The Role of Bacteria in Periodontal Disease PDF

Summary

This document discusses the changing perspectives on the role of bacteria in causing periodontal disease. It explores different hypotheses proposed over the years, along with their pros and cons and problems associated with each perspective. Some important aspects of this topic include the number of bacteria, specific pathogenic bacteria, and host immune response.

Full Transcript

# Chapter 13 Oral Biofilms ## Section 3: The Role of Bacteria in Periodontal Disease ### Changing Evidence for the Role of Bacteria - In 1683, Antonie van Leeuwenhoek used a homemade microscope to first describe oral microorganisms. - Over 700 bacterial species have been identified in the human or...

# Chapter 13 Oral Biofilms ## Section 3: The Role of Bacteria in Periodontal Disease ### Changing Evidence for the Role of Bacteria - In 1683, Antonie van Leeuwenhoek used a homemade microscope to first describe oral microorganisms. - Over 700 bacterial species have been identified in the human oral cavity. - Microbiologists have yet to identify specific bacterial pathogens that cause periodontitis. - Five hypotheses have emerged to explain the role of bacteria in periodontal disease: - Nonspecific Plaque Hypothesis - Specific Plaque Hypothesis - Ecological Plaque Hypothesis - Microbial Homeostasis-Host Response Hypothesis - Keystone Pathogen-Host Response Hypothesis ### Historical Perspectives on the Role of Bacteria - Two hypotheses focused on the role of the numbers of bacteria and the specific bacteria present in oral biofilms. - The Nonspecific Plaque Hypothesis postulated that the accumulation of bacterial biofilms leads to periodontal disease. - The Specific Plaque Hypothesis postulated that specific pathogenic bacteria and their products in the biofilm lead to periodontal disease. #### 1. Historical Perspective: Nonspecific Plaque Hypothesis - **Hypothesis**: Accumulation of plaque biofilm (an abundance of bacteria in the biofilm) adjacent to the gingival margin leads to gingival inflammation and the subsequent tissue destruction seen in periodontitis. - **Problems with the Nonspecific Plaque Hypothesis**: - This hypothesis is too simplistic. - It fails to explain why most cases of gingivitis never progress to periodontitis. - It cannot clarify why some sites in an individual's periodontium experience considerable periodontal destruction while other sites are unaffected #### 2. Historical Perspective: Specific Plaque/Microbial Shift Hypothesis - **Hypothesis**: As periodontitis develops, the oral microbiota shifts from one consisting primarily of beneficial microbes to one consisting of pathogens. - **Problems with the Specific Plaque Hypothesis**: - This hypothesis is too simplistic. - It is established that red complex organisms can be found in the absence of periodontal disease. - This hypothesis fails to explain the presence of both red complex organisms in healthy sites and the absence of these bacteria in some cases of aggressive periodontitis. ### Contemporary Perspectives on the Role of Bacteria - Rapid advances in the fields of microbiology and immunology have reshaped our previous notions about the role of bacteria in the pathogenesis of periodontal disease. - We now recognize that: - A pathogenic microbial biofilm is a prerequisite for periodontitis to develop, but the presence of a pathogenic oral biofilm alone is insufficient to cause the disease. - While red complex microorganisms are strongly associated with an inflammatory disease, there is no current evidence to support the argument that the red complex bacteria are potent initiators of the disease. - Three hypotheses have been proposed to reconcile the limitations of the Nonspecific Plaque Hypothesis and the Specific Plaque Hypothesis: - Ecological Plaque Hypothesis - Microbial Homeostasis-Host Response Hypothesis - Keystone Pathogen-Host Response Hypothesis #### 1. Current Perspective #1: Ecological Plaque Hypothesis - **Hypothesis**: The accumulation of nonspecific bacteria triggers the host inflammatory response. In turn, the host inflammatory response alters the local environment within the gingival sulcus (higher GCF flow, increased bleeding, raised pH, decreased oxygen concentration). This leads to a shift in the local environment that drives the changes in microbial composition that lead to periodontal disease. - **Support for This Hypothesis**: - Sites with bleeding upon probing and deeper probing depths are strongly associated with a higher gingival crevicular flow (GCF flow). - Subgingival periodontal instrumentation alters the subgingival ecosystem. This, in turn, reduces the number of pathogens. #### 2. Current Perspective #2: Microbial Homeostasis-Host Response Hypothesis - **Hypothesis**: While plaque biofilms are the cause of the initial inflammatory response leading to gingivitis, the pathogenic bacteria are not the direct cause of the destruction of tissues seen in periodontitis. - **Findings that support this hypothesis**: - Host-related factors, such as genetic variations and the inflammatory immune response, and environmental factors, including smoking, stress, and systemic health, are all now recognized as major factors that contribute to the initiation and progression of periodontal disease. #### 3. Current Perspective #3: Keystone Pathogen-Host Response Hypothesis - **Hypothesis**: A specific bacterial species is the key in creating the shift from symbiotic microbes to dysbiotic microbes in the biofilm community. In turn, the dysbiotic biofilm community triggers the uncontrolled host response that results in damage to the periodontal tissues. - **Support for This Hypothesis**: - Decades of research have failed to provide evidence that specific bacterial pathogens are the direct cause of the tissue destruction seen in periodontitis. - Current evidence indicates that the uncontrolled host inflammatory and immune responses cause the tissue destruction seen in periodontitis. ### Evolution of Periodontal Disease Theories |Hypothesis | Status| Theory in Brief | |---|---|---| |Nonspecific Plaque |Historical | An abundance of biofilm bacteria causes the tissue destruction seen in periodontitis. | |Specific Plaque|Historical| The presence of specific bacteria in the biofilm directly causes the tissue destruction seen in periodontitis.| |Ecological Plaque Hypothesis |Current| Changes in the subgingival environment can dictate the select the specific microbial composition of the biofilm; the pathogenic biofilm community causes the tissue destruction seen in periodontitis. | |Microbial Homeostasis-Host Response Hypothesis |Current |A shift from beneficial to pathogenic microbes triggers the host inflammatory response; the host response causes the tissue destruction seen in periodontitis. | |Keystone Pathogen Hypothesis |Current | A keystone species initiates a shift from beneficial to dysbiotic microbes in the biofilm community that in turn, trigger the host inflammatory response responsible for the tissue destruction seen in periodontitis.|

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