Normal Oral Flora 9.ppt 2l3g2

Presented by – Dr. Priyanka Singh MDS-IInd year, Department of Oral Pathology, SPIDMS.

CONTENTS            

Introduction Prokaryotic cell & eukaryotic cell Bacteria Staining of bacteria Anatomy of bacteria Growth and multiplication of bacteria Growth regulation Flora of the oral cavity Dental plaque bio film Calculus formation Role of oral flora in systemic infection Conclusion

Introduction 

Human beings like other animals, harbour a wide array of microorganisms either on or in their bodies. A knowledge of normal flora of body is essential to an understanding of the interaction between human beings and their pathogen laden environment.

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The oral cavity is accessible to the introduction of many different types of microorganisms and consist of large number of microorganisms including mycoplasma, fungi, protozoa nad viruses.

Microorganisms – A heterogeneous group of several distinct classes of living beings – Originally classified under plant and animal kingdoms – 3rd kingdom protista was formed for them – Kingdom protista –  Prokaryotes – bacteria and blue-green algae  Eukaryotes – fungi, algae, slime moulds and protozoa

Prokaryotic cell & eukaryotic cell Characteristic Nucleus

Prokaryote Absent

Diameter of cell Cytoskeleton

Present About 1µm

Absent

Cytoplasmic organelle DNA content

Eukaryote

10-100µm Present

Absent Present

Unorganized

Organized

Chromosomes Single circular Multiple linear DNA molecule DNA molecule

BACTERIA 

Prokaryotic microorganisms

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Do not contain chlorophyll

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Unicellular

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Do not show true branching except in Actinomycetes

Staining of bacteria 

Live bacteria do not show much structural detail due to lack of contrast

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Stained to produce colour contrast

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Depending upon the effect of stains on the viability of microorganisms –  Supravital staining  Toxic  Kill the cells  Intravital staining  Nontoxic  Cells remain viable

Routine methods  Simple stain – Methylene blue & basic fuchsin – Do not stain bacterial capsules – Imparts same colour to all bacteria

 Negative stain – India ink or nigrosin – Uniformly colors background – Unstained bacteria in contrast – Useful for demonstration of bacterial capsules – Spirochetes which are very slender can be stained

 Impregnation – Thin cellular structures can be seen – Thickened by impregnation of silver on the surface – Spirochetes and bacterial flagella

 Differential stains – Imparts different colour to different bacteria or bacterial structures – 2 most widely used differential stains are –  Gram stain  Acid fast stains

GRAM’S STAIN  Devised by – Christian Gram (1884)

Procedure – – Primary staining with pararosaniline dye e.g. – crystal violet, methyl violet or gentian violet – Dilute solution of iodine – Decolorisation with an organic solvent e.g.- ethanol, acetone or aniline – Counterstaining with a dye of contrasting colour e.g. – carbol fuchsin, Safranin or neutral red

Purpose of gram stain  Identification of bacteria  Therapy of bacterial infections - gram +ve bacteria are more susceptible to penicillins

Principle GRAM +ve

 Relates to the permeability of the bacterial cell wall and cytoplasmic membrane to the dye  Gram –ve cells permits the outflow of the dye during decolorisation  Gram positive cells resist decolorisation and also has got a more acidic protoplasm and so retain the primary stain, appearing violet  Gram – ve bacteria are decolorised by organic solvents and so take the counter stain, appearing red GRAM -ve

ACID FAST STAIN – Discovered by Ehrlich – after staining with aniline dyes tubercle bacilli resist decolorisation with acids – Modified by Ziehl and Neelson –  Smear stained with carbol fuchsin with application of heat  Decolorised with 20 % sulphuric acid  Counterstained with a contrasting dye i.e. methylene blue  Acid fast bacteria retain fuchsin (red) colour while others take the counter stain

SIZE OF BACTERIA

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0.2 – 1.5 m in diameter 3 – 5 m in length

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SHAPE OF BACTERIA -

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Cocci (kokkos – berry) – spherical or oval  Diplococci (in pairs)  Streptococci (in chains)  Grape – like clusters (staphylococci)

Bacilli (bacillus – rod) – rod shaped  Streptobacilli (in chains)  Corynebacteria (arranged at angles to each other, presenting a cuneiform or Chinese letter pattern)

