Dental plaque formation , What Makes Dental plaque Pathogenic ? , Microorganisms associated with periodontal diseases

1. Dental Plaque
Formation
Under the supervision
of :
Dr. Majdi Kamel

2. What’s the Dental plaque ?
Dental Plaque is an adherent intercellular
matrix consisting primarily of proliferating
microorganisms, along with a scattering of
epithelial cells, leukocytes and macrophages.

3. What’s the Dental plaque ?
CAN ALSO be defined as the soft deposits
that form the biofilm adhering to the tooth
surface or other hard surfaces in the oral
cavity, including removable and fixed
restorations.

4. Dental Plaque is a(host-
associated biofilm).

5. What’s Biofilms ?
Biofilms are defined as
“Matrix—enclosed
bacterial populations
adherent to each other
and or/to surface or
interfaces(by
Costerton).

6. What’s Biofilms ?

7. Dental Plaque As A Biofilm

8. Dental plaque Structure
Dental plaque is now considered to be a
complex and dynamic microbial community
,It contains areas of high and low bacterial
biomass interlaced with Aqueous channels
of bact. Colony.

9. Types of dental plaque
Based on its relationship to the gingival
margin, plaque is differentiated into two
categories :
1. supragingival plaque
2. subgingival plaque

10. 1- Supragingival plaque
Is further differentiated
into:
A. Coronal plaque, is only
the( tooth surface).
B. Marginal plaque, which
is( associated with the
tooth surface at the
gingival margin).

11. 1- Supragingival plaque
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 gray to yellowish-grey
to yellow.

12. Disclosing Agents

13. 1- Supragingival plaque
The rate of formation and location of
plaque vary among individuals and is
influenced by diet, age, factors, salivary
secretion oral hygiene, tooth alignment,
systemic diseases and host factors.

16. 2-Subgingival plaque
Can be further differentiated into:
A. Attached plaque
B. Unattached subgingival plaque
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

18. a-Attached plaque
Attached plaque can be:
1. tooth.
2. Epithelium.
3. connective tissue associated.

19. 1- Tooth-associated Subgingival
Plaque
The structure is similar to the supragingival
plaque.
The flora is dominated by Gram-positive
cocci, rods, filamentous bacteria and
some/few Gram-negative cocci and rods.
This flora is associated with calculus
formation, root caries and root resorption.

21. 2-Epithelium-associated
Subgingival Plaque
This type is loosely adherent because; it lacks the
interbacterial matrix and is in direct association
with the gingival epithelium, extending from the
gingival margin to the junctional epithelium.
This plaque predominantly contains Gram-
negative rods and cocci, as well as a large number
of flagellated bacteria and Spirochetes.

22. 3-Connective Tissue-associated
Plaque
It is usually demonstrated in ANUG and
localized aggressive periodontitis patients.
The clinical significance is unclear.

23. b- Unattached plaque
The unattached plaque can be seen
anywhere.

24. * Thus *
The tooth-associated subgingival plaque is
most important in calculus formation, root
caries and slowly progressive periodontal
destruction, whereas unattached bacterial
component is associated with rapid
periodontal destruction.

25. COMPOSITION OF DENTAL
PLAQUE

26. 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.
The material among the bacteria in dental
plaque is termed as intermicrobial/ cellular
matrix.
It contains organic and inorganic portions.

27. 1- The ORGANIC matrix
The ORGANIC matrix is composed of protein—
polysaccharide complex produced by microorganisms.
Carbohydrates in the form of levans (fructans)
provide smainly energy while glucans (dextran)
provide NOT only energy, but also act as the organic
skeleton of plaque.
Other carbohydrates are galactose and rhamnose.
Glycoproteins provide the protein component and
small amounts of lipids are also present.

28. 2- The INORGANIC matrix
Inorganic components include, primarily
calcium, phosphorus with small amounts of
magnesium, potassium and sodium.

29. Formation/Development of Dental
Plaque
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.
This results from the electrostatic ionic interaction
between hydroxyapatite surface which has negatively
charged phosphate groups that interacts with
opposite charged groups in the salivary
macromolecules.

