Development of Oral Micro Flora

8/3/2019 Development of Oral Micro Flora

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DEVELOPMENT OF ORAL MICROFLORA

Dr PRATHIBHA RANI .S

Post Graduate Student


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INTRODUCTION


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CONTENTS

Introduction

History

Prokaryotes and Eukaryotes

Bacteria

-Cell structure

-Bacterial physiology

-Bacterial taxonomy and classificationMicrobes of oral environment

Origins

Development of oral flora


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CONTENTS

Adhesion of oral flora

Growth of oral flora

Survival of oral flora

Distribution of oral flora

Gram positive, gram negative species of oral cavity

Fungi and viruses of oral cavity

Micro flora of Dental caries, Periodontal disease & Endodontic infections


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History of Microbiology

In 1660s Robert Hook

Microbiology began in the mouth:

Anton-van Leeuwenhoek developed

and used the first microscope to

examine material collected from teeth,

and described motile animalcules.


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Robert Koch first to prove that the

micro organisms caused disease

His postulates

Specific M.O

Should be isolated and grown

Should produce disease when

inoculated in healthy individuals

Re-isolated in pure culture

After gap of two centuries-Pasteur and

koch


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COMPARISION OF PROKARYOTES &

EUKARYOTESCHARACTERISTIC Prokaryotes Eukaryotes

Nuclear membrane Yes Yes

Cell wall Yes No

Ribosomes Yes Yes

Endoplasmic reticulum No Yes

Golgi complex No Yes

Lysosomes No Yes

Actin filaments No yes

Peroxisomes No yes

Nucleolus No Yes

Mitochondria No Yes

Chromosomes Single Multiple

Cilia/flagella No Yes

Microtubules No Yes


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Shape and size

-spherical or rod shaped, clusters/chains

Gram stain

-Gram positive-Thick amorphous cell wall,

retains fixed violet dye.

-Gram negative-Layered appearance,

stain is washed out.

Bacterial Structure And Physiology


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Surface appendages( motility &

adhesion)

Flagella

Fimbriae

The cytoplasm

Sporulation

Bacterial physiology

-Nutrition

-Energy production


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Growth of bacteria

-Definition

-Binary fission

Bacterial growth curve

-Lag phase

-Logarthmic/Exponential

phase

-Stationary phase


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Bacterial Taxonomy And Classification

Classification

Identification

Nomenclature


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THE NORMAL FLORA AND PATHOGENS OF

HUMAN BODY

Commensal flora

Pathogens

Bacterial survival in extremes

Thermophilic->45 deg c.

Psychrophilic-


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ANTIMICROBIAL FACTORS IN HEALTH

Mechanical ;Flushing action of liquids, Peristalsis of gut, skin,

cough/sneeze, mucus, shedding of epithelial cells, cilia.

Bio-chemical;Anaerobicity/ acidity, sebaceous secretions,

sweat,lysozyme,antimicrobial enzyme,digestive enzymes,bile,

detergent action,colonisation resistance.

Immunological; complement,phagocytosis,inflammation,acute

phase response,antibodies,cell mediated responses.


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ORAL CAVITY

The attainment of symbiotic status

b/w some organisms with their

host has occurred over the long

period of evolutionary change and

these organisms are referred to as

Autochthonous biota

Normant,latent,carrier state

&masking &unmasking of viruses.


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The Oral Flora

In 1979, Bowden & collegues isolated about

21 genera comprising 60 sp.

Can be recognized as three types

Indigenous flora-

Streptococcus,Actinomyces & Neisseria


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Supplemental flora;

Eg.Lactobacillus spp found in low levels in plaque,

reduced plaque ph- become dominant.

Transient flora;

- Lack of mechanisms to persist Quickly

disappear


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Host bacteria inter-relationship

Can be demonstrated in one of the three ways-

Symbiosis-

-Eg;digestive tracts of ruminants &

termites,subsist on diet in large proportion of

cellulose, gut bacteria secreting cellulase reduce

cellulose to residues absorbed by the host


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Anti-biosis;

Amphibiosis ;

E.g.; growth of S .mutans & B. gingivalis do

not compromise the survival of the host


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Growth promoting Growth limiting

Warmth,moisture,

nutrients

Antibacterial,limited

nutrients,exfoliation,swallowing.


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ORIGINS OF ORAL MICROBIOTA

In utero

During birth - Corynebacterium,lactobacilli,

coliformis,micrococci,anaerobic

strepto, anaerobic cocci, protozoa,

yeasts and some viruses.

