Dental Plaque Soft deposits that form the biofilm adhering to the tooth surface or other hard surfaces in the oral cavity, including removable & fixed restorations” Bowen , 1976 Bacterial aggregations on the teeth or other solid oral structures Lindhe, 2003

1. 1
GOOD MORNING

2. 2

3. DR. ANUJ SINGH PARIHAR
Senior Lecturer
Dept. of Periodontics
3

4. CONTENTS
• INTRODUCTION
• HISTORY
• DEFINITION OF TERMS
• CLASSIFICATION OF DENTAL PLAQUE
• COMPOSITION OF DENTAL PLAQUE
• FORMATION OF DENTAL PLAQUE
• MICROBIAL COMPLEXES
• DENTAL PLAQUE AS BIOFILM
• MICROBIAL SPECIFICITY OF PERIODONTAL DISEASE
• CRITERIAS OF IDENTIFICATION OF PATHOGENS
• PLAQUE CONTROL
• CONCLUSION
4

5. 5MICRO-
ORGANISMS
PERIODONTITIS
DENTAL CARIES

6. DEFINITIONS
• Dental Plaque
Soft deposits that form the biofilm adhering to the tooth surface or
other hard surfaces in the oral cavity, including removable & fixed
restorations”
Bowen , 1976
• Bacterial aggregations on the teeth or other solid oral structures
Lindhe, 2003
6

7. DEFINITIONS
DENTAL PLAQUE
“is a specific but highly variable
structural entity, resulting from
sequential colonization of
microorganisms on tooth surfaces,
restorations & other parts of oral cavity,
composed of salivary components like
mucin, desquamated epithelial cells,
debris & microorganisms, all embedded
in extracellular gelatinous matrix.”
WHO-1961
7

8. DentalCalculus
is a an adherent calcified or calcifying mass that forms on the
surface of natural teeth & prosthesis.
MATERIA ALBA
is a deposit composed of aggregate of microorganisms,
leucocytes & dead exfoliated epithelial cells , randomly
organized & loosely adherent to the surfaces of the teeth, plaque
& gingiva.
8

9. HISTORY
 J Leon Williams (1897) – described dental plaque
 GV Black (1899) – coined term “gelatinous dental plaque”
 Waerhaug (1950) described the importance of bacterial plaque
in the etiology of periodontal disease
9

10. HISTORY
 Schei (1959), Russel (1967) Epidemiological studies-
positive correlation between the amount of bacterial plaque
and the severity of gingivitis
 Loe et al (1965), landmark study on plaque , saying that plaque
is main etiological agent in periodontal diseaes.
 W.Loesche (1976) Modern theories of specificity
 PD Marsh (1994) Ecological plaque hypothesis
10

11. 11

12. CLASSIFICATION
12

13. SUPRA- GINGIVAL PLAQUE
• Supragingival plaque is found at or above the gingival
margin.
• Supragingival plaque in direct contact with the gingival
margin is referred to as marginal plaque
13

14. SUBGINGIVAL PLAQUE
• Sub gingival plaque
is found below the gingival
margin, between the tooth
and gingival sulcular tissue.
14

15. 15

16. 16
Tooth attached Unattached Tissue Attached
Gram positive – rods
and cocci,
Gram negative rods,
filaments, spirochetes
Gram variable
Does not extend to JE Extend to JE Extend to JE
Calculus formation,
root caries
Gingivitis Gingivitis, periodontitis
May penetrate
cementum
- May penetrate
epithelium and
connective tissue

17. 17

18. COMPOSITION OF
DENTAL PLAQUE
• Dental plaque is composed primarily of microorganisms.
• These organisms exist within an intercellular matrix.
18

19. BIOFILM
The term biofilm
describes the relatively
indefinable microbial
community associated
with a tooth surface or
any other hard, non-
shedding material.
(Wilderer & Charaklis
1989)
19

20. • Biofilm consists of one or more communities of micro-
organisms embedded in glycocalyx , that are attached to
solid surfaces.
(Costerton et al 1994)
20

21. INTERCELLULAR MATRIX
• This contains a few host cells such as epithelial cells ,
macrophages & leukocytes.
• Forms 20%-30 % of plaque mass.
21

22. ORGANIC MATERIAL
• Polysaccharides ( 30% ) produced by bacteria.
Dextran
• Protein (30%) –Albumin (originating from GCF)
• Glycoproteins from saliva.
• Lipid (15%) consists of debris from disrupted
bacteria,
host cells & food debris
22

