1. 1

2. MICROBIOLOGY OF
PERIODONTAL DISEASES
Presented by
Dr Ashish Bisane
Post Graduate Student
Dept. of Periodontics
Swargiya Dadasaheb Kalmegh Smruti Dental
College and Hospital, Nagpur.
2

3. Introduction
• The colonization of the oral cavity also starts close to
the time of birth.
• Within hours after birth, the sterile oral cavity will be
colonized by low numbers of mainly facultative and
aerobic bacteria.
• It is estimated that more than 700 different species are
capable of colonizing the adult mouth and that any
individual typically harbours 150 or more different
species. (Moore WE, 1994)
• Most oral bacteria are harmless commensals under
normal circumstances.
3

4. Bacterial Classification
• Based on Morphology : Cocci, Bacilli,
Spirochetes
• Based on Staining Characteristics
• Based on Culturing Characteristics (Aerobes,
Facultative anaerobes, Microaerophiles,
Obligate Anaerobes /Anaerobes)
4

5. Bacterial Classification Based On Shape
5

6. Gram +ve
(Purple/Blue)
Bacilli
Cocci E.g.: Clostridium,
Corneybacterium
Catalase +ve Catalase –ve
(clusters) (chains)
Staph. Strepto.
Beta Hemolysis
Coagulase +ve Coagulase –ve Alpha Hemolysis (Clear Colonies) No Hemolysis
E.g. S. aureus E.g. S.epidermis (Green Colonies) 20 Lancefield Enterococci
Groups
Capsule /Quelling
+ve No capsule,
Bacitracin Sensitive Bacitracin Resistant
Optochin resistant.
Optochin Sensitive E.g. S.pyogenes E.g. S, Agalactiae
e.g. S. viridans
e.g. S. Pneumoniae
6

7. Gram – ve
Pink
Coccobacilli
Cocci Bacilli
E.g. H.influenza
Maltose fermenter Lactose Fermenter
Lactose Non-
E.g. E.g. Klebsiella, Fermenters
N.meningtides E.coli
Maltose Non-
Oxidase +ve
Fermenter
E.g. Pseudomonas
E.g. N.gonorrhea
Oxidase –ve
E.g. Salmonella,
7
Shigella

8. Similarity between Periodontal
Diseases and Other Infectious Diseases
• Individuals may be colonized continuously by
periodontal pathogens at or below the gingival
margin and yet not show evidence of ongoing or
previous periodontal destruction.
• In spite of the presence of periodontal pathogens,
periodontal tissue damage does not take place.
• This phenomenon is consistent with other
infectious diseases in which it may be observed
that a pathogen is necessary but not sufficient for
a disease to occur.
9

9. Unique Features of Periodontal
Infection
• The major reason for this uniqueness is the unusual anatomic feature
that a mineralized structure, the tooth passes through the
integument, so that part of it is exposed to the external environment
while part is within the connective tissues.
• The tooth provides a surface for the colonization of a diverse array of
bacterial species.
• Bacteria may attach to the tooth itself, to the epithelial surfaces of
the gingiva or periodontal pocket, to underlying connective tissues,
if exposed, and to other bacteria which are attached to these
surfaces.
• Thus, a situation is set up in which microorganisms colonize a relatively
stable surface, the tooth and are continually held in immediate
proximity to the soft tissues of the periodontium.
10

10. • The organisms that cause periodontal diseases
reside in biofilms that exist on tooth or
epithelial surfaces.
• The biofilm provides a protective environment
for the colonizing organisms and fosters
metabolic properties that would not be possible
if the species existed in a free-living
(planktonic) state.
11

11. • Dynamic Equilibrium:
(1) Swallowing, Mastication, Or Blowing The Nose
(2) Tongue And Oral Hygiene Implements
(3) The Wash-out Effect Of The Salivary, Nasal, And
Crevicular Fluid Outflow
(4) Active Motion Of The Cilia (Nasal And Sinus
Walls).
• Most organisms can only survive in the oropharynx
when they adhere to either the soft tissues or the
hard surfaces (teeth, dentures, and implants).
12