Oral cavity considered sterile until

first breath is taken.

Pioneer species - St.salivarius

Others staphylo, lactobacilli

strepto, pneumo, entero, coliforms

sarcinae ,hemophili, Candida

albicans.
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Established pioneer community

By the end of third month Identifiable resident

micro-flora

At the end of one year sp. of strep, veilonella,

staphylococci, neisseria identified


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Major change at around 6

months

Organisms- hard enamel

surfaces & dento gingival margin

S.mutans & S.sanguis- enamel

surfaces.

Climax community

Around 300 species


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At Birth- Sterile,simple,aerobicStrept,Staphy,Coliforms,

Pioneer spp-Strep.salivarius

Climax community-

Staph.albus,N.spp,Veilonellaspp,Candida.albicans


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Infancy & Early childhood-

S.mitis,S.sanguis,S.mutans,Neisseria,Actinomyces,Lactobacil

li,Rothia.Fusobacterium,Veilonella.

Adolescence-Deepfissures,Large interproximalareas,Deep gingival crevice

Climax community-

Hard tissues-Strep.mutans,Strep.sanguis,Actinomyces

G C-Prevotella,Porphyromonas,Bacteroides,Spirochetes,Leptotrichia,Fusobacterium,Vibrio


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Adulthood-

Periodontal disease-

Spirochetes,Bacteroides.

Plaque-

Strep,S.mutans,S.mitior,S.sanguis,Actinomyces,Gra

m+ve,Gram-ve filaments


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Edentulous adults-

Second childhood-lossS.sanguis,S.mutans,Anaerobes,FewBacteroides,Spirochetes,

More Yeasts

Denture plaque-composition similar toplaque on the toothsurface or at the junctionof the tooth and thegingiva.


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ORAL FLORAL DEVELOPMENT

Adhesion-cell-substratum

adhesion,homotypic cell to cell &

heterotypic cell-cell

First phase - Initial reaction

-Deposition

-Extra cellular carbohydrate

influence

-Teeth and saliva

Homotypic cell adhesion

Heterotypic cell adhesion


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Adhesion factors

A range of physicochemical

positive and negative forces along

with surface features-shape,

chemical composition & charge

Weak attachment-Strengthen by

polymer bridges

Fine filaments


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Role of host polymers

Saliva-suspending medium

composed of

lipids,vitamins,ions,,polysaccharid

es & immunoglobulin

Acquired pellicle- Epithelial

surfaces & teeth, composed of

glycoprotein & antibodies.


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Role of bacterial polymers

No. of org.produce extra cellularpolysaccharides to adhere to hard

surfaces

S.mutans- glucosyl transferase

and fructosyl transferase

Type of polymers with these

interactions

first- water insoluble - mutan

second - water soluble dextran

third - unusal soluble fructan

Lipoteichoic acid bacterial

polymer - wall of +ve organism


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Site specific receptors (adhesins)

Fuzzy coat/ Glycocalyx -St.mitior ,S.salivarius Trypsin sensitive,

Polysaccharide & lipoteichoic acid.

Fimbriae (pili)

Sex pilus - Mating b/w cells

Somatic pilus Adhesion

Lectins-Receptors on tooth surface.


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Physical Retention

Organisms that lack good adhesive properties - Veilonella,

Bacteroids & Spirochetes take refuge in dental plaque


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Growth of oral flora

Temperature- Psychrophils;0-30 dg C

-Mesophils;10-45 dg C

-Thermophils-25-75 dg

Temp. affects-Ph,ion activity, solubility of gases & aggregation

of macromolecules

Oral cavity-stable heaven


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Acidity;

-Most org require ph close to neutrality

-Saliva regulates ph

-Ph of plaque falls following consumption of sugar to values - 5

or 4

-Aciduric

-Acidogenic

-Saliva - neutralising effect

-Depth of penetration of saliva into dental plaque is doubtful


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Oxidation reduction potential (Eh);

1. Obligate anaerobes

2. Facultative bacteria

3. Obligate aerobes

4. Micro aerophilic

OxidationReduction potential(Eh)

Represented by positive and negative symbol

Healthy gingival crevice +73mv

Disease - 300mv


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Carbon di oxide;needed for growth initiation & continued

growth

Atmospheric co2 is 0.03%Many bacteria require increased levels ofco2

E.g. - Actinobacillus & capnocytophaga linked with priodontal

diseases.