Vibrios (comma shaped, curved rods) –  characteristic vibratory motility Spilrilla – rigid spiral forms Spirochetes (speira=coil ; chaite=hair) – flexuous spiral forms

Actinomycetes (actis = ray, mykes = fungus) – branching filamentous bacteria – radiating rays of the sun like appearance - due to presence of rigid cell wall

Mycoplasma – Do not posses a stable morphology – protoplasts, spheroplasts or L-forms – Deficient cell wall due to drugs like penicillin – Round or oval bodies 

Some are pleomorphic (pleo : many, morphic shaped)

ANATOMY OF BACTERIA 

Consists of – Outer layer or cell envelop  Cell wall  Plasma membrane

Inner cytoplasm and cytoplasmic inclusions  Ribosomes and Mesosomes  Granules  Vacuoles  Nuclear body

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Some bacterial cell – – Enclosed by a viscid slimy layer or organized as a capsule – Filamentous appendages protruding from the cell surface – flagella – organs of locomotion – Fimbriae – organs of locotion

STRUCTURES EXTERNAL TO CELL WALL Flagella     

 

Whip like long filaments Used for locomotion Guide the bacteria towards nutritional and other sources Composed of subunits of a single protein flagellin 3 parts –  Filament  Hook  Basal body 3-20 m long 0.01-0.013 m in diameter

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Flagella of different bacteria have same chemical composition but are antigenically different

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Flagellar antigens induce specific antibody in high titers

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Flagellar antibodies are useful in serodiagnosis

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Flagella – – Peritrichos – Polar – Monotrichos – Lophotrichos – Amphitrichos

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Presence is usually detected by motility of bacteria

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Motility – spreading type of growth on a semisolid agar medium

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Present in all motile bacteria except in spirochetes (move with axial filament – a flagellum like structure)

Fimbriae & Pili – – Fine hair like surface appendages – Shorter than flagella – 0.5 m long and 10 nm thick – Present mainly on gram –ve bacteria

– Consists of self aggregating monomers of pilin – Adhesion of bacteria to receptors on human cell surface – first step in initiation of infection – Cause hemagglutination – a method of detection – Antigenic in nature

Sex pili – – A specialized type of fimbriae – Forms attachment between male (donor) and the female (recipient) through conjugation tube – Genetic material is transferred from donor to recipient cell

Glycocalyx (slime layer) 

Loose undemarcated

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Polysaccharide or polypeptide covering

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Adhesion of bacteria to structures like oral mucosa, teeth, etc.

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E.g. - leuconostoc

Capsule 

An amorphous gelatinous layer

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Surrounds entire bacteria

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Composed of mainly polysaccharides

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Antigenic

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Demonstrable by serological methods by antigenic differences of sugar in polysaccharide capsule

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Mediates adhesion of bacteria to human tissues

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Hinders or inhibits phagocytosis

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Quelling reaction – – Described by Neufeld (1902) – Presence of antiserum against capsular polysaccharide, swelling of the capsule – Protects the bacteria from deleterious agents in nature. – Helps in virulence of pathogenic bacteria – Inhibits phagocytosis – E.g. – streptococcus mutans

Spores 

E.g. – bacillus & clostridium

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Highly resistant resting stages

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One bacteria forms one spore – on germination forms one vegetative cell

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Not a method of reproduction

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Called endospores as are formed inside the parent cell

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Cause – in response to adverse conditions

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Contains bacterial DNA, cytoplasm, cell membrane, peptidoglycan, water and a thick, keratin like coat –  Consists of calcium dipicolinate  Resistant to heat, dehydration, chemicals

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Metabolically inert

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Remain dormant for many years

Types of spores – Central, budging – Central, not budging – Sub terminal, budging – Sub terminal, not budging – Terminal, budging – Terminal, not budging

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When spores are transferred to favorable conditions

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Spore loses its refractility

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Swells

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Spore wall is shed

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Germ cell appears

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Elongates to form vegetative bacterium

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Can be destroyed by autoclaving at 120 for 15 mins

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Bacillus stearothermophilus – ensures sterilization efficacy of autoclaves

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Appears unattained in gram stain

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Can be stained by Ziehl-Neelson stain due to its acid fast nature

Cell wall

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Confers rigidity upon bacterial cell

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Multilayered structure outside protoplasmic membrane

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Porous and semi permeable

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Important in virulence and immunity

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Demonstrable by plasmolysis –  Hypertonic solution  Osmosis  Cytoplasm loses water  Shrinkage of cell  But cell wall retains its original shape