12. • Several different types of surfaces are available for bacterial adhesion: soft
tissues, such as mucosae, skin, and cornea, and hard tissues, such as teeth and
nails.
• On the basis of physical and morphologic criteria, the oral cavity can be
divided into six major ecosystems (also called niches), each with the following
distinct ecologic determinants:
1. The intraoral, supragingival, hard surfaces (teeth, implants, restorations, and
prostheses)
2. Subgingival regions adjacent to a hard surface, including the periodontal/peri-
implant pocket (with its crevicular fluid, the root cementum or implant
surface, and the pocket epithelium)
3. The buccal, palatal epithelium, and the epithelium of the floor of the mouth
4. The dorsum of the tongue
5. The tonsils
6. The saliva
13

13. Historical Perspective
• Investigators in the period from 1880–1930
suggested four distinct groups of microorganisms
as possible etiologic agents; amoeba,
spirochetes, fusiforms, and streptococci.
• The basis of this determination was primarily the
seeming association of these organisms with
periodontal lesions.
• The major techniques : wet mount or stained
smear microscopy and limited cultural techniques.
15

14. Amoeba
• They found higher proportions of amoeba in lesions of
destructive periodontal diseases than in samples taken
from sites in healthy mouths or mouths with gingivitis.
• Treatment was done using systemic or local Emitin
and/or Emitic.
• The role of amoeba in periodontal disease was
questioned by some authors because amoeba were
found in sites with minimal or no disease and could not
be detected in many sites with destructive disease and
because of the failure of emitin to ameliorate the
symptoms of the disease.
16

15. Spirochetes
• Investigators reported higher proportions of
spirochetes and other motile forms in lesions of
destructive disease when compared with control
sites in the same or other individuals.
• Neosalvarsan (compound 606), the anti-
spirochetal agent used to treat syphilis, coupled
with the use of subgingival scaling to control
destructive periodontal disease.
• Other investigators employed bismuth compounds
to treat oral spirochetal infections.
17

16. Fusiforms
• The third group of organisms that were frequently
suggested to be etiologic agents of destructive
periodontal diseases, including Vincent’s infection, were
the spindle-shaped fusiforms.
• These organisms were originally recognized on the basis
of their frequent appearance in microscopic examination
of subgingival plaque samples.
• The organisms were first related to periodontal disease
by Plaut (1894).
• Vincent (1899) distinguished certain pseudomembranous
lesions of the oral cavity and throat from diphtheria and
recognized the important role of fusiforms and
spirochetes in this disease.
• In honour of this investigator the infection became
known as Vincent’s infection.
18

17. Streptococci
• These microorganisms were proposed on the
basis of cultural examination of samples of
plaque from subgingival sites of periodontal
disease.
• The selection of the streptococci may have
been predicated upon the fact these were the
only species that could be consistently isolated
from periodontitis lesions using the cultural
techniques of that era.
19

18. • Invasion of the periodontal tissues by bacteria, was thought
to be important in the pathogenesis of periodontal diseases
in the early 1900s, forgotten and then rediscovered.
• The initial enthusiasm for the hunt for the etiologic agents
of destructive periodontal diseases slowly subsided and by
the mid 1930s there were virtually no workers involved in
this quest.
• This state was eloquently described by Belding and
Belding (1936) in the aptly titled “Bacteria – Dental
Orphans”.
• In between 1920 to 1940 it was thought that periodontal
disease was due to some constitutional defect on the part of
the patient, trauma from occlusion, disuse atrophy or some
combination of these factors.
21