Nutrients; Can be obtained from saliva & GCF

Saliva - Provide org sub AA, proteins, sugars, glycoprotein whichcan promote the growth

Conversely no. of components may inhibit the growth

E.g. Lysosomes, peroxidases & IgA


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Nutrients;

GCF contains no. of factors ,IgA ,IgG ,IgM & albumin

Hemin & alpha-2 globulin for Bacteroides & Treponema

denticola resp.

GC harbors a lot of enzymes.

Primary feeders

Secondary feeders


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SURVIVAL OF THE FLORA

Depends on the ability to withstand the defensive system of

the body.

Some inhibit phagocyte engulfment while others prevent

phagocyte digestion.

Can be related to bacterial capsule Polysaccharides

surface components such as Hyaluronic acid.

Intracellular pathogens-Offer no resistance but after

ingestion exist in balance with the phagocyte.

Extra cellular pathogens-Destroyed as soon as engulfed.


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Strepto pyogenes evolved anti phagocytic capsule

Bacteroids- factors that inhibit migration & phagocytosis of

PMNS. catalase, super oxide dismutase

Strepto& Actino Leukocidin

Capnocytophaga -changes in PMNS morpho.& impair

complement induced PMNS chemo taxis.

Bacteroides-non-specific fibrolysin


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ORAL FLORA DISTRIBUTION

Depends on certain factors

Salivary secretions, GCF, microbial nutrition & metabolism,

oral hygiene practices, systemic diseases ,oral habits ,diet,Eh,

microbial interactions ,oral & dental diseases, racial & genetic

factors , hormonal secretions, anatomical factors, drugs & anti

microbial agents , microbial adhesions, dental treatment.


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ORAL FLORA ENVIRONMENTAL FACTORS

Two specific surfaces, Hard teeth & soft -epithelial surfaces

Tongue - specialized surface

1)Lips-

Transitional zone

Skin flora Staphylo.aureus , micro, gram positive rods,

Oral flora-gram negative spp.also,Neisseria & Veilonella


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Cheeks-Three predominant spp strept. mitior, strepto.

sanguis, S.salivarius

Palate -Similar to that of cheeks, no of strepto ,lacto,&

hemophilus

Tongue-Due to presence of crypts and papillae-greater

bacterial density than elsewhere

S.salivarius(50%), S.mitior, S.milleri & S.sanguis,Hemophili,

Neisseria, Veilonella, Lactobacilli, Bacteroides, Fusobacterium

to certain extent

S.mucilagenosus - throat & nasopharynx produce

polysaccharide slime.


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Saliva - Mucin an organic content favours the

aggregation & adherence of bacteria such S.sanguis

& S.mitisCarbohydrate do not influence the bacterial growth

20 AA ,Urea by filtration from blood

Ammonia derived from urea-Provide source of

nitrogenous sub for bacterial growth

Teeth- S.mutans, S.sanguis, S.mitior,

S.milleri,Actinomyces.


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Gingival crevice

1. Differs considerably from saliva

2. Harbors a community of M O3. Flushing action provides a protective action ( as in periodontal

diseases )

4. Proteins such as albumin, immunoglobulin IgG IgA & IgM as

well as complement ,monocyte, lymphocytes of T & B type.

5. As depth increases the Eh & mixture of organisms gets

altered.

6. S.mitior, S.sanguis ,S.salivarius ,Entero cocci, gram +ve org,

Veilonella & Neisseria,

MEMBERS OF ORAL FLORA


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MEMBERS OF ORAL FLORA

Gram positive

Gram negative

Fungi

Viruses

G iti


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Gram positive

Facultative anaerobic cocci-

G.Enterococcus,Stomatococcus,Streptococcus

Obligate anaerobic cocci-

G.Peptostrepto

Regular non-sporulating & facultative anaerob.rod-

G.LactobacillusIrregular,non,facultatively anaerobic rods-

G.Actinomyces,G.Arachnia,G.Bacterionema,G.Rothia

Irregular,non,obligate,anaero,rods-

G.Bifidobacterium,G.Eubacterium,G.Propionibacterium

G ti


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Gram negative

Facultative anaerobic cocci-

G.Neisseria,

Obligate anaerobic cocci-G.veilonellaF.anaerobic,rods-

G.Actinomyces,g.Capnocytophaga,G.Eikenella,G.Hemophilus

Obligate anaerobic,straight,curved,helicalrods-

G.Bacteroides,G.Fusobacterium,G.Leptotrichia,G.Selenomonas,G.Wolinella

Spirochetes-G.Treponema

Fungi- G.Candida

Viruses- Herpes V


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Gram positive bacteria

Streptococci;

pairs/chains, non

sporulating, non-

motile,

most numerous

single group(25-50%)

Occur in oral cavity,upper res. tract


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Mutans Group Of Streptrococci

Species Serogroup Mannitol Sorbitol

S. mutans c e f + +

S. sobrinus d g + +

S. rattus b + +

S. cricetus a b + +

STREPTOCOCCUS MUTANS


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First discovered Clarke in 1924

Primary habitat Tooth surface of

man

Gram positive cocci which occur

in pairs or as short or medium

length chains-mutans refer to

ability to form long chains when

grown in sucrose medium.