30. The mean pellicle thickness varies from 100 nm
at 2 hours to 500 to 1,000 nm.
e transition from pellicle to dental plaque is
extremely rapid.
The FIRST components include mainly cocci
with small number of epithelial cells and
PMNL’s  they form a monolayer within a
few hours, and the attached bacteria proliferate
and form small colonies of cocci.
With time other types of microorganisms
proliferate and form different microcolonies

31. Hence, in dental plaque development, two
adhesion processes are required.
First, bacteria must adhere to the Sl. No.
Tooth-associated subgingival plaque
Epithelium-associated plaque

32. 1. Gram-positive bacteria predominates Gram-
positive and Gram-negative bacteria.
2. Does not extend to junctional epithelium
Extends to junctional epithelium.
3. May penetrate cementum May penetrate
epithelium and connective tissue.
4. Associated with calculus formation and
root caries Associated with gingivitis and
periodontitis.30

33. Bacterial attachment via electrostatic
interactions pellicle surface and become
sufficiently attached to withstand oral
cleansing forces.
Second, they must grow and adhere to each
other to allow plaque accumulation.

34. First step in plaque
formation is:
Adhesion and attachment Of Bacteria

35. Bacterial Adherence
During initial adherence, interactions occur
mainly between specific bacteria and the pellicle.
They are:
1- Bacterial Attachment via Electrostatic
Interactions
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

36. 2- Bacterial Attachment via Hydrophobic Interactions
These interactions are based on the close structural fit
between molecules on the pellicle and bacterial
surfaces.
The nature of the hydrophobicity of the cell is not
clearly known.
The contributing factor might be lipoteichoic acid
(LTA), which may provide a long hydrophobic area .
Lectins in the bacterial surfaces recognize specific
carbohydrate structure in the pellicle and become
linked.

37. Adhesion and attachment
Adhesion and attachment occurs between:
1. Bacteria and clean tooth surface
2. Bacteria and pellicle
3. Bacteria and same species
4. Bacteria and different species
5. Bacteria and matrix.

38. Next step in plaque
formation is:
Growth and Accumulation Of
Bacteria

39. Growth and Accumulation of
Bacteria
Once the bacteria is adhered to the pellicle,
subsequent growth leads to bacterial
accumulation and increased plaque mass.
Dental plaque growth depends on:
1. Growth via adhesion of new bacteria
2. Growth via multiplication of attached
bacteria.

40. • The initial bacteria that colonize the pellicle
surface are mostly gram-positive facultative
microorganisms such as morphologic
arrangement of the flora in supragingival
plaque described as “corncob” formations,
characterized by central core consisting of rod-
shaped bacterial cells, e.g. Fusobacterium-
nucleatumand coccal cells, e.g. streptococci
which attaches along the surface of the rod-
shaped cell.

41. The subgingival plaque differs from
supragingival plaque, in that it contains
many large filaments with flagella and is
rich in Spirochetes.
Tooth-associated plaque is similar to
supragingival plaque; whereas tissue-
associated plaque is covered with flagellated
bacteria without a well-defined
extracellular matrix and numerous bristle—
brush formations.

42. This arrangement is also called as “test tube
brush” formation characterized by large
filaments that forms the long axis; and
short filaments or gram-negative rods
embedded in a amorphous matrix

43. Structural and Microscopic
Prosperities Of Dental
Plaque
1-Supragingival Plaque

44. 1- Supragingival Plaque
It is usually adherent to the tooth surface.
It contains gram positive cocci and gram-
negative rods and filaments.
The strongly influences the growth,
accumulation and pathologic potential of
subgingival plaque, especially in the early
stages of gingivitis and periodontitis.

45. Clinical Significance Of Dental
Plaque
The microbial aggregations on the tooth
surface if prevented from maturing may
become compatible with gingival health.
Supragingival plaque if allowed to grow
and mature, may induce gingivitis and can
lead to the formation of a microenvironment
that permits the development of subgingival
plaque.