19. Non – Specific Plaque Hypothesis
• Clinicians recognized that plaque control was essential in the
satisfactory treatment of periodontal patients.
• According to this “nonspecific plaque” hypothesis, any
accumulations of microorganisms at or below the gingival margin
would produce irritants leading to inflammation.
• The non specific plaque hypothesis maintains that periodontal
disease results from the elaboration of noxious products from
the entire plaque flora. (Loesche, 1976)
• The inflammation in turn was responsible for the periodontal tissue
destruction.
• The specific species of microorganisms that accumulated on the
teeth was not considered to be particularly significant, providing that
their numbers were sufficiently large to trigger a destructive process.
22

20. • At first, a direct relationship was often assumed to exist
between the total number of accumulated bacteria and the
amplitude of the pathogenic effect; biologically relevant
differences in the composition of plaque were not usually
considered.
• This bacterial mass, termed plaque, was shown to produce a
variety of irritants, such as acids, endotoxins, and antigens,
which, over time, invariably dissolved teeth and destroyed
the supporting tissues.
• Consequently, the need to discriminate among bacterial
deposits from different patients or at healthy or diseased
sites was not yet recognized in detail.
• Individuals with extensive periodontal disease were either
suspected of having a weak resistance to bacterial plaque as
a whole or were blamed for inadequate home care.
• Such a view of dental plaque as a biomass is referred to as
the non specific plaque hypothesis. (Theilade 1986).
23

21. Mixed Infections
• In the early 1930s, investigators found that mixtures of microorganisms
isolated from lung infections or subgingival plaque would induce lesions
when injected subcutaneously into various experimental animals.
• A combination of a fusiforms, a spirochete, an anaerobic vibrio and an
alpha haemolytic streptococcus could cause transmissible infections in the
guinea pig.
• Macdonald and co-workers (1956) were later able to produce transmissible
mixed infections in the guinea pig groin using combinations of pure
cultures.
• The critical mixture of four organisms included a Bacteroides
melaninogenicus strain, a Gram positive anaerobic rod and two other
Gram-negative anaerobic rods.
• These results led to the concept that mixed infections might be
“bacteriologically non-specific but biochemically specific”.
24

22. Return To Specificity In Microbial Etiology
Of Periodontal Diseases
• In the 1960s, interest in the specific microbial etiology of
periodontal disease was rekindled.
• It was demonstrated that periodontal disease could be transmitted in
the hamster from animals with periodontal disease to animals
without periodontal disease by caging them together.
• Swabs of plaque or faeces from diseased animals were effective in
transmitting the disease to animals free of disease. It was
demonstrated that a pure culture of a Gram-positive pleomorphic
rod that later became known as Actinomyces viscosus was capable
of causing destructive periodontal disease in animals free of disease.
• Other species isolated from the plaque of hamsters with periodontal
disease did not have this capability.
25

23. • At about the same time, it was demonstrated that spirochetes with a unique
ultra structural morphology could be detected in practically pure culture in
the connective tissue underlying lesions of ANUG and within the adjacent
epithelium.
• Control tissue taken from healthy individuals and individuals with other
forms of disease did not exhibit a similar tissue invasion.
• To date, the spirochete associated with ANUG has not been cultivated.
• Such findings suggested that there might be more specificity to the
microbial etiology of periodontal disease than had been accepted for the
previous 4decades.
• Human isolates of Actinomyces species were shown to have this ability in
vitro and led to plaque formation and periodontal destruction in animal
model systems.
• These findings reinforced the notion that organisms that formed abundant
plaque were responsible for destructive periodontal disease.
26

24. From Non-Specific to Specific
Plaque Hypothesis
• By the end of the 1960s it was generally accepted that dental plaque
was in some way associated with human periodontal disease.
• It was believed that the presence of bacterial plaque initiated a series
of as yet undefined events that led to the destruction of the
periodontium.
• It was thought that the major event triggering destructive
periodontal disease was an increase in mass of bacterial plaque,
possibly accompanied by a diminution of host resistance.
• Indeed, in the mid 1960s the classic studies of Loe et al. (1965,
1967) and Theilade et al. (1966) convincingly demonstrated that
plaque accumulation directly preceded and initiated gingivitis.
27