S.mutans carious lesions

Can be divided into 8 serotypes

a to h

Supported on cell wall analysis,

poly acrylamide gel,

electrophoresis of proteins ,DNA

content ,DNA hybridization studies

Can synthesise soluble &

insoluble extra cellular polymer

from sucroses (glucan,

mutan,fructan)


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Streptococcus sanguis Pri. habitat dental plaque

Colonization-after eruption of

deciduous teeth

Can be isolated from blood &

heart valves in SBE

Spherical, oval cells occur in

medium or long chains

Extracelluar soluble and insoluble

glucans from sucrose

Properties common S.mutans

Not an instigator of D.C

Asso. with Aphthous stomatitis.

St t iti


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Streptococcus mitior

Group of alpha hemolytic strep.

Spherical or oval cocci found singly/pairs/chains

Alpha or beta hemolysis on blood agar

Extra cellular polysaccharide very little

Found to be adherent to non keratinized cells (tongue, cheek &

lips)

Role in DC not proved

Streptococcus milleri


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Streptococcus milleri

S. angionosus

Spherical,/ovoid cells in pairs/chains, long/short chains

Hemolysis alpha ,beta, gamma

Do not produce polymers from glucose

Normal in habitat isolated from plaque, gingival crevice &

throat. Cariogenic in gnotobiotic animals

Isolated from infections abscesses of mouth, brain, liver

appendix & blood stream


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Streptococcus rattus

Gram positive coccus, pair/chains

Fermentation occurs with mannitol, sorbitol, raffinose, sucrose,

lactose, maltose not with glycerol or xylose

Extra cellular glucan from sucrose

Less common in humans

Streptococcus salivarius


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Streptococcus salivarius

Spherical/ovoid cells variable chain

length

Majority are non hemolytic on blood

agar some alpha and beta hemolytic

Do not produce sticky dextrans -thus

does not colonize plaque/tooth

surfaces.

One of the first organisms to colonize

the infants mouth

In habitat-tongue fissures,

Isolated from blood-Infective

endocarditis

No caries inducing properties

Regarded as the True commensal

St t i t


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Streptococcus cricetus

Cocci are gram positive pairs/chains

Some produce alpha hemolysis majority are non hemolytic

Best grown in reduced atmosphere

Fermentation Mannitol sorbitol, rafinose, mannose, sucrose&

lactose

Originating from serovar type a

Can not produce ammonia from arginine

Isolated occasionally in man

Streptococcus sobrinus


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Streptococcus sobrinus

Gram positive in pairs/chains of varying length

Some alpha hemolysis others non-hemolytic

Fermentation of mannitol, insulin &lactose

Ammonia is not produced from arginine

Habitat- tooth surface induce DC in gnotobiots

Streptococcus ferus


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Streptococcus ferus

Gram positive in pairs/chains

Can produce extra cellular & intracellular glucans

Ferment- mannitol & sorbitol

No fermentation of rafinose

Not isolated from human mouth

Streptococcus mitis


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Streptococcus mitis

Appear spherical/ellipsoidal form long chains

Ferment-glucose, sucrose, maltose, lactose

No fermentation of mannitol, inulin, glycerol or xylose

Isolated from human saliva, respiratory tract & feces.

Serologically-similar to S.sanguis

DNA hybridization show links with S.mitior

Actinomyces


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Actinomyces

Are filamentous bacteria

Obligate or facultative

anaerobic, capnophilic, grm

positive & non acid fast

A.viscosus , A.naesludi &

A.odontolyticus have limited

patogenecity

A .israeli & A. bovis implicated

in actinomycosis of man &

lumpy jaw in cattles


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A. viscosus - facultative anaerobic, grow in presence of

CO2,produces pdl disease, isolated from dental calculus, related

to root surface caries

A. naeslundii - common in habitat of oral cavity, tonsillar crypts,

plaque & calculus, produce pdl disease

A. odontolyticus- located carious teeth on blood agar produce

green area similar to hemolytic strep


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A .israeli- normal member of

oral flora, tonsillar crypts &

dental calculus

Actinomycosis a true

opportunistic infection invading

tissues & regions of body as

portals of entry occur

A bovis- lumpy jaw of cattles

not transmitted to humans


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Propionibacteria;

1. Anaerobic gram positive rods

which produce a high peak ofpropionic acid in glucose broth.