23. INORGANIC MATERIAL
•Predominantly – calcium, sodium, phosphorous,
potassium & fluorides (in traces)
•Source of inorganic material in supragingival plaque
is primarily saliva
• source of inorganic material in sub gingival plaque is
GCF
23

24. EXOPOLYSACCHARIDES –
the backbone of the biofilm
The bulk of the biofilm consists of the matrix, composed
predominantly of water and aqueous solutes.
24

25. Maintaining the integrity & protecting
microbial cells within the biofilm by
preventing desiccation and attack by
harmful agents.
They bind essential nutrients such as
cations to create a nutritionally rich
environment favouring specific micro-
organisms.
Act as a buffer and assist in retaining
extracellular enzymes (and their
substrates), enhancing substrate
utilization by bacterial cells.
25

26. •
One gram of plaque contains approximately
2 X 1011 bacteria.
(Socransky SS,1953), (Schroeder, De Boever-
1970)
26

27. NON BACTERIAL ORGANISMS IN PLAQUE
MYCOPLASMA
SPECIES
YEAST
PROTOZOA VIRUSES
NON
BACTERIAL
27

28. 28

29. Dental plaque may be readily visualized on teeth after 1-2 days of
no oral hygiene.
FORMATION OF
DENTAL
PELLICLE
INITIAL
ADHESION &
ATTACHMENT
COLONIZATION
& PLAQUE
MATURATION
29

30. I. FORMATION OF DENTAL
PELLICLE
• Acquired pellicle may be defined as a homogenous,
membranous, acellular film that covers the tooth surface and
frequently form the interface between the tooth ,the dental
plaque and calculus . (SCHLUGER)
• `A fully established pellicle is found within 30 min.
Within 24 hr, the pellicle is around 0.1-0.8 µm in diameter.
• Derived from components of saliva and crevicular fluid as well
as bacterial and host tissue cell products and food debris. 30

31. • Consists of numerous components, including glycoprotein
(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
bacterial receptors.
31

32. FUNCTIONS OF DENTAL PELLICLE
Protective
barrier
Lubrication
Preventing
tissue
desiccation
Substrate to
which
bacteria
attaches
32

33. II. INITIAL ADHESION &
ATTACHMENT
OF BACTERIA
• We cannot conclude a single mechanism that dictates the
adhesiveness of micro-organisms .
TRANSPORT TO
SURFACE
INITIAL
ADHESION
ATTACHMENT
COLONIZATION
OF SURFACE &
BIOFILM
FORMATION 33
SCHEIE ( 1994)

34. A) TRANSPORT TO SURFACE
• The first stage involves the initial transport of the bacterium to
the tooth surface.
• Random contacts may occur
o Brownian motion (average displacement of 40 µm/hour)
o Sedimentation of microorganisms,
o Liquid flow
o Active bacterial movement (chemotactic activity).
34

35. B) INITIAL ADHESION
• There is an initial, reversible adhesion of the bacterium.
• It is 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.
• The total interaction energy, also called the total Gibbs energy
(GTOT).
• (GTOT = GA + GE)
35

36. INITIAL ADHESION
• For most bacteria, GTOT consists of a
o Secondary minimum (where a reversible binding takes
place: 5-20 nm from the surface)
o A positive maximum (an energy barrier B) to adhesion
o A steep primary minimum (located at <2 nm away from
the surface), where an irreversible adhesion is established.
36

37. C) ATTACHMENT
• After initial adhesion, a firm anchorage between bacterium and
surface will be established by specific interactions (covalent,
ionic, or hydrogen bonding).
• The bonding between the bacteria & pellicle is mediated by
specific extracellular components of organisms &
complementary receptors on pellicle surface.
37

38. ATTACHMENT OF BACTERIA
• The attachment to tooth surface is the essential first step in
the development of a biofilm.
• Many bacterial species possess surface structures such as
FIMBRIAE and FIBRILS that aid in their attachment to
different surfaces.
38

39. • The fimbriae of A. naeslundii are the best characterized of the
gram-positive oral bacteria.
39
• Associated with adhesion of
A. naeslundii to salivary
acidic proline- rich proteins
and to statherin deposited
within the salivary pellicle.
Type I fimbrae
• Associated with attachment of
A. naeslundii to glycosidic
receptors on epithelial cells,
polymorphonuclear leukocytes
and oral streptococci .
Type II fimbrae

