dental plaque

1. Dr. Enas Elgendy

2. • Dental plaque is dense, non calcified bacterial
masses, firmly adherent to tooth surface and
resists wash by salivary flow or forceful rinsing.
• Dental plaque represents a biofilm which
consists of bacteria in an intermicrobial matrix
that can adhere to any hard non shedding
surface (tooth, fixed and removable appliance
and restorations).
• Dental Plaque is a host-associated biofilm.

3.  Biofilms are defined as "Matrix-enclosed
bacterial populations adherent to each other
and or/to surface or interfaces.
 Biofilm is defined as the relatively un-definable
microbial community associated with a tooth
surface or any other hard, non-shedding
material.

4. Based on its relationship to the gingival margin, plaque is
differentiated into two categories.
Tooth Attached plaque
 Tissue Attached plaque
(epithelium and / or
connective tissue)
Unattached
Coronal plaque, which is
in contact with only the
tooth surface
 Marginal plaque, which
is associated with the
tooth surface at the
gingival
 Fissural

5.  It can be detected clinically only after it has reached a certain thickness.
Small amounts of plaque can be visualized by using disclosing agents.
 The color varies from grey to yellowish-grey to yellow.
 The rate of formation and location of plaque vary among individuals and
is influenced by diet, age, salivary factors, oral hygiene, tooth alignment,
systemic diseases and host factors.

6.  It is usually thin,
contained within the
gingival sulci or
periodontal pocket and
thus cannot be detected
by direct observation.
 Its presence can be
identified only by running
the end of a probe around
gingival margin

7.  Bacteria make up approximately 70 to 80 percent of total
material.
 One mg of dental plaque is estimated to contain 250 million
bacteria.
 Other than bacteria, mycoplasma, fungi, protozoa and viruses
may be present.
 microbial/cellular matrix contains organic and inorganic
portions and accounts for approximately 30% of the plaque
volume.
 The intermicrobial matrix is derived from bacteria, saliva and
gingival fluid.

8.  Intercellular matrix forms a hydrated gel function as a barrier
to protect bacteria from antimicrobial agents which cannot
diffuse through the matrix to each bacterium.
 Moreover, the inter-microbial matrix is penetrated by fluid
channels that conduct the flow of nutrient and waste products

10. Structure of supragingival plaque
Organic component Inorganic component
The intermicrobial matrix
glycoproteins
derived from
saliva
glycoproteins
serve also in
bacterial adhesion
polysacchrides derived
from bacteria serve as
1- energy storage for
bacteria (such as
dextran)
2- bacterial adhesion
(such as mutan).
Calcium
derived
from saliva
Phosphorus
derived from
saliva

11. Supragingival plaque = bacteria +
intermicrobial matrix
Intermicrobial matrix = organic + inorganic
material
Organic material = polysaccharides (bacteria)
+ glycoprotein (Saliva)
Inorganic material = calcium + phosphorous

12. Structure of subgingival plaque
Between the subgingival
plaque and the tooth there
is an organic material
known as cuticle. This
cuticle originates from
remnant of epithelial
attachment lamina and
material deposited from
gingival fluid.
Between the sub-gingival
plaque and the epithelial
lining of gingival sulcus or
pocket there are
leukocytes.

13. Structure of subgingival plaque
Organic material
Derived from
bacteria
where small
vesicles that
contain bacterial
endotoxins and
enzymes are found.
Inorganic material
derived from gingival
fluid which contains
calcium and phosphorus
The intermicrobial matrix

14. Subgingival plaque = bacteria + intermicrobial
matrix.
Intermicrobial matrix (if present) = Organic +
inorganic material
Organic material = vesicles (derived from Gram –
ve bacteria and they contain endotoxin and
enzymes)
Inorganic material = calcium + phosphorus
(derived from gingival fluid)

15. Structure of subgingival plaque

18. Plaque formation occurs in four steps:
1.Acquired enamel pellicle formation.
2.Initial adhesion and attachment of
bacteria
3.Bacterial colonization.
4.Plaque maturation.

19.  Pellicle is the initial organic structure that forms on the
surfaces of the teeth and artificial prosthesis.
 The first stage in pellicle formation involves adsorption of
salivary proteins to apatite surfaces. The acquired enamel
pellicle provides a substrate on which bacteria can attach.
 The mechanism of selective adsorption includes electrostatic
forces between negatively charged hydroxyapatite and
positively changed salivary glycoproteins.
 The mean pellicle thickness varies from 100 nm at 2 hours to
500 to 1,000 nm.
 The acquired enamel pellicle alters the charge and free
energy of the surface which in turn increases the efficiency of
bacterial adhesion (attachment).