2. Isolated from dental plaque&

oral cavity.Primary habitat-skin.

3. P.acnes isolated from oral

cavity in association with dental

plaque,carious dentine &

necrotic pulp tissue.

4. Association DC,pdl diseases

not proven


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Bacterionema B .matruchotii; identified in oral cavity

gram positive, on acid fast, on motile, facultative

Cells - pleomorphic whip-handle cells

Ferment carbohydrates to acetic, propionic & lactic acid acts as

an important focus for the calcification of plaque


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Lactobacilli

Currently 43 species of this genus

have been listed

long, slender, bent rods chain

formation observed

most are non motile& non sporulating

gram positive, later become gram

negative -age

They are both acidogenic and aciduric

Homo fermentative -lactic acid

Hetero fermentative when less oflactic acid is produced.

In oral cavity L. acidophilus & L.

salivarius homo fermentors break

down glucose via emb meyerhof

pathway & high lactic acid production


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Other two sp L .fermentum, L .breve's Hetero fermentors

degrading glucose by a 6- phospho gluconate pathway

producing lactic acid,ethanol or acetic acid

Other two species L. casei & L .plantarum use both pathways

called facultative hetero fermentors.

GRAM NEGATIVE BACTERIA


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GRAM NEGATIVE BACTERIA

Neisseria-Gram negative aerobic/

facultatively anaerobic cocci ,isolated from

the tongue, lips & cheek, plaque & saliva. N.

sicca & N. catarrhalis in oral cavity.

Infection of oral mucous membrane


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Veilonella-strictly anaerobic cocci

comprise 5-10% from saliva &

tongue surfaces. V. parvula &V

.alcaseus.

Lack glucokinase &

fructokinase..Use pyruvate,

lactate, maltate, fumarate or

oxaloacetate for their growth

Cause few infections &

Is protective to the oral cavity.


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Hemophili -aerobic/ fac. anaerobic

gram negative rods , isolated from oral

cavity. Enter oral cavity during infancy

but have low toxicity.

Opportunistic cause

endogenous infections, otitis media &

infective endocarditis

H .segnis common mem of dental

plaque.


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Eikenella corrodens -Due to its property to

pit/corrode the surface of agar plates .

Small, non sporulating, non encapsulated, non motile

micro aerophilic, gram negative.

Isolated from oral cavity, abscesses of various parts

of the body.


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Bacteroids -30 species, occur

in large bowel & faces. In oral

cavity divided into pigmented &

non-pigmented.

B. melaninogenicus is further

subdivided

isolated from periodontal

pockets.


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Fusobacteria Anaerobic,

sporulating, gm ve rods, with

fusiform shape. paired rods

giving elongated cigar app.

first noted in ulcerative

gingivitis in 1880,later linked to

the presence of spirochetes in

vincets infection.

F. nucleatum -oral cavity its

increase associ.with

periodontitis


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Wolinella -gm ve curved anaerobic rods with single polar

flagellum.

W.succinogenes-abdominal inf. Dental abscess .

W .recta in gingival crevice.

Capnocytophaga-gm ve fusiform rods, capnophilic, Possible

role in periodontitis & juvenile periodontitis

FUNGI


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FUNGI Candida only fungal spp

accepted as members of the oral

commensal flora

Candidiasis local/systemic

Yeast like fungus

In oral cavity no. of sp isolated-

C.albicans, C.tropicalis,

C .krusei, C .parapsilosis, C

guilliermondii & C. glabrata

C .albicans-Acute/Chronic

candidiasis

Acute pseudo membranous atrophic candidiasis


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Acute-pseudo membranous ,atrophic candidiasis

Chronic-Atrophic ,hyper plastic, muco cutaneous

Acute pseudo membranous seen in young childrenconsist

of dead mucosal cells with fungal hyphae.

Acute atropic Imbalance of normal flora due to use of

antibiotics


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Chronic atropic swollen inflamed mucosa in denture

wearers linked with angular chelitis

Chronic hyperplastic-firm white, persistent plaques on the

lips, tongue & cheeks

Oral candidiasis remain localized or get extended to include

esophagitis

Systemic candidiasis-C.albicans, C.glabrata & C.tropicalis -

three target organs ,eyes, kidneys & skin.

