This document discusses dental plaque and the role of bacteria in periodontal diseases. It begins by describing how the oral cavity is colonized by bacteria from birth and how plaque forms on teeth. Plaque is made up of over 500 types of bacteria embedded in an extracellular matrix. The document then discusses plaque structure and composition, the diversity of surfaces in the oral cavity that bacteria can adhere to, and factors that influence individual plaque formation. It describes the ultrastructure of plaque formation over time, as early colonizers attach followed by maturation into a biofilm. Physiological properties and growth dynamics of plaque are also summarized.

1. Periodontal microbiology
Dr.D.Navya, MDS

2. Role of dental plaque in etiology
of periodontal diseases
 Introduction:
 Sterile fetus within short period of birth starts inoculating micro
organisms, by the weaning period inoculated with app 10 14
microorganisms consisting of more than 400 different types of
bacteria.
 Balance
 Beneficial role
 Plaque structure and composition.
 Identification.
 Removal.

3. Diversity of intra oral; surfaces for
bacterial adhesion
 Ecological point of view oral cavity considered as “open growth
system.
 Oral cavity divided in to five major ecosystems:
 Intraoral, supragingival, hard tissues.
 Periodontal / periimplant pockets.
 Buccal epithelium, palatal epithelium, and epithelium of floor
of mouth.
 Dorsum of tongue.
 Tonsils.

4. Diversity of intra oral; surfaces for bacterial
adhesion:
 Bacterial adhesion to epithelial cells generally shows large
intersubject variability.
 Positive correlation between the adhesion rate of pathogenic
bacteria to different epithelia and the susceptibility of that
patient to certain infections*.
 Lower adhesion rates of P. gingivalis and P. intermedia stains to
gingival epithelial cells in rats*
 High turn over rate of intra oral epithelial cells prevents the
permanent accumulation of large masses.

5. Diversity of intra oral; surfaces for bacterial
adhesion:
 Teeth can be considered as a “ Port of entry” for
periopathogens.
 Key pathogens such as Actino-bacillus actinomycetemcomitants
and P. gingivalis will disappears from all other intra oral
habitants after full mouth extraction .*
 P. intermedia and other black pigmented prevotella species can
remain, but at lower frequencies and numbers.
 Micro biological point of view, teeth and implants are unique for
two reasons: Provide hard and nonshedding surfaces and they
form unique ectodermal interruption.

6. Structure and composition of plaque
 Dental plaque as defined
clinically as a structured,
resilient, yellowish grayish
substance that adhere
tenaciously to the intra oral
hard surfaces, including
removable and fixed
restorations.*
Plaque on the enamel
surface of central incisor

7. Structure and composition of plaque
Plaque
 Primarily Micro organisms.
 1gm of - app 10 11bacteria.
 Single tooth surface -10 9.
 Healthy sulcus - 10 3.
 Deep periodontal pockets- 10 8
 More than 500 distinct species.
 Non bacterial may be mycoplasm, viruses, ect
Inter cellular matrix:
Organic :
polysaccharides (Dextran - Bacteria).
Protein ( Albumin – GCF).
Glycoprotein ( Saliva) .
Lipid (Cell membranes).
In organic:
predominantly by calcium and phosphates.
Trace amount by sodium, calcium etc.

8. Structure and composition of plaque
Plaque classified as
Supra gingival:
Gram +ve cocci and short rods predominant at tooth
surfaces.
Gram –ve rods, filaments, spirochetes, at outer surfaces.
Sub gingival plaque:
Local availability of blood products and
low redox potential makes differ
environment
Gingival crevice bathed by GCF, contains
host inflammatory cells and mediators.
Tooth associated Tissue associated

9. Structure and composition of plaque
Sub gingival plaque
Tooth associated:
Adhering to the root cementum.
Filamentus microorganisms dominate.
Cocci and rods also present .
Gram +ve rods and cocci:
St. mitis
St. sangius
A. Viscosus
A. naeslundii
Eubacterium.
Tissue associated:
Lack of definite intermicrobial matrix, gram -ve rods and
cocci.
Large number filaments, flagellated rods, and spirochetes.
Predominate organisms:
St. oralis
St. intermedius
Peptostreptcoccus micros
P. gingivalis
P. intermefia
T. Forsythia
F. Nucleatum

10. Structure and composition of plaque

11. Structure and composition of plaque
Site specificity of plaque
Marginal
plaque:
Gingivitis.
Tooth
associated and
supragingival
plaque
Calculus formation and
root caries.
Tissue
associated
plaque:
Periodontitis

12. Plaque as Biofilm
 In general, have an organized structure.
 They are composed of micro colonies of bacterial cells non- randomly distributed in
a shaped matrix or glycocalyx.
 Having fluid filled channels running through the plaque mass (Acting as a primitive
“ circulatory” system).
 Bacteria exist and proliferate within the intercellular matrix through which the
channels are run.
 Channels permit the passage of nutrients and other agents.
 Biofilm functions as a barrier.