20. Oral bacteria bear an overall net
negative charge, negatively-charged
components of the bacterial surface
and negatively-charged components of
pellicle become linked by cations such
as calcium.
During initial adherence, interactions occur mainly between
specific bacteria and the pellicle. They are:

21.  These interactions are based on
the close structural fit between
molecules on the pellicle and
bacterial surfaces.

22.  Lectins in the bacterial surfaces recognize specific
carbohydrate structure in the pellicle and become linked.
Bacterial attachment via specific lectin-like
interactions

23. Adhesins are protein in nature and have been
identified on fimbriae of bacteria. Fimbria are
fibrous protein structure extending from
bacterial cell surface.
Adhesins are able to bind to protein in
acquired enamel pellicle so help in bacterial
adhesion.
Another mean of bacterial adhesion to the
tooth surface is the formation of extra-cellular
polysaccharides produced by streptococci.

25.  Bacteria and pellicle
 Bacteria and same species
 Bacteria and different species
 Bacteria and matrix

26. Once the bacteria is adhered to
the pellicle, subsequent growth
leads to bacterial accumulation
and increased plaque mass.
Dental plaque growth depends
on:
A. Growth via adhesion of new
bacteria
B. Growth via multiplication of
attached bacteria

27. They include Gram +ve facultative cocci [streptococcus sanguis]
and Gram +ve facultative rods [actinomyces viscosus]. These initial
colonizer adhere to the pellicle.
Initial colonizers

29.  These bacteria are not able to initially
colonize the tooth surface.
 Secondary colonizers include Gram –ve
anaerobic bacteria such as P. gingivalis,
P. intermedia, F. nucleatum.
 They adhere to bacteria already
adherent to the tooth. The ability of
bacteria to adhere to one another is
termed coaggregation.
 The mechanism of coaggregation
appears to be mediated by specific
receptor-adhesin interaction. i.e.
specific protein on the surface of one
species (adhesins) attach to specific
carbohydrate on the surface of the
other (receptor).
Secondary colonizers

31. After colonization, a phase of rapid growth of
colonizing microorganisms occurs. In addition to
the continued growth of the adhering bacteria,
adhesion of new bacteria occurs leading to the
complexity of plaque maturation.

32. Factors that influence complexit of
plaque maturation and ecology
• Oxygen levels: With increasing thickness of
dental plaque diffusion of oxygen into the biofilm
becomes more and more difficult so favor the
growth of anaerobic bacteria.
• Nutritional sources: Dietary products dissolved
in saliva are an important source of nutrients for
bacteria in the supragingival plaque. Saccharolytic
bacteria can ferment sugar to provide energy for
their growth and multiplication.

33. Inter-bacterial relation
Beneficial interactions between bacteria may be in the form of:
 One species provides growth conditions favorable to another.
Obligate aerobes utilize oxygen for growth so provide suitable
environment for growth of anaerobes.
 One species facilitates attachment of another resulting in the
formation of different morphological structures as corn-cobs
(adherence of cocci to rod-shaped bacteria).
 One species provides growth factor utilized by other species
such as analogs of vitamin K.

34. Antagonistic interactions between
bacteria may be in the form of
Competition for nutrients.
Competition for binding sites.
Production of substances by one species
which limit growth of another one:
Streptococcus sanguis produces H2O2 which
inhibits the growth of A. actinomycetem
comitans, while A. actinomycetem comitans
produces bacteriocin that inhibits S. sanguis.

35. Accumulation of plaque along the gingival
margin leads to an inflammatory reaction of the
soft tissue. The presence of this inflammation
has a profound influence on local ecology. The
availability of blood and gingival fluid
components, associated with inflammation,
promotes the growth of Gram –ve bacterial
species. The bacteria breakdown these host
molecules to amino acids and utilize them for
growth.

36. Evidence for the role of bacteria as initiating factor in
the etiology of periodontal disease
• The relation between plaque levels and periodontal disease: There is a
positive correlation between the amount of bacterial plaque and the
severity of periodontal disease proper plaque control result in elimination
of signs of inflammation.
• Efficacy of antibiotics in treatment of periodontal disease: The use of
antibiotics in the treatment of periodontal disease improves the outcome.
• Host immunologic response: Patients with destructive periodontal
diseases show an elevated serum antibody response to subgingival
organisms.
• Pathogenic potential of bacterial plaque: A number of products that can
destroy periodontal tissues can be detected in dental plaque e.g.
endotoxins, leukotoxin, enzymes and low molecular weight substances.
• Studies on experimental animals: Certain microorganisms isolated from
human periodontal pockets can initiate periodontal destruction in
animals.

