Introduction…… Uterus……..Sterile After birth……… few facultative & aerobic microorganisms Second day……... anaerobic 2 weeks …….. Nearly mature microbiota > 2 years …….. 400 different spp (10 14 ) After tooth eruption …… > 500 spp. Any individual contains ≥150 spp. 6 Ecological niches Or Microbial habitats within the mouth EARLYCOLONIZERS Dental plaque Formation 2. Specific Plaque Hypothesis 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 periodontal disease because these organisms produce substances that mediate the destruction of host tissues. 3. Ecological plaque hypothesis In 1990, PD Marsh et al developed the ecologic plaque hypothesis According to this, both the total no. of dental plaque and the specific microbial composition of plaque may contribute to the transition from health to disease. A change in the nutrient status of a pocket or chemical and physical changes to the habitat are thus considered the primary cause for overgrowth by pathogens.

1. Dental
plaque
Dr. Rebicca Ranjit

2. Introduction……
Uterus……..Sterile
After birth……… few facultative & aerobic microorganisms
Second day……... anaerobic
2 weeks …….. Nearly mature microbiota
> 2 years …….. 400 different spp (10 14 )
After tooth eruption …… > 500 spp.
Any individual contains ≥150 spp.
Human
bacteria=2
k.g.
Human
brain=1.4
k.g.

4. Most oral bacteria are harmless commensals under normal
circumstances.
Under specific conditions
Increased mass and/or pathogenicity,
Suppression of commensal or beneficial bacteria and/or
Reduced host response
Disease can occur
Long-term systemic antibiotic use…normal oral microbiota reduced
......yeast infection
Aggressive periodontitis is associated with a loss of colonization of
S. sanguinis.

5. Beneficial Species modify the disease process, as follows:
(1)by passively occupying a niche that may otherwise be colonized
by pathogens,
(2)by actively limiting a pathogen’s ability to adhere to appropriate
tissue surfaces,
(3)by adversely affecting the vitality or growth of a pathogen
(4)by affecting the ability of a pathogen to produce virulence
factors, or
(5)by degrading virulence factors produced by the pathogen.

6. Microbial Shift during Disease
• From gm +ve to gm –ve
• From non-motile to motile organisms
• From cocci to rods (at a later stage to spirochetes)
• From facultative anaerobes to obligate anaerobes
• From fermenting to proteolytic species

7. 6Ecological niches
Or
Microbial habitats within
the mouth

8. 1. Swallowing,
mastication,
or blowing
the nose
2. Tongue &
OH
implements
3. Wash-out
effect of the
salivary,
nasal, & GCF
4. Active
motion of
surfaces (teeth,
implants,
restorations &
prosthesis)
#Periodontal/periimpla
nt pocket
(with GCF, cementum
or implant
surface, & the pocket
epithelium)
# Buccal epithelium,
palatal
epithelium &
epithelium of floor
of mouth.

9. S. mitis
S. oralis
S. sanguis
Streptococcus spp.E
A
R
L
Y
CO
L
ON
I
Z
E
R
S
A. Odontolyticus
Veilonella parvula
Eikenella corrodens
Capnocytophaga spp
A. actinomycetemcomitans
Porphyromonas gingivalis
Tanerella forsythus
Treponema denticola
CLOSELY ASSOCIATED
COMPLEXES IN THE ORAL CAVITY
LATE COLONIZERS
Prevotella intermedia
Campylobacter rectus
Fusobacterium nucleatum
Socransky & Haffajee 2002

10. NON-BACTERIAL INHABITANTS OF THE
ORAL CAVITY
Viruses: Herpesviruses (HSV-1,2; Varicella zoster
virus, etc)
Human papillomaviruses
Picornaviruses (Coxsackie; Echo; Entero
virus)
Retroviruses (HIV-1,2)
Yeasts : Candidiasis, Aspergillosis, Cryptococcosis
Protozoa: Entamoeba gingivalis & Trichomonas
tenax
Archaea

11. Materia alba Dental plaque calculus
- White cheese like
accumulation.
- A soft accumulation
of salivary proteins,
bacteria, desquamated
epithelial cells, food
debris.
- Lacks an organized
structure.
- Easily displaced with a
water spray.
- Resilient clear to
yellow grayish
substance.
- Composed of bacteria
in a matrix of salivary
glycoproteins &
extracellular
polysaccharides.
- Considered to be a
biofilm.
- Impossible to remove
by rinsing or water
spray.
- Hard deposit that
forms by
mineralization of
dental plaque.
- Generally covered
by a layer of
unmineralized
dental plaque.

