PART I: HOST-PARASITE INTERACTIONS IN PERIODONTAL DISEASE

COURSE DESCRIPTION

“PART I: HOST-PARASITE INTERACTIONS in PERIODONTAL DISEASE” (8 CE Units) provides a comprehensive review of the periodontal subgingival infection and the mechanisms utilized by the host to sense and respond to bacterial invasion. It discusses how bacteria adhere to the host to form subgingival biofilms while regulating biofilm growth and gene expression, and the proposed bacterial-viral interaction. Finally, it explores how the host and bacteria participate in the invasion of epithelial cells and spread in periodontal tissue, and the transport of intracellular oral pathogens. It concludes with a discussion of therapeutic possibilities and the likelihood that the fundamental framework for the pathogenesis of periodontitis is established by host–parasite interactions.

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Introduction: Subgingival Infection and Host Sensing 

There are more than 700 bacterial species in the oral cavity and they probably coexist with millions of copies of viral genomes.  Research has confirmed that the cause of periodontitis is a series of aberrant inflammatory responses induced by a subset of endogenous gram-negative periodontopathic bacteria, for example, Porphyromonas gingivalis, Tannerella forsythia (forsythensis) and Treponema denticola.1

These microbes possess a microbial arsenal of many potent virulence factors that neutralize the local defenses of the host and destroy the periodontium. Investigators have proposed that an interaction between the herpes virus and bacteria is also a component of the etiopathogenesis of periodontitis. Destruction of tissues surrounding and supporting the teeth, with subsequent loss of tissue, bone, and teeth occurs after a long period of continuous interaction between these microbes and the host.1

Regardless of the amazing fact that 90% of cells in the body are bacteria, humans generally remain in good health. The theory is that endogenous microbes are capable of minimizing inflammatory responses by influencing the immune system of their host. Unfortunately this relationship renders periodontitis a disease that is both complex and perplexing.1

Bacterial virulence factors, host immune repertoires and the pathways involved in periodontal destruction have recently been described in detail by genetic and molecular analyses. Researchers have also identified several strategies that enable periodontal pathogens to persist and overcome host immune defenses. Not only do these results suggest therapeutic possibilities but also indicate that the fundamental framework for the pathogenesis of periodontitis is established by host–parasite interactions. The focus is on subgingival infection in periodontitis and how the host senses and responds to bacterial invasion.1

COURSE OBJECTIVES

1. Understand the mechanisms used by bacteria to adhere to and enter host cells in periodontitis.

2. Discuss the role of endogenous gram-negative periodontopathic bacteria in the etiology of periodontitis.

3. Discuss how the host senses and responds to bacterial invasion with regard to subgingival infection in periodontitis.

4. Explain the mechanism by which organisms colonize their preferred subgingival area and eventually give rise to periodontal disease.

5. Understand how biofilms regulate growth and gene expression through quorum sensing.

6. Discuss the mechanisms used by pathogenic bacteria to spread in periodontal tissues.

7. Explain, in general, how intracellular oral pathogens are transported inside the host by the host cell membrane.

8. Discuss the mechanisms by which these organisms enter the host cell and their fate after entry: Porphyromonas gingivalis and Aggregatibacter (Actinobacillus) actinomycetemcomitans.

9. Understand the systemic impact of periodontal pathogens on human health.

10. Discuss the potential for developing vaccines against periodontal pathogens.

Intended Audience – Dentists

Released: 5-13-10 Reviewed: Aug 2012 Expiration: Aug 2015

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