dental plaque by Dr Divjot

1. DENTAL PLAQUE
PRESENTED BY: Dr Divjot Kaur Narula ( PG 1st year)
Guided by: Dr Shweta Bali (Professor, HOD)

2. CONTENTS
• Definition
• Classification
• Content
• Biofilm
• Plaque attachment at ultrastructural level
• Colonizers (bacteria involved)
• Plaque control methods

3. DEFINITION
• Dental plaque is defined clinically as a structured, resilient, yellow-grayish substance that adheres tenaciously to the
intraoral hard surfaces, including removable and fixed restorations(Carranza, 10th)
• 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, microorganisms all embedded in a gelatinous extracellular matrix.( WHO,1961)
• It is soft amorphous granular deposists which accumulate on surfaces of teeth, dental restoration and dental
calculus. (Glickman)

4. • contains a complex of bacterial matrix consisting of salivary
glycoproteins and extracellular polysaccharides
• Materia alba refers to soft accumulations of bacteria and tissue cells that
lack the organized structure of dental plaque, and it is easily displaced
with a water spray.
• Calculus is a hard deposit that forms by mineralization of dental plaque,
and it is generally covered by a layer of unmineralized plaque.
1mm of dental plaque, weighing
about 1mg contains more than 200
million bacteria

5. PATHOGENIC EFFECTS
45%
GRAM
NEGATIVE
23%
GRAM
POSITIVE
55%
GRAM
POSITIVE
77% Gram
Negative
GINGIVITS PERIODONTITIS

6. MATERIA ALBA DENTAL PLAQUE CALCULUS
White cheese like
accumulation
Resilient clear to yellow-
grayish substance
Hard deposits that forms
by mineralization of
dental plaque
A soft accumulation of
salivary protein, some
bacteria, desquamated
epithelial cells and
occasional food debris
Composed of bacteria in a
matrix of salivary
glycoproteins and
extracellular
polysaccharides
Generally covered by a
layer of unmineralized
dental plaque
Lacks and organized
structure and is therefore
not as complex as plaque
Considered to be a biofilm
Easily displaced with a
water spray
Impossible to remove by
rinsing or the use of
sprays

7. CLASSIFICATION(BASED ON THE POSITION)
SUPRAGINGIVAL
• Found at or above the gingival margin
SUBGINGIVAL
• Between the gingiva and the pocket epithelium
1) Marginal
2) Coronal
3) Fissural
1)Tooth associated
2)Unattached
3)Tissue associated

8. SUPRAGINGIVAL SUBGINGIVAL
Coronal Apical
Originates from salivary glycoprotein Exacerbation from the supra-gingival plaque
Lingual surfaces of mandibular incisors
Buccal surfaces of maxillary molars
Interproximal areas
In the shallow pockets
Firmly attached to acquired pellicle Adhere to the attached plaque, tissue side
Rough surfaces of teeth Pocket hold plaque against tooth surfaces.

10. • Supragingival plaque typically
demonstrates a stratified
organization of a multilayered
accumulation of bacterial
morphotypes .Gram-positive
cocci and short rods
predominate at the tooth
surface, whereas gram-negative
rods and filaments, as well as
spirochetes, predominate in the
outer surface of the mature
plaque mass
• The subgingival differs in
composition firstly due to the
anaerobic environment secondly
due to low availability of blood
products.

11. Plaque mostly consists of filamentous bacteria, dominantly contains cocci and rods:
1) Streptococcus mitis,
2) S. sanguis,
3) Actinomyces viscosus,
4) A. naeslundii,
5) Eubacterium
The layers of microorganisms facing the soft tissue lack a definite intermicrobial matrix and contain primarily
gram-negative rods and cocci, as well as large numbers of filaments, flagellated rods, and spirochetes.
Species such as
1) Streptococcus oralis,
2) Streptococcus intermedius,
3) Peptostreptococcus micros,
4) Porphyromonas gingivalis,
5) Prevotella intermedia,
6) Tannerella forsythia,
7) Fusobacterium nucleatum.
COMPOSITION

12. NON- BACTERIAL COMPOSITION
• Mycoplasma species
• Yeast
• Protozoa
• Viruses
• Macrophages
• Leukocytes

14. Organic Inorganic
Intercellular matric

15. Organic
1. Polysaccharides(30%) produced by bacterial dextran
2. Protein (30%)- Albumin (orginating from GCF )
3. Gycoproteins from Saliva
4. Lipid (15%) consists of debris from disrupted bacteria,
host cells and food debris.
Inorganic
1. Predominantly –calcium, sodium, phosphorus,
potassium, fluorides(in traces)
2. Sources of inorganic material in supragingival plaque
in primary saliva
3. Sources of inorganic material in subgingival palque is
GCF