12. Biofilm are organized structures
composed of microcolonies of
bacterial cells non-randomly
distributed in a shaped matrix or
glycocalyx.

13.  Contains microcolonies of bacterial cells
 Presence of water-filled channels (primitive
circulatory system); Removes potential harmful
metabolic products ( utilization by other species)
Cross feeding (one species providing nutrients for
another)
Facilitate processing & uptake of nutrients (Metabolic
Interaction)

14. Biofilms are found in…..
Pipe
Plaque on
the teeth
Creek

16. Dental plaque
Defined as a specific but highly variable
structural entity resulting from sequential
colonization of micro-organisms on the
tooth surfaces, restorations & other parts
of oral cavity & consists of mucin,
desquamated epithelial cells, debris &
micro organisms all embedded in the
gelatinous extra cellular matrix.

17. Methods of detecting plaque
Probing with a
periodontal
probe.
Disclosing
solution.

18. PLAQUE
Micro-
organism
Intermicrobial
matrix
70-90% by volume

19. Intermicrobial
matrix (25%)
Solid Water 70-80%
Inorganic Organic
• Mainly Ca , PO4
• Traces-Na ,F,
Mg ,P, K
• Carbohydrates(polysaccharides,
fructans,glucans,
levans,dextrans)
• Proteins(albumin)
• Lipids(LPS , endotoxin from Gm
–ve bacteria)
• Glycoproteins

20. Supra-gingival plaque Sub-
gingival plaque
Coronal Marginal Attached
Unattached
Tooth asso.
Tissue asso.
PLAQUE

24. Supragingival plaque Subgingival plaque
Location Coronal to margin of gingiva Apical to margin of gingiva
Origin Salivary glycoprotein &
salivary microorganisms
Downgrowth of bacteria from
supragingival plaque
Retention Rough surface of
teeth/restoration/
malpositioned teeth/carious
lesion
Overhanging margins,
periodontal pockets
Microorganisms Early plaque: Gram +ve
Older plaque:
rods,filamentous,fusiforms,
spirochetes
Anaerobic population:
Gram –ve, motile, spirochetes ,
rods
Source of nutrients Saliva & ingested food GCF, exudate
Significance Causes gingivitis,
supragingival calculus, dental
caries
Causes periodontitis
(tissue destruction)

25. Dental plaque
FORMATION

26. 1)
2)
3)

27. Within nanoseconds after vigorously
polishing the teeth, a thin, saliva‐derived
layer, called the acquired pellicle, covers
the tooth surface.
Contents:
• Glycoproteins (mucin)
• Histidine‐rich proteins
• Proline‐rich proteins,
• Ezymes (α amylase)
• Phosphoproteins
(Statherin)
I. Formation of pellicle on the
tooth surface

28. Components of
saliva
GCF
Debris
Bacterial & host
tissue cell
products
Glycoprotein pellicle

29. II. Initial Adhesion &
Attachment of Bacteria
Transport
to surface
Initial adhesion
Attachment
Colonization of
surface & biofilm
maturation

30. Browni
an
motion
Sedimenta
tion of
micro-
organism
Liquid
flow Chemota
ctic
moveme
nt
Transport to the
surface
TOOTH
SURFACE

31. Initial adhesion
(reversible)
• Due to interaction between bacteria &
the tooth surface at the distance of
50nm.
• Long range & short range forces
including Vanderwaal attractive
force(GA) & electrostatic repulsive
force(GE).

32. LVO ( Derjaguin , Landau , Verwey , Overbee
“Theory of Colloid Stability”, 1999
For some bacteria , Gibb’s total energy (Gtot=GA +
• Secondary (net energy) minimum (5-20nm fro
• Positive maximum (An energy barrier to adhes
• Steep primary minimum (<2nm distance from s

33. Strong
attachment
After initial adhesion , a strong anchorage
is established between bacteria & tooth
surface by specific interaction (covalent ,
ionic , H2 bond)
Direct contact/Bridging
Reversible to irreversible bondi

34. Some molecules from the pellicle (eg-
PRP) evidently undergo conformational
change so that new receptors become
available.
Such hidden receptors (on pellicle
surface) for bacterial adhesions
Cryptitopes (cryptic-hidden ;
topo-place)

35. Colonization of the surface &
biofilm formationCo-
adhesion
Primary colonizers adhered to tooth surfaces
provide new receptors for attachment by other
bacteria (act as bridge for secondary
colonizers)
Development of microcolonies & eventually
to a mature biofilm