25. • If all plaques were more or less alike and induced a particular tissue
response in the host, why was periodontal destruction localized,
taking place adjacent to one tooth but not another?
• If plaque mass was a prime trigger for periodontal destruction, why
did certain subjects accumulate much plaque, frequently
accompanied by gingivitis, but fail, even after many years to
develop destruction of the supporting structures?
• On the other hand, why did some individuals with little détectable
plaque or clinical inflammation develop rapid periodontal
destruction?
• If inflammation was the main mediator of tissue destruction, why
were so many teeth retained in the presence of continual gingivitis ?
28

26. • One explanation may have been that there were inconsistencies
in the host response, or disease required the superimposition of
local factors such as trauma from occlusion, overhanging
fillings etc.
• Newman et al. (1976, 1977) and Slots (1976) demonstrated that
the microbial composition of subgingival plaque taken from
diseased sites differed substantially from the samples taken
from healthy sites in subjects with localized aggressive
periodontitis (LAP).
• Tanner et al. (1979) and Slots (1977) demonstrated that the
microbiota recovered from lesion sites from subjects with
chronic periodontitis differed from the microbiota from healthy
sites in the same subjects and also from lesion sites in LAP
subjects.
• Such a view of periodontitis being caused by specific
pathogens is referred to as the specific plaque hypothesis
(Loesche 1979).
29

27. Biofilm
• The term biofilm describes the relatively
indefinable microbial community associated with
a tooth surface or any other hard, non-shedding
material (Wilderer & Charaklis 1989).
• Biofilms consist of one or more communities of
microorganisms, embedded in a glycocalyx, that
are attached to a solid surface.
• The biofilm allows microorganisms to stick to and
multiply on surfaces.
30

28. • This method of growth provides a number of
advantages to colonizing species.
• A major advantage is the protection that the
biofilm provides to colonizing species from
competing microorganisms, from environmental
factors such as host defence mechanisms, and
from potentially toxic substances in the
environment, such as lethal chemicals or
antibiotics.
• Biofilms also can facilitate processing and uptake
of nutrients, cross-feeding (one species providing
nutrients for another), removal of potentially
harmful metabolic products (often by utilization
by other bacteria), as well as the development of
an appropriate physicochemical environment (e.g.
a properly reduced oxidation reduction potential).
31

29. • In the lower levels of most biofilms a dense
layer of microbes is bound together in a
polysaccharide matrix with other organic and
inorganic materials.
• On top of this layer is a looser layer, which is
often highly irregular in appearance and may
extend into the surrounding medium.
• The fluid layer bordering the biofi lm may
have a rather “stationary’’ sub layer and a fluid
layer in motion.
• Nutrient components may penetrate this fluid
medium by molecular diffusion.
32

30. • Communication between bacterial cells within a
biofilm is also necessary for optimum community
development and is performed by production of
signalling molecules such as those found in
“quorum sensing” or perhaps by the exchange of
genetic information.
• The long-term survival of the human species as
well as a species in a biofi lm becomes more
likely if that species (or the human) colonizes
multiple sites.
• Thus, detachment of cells from biofilms and
establishment in new sites is important for
survival of biofi lm dwellers.
• Thus, we may regard mixed species biofilms as
primitive precursors to the more complex
organizations observed for eukaryotic species.
33

31. Structure of Biofilm
• Biofilms are composed of micro colonies of bacterial cells (15–20% by
volume) that are non-randomly distributed in a shaped matrix or glycocalyx
(75–80% by volume).
• The water channels permit the passage of nutrients and other agents
throughout the biofi lm acting as a primitive “circulatory” system.
• Nutrients make contact with the sessile (attached) microcolonies by
diffusion from the water channel to the microcolony rather than from the
matrix.
• Microcolonies occur in different shapes in biofilms which are governed by
shear forces due to the passage of fluid over the biofi lm.
• At low shear force, the colonies are shaped liked towers or mushrooms,
while at high shear force, the colonies are elongated and capable of rapid
oscillation.
34

