Endodontics microbiology

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ENDODONTICS MICROBIOLOGY

BYPROF.MAGED NEGM

Infection occurs if an organism damage the host & produce clinical signs & symptoms.

Pathogenicity the capacity of organisms to produce disease within the host.

Virulence Degree of pathogenicity in a host.

Stages in development of an endo-infection microbial invasion Colonization multiplication & pathogenic activity.

Portal of entry of microorganisms:

Dentinal tubules

Pulp

exposure

Microbes invade the pulp through

Fractures & cracks

Lateral & accessory canals Blood circulation (anachoresis)

Pulpal Reaction to Bacteria: Caries without pulp exposure

chronic pulpal response. Caries with pulp exposure acute

or chronic pulpal response. Pulp exposure Pulp abscess. Pulp

necrosis. Periradicular

inflammation. Pulp exposure without

microorganisms minimal inflammation.

Polymicrobal infections: Normal oral flora contains more than

350 bacterial species. A relatively small group is isolated from

infected pulp cavities.  Infected pulp Mainly

anaerobic bacteria

(strict). Some facultative

anaerobes.

Rarely aerobes.

No absolute correlation between species of bacteria & endo. signs & symptoms.

Black Pigmented Bacteria( BPB) associated with endo-infections.

Most canals containing BPB associated with acute periapical abscess.

Purulent lesions are induced by strains of BPB.

Porphyromonas gigivalis

Isolated from acute

infections.

Porphyromonas endodontalis  Prevotella intermedia found in

both symptomatic & asymptomatic cases. Yeasts & viruses were also

found in pulp cavity. Even the human immunodeficiency virus

(HIV) was isolated from the pulp.

Microbal Ecosystem in the Root Canal: Necrotic pulp cavity becomes

a reservoir for microbes. Disintegrated tissues & fluids

nutrients for microorganisms. Nutrients are polypeptides & amino

acids. Nutrients Low 02

tension + Bacterial interactions+

Determine the type of predominant

bacteria

Growth of anaerobes able to metabolize peptides & amino acids.

Some species produce metabolic byproducts

essential nutrient for other species.

Antagonistic relationships may occur among

bacteria. Some by products (eg. Ammonia)

could be either a nutrient or toxin. Bacteriocins (antibiotic-like proteins)

inhibit growth of other species. 

Chemomechanical RC. Preparation disrupt & destroy microbial ecosystem.

  Perfect obturation

eliminate the pulp cavity as a reservoir.

 

Association of bacteria with periradicular disease:

Contents of infected canals are potent irritants periradicular pathosis.

Bacteria &/or bacterial by products apical periodontitis.

Virulence Factors: Fimbrae (pili).

Capsules.

Extracellular

vesicles. Virulence factors

lipopolysaccharides (LPSs).  Enzymes.  Low-molecular weight

products.  Short chain fatty

acids.  Polyamines. 

1-Fimbrae synergistic relationship between bacteria.

2-Capsules resistance against phagocytosis.

3-Extracellular vesicles affect host cells & protect bacteria against antibodies.

4-LPSs are endotoxins induce periradicular inflammation.

5-Enzymes spreading factors + proteases that neutralize immunoglobulins.

6-Low-molecular weight products (ammonia & hydrogen sulfide) bacterial nutrients.

7-Short chain fatty acids propionic, butyric & isobutyric acids.

These fatty acids affect phagocytosis, production of interleukin 1 & intracellular changes.

8-Polyamines putrescine, cadaverine & spermidine.

Correlations with Pathoses & Treatment:

-Endo. infections are polymicrobial.

Excellent collateral circulation.

-Periradicular tissues posses

Lymphatic drainage.

Vast amount of undifferentiated cells.

Periradicular pathoses develop in response of microorganisms

Microorganisms.

Microbial by product.

Microbial breakdown products.

Inflammatory mediators.

Instrument trauma. Chemicals.

Acute periapical abscess .

Necrotic tissues.Phoenix abscess.

Contain

Bacteria.Suppurative apical

periodontitis.

Numerous PMNs

Infection Control:All patients should be treated as if they

have transmissible disease.

Use physical barriers

Disinfect tooth surface & rubber dam with Chlorhexidine or Na OCL.

Rubber dam Safety glasses face shields Masks Gowns Gloves

Treatment of endodontic infections:

Removal of source of irritation healing of periradicular lesion.

Source of irritation reservoir of infection (pulp cavity).

Achieved by thorough debridement of root canals.

Debridement of the root canal system:

RC debridement instrumentation + irrigation.

  Flush out

debrisIrrigants Dissolve organic

remnants Antimicrobials Lubricants

Sodium hypochlorite ( Na OCL 0.5 to 5.25%)

irrigant of choice Na OCL dissolves organic

debris & an excellent antimicrobial agent.

Bacteria stay in fins, irregularities & cul-de-sacs of RC. walls.

Sonic and ultrasonic devices improve the irrigant effects.

Irrigant should be passively delivered with a blunt end needle.

Smear layer amorphous layer of dentin & other debris + viscous material.

