This document discusses dental plaque/biofilm, including its definition, classification, composition, properties, and factors that affect its composition. It begins by defining dental plaque as a host-associated biofilm that adheres tenaciously to intraoral hard surfaces. Plaque is classified as supragingival or subgingival based on its location relative to the gingival margin. The composition of plaque includes water, organic constituents like bacteria and carbohydrates, and inorganic constituents like calcium and phosphorus. Properties include its structure, exopolysaccharides that form its backbone, physiological heterogeneity, quorum sensing, and increased antibiotic resistance of bacteria within it. Factors like periodontal disease status, the local environment, transmission from other individuals,

1. DENTAL
PLAQUE/BIOFILM

2. SOFT TOOTH
ACCUMULATED
MATERIAL (TAM)

3. INDEX
1. Introduction
2. Definition
3. Classification
4. Composition
5. Properties
6. Factors that affect composition of subgingival
biofilm
7. Plaque formation
8. Clinical Consideration

4. TOOTH ACCUMULATED MATERIAL
(TAM)
Non-mineralized (Soft TAM)
Acquired pellicle
Dental plaque
Material alba
Food debris
Dental stains
Mineralized (Hard TAM)
Calculus

5. INTRODUCTION

6.  Gingivitis and Periodontitis are considered as
Diseases that are
initiated by bacteria.

7. HOW DOES BACTERIA APPEAR IN ORAL CAVITY?
After tooth eruption, a more complex oral flora develop,
comprising of 500 different species colonizing the adult
mouth
>2 years - oral cavity consists of 400 different types of
bacteria
2nd day - anaerobic bacteria can be detected
Within hours - facultative and aerobic bacteria develop
At Birth (oral cavity is sterile)

8. INTRAORAL NICHES FOR BACTERIAL
ADHESION
 Supragingival hard surfaces - teeth,
implants, restorations, and prosthesis.
 Periodontal/Peri-implant pocket
 Buccal epithelium, palatal epithelium
and epithelium of the floor of the mouth
 Dorsum of the tongue
 Tonsils

9.  In intraoral epithelial cells  High
turnover rate prevents the permanent
accumulation of microorganisms 
NATURAL DEFENSE.
 On hard and non shedding surfaces i.e.
Teeth & Implants extensive bacterial
deposit develop  primary cause of
caries, gingivitis, periodontitis,
periimplantitis, & bad breath.

10. Acc.To Dawsen (1994), Teeth are the primary habitats of
periopathogens. After full mouth extraction 
Actinobacillus actinomycetemcomitans and P. gingivalis
disappear
P. intermedia and other Prevotella species can remain, but
at lower numbers
So, teeth can even be considered as ‘port of entry’ for
periopathogens.

11. DEFINITION

12. DENTAL PLAQUE
Host associated biofilm
Structured, resilient, yellow grayish
colored substance that adheres
tenaciously to intra oral hard surfaces
including restorations
The term plaque is derived from French
word, meaning ‘to form a coverage’.

13. J.Leon Williams- described Bacterial
plaque in 1897
Adolph Witzel- first identified bacteria
as the cause of periodontal disease.
G.V.Black in 1899 coined the term
‘gelatinous microbic plaque’.

14. CLASSIFICATION

15. PLAQUE
Supragingival Subgingival
plaque plaque
found at or above found below the
gingival margin gingival margin

16. TABLE: CHARACTERISTICS OF SUPRAGINGIVAL & SUBGINGIVAL BIOFILM
CHARACTERISTIC SUPRAGINGIVAL BIOFILM SUBGINGIVAL BIOFILM
1) Location Coronal to free gingival margin Apical to free gingival margin
2) Origin
Salivary glycoprotein forms pellicle
and then micro-organisms get attached
on pellicle
Downgrowth of bacteria from
supragingival biofilm
3) Distribution
- Starts on proximal surfaces and other
protected areas
- Pit and fissure
-Shallow pocket
- Attached biofilm covers calculus
- Unattached biofilm extends to the
junctional epithelium
4) Adhesion
- Firmly attached to acquired
pellicle, other bacteria, and tooth
surfaces.
- Adheres to tooth surface,
subgingival pellicle, and calculus
- loose, floating, motile organisms in
deep pocket that do not adhere;
present between biofilm on tooth and
the pocket epithelium.

