This document discusses oral microbiology and dental plaque. It begins by introducing the types of microorganisms found in the oral cavity, including bacteria, fungi, and protozoa. It then discusses the normal oral microflora, including indigenous, supplemental, and transient flora. Key topics covered include the various types of oral bacteria; factors that affect bacterial growth such as temperature, pH, nutrients, and host defenses; bacterial metabolism of carbohydrates, proteins, oxygen, and nitrogen; and the definition and formation of dental plaque.

1. ORAL MICROBIOLOGY:
NORMAL ORAL MICROFLORA;
DENTAL PLAQUE
KARISHMA.S
II MDS

2. CONTENTS
 INTRODUCTION
 TERMINOLOGIES
 TYPES OF ORAL FLORA
 HOST BACTERIAL INTERACTIONS
 FACTORS EFFECTING THE GROWTH OF MICRO ORGANISMS
 METABOLISM OF ORAL BACTERIA
 DENTAL PLAQUE
 CONCLUSION
 REFERENCES

3. INTRODUCTION
Microrganisms are living structures of microscopical size which
were first discovered by “AV Leeuwenhock”(1674) in his own
dental plaque & reported ‘ little living animalcules prettily
moving’.
These organisms are classified under PROTISTA, which are
further classified into
- Prokaryotes
- Eukaryotes

4.  Prokaryotes - Bacteria
 Eukaryotes - Fungi,Algae,Protozoa and
Slime moulds are included
in this group
The human body is continuously inhabited by many different
micro-organisms mostly bacteria, some fungi and other micro-
organisms, which under normal circumstances in a healthy
individual, are harmless, and may even be beneficial. These micro-
organisms are termed, the normal micro flora.

5. ACTINOMYCETES

6. TERMINOLOGIES
AEROBES: These organisms require oxygen for aerobic cellular respiration to
obtain energy.
OBLIGATE AEROBE: Is an organism that can survive and grow only in an
oxygenated environment.
FACULTATIVE ANAEROBES: Can use oxygen, but also have anaerobic
methods of energy production.
CAPNOPHILES: Are which require high concentrations of carbon dioxide.
for their growth.

7. OLIGOTROPH: An organism that can live in an environment that offers
very low levels of nutrients.
MICROAEROPHILES: Organisms that may use oxygen, but only at low
concentrations
PATHOGENS: Microorganisms that have the potential to cause disease.
OPPORTUNISTIC PATHOGENS: Micro-organisms that cause disease only
under exceptional circumstances .
TRUE PATHOGENS: Micro-organisms that are consistently associated with a
particular disease.

8. TYPES OF ORAL FLORA
Indigenous Flora (resident): It comprises those indigenous species that are
almost always present in high numbers, greater than 1 per cent of the total
viable count.
Eg : Streptococci, Actinomyces & Neisseria.
Supplemental Flora: The supplemental flora are those bacterial species that
are nearly always present, but in low numbers, less than 1 per cent of total
viable count
Eg : Lactobacilli, P. gingivalis
Transient Flora: Comprise organisms "just passing through" a host. At any
given time a particular species may or may not be represented in the flora.

9. HOST - BACTERIAL INTERACTIONS
SYMBIOSIS: When both the host and the bacteria benefit from their inter-
relationship, it is termed symbiotic.
ANTIBIOSIS: It is the opposite of a symbiotic relationship. Instead of helping
each other, the bacteria and the host are antagonistic to each
other.
AMPHIBIOSIS: An intermediate stage in which the host and its flora exist in a
stable balance with each other

10. FACTORS AFFECTING THE GROWTH OF MICRORGANISMS
IN THE ORAL CAVITY
 TEMPERATURE
 REDOX POTENTIAL
 PH
 NUTRIENTS :
- Exogenous
- Endogenous
 HOST DEFENSES
 HOST GENETICS
 ANTIMICROBIAL AGENTS & INHIBITORS

11. TEMPERATURE
 Human mouth has constant temp. which provides
stable conditions for growth.(35-36 oC)
 Periodontal pockets with active disease have
higher temp. as compared to healthy sites.
 Even small rise in temperature can significantly
alter gene expression and competitiveness of
bacteria

12. pH
 Many microorganisms require, normal
pH and are sensitive to acid/alkali.
 After consumption of sugars pH falls
rapidly below 5 and then rises again.
 Many bacteria of healthy sites may get
killed due to prolonged exposure to pH.
 pH of gingival crevice rises in response
to inflammation.