36.  Described by Gibbsons & Nygaard
 Cell to cell recognition of genetically distinct
partner cell types
Eg:
Fusobacterium nucleatum all other
human bacteria Veilonella spp
Capnocytophaga ochracea Streptococci &/or
Actinomyces
Prevotella loeschii
Co-
aggregatio
n

38. Eg:
• Corn-cob formation Streptococci
adhere to filaments
• Test-tube brush formation Gram –ve rods
adhere to filaments
• Rosette formation Gram –ve
roods adhere to cocci

39. During night, plaque formation/growth rate
is ……………?
a) reduced by 50%
b) increased by 50%

40. WHAT WE EXPECT:
Reduced plaque removal Reduced saliv
Increased plaque growth
BUT WHAT HAPPENS:
Supragingival plaque obtain its nutrients from saliva
reduced at night
Reduced plaque formation

42. Topography of supragingival
plaque
Initial plaque formation takes place along the gingival
margin & from interdental space, later further
extension in coronal direction can be observed.
Plaque formation can also start from grooves, cracks,
perikymata, or pits.

43. Quorum
sensing
Communications between biofilm
bacteria
Biofilm cells can coordinate behaviour via
intercellular "communication“ using
biochemical signalling molecules

44. Bacteria secrete a signaling molecule that
accumulates in the local environment
Once they reach a critical threshold
concentration.
Triggers a response such as a change in the
expression of specific genes
The threshold concentration is reached only at
a high-cell density, and therefore bacteria
sense that the population has reached a

45. o Conjugation,
o Transformation,
o Plasmid transfer,
o Transposon
transfer.
Genetic transfer between
bacteria

46. Bacterial Transmission &
Translocation
Transmission: Passage of pathogens from one
person to another
: Horizontal or Vertical
Translocation: Transfer of bacteria from 1
ecological niche to the other.
: By explorer, probes, saliva flow

48. • Periodontal disease results from the - Elaboration of
noxious products by the entire plaque flora.
• Small amounts of plaque noxious products are
neutralized by the host.
• Large amounts of plaque large
amounts of noxious products overwhelm the host's
defenses.
Concept:- Control of periodontal disease depends on
1.Non-specific plaque Hypothesis Walter Loesche 1976

49. 2. Specific Plaque Hypothesis
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
periodontal disease because these organisms
produce substances that mediate the
destruction of host tissues.
Walter Loesche.

50. 3. Ecological plaque hypothesis
In 1990, PD Marsh et al developed the ecologic plaque
hypothesis
According to this, both the total no. of dental plaque and
the specific microbial composition of plaque may
contribute to the transition from health to disease.
A change in the nutrient status of a pocket or chemical
and physical changes to the habitat are thus considered
the primary cause for overgrowth by pathogens.

52. Criteria for Identification of
PeriodontopathogensKoch’s postulate (1870s, Robert Koch)
1. Be routinely isolated from diseased individuals.
2. Be grown in pure culture in the laboratory.
3. Produce a similar disease when inoculated into
susceptible laboratory animals.
4. Be recovered from lesions in a diseased laboratory
animal

53. In the case of periodontitis, three primary
problems are
(1)the inability to culture all the organisms that
have been associated with disease
(2)difficulties inherent in defining and culturing
sites of active disease, and
(3)the lack of a good animal model system for
the study of periodontitis.

54. Socransky proposed criteria by which periodontal micro-o
may be judged to be potential pathogens.

55. 1. Be associated with disease, as evident by
increases in the no. of organisms at diseased
sites
2. Be eliminated / decreased in sites that
demonstrate clinical resolution of disease with
treatment
3. Induce a host response, in the form of an
alteration in the host cellular or humoral
immune response
4. Be capable of causing disease in
experimental animal models

56. VIRULENCE FACTORS OF PERIODONTOPATHOGENS
Porphyromonas
gingivalis:
1) Proteases:-
Gingipains
2) Major & minor
fimbriae
3) Hemagglutinins
Aggregatibacter
actinomycetemcom
itans:
1) Leukotoxin
2) Chemotactic
inhibitors
3) Adhesins
4) Bacteriocin
5) Invasin
6) Collagenases

57. Source of nutrition for subgingival
Human adult contains about………
Virulence factor of A.a……
Red Complex?? Green Complex

58. Virulence factor of
Porphyromonas gingivalis?
Fusobacterium nucleatum belongs to
…… complex??
Example of Co-aggregation??
Tissue associated plaque leads to……

59. Important features of a biofilm???