13. Plaque formation at the ultra structural
level.
 Three major phases:
I. The formation of the pellicle on the tooth
surfaces.
II. Initial adhesion and attachment of bacteria.
III. Colonization and plaque maturation.

14. Plaque formation at the ultra structural
level.
The formation of the pellicle on the tooth
surfaces
Tooth surface
Electrostatic forces.
Van der wals.
Hydrophobic forces
Selective absorption
Pellicle
Glycoprotein
Proline rich protein
Histidine rich protein
Phospho protein
Enzymes
Statrs forming within the nano seconds
of polishing.
Composition act as adhesive sites for
bacteria( receptors).
Physical and chemical nature of solid
substratum significant;y affect the
composition.

15. Plaque formation at the ultra structural
level.
Initial adhesion and attachment of bacteria:
Microbial adhesion to surfaces in an aquatic environment as a four stages sequences:
I. Trans port to the surface.
II. Initial adhesion.
III. Attachment.
IV. Colonization of the surface and biofilm formation.
Phase I: Trans port to the surface:
- Transport of bacterium to the tooth surface.
-Random contact may occur, through:
- Brownian motion.
- Sedimentation of microorganisms
- Liquid flow
- Active bacterial movement.

16. Plaque formation at the ultra structural
level.
Phase II : Initial adhesion.
- Initially adhesion of bacterium by long range force (50nm) ie, Reversible.
- Later by short range forces ( less than 2 nm) ie, irreversible.
- These includes Electrostatic repulsive forces( E) and Van der wals attractive forces ( A).
- Application of formula given by Derjaguin, Landau, Verwey, and Overbeek (DLVO).
- Total interaction energy : G TOT = GA +GE.
- G TOT consists of :
- secondary minimum.( Reversible adhesion).
- Positive maximum .(Energy barrier B).
- Primary minimum. ( Irreversible adhesion).

17. Plaque formation at the ultra structural
level.
I. Transport to the surface.
GA
50nm Long range scale forces , reversible
GA
GE
Short range forces, Irreversible
Less than 2nm
(Secondary minimum)
(Primary minimum)
Mediated only by the
electrostatic repulsive and
van der wals attractive
forces.
Along with above forces:
Hydrogen bonding .
Ion Pair formation.
Steric interactions.

18. Plaque formation at the ultra structural
level.
 Phase III: Attachment:
- Here firm anchorage between bacterium and surface will be
established by specific interactions ( covalent, ionic, or hydrogen
bonding).
- This is fallowed by direct contact or bridging true extra cellular
filamentous appendages.
- The bonding between bacteria and pellicle is mediated by specific
extrcellular proteinaceous components ( adhesions) of the organisms
and complementary receptors( ie proteins, glycoprotein, or
polysaccharides) on the surfaces ( e.g., pellicle) and is species specific.

19. Plaque formation at the ultra structural
level.
Phase III: Attachment:
Streptococci bind to Proline
rich protein
Streptococci bind to amylase enzyme
A.Viscous binds proline rich protein with its
fimbrea
Streptococci and
Actinomyces considered as
early colonizers and binds
to salivary molecules of
pellicle.
Some molecules from
pellicle under goes
conformational changes
when they absorbed on
tooth surfaces so that new
receptors become available

20. Plaque formation at the ultra structural
level.
Phase IV: colonization and plaque maturation
Here early colonizers start growing and allow for newly formed bacterial
clusters remain attached, micro colonies and biofilm can develop.
New mechanism involved characterized by inter bacterial connections.
Here shows the 18 genera from the oral cavity shows coaggregation ( Cell-to-
cell recognition of genetically distinct partner cell types).
Coaggregation is interaction of protein and carbohydrate molecules located on
the bacterial cell surfaces, Hydrophobic, electrostatic, van der wals forces also
participates.