13. pH drop after sugar consumption
Enhanced growth/colonization of
acid-tolerant species (strep
mutans,lactobacillus)
Change in bacterial composition
leads to predisposition of caries
 Ph of healthy gingiva crevice is
approx. 6.90
 Rises to 7.2 – 7.4 during disease
 In Periodontal pockets 7.8

14. EFFECT OF NONFLUORIDATED MILK AND FLUORIDATED MILK ON ACIDIC
DENTAL PLAQUE
Varangkanar Jirarattanasopha a,* , Nunthiya Pruetpongpun b , Chutima Amornpipithkul a , Sirima Sanguansin c a
Department of Pediatric Dentistry, Faculty of Dentistry, Mahidol University, Bangkok, Thailand b Dental Department, Bangkok
Hospital Phitsanulok, Phitsanulok, Thailand c Department of Oral Biology, Faculty of Dentistry, Mahidol University, Bangkok, Thailand
Purpose: Recovering the acidic plaque pH to its resting value as soon as possible after exposure to a sugary beverage might
reduce the risk of dental caries. Milk contains nutrients that help to buffer acid. Adding fluoride to milk might enhance this
effect. Accordingly, this study investigates the effect of milk and fluoridated milk on acidic dental plaque.
Methods: The study was a randomized crossover design. Ten subjects were asked to rinse for 2 min with the following
solutions: (1) water, (2) 10% sucrose, (3) milk, (4) fluoridated milk, (5) 10% sucrose followed by water, (6) 10% sucrose
followed by milk, or (7) 10% sucrose followed by fluoridated milk. The supra-gingival plaque was collected before rinsing and
every 5 min after rinsing to measure the plaque pH.
Results: The results showed that rinsing with 10% sucrose caused acidic dental plaque. After rinsing with 10% sucrose
followed by milk, fluoridated milk, or water, the maximum plaque pH dropped and the area under the curve was
significantly less than that after rinsing with 10% sucrose alone (p ¼ 0.001). The maximum change in the plaque pH and the
area under the curve in the group challenged with 10% sucrose followed by fluoridated milk were significantly lower than
those in the group followed by nonfluoridated milk (p ¼ 0.04).
Conclusion: Rinsing with milk could raise the acidic plaque pH to the resting value faster than individual's natural capacity to
do so. Adding fluoride to milk can enhance this effect.

15. Redox potential (Eh)
 Oral microflora has few aerobic species and majority are anaerobic
in addition to being capnophilic and microaerophilic.
 O2 conc is the main limiting factor for the growth. Anaerobic species
require reduced conditions for their normal metabolism
 The degree of oxidation-reduction governs the survival and relative
growth of these organisms
During plaque development the redox potential falls from +200 to
-141mV after 7 days

16.  O2 tension of the anterior surface of the tongue was 16.4%, the
posterior surface 12.4%, and the buccal folds of the upper and
lower jaw only 0.3–0.4%. Microelectrodes have enabled the
redox potential to be measured at specific sites in the oral
cavity.
 Early colonizers will use the oxygen
 Late colonizers may produce H2
an other reducing agents like Sulphur.