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Inner layer – Peptidoglycan – Scaffoldings formed by Nacetyl glucosamine and Nacetyl muramic acid – Present in chains which are cross-linked by peptide chains

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Outer layer – Depends upon gram staining property of bacteria

Bacteria with deficient or defective cell walls

Mycoplasma – Do not posses cell wall – May cause human disease e.g. – pneumonia

L - forms – – – –

E.g. – streptobacillus moniliformis Swollen cells Named after Lister Institute, London Develops –  Spontaneously  Presence of penicillin  Other agents that interfere with cell wall synthesis  Cause urinary and suppurative infections

Spheroplasts (gram –ve bacteria) & protoplasts (gram +ve bacteria)  Lack cell walls  Cannot replicate on laboratory media  Unstable  Osmotically fragile  Require hypertonic conditions for maintenance  Produced in laboratory by action of enzymes or antibiotics Spheroplast

Protoplast

Conversion of bacteria into protoplast and spheroplast

Cytoplasmic membrane 

Thin inner layer lining the inner surface of the cell wall

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5 – 10 nm thick

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Separates cell wall from cytoplasm

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Semi permeable membrane

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age through the membrane depends upon– Molecular size of the particles – Presence of specific enzymes (permeases)

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Consists of – – Lipoprotein with small amounts of carbohydrate – Sterols are absent except in mycoplasma

Cytoplasm 

Colloidal system of organic and inorganic solutes in a viscous watery solution

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Differs from eukaryotic cytoplasm – – Absence of protoplasmic streaming – Absence of endoplasmic reticulum and mitochondria – Stains uniformly with basic dyes – Contains ribosome, mesosome, inclusions (volutin granules or Babes Ernst granules) and vacuoles, metabolites and various ions

Ribosomes 

Centers of protein synthesis

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Smaller than in eukaryotes

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Sedimentation rate – 70 s

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Integrated in linear strands of mRNA to form polysomes

Mesosomes (chondroids) 

Convoluted or multilaminated structures

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Invaginations of plasma membrane into the cytoplasm

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More prominent in gram + ve bacteria

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Principal site of respiration

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Analogous top mitochondria of eukaryotes

Nucleus 

Demonstrated by acid or ribonuclease hydrolysis and subsequent staining

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Oval or elongated

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No nuclear membrane or nucleolus

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Genome consists of a single molecule of double stranded DNA arranged in a form of a circle

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Chromosome is haploid and replicates by simple binary fission

Plasmids or episomes – Extra nuclear genetic material – Carried by some bacteria – Consists of DNA – Cytoplasmic carriers of genetic information

GROWTH AND MULTIPLICATION OF BACTERIA 

Divide by binary fission

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On reaching certain size  Nucleus divides  Cell divides to form 2 daughter cells

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Generation time or population doubling time – time interval between two cell divisions –generally vary from 20 mins in E. coli to 24 hrs in M. tuberculosis

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Can be arrested by  deficiency of nutrients  Accumulation of toxins  Antibiotics like penicillin and acriflavin

Bacterial growth curve

Growth regulation 

Regulated by nutritional environment –  Intracellular  Extracellular

Intracellular  End-product inhibition – first enzyme in metabolic pathway is inhibited by end product of that pathway  Catabolic repression – enzyme synthesis is inhibited by catabolites

Extracellular factors 

Temperature – – Can grow in a wide range of temperature –  Mesophiles – 25 – 40 C – majority of bacteria  Thermophiles – 55 – 80 C  Psychrophiles – below 20 C

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pH –  Optimal growth at physiological pH – 7.2 – 7.4  Vibrio cholera – high degrees of alkalinity

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Oxygen requirement –  Obligate aerobes – require oxygen – ATP generating system is oxygen dependent – e.g.-M. tuberculosis  Facultative anaerobes – can survive in the absence of oxygen - e.g.- Strep. Mutans & E. coli  Obligate anaerobes – do not require oxygen e.g. – Porphyromonas gingivalis  Microaerophiles – grow best at low oxygen concentration e.g. – Campylobacter fetus

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Light  Grows well in absence of light  Sensitive to ultraviolet and other radiations

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Osmotic effect –  More tolerant to osmotic variation  Due to mechanical strength of the cell walls  Sudden exposure to hypertonic solutions – plasmolysis – mostly in gram –ve bacteria  Plasmoptysis – sudden transfer from conc. Solution to distilled water – swelling and rupture of cell