40. 40

41. FORMATION
OF DENTAL
PELLICLE
• TRANSPORT
• INITIAL ADHESION
• ATTACHMENT
• COLONIZATION
INITIAL
ADHESION &
ATTACHMENT
41

42. III. COLONIZATION
&
PLAQUE MATURATION
• The early colonizers (e.g., streptococci and Actinomyces
species) use oxygen and lower the reduction-oxidation potential
of the environment, which then favors the growth of anaerobic
species.
42

43. 43

44. • Secondary colonizers are the microorganisms that do not
initially colonize clean tooth surfaces, including Prevotella
intermedia, Prevotella loescheii, Capnocytophaga spp.,
Fusobacterium nucleatum, and Porphyromonas gingivalis.
44

45. `
45

46. COAGGREGATION
• Coaggregation is referred to as cell-to cell recognition of
genetically distinct partner cell types.
• Occurs primarily through the highly specific stereo chemical
interaction of protein and carbohydrate molecules located on
the bacterial cell surfaces.
• Also by the less specific interactions resulting from
hydrophobic, electrostatic, and van der Waals forces.
46

47. COAGGREGATION
• Well characterized interaction include the coaggregation of:
• Fusobacterium nucleatum S. sanguis,
• Prevotella loescheii A. viscosus
• Capnocytophaga ochraceus A. viscosus
• Streptococci show intrageneric co-aggregation  bind to
the nascent monolayer of already bound streptococci.
• Later stages – coaggregation between different Gram negative
species seen – F. nucleatum & P. gingivalis or T. denticola.
47

48. COAGGREGATION BRIDGES
• A co-aggregation 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
48

49. • Thus most coaggregation
among strains of different
genera are mediated by
lectin-like adhesin & can be
inhibited by lactose & other
glycosides.
49

50. CORN COB formation – streptococci adhere to
filaments of Bacterionema.matruchotti or F.nucleatum.
50
CORNCOB STRUCTURE TEST TUBE BRUSH

51. MICROBIAL COMPLEXES
Socransky et al. in 1998 examined over 13,000 subgingival
plaque samples from 185 adult subjects and DNA
hybridization methodology described the presence of
specific complexes of periodontal microorganisms.
51

52. 52
ACTINOMYCES
SPECIES
V. Parvula
A.odontolyticus
S.Mitis
S.Oralis
S.Sanguis
Streptococcus sp.
S.gordonii
S.intermedius
PRIMARY COLONIZERS

53. 53
P.Intermedia
P.Nigrescens
P.Micros
F.nucleatum
C.rectus
E.nodatum
C.showae
E.Corrodens
Capnocyptophaga spp
A.actinomycetemcomitans
P.Gingivalis
B.Forsythus
T.denticola
SECONDARY
COLONIZERS

54. ACTINOBACILLUS
ACTINOMYCETEMCOMITANS
• It is non motile & gram negative.
• This bacteria is small, short ,straight or curved with rounded
ends.
AGGREGAGIBACTER. ACTINOMYCETUMCOMITANS
(LAURITSON & KILION,2006)
54

55. 55

56. VIRULENCE FACTORS OF
A. ACTINOMYCETEMCOMITANS
FACTOR EFFECT
LIPOPOLYSACCHARIDE Release of endotoxin
LEUKOTOXIN • forms pores in the
membranes of Pmns,
monocytes and lymphocytes
causing osmotic imbalance
leading to cell death
COLLAGENASE reduce collagen density
PROTEASE Able to cleave Ig G
56

57. PORPHYROMONAS GINGIVALIS
• It is a gram negative , non-motile & obligate anaerobe.
57

58. VIRULENCE FACTORS OF
PORPHYROMONAS GINGIVALIS
FACTOR EFFECT
FIMBRIAE attach to epithelial cells, fibroblasts,
hemoglobin
PROTEINASES provide nutrients for
bacterial growth
degrade type I and IV
collagen and extracellular
matrix proteins
FIMBRILLIN bind to proline rich proteins
PROTEASE Able to cleave Ig G
HAEMOLYSIN & COLLAGENASE 58

59. GINGIPAIN
• Trypsine like protinases
59
ARGININE
LYSINE
GINGIPAINS

60. BACTERIODS FORSYTHUS
• It is a non-motile , spindle shaped & gram negative obligate
anaerobe.
TANNERELLA.FORSYTHENSIS
(SAKA MOTO et al ,2002)
TANNERELLA.FORSYTHIA
(MAIDEN et al,2003)
60