16. INTERMICROBIAL MATRIX
• Plaque microorganisms
• Saliva
• Gingival exudates.
• Degenerating or dead bacteria

17. PLAQUE AS A BIOFILM
Biofilms are composed of micro-colonies of bacterial cells (15-20% by volume) that are non-randomly distributed in a
shaped matrix or glycocalyx (75-80% volume)
Socransky SS, Haffajee AD. Dental biofilms: Difficult therapeutics target. Periodontol 2000. 2002;28:12–55
In the lower plaque layers, which are dense, microbes are bound together in a polysaccharide matrix with other
organic and inorganic materials
• The fluid layer bordering the biofilm has a stationary sublayer and a fluid layer in motion.
• Nutrient components penetrate this fluid medium by molecular diffusion.
• The dental plaque biofilm has a similar structure. It is heterogeneous in structure, with clear evidence of open
fluid-filled channels running through the plaque mass.
• These water channels permit the passage of nutrients and other agents throughout the biofilm, acting as a
primitive “circulatory” system Wood et al, 2000

19. • 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)

20. CHARACTERISTICS OF BIOFILM
• 1) physiologic heterogenicity- cells of the same microbial species can exhibit extremely different physiological
states in a biofilm through separated little by distance of 10mm.
• pH can vary quite remarkably over short distances within a biofilm.
• Bacteria present: beta-lactamase
• Superoxidase dismutase
• Elastase
• Cellulase
• Exopolysaccharides (EPS) are produced by the bacteria in the biofilm and are the major components of the biofilm
making up 50-95% of the dry weight. They play a major role in maintaining the integrity of the biofilm and as well
as preventing desiccation and attack by harmful agents.
• Lindhe J, editor. 4th ed. Oxford, UK: Blackwell Publishing Company; 1998. Clinical Periodontology and implant dentistry
book

21. QUOROM SENSING
• Qurom sensing in bacteria “involves the regulation of expression of specific genes through the accumulation of
signalling compounds that mediate intercellular communication” (Socransky SS, Haffajee AD. Dental biofilms:
Difficult therapeutics target. Periodontol 2000. 2002;28:12–55.)
• The stimuli of quorum-sensing systems are signal molecules, called autoinducers. Frias J, Olle E, Alsina M.
Periodontal pathogens produce quorum sensing signal molecules. Infect Immun. 2001;69:3431–4
• It depends on cell density, once signalling compounds reach a threshold level, gene expression is activated.
1) Expression of genes for antibiotic resistance at high cell densities may provide protection.
2) Has the potential to influence community structure, by encouraging the growth of beneficial species (to the
biofilm)and discouraging the growth of competitors.
3) Alteration of physiologic properties of bacteria in the community through quorum sensing.

22. • Acyl homoserine lactones (AHLS): AHLs are the major group of autoinducer signals in
gram-negative bacteria. They have a conserved homoserine lactone (HSL) ring with a
variable acyl side chain. Based on the length of the acyl groups, AHLs can be broadly
classified as short- or long chain molecules.
• Autoinducer-2 (AI-2): AI-2 was first recognized as a quorum-sensing signal in Vibrio
harveyi by Bassler et al. This type of signaling has been discovered in many gram-
negative bacteria.

24. COUNTERMEASURES
• (1) enzymatic degradation of the signal molecule,
• (2) blocking signal generation
• (3) blocking signal reception
• Hentzer M, Givskov M. Pharmacological inhibition of quorum sensing for the
treatment of chronic infections. J Clin Invest 2003;112:1300-07.

25. ANTIBIOTIC RESISTANCE
• Resistance of bacteria to their antibiotics or preventives is affective by their
1) Position of bacteria
2) Growth rate
3) Temperature & pH

26. • Gene transfer: Horizontal gene transfer among bacteria is recognized as a major contributor in the
molecular evolution of many bacterial genomes.
• Transformation: Transformation is defined as the uptake and maintenance of DNA.
• Some oral bacteria, including members of genus Streptococcus, Neisseria and Actinobacillus are naturally
competent and have specialized systems for DNA uptake.
• Transduction: Transduction is a process where bacterial DNA is packaged into phage heads.
• Conjugation: Conjugation is the polar transfer of genetic material through direct cell-to-cell contact and
is mediated by a variety of specialized genetic elements, such as conjugative transposons and conjugative
plasmids.