21. Plaque formation at the ultra structural
level.
Coaggregation between certain bacterias:
Streptococci show intrageneric
Coaggregation bind to already
present nascent monolayer of
streptococci.
Secondary colonizers with early colonizers.
F.Nuceatum with St. sanguis
P. Loescheii with A. viscosus.
Capnocytophaga with A. viscosus.
Later stage Coaggregation
between the Gram –ve
species predominate:
F. Nuleatum with P. gingivalis or T. denticola.
“Corncob” formation (Streptococci with B.
matruchotii or actinomyces.
“Test tube brush” filamentous to gram –ve
rods.

22. Plaque formation at the ultra structural
level.
Recent analysis of more than 13000 plaque samples, looking for 40 sub
gingival microorganisms using DNA hybridization technologies, defined
complexes of periodontal micro organisms as follows:
A.naeslundii, A.
viscosus.
Streptococcus spp.
E. Corrodens.
A. actinomycetemcomitans-a.
Capnocytophaga.
Fusobacterium.
Prevotella.
Campylobacter species.
P. gingivalis.
T. forsythia.
T. denticola

23. Plaque formation at the ultra structural
level.
Over view of bacterial interactions during plaque formation:

24. Physiological properties of dental plaque
The transition from gram +ve to gram –ve microorganisms observed in the
structural development of plaque is paralleled by a physiologic transition in the
developing plaque.
The early colonizers use oxygen and lowers the redox potential of the
environment which than favors the growth of anaerobic organisms.
Gram +ve organisms use the sugars as an energy source and saliva as carbon
source.
The bacteria that predominate in mature plaque are anaerobic and asscharolytic
and use amino acids and small peptides as energy sources.
Laboratory studies have shown that many physiologic interactions among the
different bacteria found in the dental plaque.

25. Physiological properties of dental plaque
Streptococcus.
Actinomyces
Formate
Veillonella
Campylobacter
Protoheme
P. gingivalis.
P. intermedia
P-Aminobenzoate
Streptococcus mutants
Capnocytophaga
Fusobacterium
Treponema
NH4+ Co2
H2
Menadione
Succinate
Isobutyrate
hemin Host A- Globulin
Lactate

26. Growth and dynamics of dental plaque:
Ultra structural aspects:
.
Important changes in
the plaque growth
rate can be detected
within the first 24
hours
2-8 hours streptococci
saturate the salivary
pellicular binding sites and
thus covers 3% to 30% of
enamel suface
Short period of rapid
growth .4-6 hours
generation time
After one day
biofilm is
deserved.
Bacterial densities approaches 2-6
million bacteria/mm2 than marked
increase in growth rate up to 32
million bacteria/ mm2.
Further growth by self
multiplication of already existing
rather than new organisms
By the 3rd day increases
up to 30mm .Later starts
maturation
Loeshe et al
1988

27. De Novo supragingival plaque formation
Clinical aspects:
By the 3 days, plaque growth increases at
rapid rate ,then slow down from that point
onward.
After 4th days composition of plaque alters
shifts towards more anaerobic and gram –
va flora, including and influx of fuso
bacteria, filaments, spiral forms, and
spirochetes.
During night plaque growth rate is
reduced by about 50%.
Dark field microscopic
appearance of 14 hours
plaque:

28. Topography of supra gingival plaque:
Initial growth along the gingival margin and from inter dental spaces.
Later extended in to coronal direction.
This can be altered by surface irregularities such as pits, grooves,
perikymeta, cracks.
Scanning electron microscopy revealed early colonization of the enamel
surfaces starts from surface irregularities, where bacteria escapes shear
forces, allowing time needed to chanhe from reverisble to irreversible
binding.*

29. Surface micro roughness:
Rough intra oral surfaces accumulates and retain more plaque and calculus in
terms of thickness, area, and colony forming units.*
Shown increase maturity and pathogenicity of its bacterial components and
characterized by an increase proportions of motile organisms and spirochetes, or
denser packing of bacteria.
There seems to be a threshold level for surface roughness Ra about 0.2 mm ,
above which bacterial adhesion will be facilitated.*

30. Individual variables influencing plaque
formation.
Plaque formers
Heavy ( Fast): Light ( Slow):
•* Noticed only minor differences between the groups, and no single variable
considered
•*After one day, the heavy plaque formers showed more plaque with a more complex
supragingival structure.
•From 1- 14 days, there were no discernible differences between both groups, except
for a more prominent inter microbial matrix in the group of fast growers.
•* Notice higher level of Gram –ve rods in 4 day old plaque.
•* Factors such as diet, chewing fibrous foods, smoking, restorations, tongue and
palate brushing, the colloidal stability of bacteria in the saliva, antimicrobial factors
present in the saliva, chemical composition of pellicle.
Zee KY et al ( 1996,97)
Simonsson et al ( 1987)
Ainamo J et al ( 1979)

31. Variation within the dentition:
* Early plaque formation occur fasters in:
- In the lower jaw compare to the upper jaw.
- In the molar areas.
- On buccal tooth surfaces compare to oral sites.
- In the interdental areas compare to strict buccal on
oral surfaces.