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Moisture and drying –  Moisture is essential  Drying – lethal  Highly sensitive for drying – Treponema palladium

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Antimicrobial therapy –  Broad-spectrum antibiotics  Wipe out most of the endogenous flora  Favor fungal infection

FLORA OF THE ORAL CAVITY 

Gram positive cocci Streptococcus  Gram positive  Non motile, flagella usually absent  Occur in chains  Generally non capsulated  Facultative anaerobes  Causes α haemolysis  Selective medium – mitis salivarius agar  Various types are – – Mutans group    

High, convex, opaque colonies Produce extra cellular polysaccharide Site – tooth surfaces Causes – Dental caries

– Salivarious group   

Appear in mouth of infants as early as 18 hrs to 1 month after birth. Large mucoid colonies Produce extra cellular fructans (polymer of fructose with a levan structure)  Site – dorsum of tongue and saliva (especially in infants)  Not a major oral pathogen – Mitis group   

Small, rubbery or non adherent colonies Site – tongue and cheeks Causes – Dental plaque bio films, Dental caries, Infective endocarditis

– Anaerobic streptococci     

Strict anaerobes Slow growing Usually non hemolytic Site – teeth (carious dentin) Causes – Periodontal or Dentoalveolar abscess

 Gram positive rods and cocci – Actinomyces   

Strict and facultative anaerobes Branched – sun ray appearance Ferments glucose – characteristic patterns of short chain carboxylic acids  Causes – Dental caries (especially root caries) & Gingivitis Actinomycosis

– Lactobacillus  Micro-aerophiic  Aciduric (optimal ph=5.5-5.8)  Selective medium – Rogosa agar  Catalase negative  Site – common oral inhabitats  Causes – Dental plaque bio film Advancing front of dental caries – Eubacterium  Pleomorphic  Obligatory anaerobes  Site – plaque bio films and calculus  Causes – Role in dental caries

– Propionibacterium   

Strict anaerobe Produces propionic acid from glucose Causes – Root surface caries and Dento-alveolar infections

 Gram negative cocci – Neisseria  Facultative anaerobe  Site – tongue, oral mucosa, saliva and early plaque  Causes - not a major oral pathogen – Veillonela  Strict anaerobe  Site – tongue, saliva and plaque bio film

 Gram negative rods (Facultative anaerobe an capnophilic genera) – Hemophilus    

Growth on heated blood agar Requires X (haemin) and V (NAD) for growth Site - oral mucosa, saliva and plaque bio film Causes – Dentoalveolar infections, Acute sialadenitis Infective endocarditis

– Actinobacillus  Produces virulent factors – leucotoxin, epitheiotoxin, cardotoxin  Site – periodontal pockets  Causes - Periodontal disease

 Gram negative rods (obligate anaerobic genera) Produce brown black pigment on blood agar Black pigmented anaerobes – Prevotella      

Pleomorphic rods Non-motile Strict anaerobe Require Vit. K and haemin for growth Site – gingival crevice and sub gingival plaque Causes – Chronic periodontitis and Dentoalveolar abscess

– Fusobacterium  Sender, cigar shaped Gm –ve rods with rounded ends  Site – gingival crevice and tonsils  Causes – periodontal infections acute ulcerative gingivitis dentoalveolar abscess

– Treponema       

Motile Helical cells (large, medium, small) Strict anaerobes Require enriched media with serum to grow Site – gingival crevice Causes - acute ulcerative gingivitis destructive periodontal disease

Other bacterial genus present are –        

Angiogenous group Stomatococcus group Propionibacterium group Actinobacillus group Eikenella group Capnocytophaga group Leptotrichia group Wolinella

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Fungi and protozoa present in the oral cavity are – – Fungi –  Candida albicans  Candida tropicalis  Candida pseudo tropicalis  Cryptococcus – Protozoa  Entameoba gingivalis

Factors in the oral cavity affecting growth of micro flora 

Anatomical factors  Shape of teeth  Malalignment of teeth  Poor quality of restorations  Non-keratinized sulcular epithelium – Difficult to clean – Favors accumulation of bacteria