32. Exopolysaccharides – The
Backbone of Biofilms
• The bulk of the biofi lm consists of the matrix or glycocalyx and is
composed predominantly of water and aqueous solutes.
• The “dry” material is a mixture of Exopolysaccharides, proteins, salts, and
cell material.
• Exopolysaccharides (EPS), which are produced by the bacteria in the
biofilm, are the major components of the biofi lm making up 50–95% of
the dry weight.
• They play a major role in maintaining the integrity of the biofi lm as well
as preventing desiccation and attack by harmful agents.
• In addition, they may also bind essential nutrients such as cations to create
a local nutritionally rich environment favouring specific microorganisms.
• The EPS matrix could also act as a buffer and assist in the retention of
extracellular enzymes (and their substrates) enhancing substrate utilization
by bacterial cells.
• The EPS can be degraded and utilized by bacteria within the biofi m.
• One distinguishing feature of oral biofilms is that many of the
microorganisms can both synthesize and degrade the EPS.
35

33. • Bacterial cells within biofilms can produce
enzymes such as beta-lactamase against
antibiotics, catalases, and superoxide dismutases
against oxidizing ions released by phagocytes.
• These enzymes are released into the matrix
producing an almost impregnable line of defense.
• Bacterial cells in biofilms can also produce
elastases and cellulases which become
concentrated in the local matrix and produce
tissue damage.
36

34. Quorum Sensing and Exchange of
Genetic Information
• Quorum sensing in bacteria “involves the regulation of
expression of specific genes through the accumulation of
signalling compounds that mediate intercellular
communication” (Prosser 1999).
• Quorum sensing is dependent on cell density.
• Once the signalling compounds reach a threshold level
(quorum cell density), gene expression is activated.
• Quorum sensing may give biofilms their distinct properties.
• For example, expression of genes for antibiotic resistance at
high cell densities may provide protection Or influence
community structure by encouraging the growth of
beneficial species (to the biofilm) and discouraging the
growth of competitors.
37

35. • The high density of bacterial cells growing in
biofilms facilitates exchange of genetic
information between cells of the same species
and across species or even genera.
• Conjugation, transformation, plasmid transfer,
and transposon transfer have all been shown to
occur in naturally occurring or in vitro
prepared mixed species biofilms.
39

36. Attachment of Bacteria
• The key characteristic of a biofilm is that the microcolonies within
the biofilm attach to a solid surface.
• In the mouth, there is a wide variety of surfaces to which bacteria
can attach including the oral soft tissues, the pellicle coated teeth,
other bacteria, as well as prosthetic replacements such dentures and
implants.
• Many bacterial species possess surface structures such as fimbriae
and fibrils that aid in their attachment to different surfaces.
• Fimbriae have been detected on a number of oral species including
Actinomyces naeslundii, P. gingivalis, A. actinomycetemcomitans
and some strains of streptococci such as Streptococcus salivarius,
Streptococcus parasanguinis, and members of the Streptococcus
mitis group.
40

37. Dental Plaque
• Dental Plaque is defined clinically as a structured, resilient,
yellow-grayish substance that adheres tenaciously to the
intraoral hard surfaces, including removable and fixed
restorations. (W H Bowen, 1976)
• Dental plaque may accumulate supragingivally, i.e. on the clinical
crown of the tooth, but also below the gingival margin, i.e. in the
subgingival area of the sulcus or pocket.
• Differences in the composition of the subgingival microbiota have
been attributed in part to the local availability of blood products,
pocket depth, redox potential, and pO2.
• Supragingival plaque typically demonstrates a stratified organization
of a multilayered accumulation of bacterial morphotypes.
• Gram-positive cocci and short rods predominate at the tooth surface,
whereas gram-negative rods and filaments, as well as spirochetes,
predominate in the outer surface of the plaque mass.
41