VIRUSES RNA group DNA group


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VIRUSES

Herpes virus hominis(Herpes

simplex)

Virus division on the basis of

viral nucleic acid, the size of

virus, shape, presence of an

envelope, chemical &

physical nature of the virus &

site of assembly

RNA group DNA group

Paramyxo v

Rubeola(measles)

Mumpsvirus

Picorna v

Poliovirus

Coxsackievirus

Aphthovirus

Toga v

Rubellavirus

Herpes v

Herpes simplex

Varicella- zooster

Cytomegalo v

Epstein barr

Pox v

(molluscum

contagiosum)

Papovirus

Papillomavirus(warts

)


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Clearly, the normal bacterial flora of the

oral cavity benefit from their associations

with their host. Are there benefits as well

to the host?


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DENTAL PLAQUE

Definition- Soft deposit that forms thebiofilm adhering to the tooth surface orother hard surfaces in the oral

cavity,including removable & fixedrestorations.

DENTAL PLAQUE


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Classification-Supragingival / Subgingival

- Adherent/Non-adherent

- Cariogenic / Periodontopathic

Supragingival - adherent & gram positive org.-

Cariogenic

Subgingival less adherent & gm ve org

-Periodontopathic

DENTAL PLAQUE

DENTAL PLAQUE


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DENTAL PLAQUE

Composition

Micro organisms

70-80%

1Gm

500 distinctmicrobial spp

Organic & inorganiccomponents

20-30%

FORMATION, STRUCTURE AND


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ORGANISATION OF DENTAL PLAQUEAcquiring the pellicle.

Transport of microorganisms.

Long range physicochemical interactions.

Short range interactions.

Co aggregation of microorganisms.

Multiplication of attached organisms.

DENTAL PLAQUE


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DENTAL PLAQUE

Pellicle formation- Distinct organicstructure on surface of teeth prior to

colonisation by bacetria,consists of

glycoproteins derived from salivaThickness-100nm-2hrs

-500-1000nm-24hrs


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Early plaque principally composed of cocci


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y p q p p y p

Salivary pellicle-Specific attachment site

Increase in size by multiplication than by

apposition

Surface of early plaque-rod shaped

bacteria-next phase filamentous bacteria


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Streptococci and

Actinomyces are

early colonizers

S.sanguis is the first

to be discovered


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Secondary colonisers-Prevotella,Capnocytophagaspp,F.nucleatum,P.gingivalis

Coaggregation


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One day old plaque Non-bacterial components


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Developed Supragingival plaque Long Standing supra gingival plaque

MICROBIAL COMPOSITION OF DENTAL


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PLAQUE IN HEALTH

Bacterium Fissures Approximal GingivalCrevice

Streptococcus + + + + + + + + + +

Actinomyces + + + + + + + + + +

Lactobacilli + / - + / - + / -

Veilonella + + + + + + +

Fusobacterium - + + +

Spirochetes - - +

Gm veAnaerobes

+ / - + + +

HYPOTHESIS RELATING PLAQUE TO CARIES


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Specific plaque hypothesis: only a very limitednumber of species are involved in disease.

-specific pathogens.

Non-specific plaque hypothesis:plaque is amicrobial community.

Ecological plaque hypothesis: shifts in the

balance of the resident plaque microflora.

ECOLOGIC PLAQUE HYPOTHESIS


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EXCESS

SUGAR

NEUTRAL

pH

S. sanguis

S.oralis

ACID

PRODUCTION

LOW

pH

MS

LACTOBACILLI

STRESS ENVIRONMENTALCHANGE

ECOLOGICAL

SHIFTDISEASE

REMINERALISATION

DEMINERALISATION

BACTERIA AND DENTAL CARIES


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BACTERIA AND DENTAL CARIES

Dental caries- Slow decomposition ofteeth resulting from loss of hydroxyapatite crystals

Host

Plaque

Substrate

PATHOGENIC DETERMINANTS


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Rapid transport of dietary sugars: Mutans streptococci possess

more than one sugar transport system.

Rapid rates of glycolysis (acidogenicity):can result in a terminal

pH of below 4.5 in only a few minutes.

Tolerance of, and growth at, low pH (aciduricity):the growth of

many of the bacteria found on sound enamel (e.g.. Strep.