61. VIRULENCE FACTORS OF
TANNERELLA FORSYTHIA
FACTOR EFFECT
LIPOPROTEINS bind to other bacteria and host cells
PROTEINASES degrades benzoyl arginine
naphthylamide, activity of which
appears related to sites of periodontal
infection
ENVELOPE
LIPOPROTEIN
activate gingival fibroblasts
to produce elevated levels
of IL-6 and TNF α
61

62. TREPONEMA.DENTICOLA
• This is a classified species of SPIROCHAETES.
• These organisms are gram negative spiral , motile organisms
• It is difficult to grow these organisms on culture media , as
these require strict anaerobic conditions.
PATHOGENIC CHARACTER
• Ability to travel in viscous environment & penetrate both
epithelium and connective tissue.
• These can degrade collagen & dentine.
• Produce proteolytic enzymes that destroys immunoglobulins.
62

63. 63

64. 1) PHYSIOLOGICAL HETEROGENECITY
WITHIN BIOFILM
• Cells of same microbial species can exhibit extremely different
physiological states in a biofilm though separated by little
distance of 10 micrometer.
• pH can vary quite remarkably over short distances within a
biofilm .
• Bacteria in biofilm several enzymes Beta- lactamase,
Superoxide dismutase, Elastases, Cellulases.
64

65. 65

66. 2) QUORUM SENSING
• Quorum sensing in bacteria , ‘‘involves the regulation of
expression of specific genes through the accumulation of
signaling compounds that mediate intercellular communication.”
(Prosser 1999)
• This is a method of intercellular communication.
Quorum sensing depends on cell density.
• Once signaling compounds reach a threshold level, gene
expression is activated.
66

67. 67

68. Quorum sensing may give biofilms their distinct properties:
Alteration of physiological properties of bacteria in the
community through quorum sensing.
Has the potential to influence community structure, by
encouraging the growth of beneficial species (to the biofilm)
and discouraging the growth of competitors.
Expression of genes for antibiotic resistance at high cell
densities may provide protection.
68

69. 3) ANTIBIOTIC RESISTANCE:
• Resistance of bacteria to antibiotics, or preservatives is affected
by their
- position of bacteria
- growth rate
- temperature & PH
69

70. PROPERTIES OF BIOFILM
• Cooperating community of various types of micro-organisms.
• Micro-organisms are arranged in microcolonies.
• Micro-organisms are surrounded by protective matrix.
• There is differing environment within micro-colonies which
impact the property of PHYSIOLOGICAL HETEROGENICITY.
• Micro-organisms have antibiotic resistance mainly due to
phenomenon of QUORUM SENSING.
70

71. 71

72. EXPERIMENTAL GINGIVITIS MODEL
( SAYED, LOESCHE, 1978)
72

73. TOPOGRAPHY OF SUPRA GINGIVAL PLAQUE
73

74. PLAQUE RETENTIVE FACTORS
Surface
irregularities
Restorative
materials
Removable
partial
denture
Calculus
Abnormal
tooth
position
Erupting
teeth
Carious
lesion
Orthodontic
therapy
74

75. VARIATIONS IN DENTITION
Molar > front region
Increased plaque formation
in the lower jaw compared
to the upper jaw
Buccal surfaces more
especially in the upper jaw
Interdental areas compared
to strict buccal or oral
surfaces
Plaque growth
rate
75

76. 76

77. NON-SPECIFIC
PLAQUE
HYPOTHESIS
SPECIFIC
PLAQUE
HYPOTHESIS
ECOLOGICAL
PLAQUE
HYPOTHESIS
77

78. NON SPECIFIC PLAQUE
HYPOTHESIS
• Non specific plaque hypothesis was proposed by
WALTER LOESCHE(1976).
• In the mid-1900s, periodontal disease was believed to
result from an accumulation of plaque over time in
conjunction with a diminished host response and
increased host susceptibility with age.
• This thinking is referred as
“NON-SPECIFIC PLAQUE HYPOTHESIS”
78

79. • The nonspecific plaque hypothesis maintains that
periodontal disease results from the “elaboration of
noxious products by the entire plaque flora.”
• Thus it lead to concept that control of periodontal
disease depends on control of the amount of plaque
accumulation.
• Treatment of periodontitis by debridement (nonsurgical
or surgical) and oral hygiene measures focuses on the
removal of plaque and its products
79

