Podcast
Questions and Answers
What is the primary mechanism involved in the aetiology of periodontal disease?
What is the primary mechanism involved in the aetiology of periodontal disease?
Which microbial component is commonly associated with periodontal disease?
Which microbial component is commonly associated with periodontal disease?
Which process best describes the transition from gingival health to periodontal disease?
Which process best describes the transition from gingival health to periodontal disease?
What role do virulence factors play in periodontal disease?
What role do virulence factors play in periodontal disease?
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What immune response is primarily activated due to pathogens in periodontal disease?
What immune response is primarily activated due to pathogens in periodontal disease?
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What characterizes dental plaque as a biofilm?
What characterizes dental plaque as a biofilm?
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Which type of bacteria are predominantly found subgingivally?
Which type of bacteria are predominantly found subgingivally?
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What happens to the equilibrium between dental plaque and host defenses in periodontitis?
What happens to the equilibrium between dental plaque and host defenses in periodontitis?
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What can disturb the equilibrium in periodontitis?
What can disturb the equilibrium in periodontitis?
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Which of the following is a recognized periodontal pathogen?
Which of the following is a recognized periodontal pathogen?
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What role do proteinases like gingipains play in periodontal pathogens?
What role do proteinases like gingipains play in periodontal pathogens?
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How many types of bacteria are particularly likely to cause periodontal breakdown?
How many types of bacteria are particularly likely to cause periodontal breakdown?
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What type of layer is the extracellular slime layer in biofilms?
What type of layer is the extracellular slime layer in biofilms?
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What virulence factor in Porphyromonas gingivalis helps the bacterium adhere to host tissues?
What virulence factor in Porphyromonas gingivalis helps the bacterium adhere to host tissues?
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Which of the following characteristics is true for Aggregatibacter actinomycetemcomitans?
Which of the following characteristics is true for Aggregatibacter actinomycetemcomitans?
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Which virulence factor of Porphyromonas gingivalis allows it to use gingival crevicular fluid as a nutrient source?
Which virulence factor of Porphyromonas gingivalis allows it to use gingival crevicular fluid as a nutrient source?
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How does Treponema denticola disrupt host defenses?
How does Treponema denticola disrupt host defenses?
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What is a key characteristic of Tannerella forsythia in relation to periodontitis?
What is a key characteristic of Tannerella forsythia in relation to periodontitis?
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What role does haemagglutination play for Porphyromonas gingivalis?
What role does haemagglutination play for Porphyromonas gingivalis?
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What is the primary mode of nutrient acquisition for Treponema denticola?
What is the primary mode of nutrient acquisition for Treponema denticola?
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What is a factor that contributes to Porphyromonas gingivalis being able to evade host defenses?
What is a factor that contributes to Porphyromonas gingivalis being able to evade host defenses?
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What is one of the virulence factors of Gram-negative coccoid baccillus?
What is one of the virulence factors of Gram-negative coccoid baccillus?
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Which hypothesis describes the stagnation of plaque biofilm leading to periodontal disease?
Which hypothesis describes the stagnation of plaque biofilm leading to periodontal disease?
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According to the Specific Plaque Hypothesis, what occurs as periodontal disease develops?
According to the Specific Plaque Hypothesis, what occurs as periodontal disease develops?
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What is a criticism of the Non-specific Plaque Hypothesis?
What is a criticism of the Non-specific Plaque Hypothesis?
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What are some bacteria identified as specific pathogens associated with periodontal disease?
What are some bacteria identified as specific pathogens associated with periodontal disease?
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Which hypothesis focuses on the balance between microbes and host response in periodontal disease?
Which hypothesis focuses on the balance between microbes and host response in periodontal disease?
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What is a key concept of the Ecological Plaque Hypothesis?
What is a key concept of the Ecological Plaque Hypothesis?
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What do proteases produced by Gram-negative coccoid baccillus do?
What do proteases produced by Gram-negative coccoid baccillus do?
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Which microbial complexes are associated with periodontal disease?