28. PLAQUE FORMATION AT THE ULTRASTRUCTURAL LEVEL
FORMATION OF PELLICLE:
All surfaces of the oral cavity (both hard and soft tissues) are coated with a pellicle (initial phase of plaque
development)
This pellicle consists of numerous components, including glycoproteins (mucins), proline-rich proteins,
phosphoproteins (e.g., statherin), histidine-rich proteins, enzymes (e.g., α-amylase), and other molecules that
can function as adhesion sites for bacteria (receptors). The mechanisms involved in enamel pellicle formation
include electrostatic, van der Waals, and hydrophobic forces. The specific components of a pellicle also depend
on the underlying surface. The physical and chemical nature of the solid substratum significantly affects several
physicochemical surface properties of the pellicle, including its composition, packing, density, and its
configuration.
Currently the term “acquired pellicle” is less frequently used because it is misleading. Indeed, it may imply that
bacteria can colonize the tooth surface only when this pellicle is in place for some hours.

29. FUNCTIONS OF DENTAL PELLICLE
 Protective barrier.
 Lubrication.
 Preventing tissue desiccation.
 Substrate to which bacteria attaches.

32. INITIAL ADHESION OF AND ATTACHMENT BACTERIA
• Phase 1: Transport to the surface
a) Brownian motion (average displacement of 40 µm/hour),
b) Sedimentation of microorganisms,
c) liquid flow(several orders of magnitude faster than diffusion),
d) active bacterial movement (chemotactic activity)

33. PHASE 2- INITIAL ADHESION.
• reversible adhesion of the bacterium, initiated by the interaction between the bacterium and the surface, from a
certain distance (50 nm), through long-range and short-range forces, including van der Waals attractive forces
and electrostatic repulsive forces

34. • Reversible adhesion involves weak, long-range,
physico-chemical interactions between the charge on
the microbial cell surface and that produced by the
conditioning film.
• Irreversible adhesion involves interactions
between specific molecules on the microbial cell
surface (adhesins) and complementary molecules
(receptors) present in the acquired pellicle.
• Co-adhesion, secondary and late colonizers adhere
via cell-surface adhesins to receptors on already
attached bacteria

35. TOTAL GIBBS ENERGY
• the total interaction energy of the plaque is denoted by
•G(tot)= GA+GE
• Secondary minimum(where a reversible binding takes place: 5-20nm from the surface)
• A positive maximum to adhesion
• A steep primary minimum(located at <2nm away from the surface where an irreversible adhesion
takes place

36. PHASE 3: ATTACHMENT
• On a rough surface, bacteria are better
protected against shear forces.
• The bonding between bacteria and pellicle is
mediated by specific extracellular
proteinaceous components (adhesions) of the
organism and complementary receptors (i.e.,
proteins, glycoproteins, or polysaccharides) on
the surface (e.g., pellicle) and is species specific.

38. PHASE 4: COLONIZATION OF THE SURFACE AND BIOFILM FORMATION
• When the firmly attached microorganisms start growing and the newly formed bacterial clusters remain attached,
microcolonies or a biofilm can develop called coaggregation(cell to cell adhesion)
• Early colonizers: attaches on the tooth surface and uses the oxygen to lower the reduction-oxidation reaction
which later leads to excess accumulation of anaerobic microorganisms.
• Eg. Streptococci and actinomyces species
• Secondary colonizers: do not initially colonize clean tooth surface.
• Eg. Prevotella intermedia, Capnocytophaga species, fusobacterium nucleatum and porphyromonas gingivalis

39. MATRIX FORMATION
• Intermicrobial phase substances are derived from
• Supra gingival- mainly saliva
• Subgingival- gingival sulcus fluid and subgingival fluid

40. COAGGREGATION
• Referred as cell-cell recognition of genetically distinct partner cell types.
• Occurs primarily through highly specific stere chemical interaction of protein and carbohydrate molecules
located on the bacterial cell surfaces
• Also by the less specific interactions resulting from hydrophobic, Vander walls and electrostatic
• A coaggregation bridge is formed when the common partner bears two or more types of coaggregation
mediators
• These mediators can be various types of polysaccharides or various adhesin or combination of two.
a) Fusobacterium nucleatum with streptococcus sanguis
b) Prevotella loesheii with actinomyces viscous
c) Capnocytophaga ochraceus with A viscous

41. • The dental plaque has a 'corn-cob' appearance and
'test-tube brush' appearance due to the adherence of
cocci to filamentous bacteria.

