Bacterial Colonization and Plaque Formation


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Bacterial Colonization and Plaque Formation

  1. 1. Role of Biofilm In Persistant Endodontic Infection Oday Alhalasa DDS. Graduate Endodontics
  2. 2. Definitions: <ul><li>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. </li></ul> 
  3. 3. <ul><li>Planktonic Cells: Bacteria that are suspended or growing in a fluid environment </li></ul>
  4. 4. Bacterial interactions <ul><li>Coaggregation: </li></ul><ul><li>Recognition between genetically distinct cells </li></ul><ul><li>in suspension that result in clumping </li></ul><ul><li>Coadhesion: </li></ul><ul><li>Recognition between a suspended cell type </li></ul><ul><li>and one already attached to a substratum </li></ul>
  5. 5. Stages of Biofilm Formation
  6. 7. QUORUM SENSING <ul><li>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. </li></ul>
  7. 8. Mature Biofilm
  8. 9. <ul><li>Fusobacterium nucleatum : </li></ul><ul><li>The most numerous gram-negative species in healthy sites, and its numbers increase markedly in periodontally diseased sites </li></ul><ul><li>2. Acts as a bridge between early and late colonizers. </li></ul><ul><li>late colonizers coaggregate with F. nucleatum, they generally </li></ul><ul><li>do not coaggregate with each other </li></ul><ul><li>exceptions: T. denticola coaggregating with P. gingivalis, have </li></ul><ul><li>been reported </li></ul>
  9. 10. <ul><li>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. </li></ul><ul><li>4. Induces expression of B-defensin 2. </li></ul><ul><li>Although F. nucleatum is often considered a periodontal pathogen, it may instead contribute to maintaining homeostasis and improving host defense against true pathogens. </li></ul>
  10. 11. Supragingival dental plaque biofilm
  11. 12. Significance of biofilm <ul><li>I- Contributing to host tissue damage: </li></ul><ul><li>- Sessile bacterial cells release antigens ->antibodies stimulation -> immune complex activation </li></ul><ul><li>- Extracellular polymeric substances mainly polysaccharides ->constant irritation to macrophages (Frustrated Macrophages ) </li></ul>
  12. 13. II-Resistance to antimicrobial agents <ul><li>1,000- fold greater than planktonic cells </li></ul><ul><li>Failure of an agent to penetrate the full depth of the biofilm </li></ul><ul><li>Cells in a biofilm experience nutrient limitation and therefore exist in a slow-growing or starved state </li></ul><ul><li>Oral biofilms are more resistant to: </li></ul><ul><li>chlorhexidine, amine fluoride, amoxycillin, doxycycline,and metronidazole than planktonic cells </li></ul>
  13. 14. III- Potential to spread <ul><li>Seeding dispersal: </li></ul><ul><li>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 </li></ul><ul><li>clumping dispersal: </li></ul><ul><li>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. </li></ul>
  14. 17. Biofilm in root canal surfaces <ul><li>oral microorganisms are able to colonize root canals by adhering to the dentine walls </li></ul><ul><li>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 </li></ul><ul><li>Aggregations of microorganisms can be seen adhering to the inner walls of an accessory canal ,thus demonstrating the retention of these biofilm communities </li></ul>
  15. 18. Pathways of entry <ul><li>Opening in the dental hard tissue wall…. most common! </li></ul><ul><li>Caries, trauma,cracks </li></ul><ul><li>**Svensäter and Bergenholtz: </li></ul><ul><li>Invasion by planktonic oral organisms tissue breakdown fluid vehicle for planktonic organisms </li></ul><ul><li>Endo-Perio lesions </li></ul><ul><li>Anachoresis???? discredited by Moller. </li></ul>