Which microbial complexes are associated with periodontal disease?
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What has recent research shown about the red complex microorganisms?
What has recent research shown about the red complex microorganisms?
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What does the Ecological Plaque Hypothesis suggest is the role of nonspecific bacteria?
What does the Ecological Plaque Hypothesis suggest is the role of nonspecific bacteria?
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What factors are reported to change the microbial ecology in gingival sulcus?
What factors are reported to change the microbial ecology in gingival sulcus?
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What is suggested to occur following subgingival debridement in terms of microbial populations?
What is suggested to occur following subgingival debridement in terms of microbial populations?
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Which hypothesis acknowledges the role of host-related traits in periodontal disease?
Which hypothesis acknowledges the role of host-related traits in periodontal disease?
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What consequence does an uncontrolled immune response have on periodontal tissues?
What consequence does an uncontrolled immune response have on periodontal tissues?
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What underlying factor contributes to dysbiosis within the gingival environment?
What underlying factor contributes to dysbiosis within the gingival environment?
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What influences the initiation and progression of periodontal disease?
What influences the initiation and progression of periodontal disease?
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What occurs when there is a shift from beneficial to pathogenic microbes in the biofilm?
What occurs when there is a shift from beneficial to pathogenic microbes in the biofilm?
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According to Page and Schroeder, what is required for gingivitis to progress to periodontitis?
According to Page and Schroeder, what is required for gingivitis to progress to periodontitis?
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What does current evidence suggest is primarily responsible for tissue destruction in periodontal disease?
What does current evidence suggest is primarily responsible for tissue destruction in periodontal disease?
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Which of the following best describes the keystone pathogen-host response hypothesis?
Which of the following best describes the keystone pathogen-host response hypothesis?
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What role do environmental factors play in periodontal disease?
What role do environmental factors play in periodontal disease?
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Which of the following is not considered a factor in the multifactorial aetiology of periodontal disease?
Which of the following is not considered a factor in the multifactorial aetiology of periodontal disease?
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Which statement reflects the research limitations regarding bacterial pathogens and periodontal disease?
Which statement reflects the research limitations regarding bacterial pathogens and periodontal disease?
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Study Notes
Periodontal Disease Microbiology
- Module: Oral and Dental Science
- Tutor: Ms P Lazarou
- Aim: To understand the microbial components in periodontal disease and their role.
GDC Learning Outcomes
- Explain general and systemic disease and their relevance to oral health.
- Explain the etiology and pathogenesis of oral disease.
- Explain potential routes of transmission of infectious agents in dental practice.
Intended Learning Outcomes
- Revise mechanisms of periodontal disease (plaque biofilm, host immune response, inflammation).
- Recognize microbial organisms found in periodontal disease and discuss their virulence factors.
- Describe the microbial transition from gingival health to periodontal disease.
- Discuss the role of bacteria in periodontal disease etiology, comparing historical and current concepts.
Assessment
- Formative: Forum discussion
- Summative: Questions in Oral and Dental Sciences Eassessment
Pre-Session Knowledge
- Microbiology/Bacteria
- Dental plaque/biofilm
- Immunology
- Virulence factors
- Inflammation
Recall
- What is dental plaque/biofilm? How does it form on tooth surfaces?
- Explain the immune response to pathogens.
- Identify virulence factors of oral microorganisms.
- Describe the process of inflammation.
Oral Bacteria
- More than 700 species of oral microorganisms.
- Gram-positive
- Gram-negative
- Facultative
- Anaerobic
Biofilm
- Community of interdependent organisms that grow on a surface.
- Dental plaque is biofilm. Some subgingival microbes are only loosely adherent.
- Extra-cellular slime layer, Protective layer and Fluid channels.
Which type is found subgingivally?
- Gram +ve or Gram -ve? (refer to slide 10 for a list of bacteria)
Health and Stable Gingivitis
- Dynamic equilibrium between dental plaque and host defenses.
- Disturbance in this equilibrium leads to periodontitis.