17. NUTRIENTS
 The microbial community is dependent solely on the habitat
for its nutrition and growth
 Main source of ENDOGENOUS nutrients in SALIVA which
contains Amino Acids , Peptides , Proteins , Glycoproteins,
Vitamins and Gases.
 In addition, GCF in the gingival crevice contains nutrients such
as albumin, glycoproteins and other host proteins

18. EXOGENOUSLY carbohydrates and Diary Products have an effect
on Ecology of Mouth
 Carbohydrates – acids
 Additional sucrose – glucans and fructans
 Xylitol a sugar substitute cannot be metabolized by oral
bacteria, and has an inhibitory effect on the Growth of
Streptococcus mutans
 Nitrate in green vegetables may influences normal microflora
Nitrate – Nitrite – Nitric oxide

19. HOST DEFENSES
 Saliva flow , lysozymes , lactoferrins
, Histatins , Defensins and mucins
are Non Specific/Innate immunity
 Salivary IgA , IgG , IgM ,
Complement system and
Neutrophils are Specific/Acquired
immunity

20. HOST GENETICS
 P.gingivalis & anaerobic streptococci are associated more
with African American subjects and Fusobacterium
nucleatum is found mostly in Caucasian population.
 Periodontal pathogens are most likely to be detected in
Hispanic Asian American Population than Caucasians.
 Subgingival microflora of twins living together are more
similar than unrelated children of the same age.

21. ANTIMICROBIAL AGENTS & INHIBITORS
 Antimicrobials have direct inhibitory effects on the
,microorganisms than can be lethal or inhibitory.
 Chlorohexidine has been proven to be antibacterial , antiviral
& antifungal activity and has also marked Antiplaque Activity
 Flourides present in many tooth pastes
 Antibiotics given systematically

22.  Oral mucosa harbors organisms that can overcome abrasive forces
of food, tongue and teeth for retention. Due to the washing effects
of saliva, these organisms should be able to reproduce in great
numbers to ensure survival by reattachment.
LIPS - Staphylococcus albus and micro-cocci predominate
- large no. of Streptococci (S. salivarius, S. mitis)
ORAL MUCOSAL HABITATS

23. CHEEKS - Predominant bacterium is Streptococcus mitor with
Sanguis and salivarius .
- Yeasts may be isolated from carriers.
PALATE -Streptococcal flora resembling cheek
-Others like lactobacilli are common
-Yeasts and lactobacilli in denture wearers because of protected
environment.

24. TONGUE :
 Dorsal surface of the tongue is ideal for retention of
microorganisms due to the presence of surface papilla
 Predominant organisms are:
- Streptococcus salivarius, mitior, haemophilus, small number of
Candida albicans
SALIVA :
 A wide variety of microbes as most of the microbes which
get detached from the tissue / tooth surface will appear in
saliva .
 All species of streptococcus especially Streptococcus oralis
and Streptococcus salivarius are found in the saliva .

25. APPLIANCES :
 Dentures worn in mouth for a considerable period will
become colonized with microorganisms and may alter
the oral flora .
 Candida albicans can be found in large numbers in the
fitting surfaces of acrylic dentures while yeasts and
lactobacilli in particular, multiply on any mucosal
surface protected from flow of saliva .

26. 1) PIT AND FISSURES Streptococcus mutans very significant
Streptococcus Sanguis Not very significant
Other Streptococci Not very significant
Lactobacilli sp very significant
Actinomyces sp May be significant
2) SMOOTH SURFACE Streptococcus mutans Very significant
Streptococcus Salivarius Not significant

27. 3) Root surface Actinomyces viscosus Very significant
Actinomyces naeslundii Very significant
Other filamentous rods Very significant
Streptococcus mutans Significant
Streptococcus Sanguis May be significant
4) Deep dental caries Lactobacillus sp Very significant
Actinomyces naeslundii Very significant
Actinomyces viscosus Significant
Other filamentous rods Very significant

28. METABOLISM OF ORAL BACTERIA
 Nutrients are derived mainly from the metabolism of endogenous substrates
present in saliva and GCF, and these often require the concerted action of
consortia of micro organisms.
 Superimposed on these components are the exogenous nutrients that are
supplied intermittently via the diet
 The fluctuating conditions of nutrients supply and environmental change
require the oral microflora to possess biochemical flexibility

29. Various bacterial metabolisms include:
 Carbohydrate metabolism
 Sugar transport and acid production
 Acid tolerance
 Nitrogen metabolism
 Oxygen metabolism