  16. 19. <ul><li>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. </li></ul><ul><li>Sogren et al, reported a success rate of 86% in case of a necrotic pulp with a periapical rediolucency. </li></ul>
  17. 20. <ul><li>The necrotic pulp tissue becomes a </li></ul><ul><li>favorable environment for microbial </li></ul><ul><li>proliferation due to the presence of </li></ul><ul><li>organic residue or nutrients, which </li></ul><ul><li>act as substrate or culture medium. </li></ul><ul><li>Gram-negative bacteria are more </li></ul><ul><li>frequent than Gram- positive </li></ul><ul><li>bacteria. </li></ul><ul><li>Facultative or strict anaerobic </li></ul><ul><li>microorganisms are more frequent </li></ul><ul><li>than aerobic microorganisms, and </li></ul><ul><li>the presence of bacilli and filaments is equivalent to that of cocci </li></ul>
  18. 21. <ul><li>study: Nobuo Noguchi et al, Osaka University Graduate School of Dentistry-Japan </li></ul><ul><li>Early colonizers: </li></ul><ul><li>Enterococcus faecalis </li></ul><ul><li>Streptococcus sanguis </li></ul><ul><li>Streptococcus intermedius </li></ul><ul><li>Porphyromonas gingivalis : high proteolytic activity->adhere to the collagen matrix in cementum </li></ul><ul><li>F. nucleatum </li></ul><ul><li>Late colonizers: </li></ul><ul><li>Tannerella. forsythensis </li></ul><ul><li>Prevotella. intermedia </li></ul>
  19. 23. Periradicular Biofilms <ul><li>extraradicular biofilms average thickness of 30 to 40 m thickness </li></ul><ul><li>Department of Restorative Dentistry and Endodontology, Osaka University Graduate School of Dentistry, </li></ul><ul><li>1-8, Yamadaoka, Suita, Osaka 565-0871, Japan </li></ul>
  20. 31. Treatment of persistent periapical infections <ul><li>resection of the apical root tip: </li></ul><ul><li>I-To physically eradicate the biofilm layer </li></ul><ul><li>residing on the root surface </li></ul>
  21. 33. <ul><li>II-To reduce the load of bacteria residing in the lateral canals or deltas within the apical third </li></ul>
  22. 34. Conclusion <ul><li>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. </li></ul>
  23. 35. Thank you. <ul><li>Refernces: </li></ul><ul><li>1.BACTERIAL BIOFILMS: FROM THE NATURAL ENVIRONMENT TO INFECTIOUS DISEASES </li></ul><ul><li>Luanne Hall-Stoodley*‡§, J.William Costerton§ and Paul Stoodley|| </li></ul><ul><li>2.. Bacterial BioÞlms: A Common Cause of Persistent Infections </li></ul><ul><li>J. W. Costerton,1 Philip S. Stewart,1 E. P. Greenberg2* </li></ul><ul><li>3.Takemura N, Noiri Y, Ehara A, Kawahara T, Noguchi N, Ebisu S. Single species </li></ul><ul><li>biofilm-forming ability of root canal isolates on gutta-percha points. Eur J Oral Sci 2004; 112: 523–529. </li></ul><ul><li>4. Biofilm Formation of Oral and Endodontic Enterococcus faecalis </li></ul><ul><li>Jason M. Duggan, DDS, and Christine M. Sedgley, PhD , J Endod 2007;33:815– 818 </li></ul><ul><li>5. EM Evaluation of Bacterial Biofilm and Microorganisms on the Apical External Root Surface of Human Teeth </li></ul><ul><li>Ma´ rio R. Leonardo, DDS, PhD, Marcos A. Rossi, MD, PhD, Le´ a A. B. Silva, DDS, PhD, Izabel Y. Ito, PhD, and Kleber C. Bonifa´ cio, DDS, </li></ul><ul><li>J OURNAL OF ENDODONTICS, VOL. 28, NO. 12, DECEMBER 2002 </li></ul><ul><li>6. Redefining the Persistent Infection in Root Canals: Possible Role of Biofilm Communitie </li></ul><ul><li>Luis Chávez de Paz, DDS, MS, PhD . J Endod 2007;33:652– 662 </li></ul><ul><li>7.Path way of the Pulp,9 th edition </li></ul><ul><li>8. Communication among Oral Bacteria </li></ul><ul><li>Paul E. Kolenbrander,* Roxanna N. Andersen, David S. Blehert, Paul G. Egland, Jamie S. Foster, and Robert J. Palmer Jr. </li></ul><ul><li>MICROBIOLOGY AND MOLECULAR BIOLOGY REVIEWS, Sept. 2002, p. 486–505 Vol. 66 </li></ul>