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Saliva – – Consist of proteins, glycoproteins and various other ions & metabolites – Modulate bacterial growth by –  Adsorption on the tooth surfaces – pellicle – facilitates bacterial adhesion  Acts as a primary source of nutrition  Helps in aggregation of bacteria – plaque formation  Inhibits growth – Due to presence of defense factors – – Lysozyme, lactoferrin, IgA, etc – Bactericidal and fungicidal

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Gingival crevicular fluid –  Continuous but slow flow  Flushes microbes out of the crevice  Maintains pH level  Provide defense factors – IgG ( also IgM & IgA)  Causes phagocytosis due to presence of neutrophils

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Microbial factors – – Interaction of bacteria with each other may promote or suppress the neighboring bacteria by –  Competition for receptors for adhesion  Production of toxins by one may destroy same or other bacterial species  Production of metabolic end products – lowering of pH  Co-aggregation to form corn-cob formation with –  Same (homotypic) or  Different (heterotypic) species

Distribution of oral flora 

Oral micro flora does not represent a homogenous collection of organisms through out the oral cavity but it is localized in 3 different foci – – Gingival crevices – Dorsum of tongue – Areas that are not cleaned by mastication – Other areas that may be involved are –  Lips  Palate  Saliva  Cheeks or buccal mucosa

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Gingival crevices – – The gingival crevice is not sterile, but harbors a microbial flora in both health and disease – In healthy sulci, gram positive cocci are major macrophyte and compose almost 2/3rd of total flora. Filamentous forms and all spirochetes fusiforms are found. – In diseased conditions, gram positive as well a sgram negative rods such as capnocytophaga, bacteroids, compylobacter, fusobacterium can be isolated.

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Tongue – – The tongue with its complex surface structures (crypts and papilla) forms large surface areas that growth of a wide variety of bacteria and serves as a reservior of microorganisms in the mouths. – Predominant cultivative bacteria isolated from the tongue falls in the following list of microorganisms which are -

– – – – – – – – – – –

Facultative streptococci Veillonelle Facultative diptheroids Anaerobic diptheroids Bacteroides Peptostreptococcus Neisseria Vibrio Fusobacterium Provetella intermedia Provetella melanogenicus

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Lips – – The lips form the border between the skin flora and consists predominantly of staphylococcus. – Facultative anaerobic micro flora comprises a large part of flora of the lips. – Veillonella and neisseria have been found – If commissures are moistened by saliva, then Candida albicans, Staph. aureus and Strept. Pyogenes are common.

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Cheeks/buccal mucosa – – Predominant bacteria are – Strept. sanguis and Strept. salivarious. – Yeasts may also be isolated from carriers. Other organisms may be hemophilus and neisseria sp.

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Palate – – Hard palate s a streptococcal flora resembling the cheek flora – Haemophillus and lactobacilli are also found regularly – Yeasts and lactobacilli are increased dramatically, in some denture wearers and flora may alter substantially when the palate is protected from the action of tongue and saliva by denture base. – Soft palate – also harbor respiratory tract bacteria like hemophilus, corynebacterium, neisseria.

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Saliva – – Adult human saliva contains approx. 6 billion micro flora and include –  Streptococci  Peptostreptococci  Veillonella  Corynebacteria  Neisseria  Nocardia  Fusobacteria  Lactobacilli  Actinomycosis  Spirochetes  Fungi like Candida and Cryptococci

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Teeth – – On eruption, teeth are covered by organic structure of embryonic origin. – After eruption, organic deposits form on the surfaces of teeth which contain organic acids, bacterial and cytotoxic agents. – Williams demonstrated microscopically, the presence of thick mass of microorganisms covering the surface of teeth – G.V. Black introduced the term gelatinous microbial plaque to describe microbial colonies on the surface of teeth. – Microorganisms do not attach themselves directly to mineralized tooth surface as teeth are covered by teeth by an acellular proteinaceous film.

DENTAL PLAQUE BIOFILM

“Dental plaque is a tenacious microbial community which develops on soft and hard surfaces of mouth, comprising of living, dead and drying bacteria and their extra cellular products, together with host compounds mainly derived from saliva.”

