Role of Biofilm In Persistant Endodontic Infection

Oday Alhalasa DDS.

Graduate Endodontics

Definitions:

• Biofilm: A collection of microorganisms, extracellular polymeric products, and organic mater located at the interface in solid-liquid, gas-liquid, or liquid-liquid biphasic systems.

    

• Planktonic Cells: Bacteria that are suspended or growing in a fluid environment

Bacterial interactions

• Coaggregation:

Recognition between genetically distinct cells

in suspension that result in clumping

• Coadhesion:

Recognition between a suspended cell type

and one already attached to a substratum

Stages of Biofilm Formation

QUORUM SENSING

• A system by which bacteria communicate. Signaling molecules — chemicals similar to pheromones that are produced by an individual bacterium — can affect the behavior of surrounding bacteria.

Mature Biofilm

Fusobacterium nucleatum :

•The most numerous gram-negative species in healthy sites, and its numbers increase markedly in periodontally diseased sites 

2.   Acts as a bridge between early and late colonizers.         late colonizers coaggregate with F. nucleatum, they generally         do not coaggregate with each other   exceptions: T. denticola coaggregating with P. gingivalis, have           been reported 

• F. nucleatum interacts with and binds host-derived molecule plasminogen →P. gingivalis, are highly proteolytic and can activate fusobacterium-bound plasminogen→fusobacterium- bound plasmin,a plasma serine protease →new metabolic property →nutrients for fusobacteria or by other biofilm residents.

4. Induces expression of B-defensin 2.

Although F. nucleatum is often considered a periodontal pathogen, it may instead contribute to maintaining homeostasis and improving host defense against true pathogens.

Supragingival dental plaque biofilm

Significance of biofilm

I- Contributing to host tissue damage:

- Sessile bacterial cells release antigens →antibodies stimulation → immune complex activation

- Extracellular polymeric substances mainly polysaccharides →constant irritation to macrophages (Frustrated Macrophages )

II-Resistance to antimicrobial agents

1,000- fold greater than planktonic cells

Failure of an agent to penetrate the full depth of the biofilm

Cells in a biofilm experience nutrient limitation and therefore exist in a slow-growing or starved state

Oral biofilms are more resistant to:

chlorhexidine, amine fluoride, amoxycillin, doxycycline,and metronidazole than planktonic cells

III- Potential to spread

Seeding dispersal:

Programmed detachment of Planktonic bacterial cells caused by local hydrolysis of the extracellular polysaccharide matrix, and conversion of a subpopulation of cells into motile planktonic cells

• clumping dispersal:

A physical detachment pathway in which a fragment of a microcolony, simply detaches from the biofilm and is carried by the bulk until it lodges in a new location and initiates a new sessile population.

Biofilm in root canal surfaces

oral microorganisms are able to colonize root canals by adhering to the dentine walls

Biofilm formation in root canals is probably initiated at some time after the first invasion of the pulp chamber by planktonic oral organisms after some tissue breakdown. At this point, the inflammatory lesion frontage that moves successively toward the apex will provide the fluid vehicle for the invading planktonic organisms so these can multiply and continue attaching to the root canal walls . Hypothesis: Svensäter and Bergenholtz

Aggregations of microorganisms can be seen adhering to the inner walls of an accessory canal ,thus demonstrating the retention of these biofilm communities

Pathways of entry

• Opening in the dental hard tissue wall….most common!

Caries, trauma,cracks **Svensäter and Bergenholtz:

Invasion by planktonic oral organisms tissue breakdown fluid vehicle for planktonic organisms

• Endo-Perio lesions• Anachoresis???? discredited by Moller.

Molven et al, reported the microbial colonization of the external root apex of teeth with pulp necrosis and periapical lesion by cocci, bacilli, cocci-bacilli, filament, spirochetes, and also the presence of bacterial biofilm on the apical 2 mm of the external root surface in 83.3% of the cases.

Sogren et al, reported a success rate of 86% in case of a necrotic pulp with a periapical rediolucency.

The necrotic pulp tissue becomes a       favorable environment for microbial       proliferation due to the presence of     organic residue or nutrients, which      act as substrate or culture medium.

Gram-negative bacteria are more      frequent than Gram- positive       bacteria. 

Facultative or strict anaerobic      microorganisms are more frequent      than aerobic microorganisms, and     the presence of bacilli and filaments    is equivalent to that of cocci

study: Nobuo Noguchi et al, Osaka University Graduate School of Dentistry-Japan

• Early colonizers: Enterococcus faecalis

Streptococcus sanguis

Streptococcus intermedius

Porphyromonas gingivalis : high proteolytic activity→adhere to the collagen matrix in cementum

F. nucleatum

• Late colonizers: Tannerella. forsythensis

Prevotella. intermedia

Periradicular Biofilms

extraradicular biofilms average thickness of 30 to 40 m thickness

Department of Restorative Dentistry and Endodontology, Osaka University Graduate School of Dentistry,

1-8, Yamadaoka, Suita, Osaka 565-0871, Japan

Treatment of persistent periapical infections

• resection of the apical root tip:

I-To physically eradicate the biofilm layer

residing on the root surface

II-To reduce the load of bacteria residing in the lateral canals or deltas within the apical third

Conclusion

It is imperative to understand and to realize the complexity and nature of the biofilm, especially the role it plays in harboring and protecting the microorganisms, thus, contributing to persistant infections.

Thank you.

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