  Smear layer plugs dentinal

tubules to a depth of 40mm.  It affects permeability. Protects

entraped bacteria . Inhibits penetration of

irrigants & medications..Inhibits penetration of sealers. . Inhibits bacterial

colonization

Intracanal Medication (IC):

Microorganisms inside RC. multiply between appts. Intracanal medicaments exert antimicrobial action

between appts

Intracanal medicaments (phenolic products).

. Phenolics antigenic, cytotoxic & with short durations.

The current IC. Medicament of choice Ca (oH)2.

Formocresol. CMCP & CPCP. Metacresyl acetate. Eugenol . Thymol. Cresation.

Drainage: The key to managing an abscess or cellulitis

is drainage. Drainage through the canal & incision

decrease discomfort, toxins & pressure. Incision of indurated swelling releases

Blood.

Serous fluids.

Bacteria & their byproducts . Inflammatory mediators.

Drainage removes these irritants & improves local circulation.

Adjunctive Antibiotic therapy

  Antibiotics are not a

substitute for local treatment. The majority of endo. cases

can be treated without antibiotics. Pain & swelling of endo. origin are

managed by debridement & drainage.

Symptomatic pulpitis Apical periodontitis

without systemic signs & symptoms Draining sinus tract Localized swelling

do not

require antibiotics

Prophylactic Antibiotics for Medically Compromised Patients:

Distant infection are high in case of transient bacteremia.

Bacteremia puts medically compromised patients at a great risk.

Transient bacteria can result from apical extrusion of bacteria.

Procedures that may produce bleeding induce bacteremia.

Procedures that may induce bleeding

Rubber dam

Local injections

Extirpation

Surgical procedures Overinstrumentation

Prior to surgical procedures gum & mucosa should be disinfected with:

Chlorhexidine or iodine-glycerine

Medicaly compromised patients at great risk of bacteremia include:

i-Rheumatic & congentinal disease.

ii-Prosthetic cardiac valves.

iii-Valvular prolapse & regurgitation.

iv-Previous infective endocarditis.

V- Systemic pulmonary shunts.

Vi- Arterio-venous shunts.

Vii -Uncontrolled diabetes.

Viii- Immunosuppressed & immunologically deficient cases.

Medically compromised patients at risk of bacteremia must receive.

 

A regimen of antibiotics that follows the recommendations of

  American Heart Association (AHA)

Antibiotics used in treatment: Antibiotics are prescribed in conjunction

with endo. procedures. In the reservoir of microorganisms (RC

System) absence of circulation. Therefore antibiotics without endo.

procedures not effective. Antibiotics are prescribed when there is : systemic involvement Persistent

infection Spreading

infection

Signs & symptoms of systemic

iInvolvement & spread infection

alone or in combination

Antibiotics should be continued for 2 to 3 days after disappearance of signs & symptoms.

Fever 38° c Malaise Trismus Diffuse swelling Cellulitis

Selection of an Antibiotic Regimen:

Penicillin remains the antibiotic of choice.

Effective against many facultative

& strict anaerobes.

Penicillin Has low toxicity

Inexpensive

However, penicillin is allergic to approx. 10% of humans.

Adequate blood level of penicillin must be maintained.

Initial oral dose of 1000mg followed by 500 mg/6hours.

Antibiotics + proper endo. procedure signif. improvement within 48 hours.

ALL PRESCRIBED ANTIBIOTICS

MAY BE GIVEN FOR 7 DAYS.

Erythromycin alternative choice for patients allergic to penicillin.

Erythromycin effective against facultative bacteria.

Erythromycin ineffective against most anaerobes & serious infections.

Adverse effect GI upset ingestion of milk or yogurt gives relief.

Adverse effect transient deafnes.

Dose 1000mg followed by 500mg/6 hours.

Clarithromycin (Klacid)

Clarithromycin a macrolide – a semisynthetic derivative of erythromycin.

Clarithromycin has greater

antibacterial

spectrum.

less GI upset.

Dose 500 mg/8-12 hours

Cephalosporins broad spectrum but does not include anaerobes.

Cefaclor (2 nd. generation) effective against anaerobes.

Not recommended for penicillin allergic patients.

Clindamycin effective gm +ve & -ve

bacteria.

Facultative & strict

anaerobes.

Clindamycin well distributed throughout the body & bones.

Adverse effects long use pseudomembranous colitis.

Dose 150 to 300 mg/6 hours.

Metronidazole

effective against anaerobes

Ineffective against aerobes

Metronidazole + penicillin or other antibiotic

endo.infection. Dose 250 to 500 mg/ 6

hours.

Culturing Required when

empirical use of antibiotics is not effective.

Procedure: Rubber dam isolation. Disinfection with Na

OCL or other disinfectant. Access opening with

sterile instruments. Microbial sampling with

sterile paper points or aspiration.

Aspiration is done with 16 to 20 gauge needle.

In dry canals place a drop of a sterile solution before sampling.

Submucosal swellings should be sampled by aspiration before incision.

Samples are immediately placed in the media.

Antimicrobial irrigating solutions should not be used before sampling.