30. CARBOHYDRATE METABOLISM
Most attention is paid to metabolism of carbohydrates because of
the relationship between dietary sugars, acid production and dental
caries

31. Sucrose,a disaccharide is the most widely used sweetening agent,and
can be:
 Broken down by extracellular invertase and the resultant glucose
and fructose molecules are taken up by the bacteria
 Transported intact disaccharides are cleaved inside the cell by
intracellular invertase
 Utilized extracellularly by glycosyl transferase or fructosyl
transferase
 Starches are broken down by amylase
 S.Mutans possess a spectrum of enzymes with the potential to
catabolize dietary starches

32. SUGAR TRANSPORT AND ACID PRODUCTION
All substrates have to be transported across cytoplasm into bacterial cell to be
of a value for energy production ,oral bacteria can transport carbohydrate by 3
known processes:
 The phosphoenolpyruvate mediated phosphotransferase PET-PTS transport
system
 The multiple sugar metabolism system
 A glucose permease

33. OXYGEN METABOLISM
The mouth is an aerobic environment and yet majority of the
organisms are either facultative anaerobic or obligate anaerobic
organisms especially in dental plaque.
Early colonizers tend to be more tolerant to toxic effects of
oxygen, than later colonizers which may depend on inter-species
metabolic interactions with biofilm
All plaque bacteria, including obligate anaerobes are able to
metabolize oxygen, but at different rates.

34.  Areobis bacteria such as Neisseria species use cytochrome
containing electron transport for oxygen reduction
 Treponema denticola, possesses NADH oxidases and NADH
peroxidases enabling it to scavenge low levels of oxygen in the
subgingival environment

35. ACID TOLERANCE
Many sacharolytic bacteria found in dental plaque can
generate low pH from sugar metabolism,few species can
survive such conditions for prolonged periods.
Microbial survival in acidic environment depends on the
ability of a cell to maintain intracellular pH homeostasis
The mechanism by which s.mutans achieve this include:
 Proton extrusion via proton translocation ATP synthesis
 Acid end product efflux

36. NITROGEN METABOLISM
 Dietary proteins are utilized to any great extent,casein can be incorporated
into dental plaque and degraded.
 S.sanguinous has shown to have both endo and exopeptidases that can
cleave proteins such as casein into peptide fragments
 At acidic pH, decarboxylation of amino acids yield carbon dioxide and
amines
 At higher PH , deamination produces ammonia and ketoacids
 Many of the micro organisms from periodontal pocket are asaccharolytic but
proteolytic and depend on GCF for nutrients
Ex: P.gingivalis can directly transport and utilize some amino acids

37. In addition to obtaining essential nutrients from GCF many
subgingival organisms are able to degrade structural protein
and glycoprotein associated with pocket epithelium
The production of enzymes such as chondroitin
sulphate,hyaluronidase and collagenase contribute to tissue
damage and pocket formation.
The pH optimum of some of these enzymes is at neutral to
slightly alkaline pH which corresponds to that of the inflamed
periodontal pocket

38. According to BOWDEN, Dental plaque can be defined as the soft
tissue deposits that form the biofilm adhering to the tooth surface or
on the other hard surfaces in the oral cavity, including removable
and fixed restorations.
Defined clinically as a structured resilient, yellow grayish
substance that adheres tenaciously to the intraoral hard surfaces
including removable and fixed restorations (clinical
periodontology- caranza)

39. Materia Alba refers to soft accumulations of bacteria and
tissue cells that lack the organized structure of dental
plaque.
Calculus is the hard deposits that formed by
mineralization of dental plaque and is generally covered
by a layer of unmineralised plaque.