37. Association of plaque bacteria with
periodontal disease
It is clear that periodontal disease is associated
with the presence of dental plaque. However,
some individuals may show massive plaque
accumulation and signs of gingival inflammation
(gingivitis) but never change into periodontitis.
Based on these observations three theories have
been proposed to explain the association
between periodontal diseases and bacteria in
dental plaque.

38.  It states that, not all plaque is pathogenic and its
pathogenicity depends on the presence of certain specific
microbial pathogens in plaque.
 This is based on the fact that, the specific microorganisms
responsible for periodontal diseases release certain
damaging factors that mediates the destruction of the host
tissue.
 treatment would be directed toward the elimination of the
specific pathogen from the mouth with appropriate narrow-
spectrum antibiotic. Thus plaque control would no long be
necessary since plaque without the specific pathogen would
be non-pathogen.

39. • According to pure non-specific theory the
inflammatory periodontal disease develops when
bacterial proliferation exceeds the threshold of
host resistance, the composition of plaque was
not considered. i.e. there is a direct relation
between the total number of accumulated
bacteria and the magnitude of tissue destruction.
• If this was the case, why some patients have
lifelong contained gingivitis without developing
periodontitis in spite of continuous plaque
accumulation?

40.  It states that 6-12 bacterial species may be responsible for the
majority of destructive periodontal disease through synergistic
interaction.
 In acute necrotizing ulcerative gingivitis, synergy exists
between spirochetes and fusobacterium. Also, in chronic
periodontitis, synergy exists between fusobacterium
nucleatum, bacteroid forsythus and campylobacter recuts.

41. Koch's postulates, is made
to establish a caustive
relation ship between a
microbe and a diseases.
Koch's postulates are not
applicable in periodontal
disease, as more than one
organism is involved in
periodontal diseases.

42. Hence, Socransky (1977) had proposed the following criteria for
identifying the possible causative organisms in periodontal
diseases:
Association: The pathogen must be associated with the disease, as
evident by increase in the number of the microorganism at diseased
sites.
Elimination: The pathogen must be eliminated or decreased in sites
that demonstrate clinical resolution of the disease with treatment.
Host response: The pathogen must elicit host response as
demonstrated in the form of alteration in host cellular or humoral
immune response.
Animal studies: The pathogen must be capable of causing the
disease when inoculated in experimental animal.
Virulence factors: The pathogen and demonstrate virulence factors
responsible for enabling the microorganism to cause destruction of
periodontal tissues.

44.  Gram positive facultative species Actinomyces (viscosus and
naeslundii)
 Streptococcus (S. mitis and S. sangius)
 Veillonella parvula, small amounts of Gram-negative species
are also found.

45.  Gram-positive (56%), Gram-negative (44%)
organisms are found.
 Predominant Gram-positive species include, S.
sangius, S. mitis, S. oralis, A. viscosus, A.
naeslundii, Peptostreptococcus micros.

46.  Fusobacterium nulceatum
 Prevotella intermedia
 Veillonella parvula as well as Hemophilus,
Capnocytophaga and Campylobacter species

47.  Prevotella intermedia
 Spirochetes

48.  Porphyromonas gingivalis
 Bacteroides forsythus
 Prevotella intermedia
 Campylobacter rectus
 Eikenella corrodens
 Fusobacterium nucleatum
 Actinobacillus actinomycetemcomitans
 Peptostreptococcus micros
 Treponema, and
 Eubacterium species.

49.  EBV-l (Ebstein-Barr virus)
 HCMV (Human cytomegalovirus)

50.  Actinobacillus actinomycetemcomitans
 Porphyromonas gingivalis
 Eikenella corrodens
 Campylobacter rectus
 Fusobacterium nucleatum
 Bacteroides capillus
 Eubacterium brachy
 Capnocytophaga
 Herpes virus.

51.  Actinobacillus actinomycetemcomitans
 Porphyromonas gingivalis
 Prevotella intermedia
 Capnocytophaga
 Eikenella corrodens
 Neisseria

52.  Actinobacillus actinomycetemcomitans
 Bacteroides forsythus
 Porphyromonas gingivalis
 Prevotella intermedia
 Wolinella recta

53.  Fusobacterium nucleatum
 Prevotella intermedia
 Peptostreptococcus micros
 Bacteroides forsythus
 Porphyromonas gingivalis

54. The putative periodontal pathogens
Actinobacillus actinomycetemcomitans (A.a)
It's a G-ve facultative anaerobe, non-motile
coccoid bacillus. It correlates with aggressive
periodontitis. It was considered a specific
pathogen especially in LAP.