Sanguis)is inhibited at pH


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Extracelluar polysaccharide synthesis (EPS):thesepolymers help make up the plaque matrix.

Glucosyltransferases (GTF's) convert sucrose to solubleand insoluble glucans, that help consolidate bacterialattachment.

Fructosyltransferases (FTF's) convert sucrose tofructans; these polymers are labile and can be used byplaque bacteria as an energy source.

Intracellular polysaccharide synthesis (IPS): can be used during


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Intracellular polysaccharide synthesis (IPS):can be used during

starvation conditions and catabolised to acid when dietary

sugars are not available.

mutans streptococci but not lactobacilli produce EPS.


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PATHOGENIC PROPERTIES OF CARIOGENIC


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BACTERIA

Rapidly transport fermentable

sugars when in competition with

other bacteria

Conversion of such sugars to acid.

The production of extra-cellular and

intracellular polysaccharides.

The ability to maintain sugar

metabolism under extreme

environmental conditions.


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Prior to 1890 it was believed that mineral acids thatformed from food residues were responsible for toothdecay and there was no connection with bacteria.

1890 - W.D. Miller formed the chemo parasitic theoryof caries .Microorganisms attach to the tooth andproduce organic acids which dissolve the enamel.


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A diet that could produce caries in normal

animals could not cause caries in

germfree animals. caries was proven to be

caused by bacteria.

Evidence of Bacterial Role:


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Germ free animals do not develop caries.

Antibiotics fed to animals are effective in reducing the cariesrate.

Totally unerupted and unexposed teeth do not develop caries.

Oral Bacteria can demineralize enamel and dentin andproduce caries like lesions.

Microorganisms have been histologically demonstrated

invading carious enamel and dentin.


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1924 - Clarke isolated a streptococcus from

approx. 72% of carious lesions. These formed

rods in old cultures and therefore he called it S.

mutans.


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1933 - Tomato juice agar was usedto culture oral lactobacilli.

Higher numbers were found in mouthswith caries

Similar results with other media

selective for the lactobacilli gave riseto the belief that lactobacilli werethe cause of tooth decay.


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Gnotobioticwhen inoculated with enterococci,

could get caries.

Therefore, not just lactobacilli but other

organisms were also implicated!


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1967 & 1968 - Carlsson &

Edwardson worked on the

taxonomy of the various

cariogenic streptococci

They named thecariogenic streptococci

"Streptococcus mutans


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The characteristics which distinguishedthe S. mutansfrom all otherstreptococci were their ability to:

-ferment mannitol and sorbitol

-produce insoluble glucan from sucrose

Great Lake Study


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In the 1970s, DRG, in Great Lakes, Illinois Naval Training

Center studied S. mutans-free and caries-free individuals.

-60% of them became infected

-Disproved genetic basis for caries resistance

- Therefore caries was shown to be a communicable disease for

humans

WOMB TO TOMB STUDY


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Carlsson & collegues-Two phasedstudy

WINDOW OF INFECTIVITY OF


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S . m u ta n s

-Carfield(1993).

-6-12yrs


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Caries can be divided intoEnamel, Dentinal & Root surface

(cemental) cariesEnamel caries further divided into Smooth SurfacePit & Fissure

Smooth Surface most


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consistent are gram

positive facultative cocci,

S.mutans & S.salivarius.

S.mutans primary

etiologic agent

Role of S.salivarius in

cariesproduction is not

wellknown

Normal Buccal-Lingual smooth surface caries- S.


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g

mutansgroup

Normal Interproximal Smooth Surface caries - S.

mutansand lactobacilli

Rampant Smooth Surface caries-S. mutansgroup

Pit & Fissure caries- Wide


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variety is found because of the varied

environment present

S.mutans & Lactobacilli are suspected

etiologic agents.

Anaerobic rods, Bifidobacterium,

Eubacterium, & Propionbacterium

identified.

Actinomyces,& Bacillus sp.- invasive

front of the deep dentinal lesions

Root surface


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lesion High no. of

Actinomyces sp.

including A .viscosus,

A.naeslundii &

A. odontolyticus.


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Rampant Caries- Any tooth

surface.

characterized by a rapid

dissolution of the tooth

It is not due to different

organisms

The rapid progression is due to the frequency of

ingestion of sucrose or other fermentable sugar!

Endodontic infections


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Endodontic infections

Vital dental pulp-Sterile

Endodontics disease of pulp

& periapical tissues

W.D.Miller- bacterial

involvement

Object of many errors

Evidence experiments on

germ free rats.