17. 5) Retention - Rough surfaces of
teeth
- Overhanging
margins of
restorations
- Malpositioned teeth
- Carious lesions
- Pocket holds
biofilm against
tooth
- Overhanging
margins of
restorations

18. 8) Microorganisms
Early: primarily gram-positive cocci,
then increased numbers of gram-
negative anaerobic bacteria
- Environment conducive to
growth of anaerobic population
9) Sources of
nutrients for
bacterial
proliferation
Saliva, food GCF
10) Etiological
factor/ Causes
Gingivitis
Supragingival calculus
Dental caries
Gingivitis,
Periodontitis
Subgingival calculus

19. SUBGINGIVAL
PLAQUE
Tooth
associated
Tissue
associated

21. SUBGINGIVAL PLAQUE
Tooth associated Tissue
associated
Streptococcus mitis Streptococcus
oralis
S.Sanguis S.intermedius
A.Viscosus P.gingivalis
P.intermedia
T.forsythia
F. nucleatum

22. Dental plaque
Supragingival plaque Subgingival plaque

23. Tooth attached Unattached Epithelial
Associated
Organism:
Gram positive
bacteria
Gram negative
rods, cocci,
filaments &
spirochaetes
Anaerobic
bacteria mainly
Not extent to
junctional
epithelium
Extent to junctional
epithelium
Extent to
junctional
epithelium
Cause root
caries and
calculus
Cause gingivitis Cause gingivitis,
periodontitis
with alveolar
bone loss by
activating
osteoclasts

24. Marginal plaque – cause gingivitis.
Supragingival plaque and tooth-associated
subgingival plaque – cause calculus formation
and root caries,
Tissue-associated subgingival plaque- cause
tissue destruction in periodontitis.

25. COMPOSITION

26. COMPOSITION OF DENTAL
PLAQUEDental plaque
Water Solids
(80%) (20%)
Organic constituents Inorganic constituents
(microorganisms) (intercellular matrix)
(70%) (30%)
1) Carbohydrates (30%) 1) Calcium
2) Proteins (30%) 2) Phosphorous
3) Lipids (10%) 3) Magnesium
4) Sodium
5) Potassium
6) Fluoride

27. ROLE OF CARBOHYDRATES IN
BIOFILM
Help in adherence of microorganisms to each other and the
tooth. Eg. Streptococcus mutans, which may be linked to
glucans.
Energy source to be used by biofilm bacteria.
If dextran concentration is high in biofilm, more chances of
caries occur.
If levan concentration is high, then there more chances of
periodontal destruction.

28. ROLE OF PROTEINS IN BIOFILM
Albumin, probably originate from
gingival crevicular fluid.
Supragingival biofilm contains
proteins derived from saliva.
Subgingival biofilm contains proteins
from gingival crevicular fluid.

29. ROLE OF LIPIDS IN BIOFILM
• The lipid material (15-30%)
consists of membranes of
disrupted bacterial cells, host
cells; and possibly food debris.
• It may include lipopolysaccharide
endotoxin from gram negative
bacteria, neutral fats, fatty acids,
cholesterol and phospholipids.

30. ROLE OF CALCIUM &
PHOSPHOROUS
Its conc. is higher in biofilm than saliva
• Higher concentration is seen on
lingual surface of the mandibular
anterior teeth because of action of
saliva
Amount is even higher in heavy
calculus formers.

31. SUPRAGINGIVAL PLAQUE
minerals (Ca, P)
calcification
CALCULUS

32. ROLE OF FLUORIDE
Fluoride  main source is
fluoridated toothpastes, mouth
rinses, drinking water.
Actions:
1) aid in remineralization of tooth
structure
2) Prevention of dimeneralization
of tooth structure.
3) Inhibition of growth of plaque
microorganisms.

33. PROPERTIES

34. PROPERTIES OF BIOFILM
1. Structure
2. Exopolysaccharides – the backbone
3. Physiological heterogeneity within
biofilm
4. Quorom sensing
5. Attachment of bacteria
6. Mechanisms of increased antibiotic
resistance of microorganisms in biofilm
7. Microbial complexes

35. 1. STRUCTURE OF BIOFILM
Biofilms are composed of microcolonies of bacterial cells
(15-20% by volume) that are distributed in matrix called
glycocalyx (75-80% volume).