55. Virulence factors of Actinobacillus
actinomycetemcomitans
• Leukotoxins, which kill or impair neutrophils &
monocytes function, Epitheliotoxins &toxins affecting
fibroblast function.(Fibroblast cytotxicity factor)
• Capsule which resist phagocytosis & lysis by the
complement.
• They possess fimbrae (adhesion factor)& attach well to
oral surfaces.
• Lipopolysaccharide endotoxin which has a potent bone
resorbing activity & interfere with neutrophil function.
• Hydrolytic enzymes & collagenase.

56. Virulence factors of Porphyromonas
gingivalis
G-ve, anaerobic, non-motile assachrolytic short
rods. It forms black-brown colonies on blood
agar. It's isolated from diseased mouth.

57. Virulence factors of Porphyromonas
gingivalis
 It produces numerous virulence factors or damaging toxins
including; collagenase, protease (which destroys
immunoglobulin &complement).
 It forms membrane vesicles (20 nm) which are shed in large
numbers & may directly penetrate the epithelium & into the
connective tissues, carrying with them the secreted proteases.
 It has the ability to attach to epithelial cells, and invade soft
tissues.
 It has a carbohydrate capsule which prevents opsonization by
complement & inhibit phagocytosis by neutrophils.
 It has the ability to inhibit polymorphonuclear leukocytes
(PMNs).

58. Virulence factors of Porphyromonas
gingivalis
• Porphyromonas gingivalis releases gingipains.
• Gingipains specifically cleave protein and cable of
disrupting normal host system.
• The ability of gingipains to stimulate the release of
bradykinin, resulting in increased vascular permeability.

59. Tannerella forsythia (Bacteroides
forsythus)
It's a G–ve anaerobic, spindle shaped pleomorphic
rod, found in higher numbers at sites of
periodontitis rather than gingivitis. It produces
proteolytic enzymes that are able to destroy
immunoglobulins and complement components.

60. Prevotella intermedia
• Previously known as bacteroid intermedius, a G-
ve anaerobic, black pigmented, short rod that
can ferment both carbohydrates & proteins. It
resist phagocytosis (probably by its capsule).
• Its lipopolysaccharide (cell wall) contains unusual
fatty acids having marked effects on immune &
bone cells. It also secretes toxins acting on
epithelial cells. It correlates with ANUG, chronic
periodontitis.

61. Spirochetes (Treponema denticola &
T. vencentii)
• They are spiral, anaerobic motile microorganisms. In
advanced periodontal disease may constitute up to
47% of the observable bacteria in plaque. It's
associated with ANUG (invading the superficial tissues),
chronic periodontitis, & LJP.
• They produce potent hydrolytic enzymes, including
collagenase, proteases, & peptidase.
• T. denticola produce extracellular membrane vesicles,
which have protease & haemagglutinating activity.
Spirochetes release destructive metabolic end products
as ammonia & H2S, which easily, permeates the
tissues.

62. Campylobacter rectus
It's a G–ve anaerobic short motile vibrio, present
in high numbers in diseased sites than healthy
sites, especially in active diseased sites. It
produces potent leukotoxins like A. a.

63. Fusobacterium nucleatum
• G-ve anaerobic rod, regarded as an important
periodontal pathogen, it correlates with ANUG
and chronic periodontitis. It has a potent
lipopolysaccharide endotoxins, & produces
butyric acid as metabolic end product, which
could invade the tissues. It may act synergistically
with P. gingivalis to increase protease secretion.
• Adhesins on its surface enables it to adhere to
epithelial cells, leukcocytes, fibroblasts, & other
bacterial species. It's of low virulence but highly
antigenic i.e. produce immune response.

64. Capnocytophaga species
• They are G –ve facultative anaerobic rods, move
by gliding action i.e. slowly motile. It has been
linked with JP & chronic periodontitis. It's highly
virulent. It produces lipopolysaccharide with
bone resorbing activity, proteases, & has
capsular material which inhibit phagocytosis &
chemotaxis by PNLs.
• Recent studies indicate that it's isolated from 80%
of healthy sites & shouldn't be regarded as a
significant pathogen.

65. Peptostreptococcus micros
It's a G +ve anaerobic small asacchrolytic cocci.
It's associated with anaerobic mixed infections.
It has been detected more frequently at sites of
periodontal destruction. It's present with high
virulence in 55% of periodontitis in young
Egyptian population.

66. Actinomyces species (A. viscosus & A.
naeslundii)
It's G +ve facultative anaerobes. It plays an
important role in calculus formation & bacterial
adhesion, where they adhere through surface
fimbriae to a polysaccharide receptor on cells of
S. sanguis, where they become perpendicularly
arranged on the filaments, hence adhering to
the tooth surface.