40. i. Based On Location
a) Supragingival
Coronal
Marginal
b) Subgingival
- Attached plaque
- Unattached subgingival plaque
- Attached plaque can be tooth, epithelium
and/or connective tissue associated.
ii. Based on time
- Early plaque
- Mature or late plaque
CLASSIFICATION

41. DIFFERENCES BETWEEN SUPRA AND SUBGINGIVAL PLAQUE
Supra gingival
 Certain thickness
 Disclosing agents
 Grey to yellow
 Influence by diet,saliva,oral
hygeine,
 Teeth alignment,systemic factors
Subgingival
 Thin
 Within sulcus
 Cannot be detected by observation
 Running probe along the margin

42. COMPOSITION OF DENTAL PLAQUE
Bacteria + Intercellular matrix = Dental plaque
• Bacteria -- 70 to 80 per cent of total material.
• Mycoplasma, fungi, protozoa and viruses
• Intercellular matrix
Organic components Inorganic components
 Carbohydrates:
 Levan
 Glucan
 Galactose
 Glycoproteins
 Calcium
 Phosphorus
 Magnesium
 Potassium
 Sodium
 Host cells- Epithelial cells, macrophages & leucocytes

43. NATURE AND PROPERTIES OF BIOFILM
 Biofilms are composed of microcolonies of bacterial
cells(15-20%by volume) that are randomly distributed in
shaped matrix or GLYCOCALYX
 Earlier studies of thick biofilms have demonstrated
presence of voids and water channes between the
microcolonies
 These water channels permit the passage of nutrients and
other agents throughout the biofilm acting as a primitive
CIRCULATORY SYSTEM
.
.
.
.
.

44. The micro organisms present in the biofilm can exhibit different shapes
which are governed by shear forces caused by passage of fluid over the
biofilm
Some of the functions of the biofilm are dependent on the ability of
bacteria and microcolonies within the biofilm to communicate with one
another which is called as QUORUM SENSING.
Which is being able to respond to products or signals from other biofilm
organisms or the host and to use these to grow and prosper.
Quorum sensing signaling molecules are produced by putative
periodontal pathogens like p.gingivalis,p.intermedia,fusobacterium
nuclestum

45. FORMATION OF DENTAL PLAQUE
STAGE 1:
 Acquired pellicle formation: Involves the adsorption of salivary
proteins and glycoproteins forming pellicle
 Major constituents are glycoproteins, PRP’s, statherin,amylase
and host defence components
 Formation starts within seconds,and
equilibrium between adsorption and
deposition occurs after 90-120 minutes.

46. STAGE 2:
 Transport and Adherence of pioneering organisms: Transition
between pellicle to plaque is rapid.
 The first constituents are cocci with small numbers of epithelial
cells and PMNL’s which initially adhere via electrostatic
interactions (reversible).
 A little later specific interactions between adhesins on microbial
surface and receptors in the pellicle result in irreversible
adhesions.

47. Hence, in dental plaque development two adhesion processes are
required
 First – Bacteria must adhere to the pellicle surface and
become sufficiently adhered to withstand oral
cleansing forces
 Second – They must grow and adhere to each other to allow
plaque accumulation

48. STAGE 3: –
Bacterial adherence
1) bacterial attachment via electrostatic interactions
2) bacterial attachment via hydrophobic interactions
3) bacterial attachment via specific lectin like sucstances

49. STAGE 4: –
Growth and accumulation of bacteria
 Once the bacteria is adhered to the pellicle,subsequent
growth leads to bacterial accumulation and increased plaque
mass
1)growth via adhesion of new bacteria
2)growth via multiplication of attached bacteria
 Listgarten in 1976 has described highly
specific interspecies microbial interactions:
– “Corncob” formations – “Test tube
Brush”/Bristle Brush formations

51. STAGE 5:
SEEDING
Detachment of cells from this bio film into the saliva
results in colonization of fresh sites.

52.  Corncob formations have been observed between
rod-shaped bacterial cells (e.g. Bacterionema,
C.matruchotii or F.Nucleatum) that form the inner
core of the structure and coccal cells (e.g.
Streptococci or P. gingivalis) that attach along the
surface of the rod-shaped cell.
 Test tube Brush”/Bristle Brush formations
• This consists of one or several filaments aligned
perpendicular to the central filament.
• “Bristle-brush” formations are commonly seen in the
subgingival plaque of teeth associated with
periodontitis.