42. ULTRASTRUCTURAL ASPECTS OF PLAQUE FORMATION
• Important changes in the plaque accumulation occurs in the first 24 hours
• During the first 2 to 8 hours, the adherent pioneering streptococci saturate the salivary pellicular binding sites
and thus cover 3%to 30% of the enamel surface.
• Instead of slow growth in the next 20 hours, rapid growth occurs
• After 1 day, the term biofilm is fully deserved because organization takes place within it

43. DE NOVO SUPRAGINGIVAL PLAQUE FORMATION: CLINICAL
ASPECTS
• During the first 24 hours, starting from a clean tooth surface, plaque growth is negligible from a clinical
viewpoint (<3mm of the vestibular tooth surface, an amount almost undetectable if seen clinically.)
• Long-range interaction between a negatively charged bacterium and a negatively charged surface according to
the DLVO theory.
DAY MICRO-ORGANISM
DAY 1 and 2 Gram + cocci
DAY 3 and 4 Increase in filamentous microorganisms, cocci still dominating
DAY 4-7 Increase in cocci- coronally
Increase in filaments- apically
DAY 7-14 Increase in WBC(increase in inflammation)
Increase in vibrio and cocci
DAY 14-21 Evident gingivitis

44. TOPOGRAPHY OF SUPRAGINGIVAL PLAQUE
• Plaque growth initially occurs near the gingival margin and later moves in the coronal direction.
• Surface irregularities are also responsible for the “individualized” plaque growth pattern, which is reproduced in
the absence of optimal oral hygiene.
• Rough intraoral surfaces (e.g. crowns, implant abutments, denture bases) accumulate and retain more plaque
and calculus in terms of thickness, area, and colony-forming units.
• .Smoothing an intraoral surface decreases the rate of plaque formation. Below a certain surface roughness
(average roughness [Ra] no plaque accumulation or attachment is seen.

45. PRIMARY COLONIZERS
S.MITIS
S.SANGUIS
S.ORALIS
ACTINOMYCES
SPECIES
V. PARVULA
A.ODONTOLYTICUS

46. SECONDARY COLONIZERS
P.GINGIVALIS
T.DENTICOLA
B.FORSYTHIS
P.INTERMEDIA
C.RECTUS
P.MICROS
E.corodnes
canocytophaga spp.
A.actinomtcetecomitan
s

47. GINGIPAIN
Gingipains are a family of proteases secreted by Porphyromonas gingivalis.
Among other functions, it works to degrade cytokines,
thereby downregulating the host response in the form of
reduced inflammation.
Porphyromonas gingivalis is one of the principal organisms associated with
adult periodontitis. Bacterial surface proteins such as fimbriae and gingipain
hemagglutinin domains have been implicated as adhesins that actuate
colonization of epithelium lining the gingival sulcus.

48. PLAQUE RETENTIVE FACTORS
Surface irregularities, cementum overgrowth
Calculus
Incorrect restoration
Removable partial dentures
Erupting teeth
Orthodontic therapy
Carious lesion

49. PLAQUE HYPOTHESIS
• Non-specific plaque hypothesis
• Specific plaque hypothesis
• Ecological plaque hypothesis.

50. NON-SPECIFIC PLAQUE HYPOTHESIS
• In the mid-1900s, periodontal diseases were believed to result from an accumulation of plaque over time,
eventually in conjunction with a diminished host response and increased host susceptibility with age. This
thinking, termed the nonspecific plaque theory, was supported by epidemiologic studies that correlated both
the patient’s age and the amount of plaque with evidence of periodontitis.
• The nonspecific plaque hypothesis maintains that periodontal disease results from the “elaboration of noxious
products by the entire plaque flora.”
• Several observations contradicted the nonspecific plaque hypothesis.
• First, some patients with considerable amounts of plaque and calculus, as well as gingivitis, never developed
destructive periodontitis.
• Furthermore, individuals who did present with periodontitis demonstrated considerable site specificity in the
pattern of disease.

51. SPECIFIC PLAQUE HYPOTHESIS
• The specific plaque hypothesis states that only certain plaque is pathogenic, and its pathogenicity depends on
the presence of or increase in specific microorganisms.
• This concept predicts that plaque harboring specific bacterial pathogens results in a periodontal disease
because these organisms produce substances that mediate the destruction of host tissues
• Acceptance of the specific plaque hypothesis was spurred by the recognition of A. actinomycetemcomitans as a
pathogen in localized aggressive periodontitis.

52. ECOLOGICAL PLAQUE HYPOTHESIS
• A change in a key environmental factor will trigger a shift in the balance of the resident plaque microflora, and
this might predispose a site to disease.(PD marsh 1994)
• This hypothesis is based on the theory that the unique local microenvironment influences the composition of the
oral microflora.
• It also states that the disease can be treated by eliminating the specific pathogens as well as changing the
environmental factors.