38. 42

39. • In the tooth-associated cervical plaque, filamentous
microorganisms dominate, but cocci and rods also occur.
• This plaque is dominated by gram-positive rods and cocci,
including S. mitis, S. sanguinis, Actinomyces oris (a new
species containing strains that were formerly classified as A.
naeslundii), A. naeslundii, and Eubacterium spp.
• However, in the deeper parts of the pocket, the filamentous
organisms become fewer in numbers, and in the apical
portion they seem to be virtually absent.
• Instead, the microbiota is dominated by smaller organisms
without a particular orientation.
• The apical border of the plaque mass is separated from
the junctional epithelium by a layer of host leukocytes,
and the bacterial population of this apical tooth
associated region shows an increased concentration of
gram-negative rods.
43

40. • The layers of microorganisms facing the soft tissue lack a definite
inter-microbial matrix and contain primarily gram-negative rods and
cocci, as well as large numbers of filaments, flagellated rods, and
spirochetes.
• Studies on plaque associated with crevicular epithelial cells indicate
a predominance of species such as S. oralis, S.intermedius,
Parvimonas micra (formerly Micromonas micra and
Peptostreptococcus micros), P. gingivalis, Prevotella intermedia,
Tannerella forsythia and F. nucleatum.(S Dibart,1998)
• Host tissue cells (e.g. white blood cells and epithelial cells) may also
be found in this region.
• Bacteria are also found within the host tissues, such as in the soft
tissues and within epithelial cells. as well as in the dentinal tubules.
(F R Saglie, 1982,1988)
• The composition of the subgingival plaque depends on the
pocket depth. The apical part is more dominated by spirochetes,
cocci and rods, whereas in the coronal part more filaments are
observed.
44

41. Dental Plaque as a Biofilm
• Dental plaque has structure similar to biofilms.
• It is heterogeneous in structure with open fluid filled channels
running through plaque mass.
• These water channels permit the passage of nutrients and other
agents throughout the biofilm.
• The bacteria exist and proliferate within the intercellular matrix
through which these water channels run.
• In the lower levels, a dense layer of microbes is bound together in a
polysaccharide matrix with other organic and inorganic materials.
• On top of this layer is a looser layer, which is often highly irregular
in appearance and may extend into the surrounding medium.
• The fluid layer bordering the biofilm may have a rather “stationary’’
sub layer and a fluid layer in motion.
45

42. • Immediately upon immersion of a solid substratum into
the fluid media of the oral cavity, or upon cleaning of a
solid surface in the mouth, hydrophobic and
macromolecules begin to adsorb to the surface to form
a conditioning film termed the acquired pellicle.
• This film is composed of a variety of salivary
glycoproteins (mucins) and antibodies.
• The conditioning fi lm alters the charge and free energy
of the surface, which in turn increases the efficiency of
bacterial adhesion. Bacteria adhere variably to these
coated surfaces.
46

43. Inter-Cellular Matrix
• It consists of organic and inorganic materials derived
from saliva, GCF and bacterial products.
• Organic components:
 Polysaccharides (Mainly Dextran)
 Proteins
 Glycoproteins
 Lipid material (from debris of membranes of disrupted
bacterial and host cell membranes)
• Inorganic components:
 Calcium
 Phosphorus
 Traces of sodium, potassium and fluoride
47

44. Formation of Plaque
50

45. Phase – I
• Immediately upon immersion of a solid
substratum into the fluid media of the oral cavity,
or upon cleaning of a solid surface in the mouth,
hydrophobic and macromolecules begin to adsorb
to the surface to form a conditioning film termed
the acquired pellicle.
• This film is composed of a variety of salivary
glycoproteins (mucins) and antibodies.
• The conditioning film alters the charge and free
energy of the surface, which in turn increases the
efficiency of bacterial adhesion.
51

