Periodontal Disease Microbiology

• The presentation is about Periodontal Disease Microbiology
• The module is Oral and Dental Science
• The tutor is Ms P Lazarou

GDC Learning Outcomes

• Explain general and systemic disease and their relevance to oral health
• Explain the etiology and pathogenesis of oral disease
• Explain the potential routes of transmission of infectious agents in dental practice

Aim

• To gain knowledge of the microbial components found in periodontal disease and realize their role

Intended Learning Outcomes

• Revise the various mechanisms involved in the etiology of periodontal disease, including plaque biofilm, host immune response, and 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 the etiology of periodontal disease with reference to historical and current concepts

Assessment

• Formative assessment includes forum discussion
• Summative assessment involves questions in Oral and Dental Sciences Eassessment

Pre-Session Knowledge

• Microbiology/Bacteria
• Dental plaque/biofilm
• Immunology
• Virulence factors
• Inflammation

Recall

• Microbiology/Bacteria
• Dental plaque/biofilm: How does it form on the tooth surfaces
• Immunology: Think about the immune response to pathogens
• Virulence factors: Which virulence factors will the oral microorganisms deploy
• Inflammation: What is the process

Oral Bacteria

• There are over 700 species of oral microorganisms, including Gram-positive, Gram-negative, facultative, and anaerobic bacteria

Biofilm

• A community of interdependent organisms grows on a surface
• Dental plaque is a biofilm, with some subgingival microbes free-floating or loosely attached in the pocket
• Biofilms have an extra-cellular slime layer which is protective and contain fluid channels

Subgingival Bacteria Types

• Subgingival bacteria can be gram-positive or gram-negative

Health vs Periodontitis

• In health and stable gingivitis, there is a dynamic equilibrium between dental plaque and the host defense
• This equilibrium is disturbed in periodontitis

Causes of Periodontitis

• Periodontitis may be due to an increased amount of plaque
• Periodontitis may be due to an increase in pathogenicity of the micro-organisms in the biofilm
• Periodontitis may be due to a compromised host defense

Recognized Periodontal Pathogens

• Includes approximately 12-15 types of bacteria which are likely to cause periodontal breakdown
• Porphyromonas gingivalis (Pg)
• Tannerella forsythia (Tf)
• Treponema denticola (Td)
• Aggregatibacter actinomycetemcomitans (Aa)

Virulence Factors

• Proteinases such as gingipains produced by Pg can digest tissue proteins and destroy host defenses like antibodies
• Endotoxins, or lipopolysaccharides, are produced by Gram-negative organisms
• Haemagglutination of red blood cells by Pg can release haem for nutrient and help the bacteria adhere

Fimbraie and Tissue Invasion

• Virulence factors can aid bacterial binding to epithelium, thus aiding tissue invasion (e.g. Pg)
• Bacterium invading a host cell can be safe from host defenses and more able to replicate

Porphyromonas Gingivalis

• Gram-negative bacillus, non-saccharolytic, non-motile anaerobe
• Has a carbohydrate capsule to resist some host defenses
• Produces gingipains that enable it to use gingival crevicular fluid (GCF) as a nutrient source
• Contains LPS (Lipopolysaccharide)
• Contains haemagglutinins and platelet aggregators and are contributors to heart disease
• Fimbrae and tissue invasion
• Suppresses the early polymorphonuclear leukocytes (PMN) response

Tannerella Forsythia

• Gram-negative, anaerobic, and fusiform bacterium, very difficult to culture
• A particular phenotype (prtH) is found much more often in periodontitis than in health
• Produces proteases and apoptotic-inducing factor (i.e., causes cell death)

Treponema Denticola

• Uses GCF components for energy to aid multiplication
• Adherence factors which can bind to fibroblasts
• Motile and can invade tissue
• Disruption of host defenses by inducing and degrading cytokines
• May delay wound healing by inhibiting migration of PMNs