53. PLAQUE HYPOTHESIS
SPECIFIC PLAQUE HYPOTHESES was given by WALTER LOESCHE in 1976
NON – SPECIFIC PLAQUE HYPOTHESIS was proposed by THEILADE IN 1986
SPECIFIC PLAQUE HYPOTHESIS
• States that only certain plaque is pathogenic and its pathogenicity
depends on the presence of or increase in specific micro organism
• It predicts that plaque harboring specific bacterial pathogens results in
periodontal disease because these organisms produce substances that
mediate the destruction of the host tissue

54. NONSPECIFIC PLAQUE HYPOTHESES
This hypothesis proposes that collective groups of different
bacteria have the total complement of virulence factors required
for periodontal tissue destruction and that some bacteria can
substitute for others absent from the pathogenic consortium.
This hypothesis implies that plaque will cause disease
irrespective of its composition, and it is supported by the clinical
findings of numerous bacterial species in diseased periodontal
pockets

55. Ecological Plaque Hypothesis
 In the 1990s, MARSH and coworker developed the ecologic
plaque hypothesis as an attempt to unify the existing theories on
the role of dental plaque in oral disease.
 According to the ecologic plaque hypothesis, disease is the result
of an imbalance in the total microflora due to ecological stress,
resulting in an enrichment of some oral pathogens or disease
related microorganisms.
 The health associated dental plaque microflora is consider to be
relatively stable over time or in a state of dental equilibrium.

56.  The host control subgingival plaque to some extent by tempered
immune response and low levels of GCF flow.
 Host response may be brought about by the excessive
accumulation of dental plaque or by plaque independent host
factors (eg: the onset of an immune disorder, changes in
hormonal balance such as pregnancy or environmental
factors eg, smoking, diet)
 Change in the host status such as inflammation , tissue
degradation and/or high GCF flow, may lead to a shift in the
microbial population in plaque.

58. DIFFERENT COMPLEXES AND THEIR SIGNIFICANCE.
SOCRANSKY et al
SIGNIFICANCE:
 Early colonizers include members of
yellow complexes, purple complexes
and green complexes.
 Orange complex members are
thought to bridge early colonizers.

59.  Red complex members are associated with
bleeding on probing and more dominant at
late stages in plaque development.
 Green and orange complexes include species
recognized as pathogens in periodontal and
non–periodontal infection.

60. PATHOGENESIS OF PLAQUE
The main types of conditions caused are are:
1) Dental caries
2) Gingivitis
3) Chronic periodontitis(localized/generalized)
4) Necrotizing form of periodontal diseases
5) Aggressive periodontitis(localized/generalized)

61. DENTAL CARIES
Primary mechanism of caries formation involves:
 The Tooth (composition,morphology,position)
 Essentiality of oral bacteria
 The essentiality of oral substrate
 Environment(saliva,plaque)

62. Essential oral bacteria:
 A sterile oral cavity of a new born starts getting invaded within few
hours notably,
Streptococcus,Neisseria,Actinomyces,Veionella,Lactobacillus.
 Strep.mutans is the important pathogen in the initiation of dental caries
and takes about 5-6 years to penetrate the enamel of 2.7 mm
 Other organisms like Lactobacillus species,Actinomyces and certain
Strep.sanguis also have ability to produce caries
 The number of lactobacillus increase only after carious lesion has
developed

63. WINDOW OF INFECTIVITY
CAUFIELD (1993)
 The initial acquisition of strep mutans and designated the time
period as window of infectivity
 As the primary teeth erupt into the oral cavity they provide a
virgin habitat which enables mutans streptococci to colonize the
oral cavity avoiding competition with other indigenous bacteria

64.  Thus,during the window period in deciduous teeth the mutant
streptococci is established by 7-31 months of age and may have
difficulty in establishing later because it needs to compete with other
indigenous bacteria.
 Krass et al, Edrman et al reported that at 2-6 yrs of age the child is less
susceptible to acquiring Mutans streptococci
 The second window of infectivity is
present in permanent dentition between
6-12 years of age.

