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Microbiological aspects inEndodontics

Endodontics #348

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Interpretation of tests

VariesPulp statusIncreaseddensity oftrabecular bone

VariesCondensingosteitis (C.O.)

Not sensitiveNo responseApical lucencyDraining sinustract

CAA

TTP & palpationNo responseVariesSwelling/painAAA

None to mildTTP

No responseApical lucencyNone to mildCAP & Apicalcyst

TTP & palpationPulp statusNone to PDLwidened

Pain on bitingAAP

Not sensitiveRespondsNo changeNone significantNormal

Periapical

With periapicalinvolvement

No responsePeriapicalstatus

NoneNecrotic

With periapicalinvolvement

Responds(extremelingering pain)

WithCondensingosteitis.

Spontaneous orsevere lingeringpain

Irreversible

Not sensitiveRespondsNoneNone to mildReversible

Not sensitiveRespondsNoneNone significantNormal

Pulpal

Periapical testsPulp testsRadiographicSymptomsDiagnoses

Bacteria associated with Endodontic infections

Terminology• Colonization- establishment in host• Infection- damage to host tissues

causing clinical signs and symptoms• Disease- progression of infection• Pathogenicity- capacity to produce

disease• Virulence- degree of pathogenicity

under defined circumstances

Bacteria associated with Endodontic infections

Portals of entry to the pulp• Exposed dentinal tubules• Cracks• Fracture• Lateral canals• Tooth displacement• Periodontal pockets• Anachoresis

Bacteria associated with Endodontic infections

Caries and Pulpal disease

• Most common portal of entry• Bacteria in caries non-motile and advance by..

– Binary fission– Dentinal fluid movement

• Smooth-pit/fissure caries– Strep. mutans and sobrinus

• Root surface caries– Actinomyces spp.

• Surface vs. deep layer caries– After exposure, predominantly anaerobes in deeper

layers

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Bacteria associated with Endodontic infections

Reaction of pulp to bacteria

• Pulp responses – nonspecific inflammation & specificimmunologic reactions

• Initial response – chronic cellular response including:– Lymphocytes– Plasma cells– Macrophages

• Later response –– Formation of peritubular dentin and irregularsecondary dentin

– Decreased permeability of dentinal tubules

Bacteria associated with Endodontic infections

Polymicrobial infections

•500 species identified as normal Oral flora•Very few identified in infected pulp cavities•Most studies report polymicrobial system in pulpal andperiradicular diseases.•Strict anaerobes predominate with facultative anaerobesand aerobes distant 2nd and 3rd.

Bacteria associated with Endodontic infections

Polymicrobial infections

•Black pigmented bacteria (BPB) previously classified asbacteroides•BPB implicated with clinical signs and symptoms•Reclassified as Porphyromonas and Prevotella•Porphyromonas gingivalis/endodontalis in acute infections•Prevotella nigrescens most common isolated BPB fromendo infections.•Actinomyces and propionibacterium can persist inperiradicular tissues

Bacteria associated with Endodontic infections

Monomicrobial infections

•Recent studies show high incidence of Enterococcusfaecalis in root canals of teeth with failed root canaltreatment.

Other microbes•Fungi also found in root canals refractory to endodontictreatment.•Viruses including HIV (in HIV positive patients) have beenfound in the pulp canal system.

Virulence factors

• Fimbriae (pilli)– Attachment to host tissue or surfaces– Attachment to other microbes

• Capsule– Resist host immune defenses– Avoid phagocytosis (BPB)

Virulence factors

• Lipopolysaccharides (LPS)– Endotoxin on gram-negative cell surface– Induction of periradicular pathosis– Activate complement system

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Virulence factors

• Enzymes– Bacterial enzymes (proteases) may neutralize immunoglobulins and

complement components– Collagenase and metalloprotease associated with bacteria like P.

gingivalis help in spread of cellulitis.– In addition, enzymes from disintegrated PMNs in pus may destroy

surrounding tissue.

• Extracellular vesicles– Free endotoxins, blebs or outer membrane fragments– May contain enzymes– Hemagglutination, hemolysis, bacterial adhesion, and proteolytic

activities.

Virulence factors

• Fatty acids– Butyric acid can affect neutrophil chemotaxis,

degranulation and phagocytosis– Stimulate IL-1 production which is involved in

bone resorption

• Polyamines– Mostly by gram-negative bacteria– May be associated with acute symptoms like

spontaneous pain

Correlations with pathoses and treatment

• Conflicting reports of the presence ofactual bacterial colonies in acute orchronic apical periodontitis.

• On the other hand, AAA or acuteexacerbations of CAP are characterizedby PMNs, necrotic tissue and bacteriamostly strict anaerobes.

Treatment of endodontic infections

Debridement of the root canal system

• The microbial ecology of the root canal system and apical inflammatoryresponse will persist until the source of irritation is removed.

• Effective root canal debridement consists of chemo-mechanical cleaningof entire canal system including– Fins– Isthmus– Cul-de-sacs– Indentations

• NaOCl irrigant of choice. Copious Irrigation important for– Flushing loose debris– Antimicrobial action– Tissue dissolution– Lubrication

Treatment of endodontic infections

Intracanal medication

• Microbes left in canals can multiply.• Past medicaments like Formocresol, CMCP, CPCP and

halides not used due to antigenicity, mutagenicity,cytotoxicity or short duration of action.

• CaOH medicament of choice• Mix with water, anesthetic or glycerin and placed using a

lentulo spiral or reverse twisting a file in canal.– Most effective as antimicrobial– Hygroscopic.– Mild tissue dissolution capabilities– Anti-inflammatory ; and more

Treatment of endodontic infections

• When and how to culture– Wide range of bacteria in endo infections– Possibility of contamination in sample

collection, and transport– Culturing of anaerobes-difficult to keep

viable– Results of Antibiotic sensitivity and

planning other treatment may be delayedup to weeks

• Mostly for refractory cases• Medically compromised patients