Composition – – Organisms surrounded by organic matrix – 30% – Matrix acts as a food reserve – for adhesion of further bacteria – Composition varies –  At different sites on same tooth  At same site on different teeth  At different time on the same tooth site

Distribution – – Found on dental surfaces and appliances – Mainly in absence of oral hygiene – May be  Supra gingival – mainly aerobic bacteria  Sub gingival – mainly anaerobic bacteria

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Plaque has been found to contain the following microorganisms in percentages – – Supragingival plaque  Facultative streptococcus – 87%  Facultative diphtheroids – 23%  Anaerobic diphtheroids – 18%  Peptostreptococcus – 13% – Subgingival plaque  Veillonella – 6%  Bacteroids – 4%  Fusobacteria – 4%  Neisseria – 3%  Vibrio – 2%

Stages of Plaque Bio film formation Pellicle formation –  Thin layer of salivary glycoproteins  Deposited on the surface  Forms within minutes of exposure to the oral environment  Oral bacteria attach to pellicle for the initiation of plaque formation

Transport –  Bacteria are transported to pellicle site by – Natural salivary flow – Brownian motion – Chemo taxis

Long range interactions –  Between microbial cell surface and pellicle coated tooth  Called pioneer group-gram positive cocci and rods  Through Vander waals forces  Reversible

Short range interactions –  Polymer bridging between organisms and the surface  After which organisms come and accumulate – to increase the microorganism mass  Forms corn-cob arrangements  Secondary invaders - gram negative cocci and rods and later by fusobacteria, spirals, and spirochetes  Irreversible

Co-aggregation or co-adhesion – – Fresh Bacteria now attach to the primary invaders – May be of same genus or different genera – Process of plaque bio film mass reaches a critical size at which – Deposition = Loss of bacterial accumulation – Climax community – The bacteria in climax community- detached – Plank tonic phase – suspended in saliva – transported to new colonization site

Bio film formation – – – –

Due to resultant confluent growth Matures in complexity as time progresses Occurs at inert surfaces e.g.- tooth enamel, dentures, etc. Organisms may be arranged in columns or mushroom shaped structures – Water channels that carry metabolites and nutrition are interspersed within the organic matrix

“A bio film is defined as a complex functional community of one or more species of microbes encased in and exopolysachharide matrix and attached to one another or to solid surface” 

Major component of bio film is extra-cellular matrix –  Microbial polysaccharides  Salivary glycoproteins

Calculus formation 

Due to deposition of calcium and phosphate ions from saliva within dental plaque

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Bacteria in plaque as seeding agents of mineralization

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Accelerated by bacterial phosphatases and proteases – degrade calcification inhibitors (Statherin and proline rich proteins) in saliva

– Formation of insoluble calcium phosphate crystals – Coalesce to form a calcified mass of plaque – calculus – Mature calculus –  Mineralized material – 80%  Organic compounds – 20%

Structure of calculus – Predominant flora – cocci, bacilli, and filaments – outer layers – Supra gingival calculus – gram positive bacteria – Sub gingival – gram negative bacteria – Outer surfaces of calculus – cocci attach grow on surface of filamentous microorganism corn cob arrangements

– Filaments orient themselves at right angles to enamel surface – Palisade effect (like books on a shelf) – Cytoplasm of bacteria is  Reduced  Contains glycogens like food storage granules  Ready source of nutrition during periods of adversity – Has enough surface – Porous – Ideal reservoir for bacterial toxins – harmful to periodontium

Role of oral flora in systemic infection 

Plaque related oral diseases, especially periodontitis may alter – – Cardiovascular disease  Infective endocarditis  Coronary heart disease – Bacterial pneumonia – Diabetes mellitus – Low birth weight babies



According to ‘focal infection theory’ – 3 mechanisms lining oral infections to secondary systemic are –

1.

Metastatic infection  

2.

Gain entry into vascular system through breach in oral vascular barrier E.g. - bacteraemias during tooth extractions

Metastatic injury 

3.

disease

Products of bacteria (catalytic enzymes, endotoxins, exotoxins) gain access to cardiovascular system

Metastatic inflammation 

Caused by immunological injury due to antigens produced by oral organisms – enter blood stream from oral route - react with circulating antibodies - immune mediated disease

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Factors for periodontitis predispose risk for systemic disease

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Sub gingival bio films – reservoir for gram –ve bacteria – continuous source of lipopolysachharides (endotoxin) causes –  Induction of major vascular responses  Up regulates endothelial cell adhesion molecules  Secretion of interleukin-1 and tumour necrosis factor-α  Gain entry into vascular system

Although, there are various controversies regarding exact roe of oral flora in dental health, it can definitely be stated that good oral health is important not only to prevent oral disease but also to maintain good general health.