46. Therefore, supragingival plaque
Actinomycesviscosus and Streptococcus
sanguis, as the plaque matures, secondary
colonization of Prevotella intermedia,
Capnocytophaga, Porphyromonasgingivalis
takes place.
This ability of bacteria to adhere to
different species and genera of
microorganisms is known as coaggregation

47. 2- Subgingival Plaque
Structural and Microscopic
Prosperities Of Dental
Plaque

48. 2- Subgingival Plaque
In association with the presence of
supragingival plaque, there are
inflammatory changes that modify the
anatomic relationships of the gingival
margin and tooth surface.
This result in enlarged gingiva, which
increases the space for bacterial
colonization and also protects bacteria from
normal cleansing mechanisms.

49. They derive nutrients from gingival crevicular
fluid. Many of these microorganisms lack the
adherence ability and utilizes supragingival
plaque bacteria as a means of colonization of the
subgingival area.
Electron microscopic studies have demonstrated
the existence of an organic material called cuticle
between the root surface and subgingival plaque.
It is covered by a dense layer of microorganisms
and is believed to be a remnant or secretary
product of the junctional epithelial cells.

50. Microbial Specificity Of
Periodontal Diseases
Walter Loesche proposed the nonspecific and
specific plaque hypothesis in 1976. The
nonspecific plaque hypothesis states that it is
the total bulk of plaque, which determines the
pathogenicity rather than the individual
species within it.
In other words, all plaque is equally
pathogenic.

51. • According to this, when only small amounts of plaque
are present, the products released by this gets
neutralized by the host. Similarly, large amounts of
plaque would produce large amounts of noxious
products, which would overwhelm the host’s defenses.
• However, several authors have contradicted this
concept.
• First, many patients have considerable amounts of
plaque and calculus as well as gingivitis, but only a
minority suffer from destructive periodontal disease
even then in only few sites.

52. This paradox might be explained by specific
plaque hypothesis, which states that
destructive periodontal disease is a result of
specific microbial pathogens in plaque.
Thus, although the amount of plaque
present correlates well with disease severity,
it correlates poorly in individual patients.

53. But it is the nonspecific plaque hypothesis,
which forms the basis for virtually all the
current modalities for treatment, and
prevention, which relies on the principle of
reducing plaque scores to a minimum.
Thus, although the nonspecific plaque
hypothesis has been discarded in favor of
the specific plaque hypothesis, much clinical
treatment is still based on the nonspecific
plaque hypothesis.

54. Specific Plaque Hypothesis
It states that, not all plaque is pathogenic.
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.

55. This concept was accepted easily due to the
recognition of Actinobacillus
actinomycetemcomitansas a possible
pathogen responsible for localized juvenile
periodontitis.

56. What Makes Dental plaque
Pathogenic ?
The following are the possible pathogenic
mechanisms by which the plaque
microorganisms can cause periodontal disease:
a. Physical nature of plaque.
b. Invasion of tissues by bacteria.
c. Release of toxic and inflammatory substances.
d. Role of bacterial specificity.

57. Microorganisms associated with
periodontal diseases
It is well accepted that a plaque bacteria is
the primary etiologic agent in periodontal
disease.
Bacteria are seen in the oral cavity from
birth to death.
It is estimated that about 400 different
species are capable of colonizing in the
mouth.

58. Counts in subgingival sites range from about 103 in
healthy sulci to greater than 108 in deep periodontal
pockets.
It has not been possible to identify and study all the
organisms present in the bacterial plaque, of nearly
400 species; only 30 of them are considered to be
periodontopathic.
Koch’s postulates, generally used to identify the
periodontopathogenecity of a microorganism, are not
applicable in periodontal disease, as more than one
organism is involved in periodontal diseases.

59. Hence, Socransky (1977) had proposed the following
criteria for identifying the possible causative organisms
in periodontal diseases:
1. The number of etiologic organisms in the diseased site
must be increased and conversely the number o
forganisms must be reduced or absent in healthy sites.
2. If the etiologic organism is eliminated or suppressed, the
disease should stop.
3. Presence of specific antibodies to those microorganisms.
4. Presence of virulence factors associated with certain
microorganisms (e.g. toxins, enzymes, etc.).
5. In vitro or animal experiments should be able to
demonstrate the human disease process.