46. Phase – II
• Bacteria adhere variably to these coated
surfaces.
• Some possess specific attachment structures
such as extracellular polymeric substances and
fimbriae, which enable them to attach rapidly
upon contact.
• Other bacteria require prolonged exposure to
bind firmly.
52

47. Phase – III
• Behaviour of bacteria change once they
become attached to surfaces.
• This includes active cellular growth of
previously starving bacteria and synthesis of
new outer membrane components.
53

48. Phase – IV
• The bacterial mass increases due to continued
growth of the adhering organisms, adhesion of
new bacteria, and synthesis of extracellular
polymers.
• An oxygen gradient develops as a result of rapid
utilization by the superficial bacterial layers and
poor diffusion of oxygen through the biofi lm
matrix.
• Completely anaerobic conditions eventually
emerge in the deeper layers of the deposits.
54

49. Colonization and Plaque
Maturation
• When the firmly attached micro-organisms
start growing and the newly formed bacterial
clusters remain attached, microcolonies or a
biofilm can develop.
• Here onwards bacteria exhibit the phenomena
of Coaggregation (cell to cell recognition of
genetically distinct partner cell types)
(Kolenbrander 1993)
55

50. 56

51. 1. Streptococcus gordonii
Primary 2. Streptococcus intermedius
Colonizers 3. Streptococcus mitis
4. Streptococcus oralis
5. Streptococcus sanguinis
6. Actinomyces gerencseria
7. Actinomyces israelii
8. Actinomyces naeslundii
9. Actinomyces oris
10.Aggregatibacter actinomycetemcomitans serotype a
11.Capnocytophaga gingivalis
12.Capnocytophaga ochracea
13.Capnocytophaga sputigena
14.Eik enella corrodens
15.Actinomyces odontolyticus
16.Veillonella parvula
57

52. 1. Campylobacter gracilis
Secondary 2. Campylobacter rectus
Colonizers 3. Campylobacter showae
4. Eubacterium nodatum
5. Aggregatibacter actinomycetemcomitans
serotype b
6. Fusobacterium nucleatum ssp nucleatum
7. Fusobacterium nucleatum ssp vincentii
8. Fusobacterium nucleatum ssp polymorphum
9. Fusobacterium periodonticum
10. Parvimonas micra
11. Prevotella intermedia
12. Prevotella loescheii
13. Prevotella nigrescens
14. Streptococcus constellatus
15. Tannerella forsythia
16. Porphyromonas gingivalis
17. Treponema denticola
58

53. Coaggregation
• Coaggregation is a direct interaction and is distinct from agglutination,
which occurs when cells are stuck together by molecules in solution.
• At least 18 genera from the oral cavity have shown some form of
Coaggregation.(P E Kolenbrander, 1993)
• All oral bacteria possess surface molecules that foster some sort of
cell-cell interaction.
• The initial stages of coaggregation or co adhesion are essentially the
same as the first steps involved in bacterial binding to surfaces:
bacterial cells come into contact through passive or active transport
and bind weakly through nonspecific hydrophobic, electrostatic, and
Vander Waals forces.
• Strong cell-cell binding is then determined by the presence of adhesin
proteins or carbohydrates on one partner and complementary receptor
proteins or carbohydrates on the other.
• Many coaggregations between strains of different genera are
mediated by lectin-like adhesins (proteins that recognize
carbohydrates) and can be inhibited by lactose and other
galactosides.
59

54. • Fusobacteria coaggregate with all other human oral
bacteria.
• Veillonella spp., Capnocytophaga spp. and Prevotella
spp. bind to streptococci and/or Actinomyces.
• F. nucleatum with S. sanguinis
• Prevotella loescheii with A. oris
• Capnocytophaga ochracea with A. oris
• In some instances, coaggregation between non-
coaggregating species may be mediated by
cellularconstituents (e.g. vesicles) of a third species
(Ellen & Grove 1989; Grenier & Mayrand 1987b).
• In certain instances more than one type of adhesin–
receptor interaction has been detected between a
species pair.
60

