sp. use • sugars as an energy source and • saliva as carbon source • The bacteria that predominate in mature plaque are ananerobic and use amino acid and small peptides as energy source.
  • 86.
    • Lactate andFormate byproducts of metabolism of Streptococci and Actinomyces and may be used in metabolism of other plaque microorganisms The growth of P.gingivalis is enhanced by metabolic byproducts produced by other microorganisms, such as • succinate from Capnocytophaga ochraceus and • protoheme from Campylobacter rectus
  • 87.
    Factor antagonizes For example: •S. sanguis produces H2O2 which inhibits growth of A.actinomycetemcomitans (Hillman et. al. 1985 ) • A.actinomycetemcomitans produces bacteriocins that inhibits S. sanguis (Hammond et. al. 1987, Steven et. al. 1987)
  • 88.
    Sources of nutrientsavailable: Mainly 3 sources: diet, host, and other sub gingival species Certain nutrients are: • Vit K analogues (Gibbons and Macdonald 1960) • Certain growth factors like hemin (Evans 1951, Gibbons and Macdonald 1960)
  • 89.
    Host as sourceof nutrients: • Bacterial enzymes that degrade host proteins result in the release of ammonia, which may be used by bacteria as nitrogen source • Hemin iron from the breakdown of host Hb may be important in the metabolism of P.gingivalis • Increase in Steroid hormone are associated with significant increase in the proportions of P.intrmedia found in sub gingival plaque
  • 91.
  • 92.
    Suprgingival plaque • Microbialaggregations on the tooth surface if prevented from maturing may become compatible with gingival health. • Supragingival plaque if allowed to grow and mature, may induce gingivitis and can lead to the formation of a microenvironment that permits the development of subgingival plaque. • Therefore, supragingival plaque strongly influence the growth, accumulation and pathologic potential of sub gingival plaque, especially in the early stages of gingivitis and periodontitis.
  • 93.
    Subgingival plaque • Inassociation with the presence of supragingival plaque, there are inflammatory changes that modify the anatomic relationships of the gingival margin and tooth Surface. • This results in enlarged gingiva, which increases the space for bacterial colonization and also protects bacteria from normal cleansing mechanisms. They derive from GCF. • Many of these microorganisms lack the adherence ability and utilizes plaque bacteria as a means of colonization subgingival area.
  • 94.
    conclusion • Dental plaquebiofilm cannot be eliminated. However, the pathogenic nature of the dental plaque biofilm can be reduced by reducing the bioburden (total microbial load and different pathogenic isolates within that dental plaque biofilm) and maintaining a normal flora with appropriate oral hygiene methods that include daily brushing,flossing and rinsing with antimicrobial mouthrinses.This can result in the prevention or management of the associated sequelae, including the development of periodontal diseases and possibly the impact of periodontal diseases on specific systemic disorders. JADA, Vol. 137 November 2006.