32. Impact of gingival inflammation:
Plaque formation is more rapoid on tooth surfaces facing
inflammed gingival margins than on those adjecent to healthy
gingival *
Increase in crevicular fluid production enhances plaque
formation.
Impact of patients age :
* Could detect no differences in de nevo plaque formation,
either in amount or in composition between a group of young
and older subjects.

33. De Nevo sub gingival plaque formation
Cultural techniques, showed changes within the sub gingival micro biota during the first week after
mechanical debridement and reported only partial reduction of 3 logs, followed by a fast regrowth to
almost pre treatment level within 7 days.*
High proportions of treated tooth surfaces still harbored plaque and calculus after scaling, theses
remaining bacteria were considered the primary source for the sub gingival re colonization.*
Some pathogens penetrate the soft tissues or the dentinal tubules and eventually escapes
instrumentations.*
Sub gingival colonization in 6-mm pockets with smooth or rough root surfaces and concluded that
smooth surfaces harbored significantly less plaque.*

34. Principle of bacterial transmission, trans-
location, or cross infection:
Transmission
Periodontal pathogens are
transmissible within
members of families
( Zambon JJ et al ( 1996).
Noticed transmission of
cariogenic species from
mother to child.
( Kohler B et al ( 1981)
Translocation
Intra oral transmission is known as
translocation.
Ist noticed by Loesche et al (1979) St mutans
from dental inlay to neighboring teeth and
contra lateral arch .
Edman et al (1975) St mutants in two
volunteers by means of inoculated dental floss.
Christersson et al (1985) A. actinomycetem-
comitans in aggressive periodontitis by probing.

35. Principle of bacterial transmission, trans-
location, or cross infection:
Microbiology of implants in partially edentulous
patients:
Micro biota in pockets around the teeth that in
periimplant pockets in partially edentulous patents
and reported a striking similarity.*
In partially edentulous patients, teeth might act as
a reservoir for the recolonization of the sub gingival
area around implants, This hypothesis is supported
by Sumida et al (2002).

36. Principle of bacterial transmission, trans-
location, or cross infection:
Translocation and guided tissue regeneration:
Nowzari et al (1996) Noticed the healthy group significantly less
membrane contamination both immediately after insertion as well as
at removal after 6 weeks. The healthy group showed more clinical
gain in clinical attachment than the disease group.
Mombelli et al (1997) compared the clinical and microbiological
changes showed that after 6 months significant additional
improvements with the more global approach.
Authors concluded that pathogens most likely were transferred
through saliva from infected untreated periodontal lesions or other
niches to the treated sites.

37. Principle of bacterial transmission,
trans- location, or cross infection:
Translocation and mechanical debridement:
One stage, full mouth disinfection, introduced by Leuven group in the
1990s.
Purpose is to eradicate, or at least suppress, periodontal pathogens for
short time not only from the periodontal pockets, but all their intraoral
habitats.
This procedure comprises:
- Full mouth scaling and root planing within 24 hours to reduce the number of sub
gingival pathogenic organisms.
- Subgingival irrigation of all pockets with 1% chlorhexidine gel to kill remaining bacteria.
-Tongue brushing with an antiseptics to suppress the bacteria in the niche.
- Mouth rinsing with the antiseptic to reduce the bacteria in saliva and on the tonsils.

38. Principle of bacterial transmission, trans-
location, or cross infection:
Intraoral Equilibrium between Cariogenic Species and
Periopathogens:
*After the nonsurgical and surgical treatment of periodontitis, the
shift towards the more cariogenic flora was oberved .
That could be due to
-Subgingival out growth by S. mutans occupying spots that become available
after periodontal therapy
- May creation of new periodontal environment.
- Down growth of S. mutans from the supra gingival area, where the species
could survive in the saliva.