Factors leading to periodontitis
- Increased amount of plaque.
- Increased pathogenicity in biofilm microorganisms.
- Compromised host defense.
Periodontal Pathogens and their Virulence Factors
- 12-15 types of bacteria are particularly involved in periodontal breakdown.
- Include Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf), Treponema denticola (Td), and Aggregatibacter actinomycetemcomitans (Aa).
Virulence Factors
- Proteinases: e.g., gingipains, digest tissue proteins to aid nutrient uptake and help bacteria destroy host defenses (antibodies).
- Endotoxins (lipopolysaccharide): Produced by gram-negative bacteria.
- Haemagglutination: RBC clumping to obtain nutrients and adhere to surfaces.
Fimbraie and Tissue Invasion
- These virulence factors aid bacterial binding to the epithelium, enabling tissue invasion (e.g., Pg).
- Once inside host cells, bacteria are protected from host defenses, allowing replication.
Porphyromonas gingivalis
- Gram-negative, non-saccharolytic, non-motile bacterium.
- Carbohydrate capsule to evade host defenses.
- Gingipains allow for use of GCF as a nutrient source.
- Lipopolysaccharide (LPS), haemagglutins, and platelet aggregators.
- Fimbrae for tissue invasion; suppression of PMN response.
Tannerella forsythia
- Gram-negative, anaerobic, fusiform-shaped bacteria.
- Difficult to culture.
- A particular phenotype (prtH) is more prevalent in periodontitis than health.
- Production of proteases and apoptotic-inducing factors (cell death).
Treponema denticola
- Uses GCF components for energy and multiplication.
- Adheres to fibroblasts.
- Motile and invades tissue.
- Disrupts host defenses (inducing/degrading cytokines).
- Delays PMN wound healing by inhibiting migration.
Aggregatibacter actinomycetemcomitans
- Associated with aggressive periodontitis.
- Gram-negative, coccoid bacillus.
- Produces leukotoxin (kills WBC).
- Destroys fibroblasts and epithelial cells; produces proteases (collagenase).
- Invade host epithelial cells.
Role of Bacteria in Periodontal Disease
Theories on the role of bacteria in Periodontal Disease
- 5 hypotheses:
- Non-specific plaque hypothesis
- Specific plaque hypothesis
- Ecological plaque hypothesis
- Microbial homeostasis-host response hypothesis
- Keystone pathogen-host response hypothesis
Non-Specific Plaque Hypothesis
- Stagnation of plaque biofilm and large number of bacteria in the gingival sulcus leads to gingival inflammation, periodontal disease, and tissue destruction.
- Issues: Too simplistic, most gingivitis doesn't turn to periodontitis.
Specific Plaque/Microbial Shift Hypothesis
- Shift from beneficial (gram-positive) to pathogenic (gram-negative) microorganisms.
- Issues: Some red complex microorganisms are found in healthy sites; recent studies show wider variety of oral microbes impacting the severity of periodontal disease.
Socransky's Microbial Complexes
- Bacteria are color-coded into complexes, reflecting their role in periodontal disease and health.
Ecological Plaque Hypothesis
- Changes in subgingival environments, like high GCF flow and changes in pH and oxygen levels, favor the growth of pathogenic bacteria, contributing to periodontal tissue damage.
Microbial Homeostasis- Host Response Hypothesis
- Pathogenic biofilm community triggers uncontrolled immune response leading to periodontal tissue damage; host factors are essential.
- Page and Schroeder suggested that gingivitis is non-progressive without host factors.
Keystone Pathogen-Host Response Hypothesis
- Keystone species in the biofilm trigger a shift to a dysbiotic biofilm community, initiating an uncontrolled host response and subsequent damage to periodontal tissue.
Aetiology of Periodontal Disease
- Multifactorial:
- Microbial factors
- Environmental factors (e.g., smoking, poor oral hygiene, pre-existing pockets, plaque retentive factors)
- Host defense factors (e.g., PMN defects, certain genetic predispositions)
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