Bacterial Ecology Of The Infected Root Canal


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Microbial composition determined by a) the root by which

bacteria gain access to the root canal & b) the no. & quality of

ecological factors

Bacteria are in the dynamic state influenced by the

1)interactions bet. bacteria & 2) interaction with the host

Root canal is much less complex than the Subgingival flora

Experiments Initially facultative species of Streptococcus,


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Enterococcus ,Lactobacillus, Corynebacterium & Coliform rods,

anaerobic organisms, Peptostreptococcus, Propionibacterium,

Eubacterium,Prevotella & Fusobacterium.

Proportion of anaerobic bacteria increased with time

outnumbering the facultative species.

Greater anaerobes in the apical region than main canal.


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Apical region Bacteria are fastidious have strict nutritional req.

Serum nutrients-Apical region

Proteolytic bacteria Prevotella, Porphyromonas, Peptstrepto,

Fusobacterium main group

Staphylococci,Strept. ,Lacto, & Neisseria opt main canal.


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Main canal- metabolic activity is very low.

Accidental entry of instruments- periapex

blood entry can serve as nutrient for bacteria

this flares up the host response and Acute

apical periodontitis results.

Periapical abscess- 75% anaerobes


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Periapical abscess 75% anaerobes.

3 to 4 bacterial isolates-Porphyromonas, & Prevotella are the

common isolates.

Peptostrepto.-Second most frequent.

Viridans strept.-Third most common.

Veilonella, Eubacterium, Actinomyces, Lactobacillus &

Fusobacterium are also isolated.

Periodontal infections


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Periodontal disease-No. of distinct clinical entities

affecting Periodontium

Chronic bacterial infections

Nature of disease-bacterial host interactions

Host response-protective, destructive, or both


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Identification of bacterial etiology-


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1. Large no bacteria ass. with disease

2. Elimination reverses the disease

3. Elevated host responses assoc. With disease

4. Pathogenicity similar to periodontal disease occurs with

implantation into germ free animals

5. Bacteria possess potentially pathogenic mediators

Gingival health - Harbours microflora in health


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which is simple & sparse ,flora similar to early

stages of plaque formation

Gram positive- majority- constitute two thirds-

Filamentous forms are also seenDisease- are a result of one or two mechanisms

direct effect include invasion, exotoxins, cell

constituents & enzymes, indirect response are

immunologic & host responses

Localized juvenile


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periodontitisClinical-12-20 yrs

No/little gingival inflammation

Marked, localized alv. bone loss

perm 1st molar & incisors

Microbiology-cultural studies-

gram negative rods,

Actinobabacillus,

Actinomycetemcomitans.


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Generalized juvenile periodontitis

Clinically-similar to LJP

Microbial findings- B.gingivalis most common 13-

20%,Eikenella.corrodens,B.intermedius, Capnocytophaga,

Neisseria. A. actinomycetemcomitans in low no.


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Pre-pubertal periodontitisClinically-A rare form of priodontal disease occurs during or

immediately after the eruption of the primary teeth.

Females.

Generalized & localized forms

Microbiolgic findings- Fusobacterium, Wolinella, Bacteroides &

Capnocytophaga commonly found

ANUG (Acute Necrotizing

Ulcerative Gingivitis)


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Clinically-Marginal gingiva

Young people under stress &immunocompromised pts.

Necrotic lesions of one or more

interdental papilla & progress to

maximal extent associ.with pain,bleeding, fetor

exore & fever

Cancrum oris (NOMA)

Considerably beyond gingiva &can give rise to life threatening

infections.

ANUGMi bi l H b hi h


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Microbiology - Harbour high

no. of Spirochetes &P.intermedia

Early microscopic

examination identified high

levels of Fusobacteria (gram

negative rods)


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3)Necrotic zone-Spirochetes & rod shaped bacteria

4)Zone of spirochetal infiltration-inter.& largespirochetes b/w normal collagen

Four Histopathological zones-

1)Bacterial zone containing variety of bacteriasimilar to sub gingival flora

2)Neutrophil zone, rich in leukocytes


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www dentistpro org to find more
http://www.dentistpro.org/http://www.dentistpro.org/


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REFERENCES-Oral Microbiology and Immunology-

Newman & Neisengard

-Cariology-Newbrun-Contemporary oral microbiology &

immunology-Jogren Slots

-J.Nihon Univ.Sch.Dent.Vol.36,No.1,1-33,1994

I i i t & hidd i t 2005 49 4

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Development of Oral Micro Flora