39. Association of Plaque Microorganisms with
Periodontal diseases:
*Etiology of periodontitis considered three group factors that
determine whether active periodontitis occur in subjects:
I. Susceptible host.
II. The presence of pathological species.
III. The absence or small proportions of beneficial bacteria.
Susceptible host:
Mainly hereditary but can be
influenced by Environmental and
behavioral factors such as
smoking diabetes, stress.
Pathogens:
Susceptible clonal type and in
sufficient number should present.
Believe that A.
actinomycetemcomitans, T.
forsythia, and P. gingivalis Key
pathogens for periodontal
diseases.
Other organisms also participates
Eg,. P. intermedia ect.
Beneficial species:
I. Passively occupies the niche.
II. Actively prevent adherence
of pathogens.
III. Adversely affect the vitality
or growth of pathogens.
IV. Affect the ability of
pathogens to produce
virulence factors.
V. Degrades the virulence
factors produced by the
pathogens. Eg,. S. mutans

40. Microbial Specificity of Periodontal
diseases:
Non specific plaque
hypothesis:
•In the mid 1900s.
•Periodontal diseases due to accumulation
of plaque over time.
•Diminished host response.
•Increase host susceptibility with age.
• Elaboration of noxious products from the
entire plaque.
•Treatment options for periodontal
diseases based on this hypothesis that
good oral hygiene maintenance and
mechanical debridement.
Specific plaque
hypothesis:
•In 1960s.
•It states that only certain plaque is
pathogenic, and its pathogenicity
depends up on the presence of or
increase in specific micro organisms .
•Different morphophytes has been
found in healthy vs Periodontally
diseased sites.
•One example of this hypothesis
Association of A.
actinomycetemcomitans with localized
aggressive periodontitis.

41. Microorganisms Associated with Specific
Periodontal diseases:
In Periodontal health:
• Gram +ve facultative species and members of the genera Streptococcus and
Actinomyces, e.g., S.sngius, S. mitis, A.viscosus, A. naeslundii.
• Small proportions of gram –va specieses such as P. intermedia, F.nucleatum,
and Capnocytophaga, Neisseria, and Villonella.
• Few sphirochetes and motile organisms are also found.
• Certain protective or benificial organisms are also found S.sangius, V.Parvula,
and C. ochraceus.

42. Microorganisms Associated with Specific
Periodontal diseases:
In Gingivitis:
• Initial microbiota comprises of Gram+ve (56%) and gram –ve (44%), and aswell as
facultative (59%) and anarobic (41%) .
• Predominate gram +ve species S. sngius, S. mitis, S.intermedius, S.oralis, A. viscosus, A.
naeslundii, and P.micros.
• Gram –ve are F.nuleatum, P. intermedia, and V. parvula, Haemophilus, Capnocytophaga,
and campylobacter species.
• Pregnancy gingivitis associated with P. intermedia.

43. Microorganisms Associated with Specific
Periodontal diseases:
Microbial shift during diseases:
Gram +ve Gram-ve
Cocci Rods
Non motile Motile
Facultative anaerobes Obligate anaerobes
Fermenting proteolytic
Spirochetes

44. Microorganisms Associated with Specific
Periodontal diseases:
Localized Aggressive Periodontitis:
Predominate organisms composed of gram -ve, capnophillic, and anaerobic rods.
(90)% of total cultivable organisms harbors A. actinomycetemcomitans.
Other organisms includes P.gingivalis, E.corrodens, C.rectus, F.nuleatum,
B.capillus, Eubacterium brachy, capnocytophaga species, and spirochetes.
Herpes virus including EBV-1 and HCMV.

45. Microorganisms Associated with Specific
Periodontal diseases:
Necrotizing periodontal diseases:
Associated with stress and HIV infection clinically.
Microbiologically associated with P. intermedia, and especially of spirochetes.
Abscess of the Periodontium:
Microbiota associated with abscesses are P. intermedia, P. gingivalis, P. micros,
and T. forsythia.

46. Microorganisms Associated with Specific
Periodontal diseases:
Periodontitis as manifestation of systemic disease:
•Subgingival micro biota similar to other forms of periodontal diseases.
•Rapid destruction believes to be associated with some immunological
abnormality.
Periimplantitis:
Healthy periimplant pockets consists of high proportions of cocciodal cells, low ration of
anaerobic/aerobic, low number of gram anaerobic species, and low detection of frequencies for
periodontal pathogens.
Periimplantitis consists of A.actinomycetemcomitans, P.gingivalis, T. forsythia, P. micros, C.rectus,
Fusobacterium, and capnocytophaga.
Also noticed Pseudomonas aurginosa, entero bacteriaceae, candida albicans, and staphylococci.
Noticed high proportions of Staphylococci aureus and S. epidermis.