60. There are many speculations regarding the
pathogens responsible for periodontitis
whether they could be exogenous or
components of indigenous flora.
To explain this controversy, two theories
have been proposed.
1- According to the first theory,
periodontopathic organisms are a part of
indigenous flora and they tend to overgrow
during the disease progression.

61. 2- The second proposal is that, they are not
components of indigenous oral flora, but are
exogenous pathogens derived from outside
sources.
This concept hints that the quantity of
plaque is not necessary for disease onset.
Instead, the site should be contaminated
with specific periodontopathogens.

62. Recent reports have demonstrated a possibility of
viral etiology in periodontitis and implicated viruses
are Epstein Barr virus, human cytomegalovirus and
mixed herpes viral infections.
Viral infection can contribute to periodontitis by
altering the functions of neutrophil, macrophages and
lymphocytes which in turn promotes the overgrowth
of periodontopathic organisms in the subgingival
flora.
The other possibility is that, the viral infection can
destroy the oral epithelial cells thus disrupting the
barrier function of the periodontium.

63. Bacteria Associated with Periodontal
Health and Disease
Wolinella recta Campylobacter rectus (C. rectus)
Bacteroidesgingivalis Porphyromonasgingivalis (P.
gingivalis)
BacteroidesintermediusPrevotellaintermedia (P. intermedia)
BacteroidesmelaninogenicusPrevotellamelaninogenica (P.
melaninogenica)
BacteroidesforsythusTannerellaforsythus
ActinobacillusAggregatibacter
actinomycetemcomitansactinomycetemcomitans

64. Health
Actinomyces (viscosus and naeslundii)
Streptococcus (S. mitis and S. sangius)
Veillonellaparvula, small amounts of gram-
negative
Species are also found.

65. Chronic Gingivitis
 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.
 Gram-negative Organisms
• Fusobacteriumnulceatum
• Prevotellaintermedia
• Veillonellaparvulaas well as Haemophilus,
• Capnocytophagaand Campylobacter species.
• Pregnancy-associated Gingivitis
• Prevotellaintermedia.

66. Acute Necrotizing Ulcerative Gingivitis
• Spirochetes
• Prevotellaintermedia.
Adult Periodontitis
• Porphyromonasgingivalis
• Bacteroides (Tannerella) forsythus
• Prevotellaintermedia
• Campylobacter rectus
• Eikenellacorrodens
• Fusobacteriumnucleatum
• Actinobacillusactinomycetemcomitans
• Peptostreptococcus micros
• Treponema, and
• Eubacteriumspecies.

67. Acute Necrotizing
Ulcerative Gingivitis
Chronic Adult
Periodontitis

68.  Viruses
• EBV-1 (Ebstein-Barr virus)
• HCMV (Human cytomegalovirus).
 Localized aggressive Periodontitis
• Actinobacillus (Aggregatibacter) actinomycetemcomitans
• Porphyromonasgingivalis
• Eikenellacorrodens
• Campylobacter rectus
• Fusobacteriumnucleatum
• Bacteroidescapillus
• Eubacteriumbrachy
• Capnocytophaga
• Herpes virus.

69. Generalized aggressive Periodontitis
• Actinobacillus (Aggregatibacter)
actinomycetemcomitans
• Porphyromonasgingivalis
• Prevotellaintermedia
• Capnocytophaga
• Eikenellacorrodens
• Neisseria.

70. Localized
aggressive
Periodontitis
Generalized
aggressive
Periodontitis

71. Refractory Periodontitis
• Actinobacillusactinomycetemcomitans
• Bacteroidesforsythus
• Porphyromonasgingivalis
• Prevotellaintermedia
• Wolinella recta.
Abscesses of the Periodontium
• Fusobacteriumnucleatum
• Prevotellaintermedia
• Peptostreptococcus micros
• Bacteroidesforsythus
• Porphyromonasgingivalis.

72. Refractory Periodontitis
Abscesses of the Periodontium

74. Edit By :
Ghadah Abulqumsan
Reham Altayep
Noor Abdurrahman