36. Dental plaque biofilm has
open fluid channels
running through the
matrix
These fluid channels
permit the passage of
nutrients and other agents
throughout the biofilm 
Its like primitive
‘circulatory’ system

37. The nutrients make contact with the
sessile bacterial micro-colonies (attached)
through these water channels
Bacteria exist and proliferate within the
intercellular matrix through which the fluid
channels run.
The matrix provides special environment
 which distinguishes bacteria within the
biofilm than those that are free floating
(planktonic’ state of solutions eg. Saliva)

38. 2. EXOPOLYSACCHARIDES — THE BACKBONE
OF THE BIOFILM (PRODUCED BY BACTERIA)
Major roles:
 maintain integrity of the biofilm
 prevent desiccation and attack by
harmful agents (antibiotics).
 bind essential nutrients to create a local
nutritionally rich environment favoring
growth of specific microorganisms.
 Microorganisms can both synthesize and
degrade/utilize the exopolysaccharides as
needed

39. 3. PHYSIOLOGICAL
HETEROGENEITY WITHIN BIOFILMS
 Cells of microbial species exhibit
different physiological states in biofilm.
 pH can vary remarkably over short
distances in biofilm.
 Bacterial cells can produce B lactamase
against antibiotics, superoxide dismutases
(antioxidant) against oxidizing ions 
protecting the microorganisms

40.  Bacterial cells can also produce
elastases and cellulases  cause
lysis of elastic and collagen fibers
 Thus biofilms can exist in infinite
range of chemical and physical
microhabitats within microbial
communities

41. 4. QUORUM SENSING
It depend on microbial density. Less no. of
microbes, lesser is the intensity of signal produced
and vice versa.
Once the level of signalling compounds reach at
threshold level  gene expression is activated.
Quorum sensing in bacteria means “Regulation of
expression of specific genes by the accumulation of
signaling compounds that helps in inter cellular
communication” .

42. Role in biofilm:
 To change biofilm structure by
encouraging growth of beneficial species
and discouraging growth of competitors.

43. 5. ATTACHMENT OF BACTERIA
First step in formation of biofilm
Bacteria possess structures like Fimbriae and
Fibril on their surface that facilitate attachment.
Fimbriae on-
Actinomyces naeslundii,
P gingivalis,
Streptococcus salivarius,
Streptococcus parasanguis,
Streptococcus mitis
Fibrils on
S. salivarius,
S. mitis group,
P intermedia,
P nigrescens
Streptococcus mutans.

44. 6. MECHANISMS OF INCREASED
ANTIBIOTIC RESISTANCE OF
ORGANISMS IN BIOFILMS
Organism within biofilm are more resistant to
antibiotics than in planktonic (or unattached
stage)
Bacterial species in deeper layers of biofilm 
slower growth rate  so less susceptible
Slow growing bacteria often demonstrate
increased exopolymer synthesis (non specific
defense response)

45. MECHANISMS OF INCREASED
ANTIBIOTIC RESISTANCE OF
ORGANISMS IN BIOFILMS
This exopolymer retards diffusion within
biofilm
In addition, extracellular enzymes released by
bacteria in biofilm such as lactamases and
formaldehyde dehydrogenase in the
extracellular matrix, inactivates positively
charged, hydrophilic antibiotics.
Some antibiotics like macrolides, that are
positively charged but hydrophobic are
unaffected by these enzymes

46. Cells growing within a biofilm express genes
that are not observed in the same cells grown
in a planktonic state and they can retain this
resistance for some time after being released
from the biofilm. Eg. The cells of P.
aeruginosa liberated from biofilms is more
resistant to tobramycin than planktonic cells.

47. 7. MICROBIAL COMPLEXES
The association of bacteria within
biofilms is not random, but found to be
specific.
Socransky et al (1998) found six closely
associated groups of bacterial species

48. Yellow, Green, Purple complex  early colonizers of
biofilm
Orange, red complex  major etiologic agents of
periodontitis
Red is mainly associated with bleeding on probing.

49. Bacteria Complex Microorganism
EARLY
COLONIZERS
Blue complex Various Actinomyces species
Purple complex Veillonella parvula,
Actinomyces odontolyticus
Green complex Eikenella corrodens,
Capnocytophaga gingivalis,
Actinobacillus actinomycetemcomitans
Yellow complex Streptococcus mitis,
Streptococcus oralis,
Streptococcus sanguis,
Streptococcus gordonii,
Streptococcus intermedius
LATE COLONIZERS Orange complex Campylobacter rectus,
Eubacterium nodatum,
Fusobacterium nucleatum
Prevotella intermedia,
Prevotella nigrescens,
Red complex Porphyromonas gingivalis,
Tannerella forsythensis (Bacteroides
forsythus)
Treponema denticola

50. FACTORS THAT
AFFECT THE
COMPOSITION OF
SUBGINGIVAL
BIOFILMS

51. FACTORS THAT AFFECT THE
COMPOSITION OF SUBGINGIVAL
BIOFILMS
1. Periodontal disease status
2. The local environment
3. Transmission
4. Microbial composition of supra and sub
gingival biofilms

52. 1. PERIODONTAL DISEASE
STATUS
Most influential factor
The major difference between health and
periodontitis is the increased prevalence and counts
of the red and orange complex species, in patients
with periodontal disease.