80. SPECIFIC PLAQUE HYPOTHESIS
• Specific plaque hypothesis states that only certain
plaque is pathogenic, and its pathogenicity depends
on the presence of or increase in specific
microorganisms.
NEWMAN MG , SOCRANSKY SS (1977),ADI et al ,(1978)
• Plaque harboring specific bacterial pathogens results
in periodontal disease.
• A. actinomycetemcomitans as a pathogen in
localized aggressive periodontitis.
80

81. TISSUE INVASIVE PROPERTY
81

82. ECOLOGICAL PLAQUE
HYPOTHESIS
• A change in a key environmental factor (or factors) 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.
82

83. 83

84. • This hypothesis postulated dynamic relationship
between environmental cause & ecological shifts
within the biofilm.
• It also introduced the concept that the disease can be
prevented not only by inhibiting the putative
pathogens, but also interfering with the environmental
factors driving the selection & enrichment of these
bacteria.
84

85. CRITERIA FOR IDENTIFICATION OF PERIODONTAL
PATHOGENS
In the 1870s, Robert Koch
postulated the criteria by
which an organism can be
judged to be causative
agent in human infections
85

86. Pathogen must be routinely isolated from
the diseased individuals.
Must be grown in pure culture in the
laboratory.
Must produce a similar disease when
inoculated into susceptible lab animals.
Must be recovered from lesions in a
diseased laboratory animals.
86

87. 87

88. SIGMUND SOCRANSKY (1992) proposed criteria
by which periodontal microorganisms may be
judged to be potential pathogens.
88

89. • Must be associated with disease, as evident by increases in
the number of organisms at diseased site.
• Must be eliminated or decreased in sites that demonstrate
clinical resolution of disease with treatment.
• Must demonstrate host response, in form of alteration in
host cellular or humoral immune reaction.
• Must be capable of causing disease in experimental animal
models.
• Must demonstrate virulence factors responsible for
enabling the microorganisms to cause destruction of the
periodontal tissues.
89

91. DETECTION OF PLAQUE
DISCLOSING AGENTS
It is a preparation in liquid , tablet or lozenge which
contains a dye or other colouring agent. A disclosing
agent is used for identification of dental plaque which
is otherwise not visible to naked eye .
THE AGENTS THAT ARE USED AS DISCLOSING
AGENTS ARE:
• Iodine preparation
• Bismark brown
• Erythrosine
• Fast green
• Basic fuschin

93. PLAQUE CONTROL
• It is defined as the removal of microbial plaque &
prevention of its accumulation on the teeth & adjacent
gingival tissue. It also deals with prevention of
calculus formation.
MECHANICAL
CHEMICAL

94. MANUAL TOOTH
BRUSH
IONIC TOOTH
BRUSH
SONIC
TOOTHBRUSH
POWERED
TOOTH BRUSH

96. INTER DENTAL AIDS
DENTAL FLOSS

97. INTER DENTAL AIDS
INTER DENTAL
BRUSH

98. INTER DENTAL AIDS
UNITUFTED
BRUSHED

99. CHLORHEXIDINE GLUCONATE
• ADVANTAGE
• 1. anti plaque & anti bacterial
• properties
• 2. property of SUBSTANTIVITY
•
• DISADVANTAGE
• brownish staining of teeth
• MECHANISM
1. prevent pellicle formation.
2. prevent plaque maturation

100. POVIDONE IODINE
• ADVANTAGE
• 1. no staining of teeth seen
• 2. reduces inflammation
•
• DISADVANTAGE
• reduced substantivity

101. DELMOPINOL
This is a morpholinoethanol
derivative.
Inhibits plaque growth & reduces
inflammation.
But has less substantivity in
comparison to others

102. CONCLUSION

104. REFERENCES
• Clinical Periodontology - Carranza (9th & 10th edn)
• Clinical Periodontology- Jan Lindhe, Thorklid Karring , Niklaus P
Lang
• Clinical Periodontology : Listgarten
• Periodontal microbial ecology - Perio 2000,Vol. 38, 2005, 135–
187
104

105. • Are dental diseases examples of ecological catastrophes? - P. D.
Marsh - Microbiology (2003), 149, 279–294
• Dental biofilms: difficult therapeutic targets - Periodontology
2000, Vol. 28, 2002, 12–55
• Dental biofilms: difficult therapeutic targets - Periodontology
2000, Vol. 28, 2002, 12–55
105

106. 106