53. • Key concept implicit in the Ecological Plaque Hypothesis is that
disease can be prevented not only by targeting the key bacteria
directly (e.g. with antimicrobial agents) but also by interfering
with the factors that drive the disruption of the microbiota:
• (a)the oral microbiota is natural, and is beneficial to the host,
• (b)disease is a consequence of a deleterious shift in the microbiota
(dysbiosis),
• (c)these shifts are driven by a change in the local

54. H O M E O S TAT I C M E C H A N I S M S I N V O LV I N G M I C R O B I A L I N T E R A C T I O N S H E L P
M A I N TA I N A S TA B L E B E N E F I C I A L M I C R O B I A L C O M M U N I T Y T H AT I S A S S O C I A T E D
W I T H O R A L H E A LT H .
S E V E R E C H A N G E S TO T H E H A B I TAT ( E C O LO G I C A L P E RT U R B AT I O N S ) C A N A L T E R
T H I S E Q U I L I B R I U M BY S E L E C T I N G F O R O R G A N I S M S T H AT A R E M O R E C O M P E T I T I V E
I N T H E A LT E R E D E N V I R O N M E N T, A N D T H I S C A N P R E D I S P O S E S I T E S TO D I S E A S E .
Marsh PD, Martin MV. Oral microbiology,
5th edition. Edinburgh, UK: Churchill
Livingstone, 2009.

56. CRITERIA FOR IDENTIFICATION OF
PERIODONTAL PATHOGENS
• In the 1870s, Robert Koch developed the classic criteria by which a microorganism can be judged to
be a causative agent in human infections. These criteria, known as Koch’s postulates, stipulate the
following for the causative agent:
• 1. Must be routinely isolated from diseased individuals.
• 2. Must be grown in pure culture in the laboratory.
• 3. Must produce a similar disease when inoculated into susceptible laboratory animals.
• 4. Must be recovered from lesions in a diseased laboratory animal.

57. • Sigmund Socransky,(1977)
• 1. Must be associated with disease, as evident by increases in the number of organisms at diseased sites.
• 2. Must be eliminated or decreased in sites that demonstrate clinical resolution of disease with treatment.
• 3. Must demonstrate a host response, in the form of an alteration in the host cellular or humoral immune
response.
• 4. Must be capable of causing disease in experimental animal models.
• 5. Must demonstrate virulence factors responsible for enabling the microorganism to cause destruction of the
periodontal tissues.

58. LOCAL FACTORS AFFECTING PLAQUE
• Factor modifiers
• 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)

59. PLAQUE CONTROL
Removal of microbial plaque and prevention of its accumulation on the teeth and its
adjacent gingival tissue. It also deals with the prevention of calculus formation.
1) Detection of Plaque
2) Mechanical methods
3) Chemical methods

60. DETECTION OF PLAQUE
• It is a preparation in liquid, tablet or lozenge which contains a dye or other agent .A disclosing agent is used for
identification of dental plaque which is otherwise not visible to naked eye.
1) Iodine preparation
2) Bismark brown
3) Erythrosine
4) Fast green
5) Basic fuschin

61. MECHANICAL
1) MECHANICAL PLAQUE CONTROL BY SELFCARE
2) MECHANICAL PLAQUE CONTROL BY PROFESSIONAL TOOTH CLEANING

62. • Ultrasonic instrumentation appeared to maintain its effectiveness in
plaque removal in even the deepest pockets
• Professional tooth cleaning means removal of supragingival plaque but
also 1-3mm subgingival plaque from all tooth surfaces using
mechanically driven instruments and fluoride prophy paste.
• It also includes removal of calculus and deep subgingival plaque.

63. CHEMICAL
• CHLORHEXIDINE GLUCONATE
• ADVANTAGES:
1) antiplaque and antibacterial properties
2) Substantivity
• DISADVANTAGES
1) Brownish staining of teeth
• MECHANISM
1) Prevent pellicle formation
2) Prevent plaque maturation

64. DELMOPINOL
• This is a Morpholinoethinol derivative
• Inhibits plaque growth and reduces inflammation

65. CHEMICAL PLAQUE CONTROL AGENTS
• Triclosan and stannous fluoride for plaque control
• Pyrophosphates which are anti calculus agents

66. • Summary
• Clinical routines for a maintenance care appointment includes: • plaque
evaluation (disclosion)
• • oral hygiene instruction
• • probing depth measurements
• • registration of bleeding on probing
• • scaling (plaque removal) if indicated
• • tooth polishing
• • fluorides
• • radiographs if indicated
• • schedule the next appointment, the interval depending on the outcome of
the clinical examination

67. CONCLUSION
• 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

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