53. 2. THE LOCAL ENVIRONMENT
It includes pocket depth. Red complex
bacteria increases in number with increasing
pocket depth.
 Red and orange complex bacteria are
increased at sites exhibiting gingival redness,
bleeding on probing and suppuration.

54. 3. TRANSMISSION
Periodontal pathogens can be transmitted from
the oral cavity of one person to another.
Two types transmission are possible
“Vertical”- Transmission from parent to
offspring
“Horizontal”- Passage of bacteria between
persons outside the parent-offspring
relationship.

55. 4. MICROBIAL COMPOSITION OF
SUPRA AND SUBGINGIVAL
BIOFILMS
Supragingival biofilm  predominated by
Actinomyces species in both health and
disease.
Subgingival biofilm  more complex; red and
orange complex sp.
From supra to sub gingival environment 
there is significant ↓ in Actinomyces and ↑ in
Red complex sp.

56. PLAQUE FORMATION

57. PLAQUE FORMATION AT THE
ULTRASTRUCTURAL LEVEL
Three major phases:
(1) The formation of the pellicle on the tooth
surface,
(2) Initial adhesion and attachment of
bacteria, and
(3) Colonization and plaque maturation.

58. 1) FORMATION OF THE ACQUIRED
PELLICLE
Acquired pellicle is thin (0.05-1um thick),
colourless, translucent bacterial free film which is
deposited over the teeth by saliva immediately after
tooth brushing, with slightly large amount near
gingival margin.
 Pellicle is a word originated from ‘Pellicula’
meaning skin or film.
It precedes the first stage of plaque formation.

59. Composition:
-Glycoproteins
-Proline-rich proteins
-Phosphoproteins (e.g. statherin)
-Histidine-rich proteins
-Enzymes (e.g. α-amylase)
-Secretory IgA
-other molecules that can function as
adhesion sites for bacteria
All constituents are derived from saliva

60. Types of pellicle:
1. Surface pellicle, unstained – Unstained
pellicle is clear, translucent.
 Not visible until a disclosing agent is applied.
When stained by disclosing agent, it appears
thin, with a pale staining in contrast with the
thicker, darker stained dental biofilms.
 .

61. 2. Surface pellicle, stained – Unstained
pellicle can take on extrinsic stain and can
become brown, grayish, or of any other color.
3. Subsurface pellicle – Surface pellicle is
continuous with subsurface pellicle that is
embedded in tooth structure, particularly
where the tooth surface is partially
demineralized

62. Significance of pellicle:
1) Protective
2) Make enamel more resistant to dental caries.
3) Lubrication, prevent dessication
4) Nidus for bacterial attachments
5) Attachment of calculus

63. 2) INITIAL ADHESION AND
ATTACHMENT OF BACTERIA
Complex process and involves 3 stage
sequence.
Phase I : Transport to the surface
Phase II: Initial adhesion
Phase III: Attachment

64. PHASE I: TRANSPORT TO THE
SURFACE
Involves the initial transport of bacteria
to tooth surface.
Random contacts may occur, through
brownian motion, sedimentation of
bacteria or by active bacterial movement
(chemotactic activity).

65. PHASE II: INITIAL
ADHESION
 Initial, reversible adhesion of the
bacteria
Interaction between the bacteria and
the surface is mediated by Vander Waals
attractive forces and electrostatic

66. PHASE III: ATTACHMENT
After initial adhesion, a firm anchorage (irreversible
binding) between bacteria and tooth surface is
established by covalent, ionic, or hydrogen bonding
(specific interactions)
On a rough surface, bacteria are better protected  so
change from reversible to irreversible bonding occurs
more easily.

67. The bonding between bacteria and pellicle is by
specific extra-cellular proteinaceous
constituent (adhesions) of the bacteria and
complementary receptors like proteins,
glycoproteins, or polysaccharides on the
pellicle on tooth surface
It is species specific.

68. Streptococcus and Actinomyces  Main early
colonizers, bind to acidic proline-rich-proteins,
α-amylase and sialic acid of pellicle.
A. viscosus possesses fimbriae that contain
adhesins, that binds to proline-rich proteins of
the dental pellicle.

69. 3. COLONIZATION AND
PLAQUE MATURATION
Bacterial mass increases due to adhesion of new bacteria and
synthesis of extracellular matrix.
With increasing thickness of matrix, diffusion into and out of
the biofilm becomes more difficult.
A transition of Gram +ve to Gram –ve is observed during dental
plaque formation.