55. Adhesins
• Some of the adhesins that havebeen identifi ed on
subgingival species include
1. Fimbriae (cisar et al. 1984; clark et al. 1986; sandberg et
al. 1986, 1988; isogai et al. 1988)
2. Cell-associated proteins (murray et al. 1986, 1988;
mangan et al. 1989; weinberg & Holt 1990).
• Receptors on tissue surfaces include
1. Galactosyl residues (cisar et al. 1984; murray et al. 1988;
sandberg et al. 1988; mangan et al. 1989),
2. Sialic acid residues (murray et al. 1986),
3. Proline-rich proteins or statherin (clark et al. 1986),
4. Type I or IV collagens (Naito & Gibbons 1988; Winkler et
al. 1988). 61

56. 63

57. Supragingival Plaque
• During the first 24 hours starting from a clean tooth surface, plaque
growth is negligible from a clinical viewpoint.
• During the following 3 days, coverage progresses rapidly to the
point where, after 4 days, on average 30% of the total coronal tooth
area will be covered with plaque.
• In parts of the plaque with the presence of Gram-negative
organisms, the inter microbial matrix is regularly characterized by
the presence of small vesicles surrounded by a trilaminar membrane,
which is similar in structure to that of the outer envelope of the cell
wall of the Gram-negative microorganisms .
• Such vesicles probably contain endotoxins and proteolytic enzymes,
and may also be involved in adherence between bacteria (Hofstad et
al. 1972; Grenier & Mayrand 1987).
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58. Subgingival Plaque
• Between subgingival plaque and the tooth an electron-
dense organic material is interposed, termed a cuticle.
• This cuticle probably contains the remains of the
epithelial attachment lamina originally connecting the
junctional epithelium to the tooth, with the addition of
material deposited fromthe gingival exudate (Frank &
Cimasoni 1970; Lie &
• Selvig 1975; Eide et al. 1983). It has also been
suggested
• that the cuticle represents a secretory product
• of the adjacent epithelial cells (Schroeder & Listgarten
• 1977).
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59. • The subgingival plaque structurally resembles supragingival plaque,
particularly with respect to plaque associated with gingivitis without
the formation of deep pockets.
• A densely packed accumulation of microorganisms is seen adjacent
to the cuticular material covering the tooth surface.
• The bacteria comprise Gram-positive and Gram-negative cocci,
rods, and filamentous organisms.
• Spirochetes and various flagellated bacteria may also be
encountered, especially at the apical extension of the plaque.
• The surface layer is often less densely packed and leukocytes are
regularly interposed between the plaque and the epithelial lining of
the gingival sulcus.
• However, in the deeper parts of the periodontal pocket, the
filamentous organisms become fewer in number, and in the apical
portion they seem to be virtually absent.
• Instead, the dense, tooth-facing part of the bacterial deposit is
dominated by smaller organisms without particular orientation
(Listgarten 1976)
66

60. • The surface layers of microorganisms in the periodontal pocket
facing the soft tissue are distinctly different from the adherent layer
along the tooth surface, and no definite inter microbial matrix is
apparent.
• The microorganisms comprise a larger number of spirochetes and
flagellated bacteria. Gram-negative cocci and rods are also present.
• The multitude of spirochetes and flagellated organisms are motile
bacteria and there is no inter microbial matrix between them.
• This outer part of the microbial accumulation in the periodontal
pocket adheres loosely to the soft-tissue pocket wall (Listgarten
1976).
• Subgingivally located bacteria appear to have the capacity to invade
dentinal tubules, the openings of which have become exposed as a
consequence of inflammatory driven resorptions of the cementum
(Adriaens et al. 1988). Such a habitat might serve as the source for
bacterial recolonization of the subgingival space following treatment
of periodontal disease.
• The mechanisms involved in such reversed invasion of the
subgingival space are unknown.
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61. 68