65. 1)GINGIVITIS
 Chronic marginal gingivitis is a non specific,reversible inflamatory response to
dental plaque involving gingival margins.
 Generally, gingivitis is regarded as resulting from non specific proliferation of
the normal gingival crevice microflora due to poor oral hygeine
 Gingival disease can also be modified by systemic factors such as harmonal
disturbances, drug therapies,(immunosuppresent)
 The micro flora associated with gingivitis is more diverse and differs in over all
composition from that found in healthy gingiva

66.  There is an increase in plaque mass (10-20 fold)and there is shfit of
streptococci dominated plaque of gingival health to one rich in
actinomyces species and capnophillic bacteria which are obligate an
aerobic gram negative bacteria
 Not all sites with gingivitis progresses to severe form of periodontal
disease but it is accepted that gingivitis must preceed periodontitis.
 And the environmental conditions that develop during gingivitis
favour periodontitis.
 Pregnancy associated gingivitis is accompanied by dramatic increases
in levels of P. intermedia, which uses the steroid as growth factors.

67. Aggressive periodontitis
Previously it was LJP AND GJP now it comes under aggressive periodontitis
 Rare condition
 Puberty
 Girls
 Rapid loss of attachment
 Racial predilection(.west Africa and asia)
Two forms:
 Localized – bone loss is distinctive in first permanent molars and incisors
 Generalized – many teeth involved

68.  Tend to have functional abnormalities of neutroplhils associated with
signal transduction pathways, reduced chemotaxis phagocytosis
,increased super radical production
 Actino bacillus.Actinomycetemcomitans(A.A) could be recovered from
97% of affected sites.
 Five serotypes of A.A have been described of which more than one
serotype is seen in individuals mouth
 A.A produces virulence factors which include leukotoxins and endotoxins
which induces bone resorption.
 Metronidazole and amoxycillin are effective in eliminating A.
actinomycetem comitans.

69.  Serotype b strains are very common in aggressive periodontitis
 In contrast to most other forms of periodontal disease, LAP appears
to result due to the activity of relatively specific microflora
dominated by single species
 In these pockets,small Spirochaetes, Eikenella corrodens ,Wolinella
species,and Fusobacterium nucleatum are often numerous.

70. Chronic periodontitis
 Most common form of advanced periodontal disease affecting the
general population and is a major cause of tooth loss after the age of
25 years
 Differs from chronic gingivitis by loss of attachment between the root
surface, the gingiva and the alveolar bone and bone loss itself can
occur giving increased depth of probing(irreversible)
 Can be localized or generalized

71. Campylobacter rectus, Porphyromonas gingivalis, Provella intermedia,
Fusobacterium nucleatum and Tannerella forsythia were found to be
elevated in the active sites.
Sites with chronic periodontitis will be populated with greater
proportions of gram negative organisms and motile bacteria
. Five clusters were identified,the red complex was found more
frequently in periodontal pockets - Tannerella forsythus Porphyromonas
gingivalis and treponima denticola

72. NECROTIZING PERIODONTAL DISEASES
It includes bith NUG and NUP
NUG also known as vincents disease or trench mouth or acute
necrotizing gingivitis is a severe forn of necrotizing inflammation if
interdental papilla
Features:
- Spontaneous gingival bleeding
- Intense pain
- Formation of grey pseudo membrame(easily sloughs)
- Halitosis

73.  It is a true infection unlike chronic gingivitis
 More than 50% of the isolated species were strict anaerobes
with P. gingivalis and F. nucleatum accounting for 7-8% and
3.4%, respectively.
 Metronidazole is effective in elimination fusospirochaetal
complex from infected sites.

74. CONCLUSION

75. REFERENCES
 ORAL MICROBIOLOGY : 5th Ed. Philip D Marsh & Micheal V Martin.
 CARRANZA'S CLINICAL PERIODONTOLOGY : 11th Ed.
 ANANTHANARAYAN AND PANIKER'S Textbook of Microbiology 10th edition
 ORAL MICROBIOLOGY AND IMMUNITY – Nisengard and Newman
 PAEDIATRIC DENTISTRY – shobha tendon 3rd edition

76. THANK YOU