70. Another factor that modify the number of bacteria is the
presence of gingivitis. Gingival changes result in
increased accumulation of plaque, so more complex
bacterial composition is attained
18 genera in oral cavity have shown property of
coaggregation (cell-to-cell recognition of genetically
distinct partner cell types).

71.  Velionellae, Capnocytophagae and Prevotella (Secondary colonizers) bind to
Streptococci and Actinomycetes (Primary colonizers) whereas Fusobacteria
coaggregate with all other human oral bacteria
Well-characterized interactions of secondary colonizers with early colonizers
include the coaggregation of
Fusobacterium nucleatum with Streptococcus sanguis,
Prevotella loescheij with Actinomyces viscosus and
Capnocytophaga ochraceus with A. viscosus.

72. Coaggregation occurs first between gram-positive species, then
between gram-positive and gram-negative species and then
between gram-negative and gram-negative species.
Special examples of coaggregations are “corncob” formation, in
which Streptococci adhere to filaments of Bacterionema matruchtii
or Actinomyces, and “test tube brush” composed of filamentous
bacteria to which gram-negative rods get attached.

73. The early colonizers (e.g. Streptococci, Actinomyces) use
oxygen and lower the redox potential, which then favors
growth of anaerobic bacteria.
Gram-positive species utilize sugars as an energy source
and saliva as carbon source.
The bacteria that in mature plaque are anaerobic and
asaccharolytic and use amino acids and small peptides
as energy sources.

74. Many physiologic interactions among the
different bacteria found in dental plaque.
Lactate and Formate are byproducts produced
by Streptococci and Actinomycetes and may be
used in the metabolism of other plaque micro-
organisms.

75. Host also act as an important source of nutrients.
Hemin iron from breakdown of host hemoglobin,
utilized in the metabolism of P. gingivalis.
Increases in steroid hormones (Pregnancy, Puberty)
are associated with significant increase in the
proportions of Prevotella intermedia.

76. Dead and lysed bacteria may provide
additional nutrients to the viable bacteria in the
neighborhood.
In deepened periodontal pocket, the nutritional
conditions for bacteria change as the
penetration of saliva into the pocket is very
limited. Gingival crevicular fluid (GCF) provide
nutrition to bacteria in deep pocket.

77. Bacteria Complex Microorganism
EARLY
COLONIZERS
Blue complex Various Actinomyces species
Purple complex Veillonella parvula,
Actinomyces odontolyticus
Green complex Eikenella corrodens,
Capnocytophaga gingivalis,
Actinobacillus actinomycetemcomitans
Yellow complex Streptococcus mitis,
Streptococcus oralis,
Streptococcus sanguis,
Streptococcus gordonii,
Streptococcus intermedius
LATE COLONIZERS Orange complex Campylobacter rectus,
Eubacterium nodatum,
Fusobacterium nucleatum
Prevotella intermedia,
Prevotella nigrescens,
Red complex Porphyromonas gingivalis,
Tannerella forsythensis (Bacteroides
forsythus)
Treponema denticola

78. CLINICAL
CONSIDERATIONS

79. 1. TOPOGRAPHY OF
SUPRAGINGIVAL PLAQUE
 Initial growth occurs along the gingival margin, in
interdental space, pit and fissures or other surface
irregularity (areas protected against shear forces).
This illustrates the role of surface roughness in plaque
growth, which should taken care of during clinical
treatment

80. Rough surfaces accumulate more plaque
and calculus
Smoothing of surface  decrease rate of
plaque formation.

81. 2) VARIATION WITHIN THE
DENTITION
Plaque formation occurs faster
(1) In lower jaw compared to upper jaw,
(2) in molar area,
(3) on the buccal tooth surfaces (especially in the upper jaw)
(4) in the interdental regions compared to the buccal or lingual/palatal
surfaces.

82. 2 Translocation of Bacteria
 Periodontal pathogens
are transmissible within
members of a families.
 Intraoral transmission of
bacteria like S.mutans,
A.
actinomycetemcomitans
has been observed.

83. To reduce the chances for intraoral translocation, one-stage,
full-mouth disinfection has been introduced
This concept consists of
1) Full-mouth scaling and root planing within 24 hours
2) Subgingival irrigation of all pockets with 1% chlorhexidine gel
3) Tongue brushing with an antiseptic
4) Mouth rinsing with an antiseptic mouthwash to decrease bacteria in
saliva and in tonsils areas