Aggregatibacter Actinomycetemcomitans

• Associated with aggressive periodontitis, possibly Grade C, and with periodontitis that is refractory to treatment
• NOT motile and anaerobic
• Gram-negative coccoid baccillus (short rod)
• Virulence factors include Leukotoxin, which can kill WBCs and disrupt host defenses
• Other toxins can destroy fibroblasts and epithelial cells, and also produces proteases, including collagenase
• Can invade host epithelial cells

Theories on the Role of Bacteria in Periodontal Disease

• There are 5 Hypotheses: Non-specific Plaque Hypothesis, Specific Plaque Hypothesis, Ecological Plaque Hypothesis, Microbial Homeostasis- Host Response Hypothesis, and Keystone Pathogen- Host Response Hypothesis

Non-Specific Plaque Hypothesis

• Stagnation of plaque biofilm and in large numbers of bacteria
• Within the gingival sulcus, gingival inflammation
• Periodontal disease and tissue destruction

Issues with the Non-Specific Plaque Hypothesis

• Too simplistic
• Most gingivitis cases do not progress to periodontitis
• Some patients with light biofilm deposits suffer from periodontitis
• Some sites suffer periodontal destruction while others may not be affected

Specific Plaque/Microbial Shift Hypothesis

• As periodontal disease develops, there is a SHIFTING of oral microbiota
• A shift from beneficial, Gram-positive microbes to specific, Gram-negative pathogens

Socransky's Microbial Complexes

• Studies identified various periodontal diseases/conditions caused by specific INTERDEPENDENT bacteria: Tannerella forsythia, Porphyromonas gingivalis, and Treponema denticola
• Socransky grouped microbes into color-coded 'complexes'
• Orange/red complexes are major causative agents of periodontal disease
• Yellow/green/blue/purple complexes are compatible with gingival health

Issues with the Specific Plaque Hypothesis

• The red complex micro-organisms (P. gingivalis and T. Forsythia) exist in stable/healthy periodontal sites
• Can these pathogens directly cause destruction of the periodontium
• More recent research shows more varied and diverse oral microbes
• Newly recognized bacteria may be more causative than red complex.
• The concept of specific types causing periodontal destruction is less certain
• Current research shows Gram-positive bacteria found in larger amounts in periodontal pockets

Contemporary Theories on the Role of Bacteria

• The Ecological Plaque Hypothesis: Changes in subgingival environment: nonspecific bacteria trigger host inflammatory response
• The altered environment favors increase of pathogenic bacteria in biofilm as a result of higher GCF flow, increased bleeding, raised pH, and decreased oxygen concentration
• This leads to damage to the periodontal tissues

Support for the Contemporary Theories on the Role of Bacteria

• Deeper pocket sites and bleeding on probing sites have increased gingival crevicular fluid (GCF)
• GCF changes microbial ecology, enabling growth of pathogenic bacteria
• Changes in environmental factors (GCF/pH/temperature/oxygen decrease) drive dysbiosis in the gingival sulcus
• Subgingival debridement changes the ecosystem, reducing number of pathogens, and halt nutrient source of bacterial growth

Microbial Homeostasis-Host Response Hypothesis

• Pathogenic biofilm community
• Triggers uncontrolled host response and immune response
• Damages periodontal tissues

Microbial Homeostasis support

• Biofilm microbiota linked to periodontal health remains stable in a state of biological equilibrium or homeostasis
• Research has not proven that bacterial pathogens are directly responsible for periodontal destruction
• Robust evidence shows that it is the uncontrolled host inflammatory and immune response that cause the tissue destruction

Keystone Pathogen-Host Response Hypothesis

• Keystone species in biofilm
• Triggers SHIFT to dysbiotic biofilm community and uncontrolled host response initiated
• Damage to periodontal tissue

Evidence

• Previous research could not provide solid evidence to show that specific bacteria are the direct cause of periodontal destruction
• Current evidence demonstrates host inflammatory response can cause destruction to tissue and result in periodontal disease

Etiology of Periodontal Disease

• Multifactorial, involving
• Microbial factors
• Environmental factors, such as smoking, poor oral hygiene, pre-existing pockets, and plaque-retentive factors
• Host defense factors, such as PMN defects and certain inherited geno-types