Periodontics: Dental specialty deals with the supporting and surrounding tissues of the teeth. 

1. Periodontium: tissues that invest and support teeth Includes Gingiva, Alveolar mucosa  Cementum, Periodontal ligament, Alveolar bone, Support bone

2. Periodontal disease: changes to periodontium beyond normal range of variation

a. Specific plaque hypothesis: specific microorganisms cause periodontal disease; mostly anaerobes. Three implicated: Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Bacteriodes forsythus

b. Contributing factors: often a combination of factors

i. Local: calculus (tarter, home for bacteria, ­ with age), traumatic occlusal forces, caries (root caries), overhangs and over-contoured restorations, open contacts with food impaction, missing/malaligned teeth

Invasion of biological width: from free gingival margin -> attached gingiva need ~ 3 mm.  If enter this area -> problems (e.g., resorption)

ii. Host factors: exacerbate periodontal problems; e.g., smoking/tobacco use, pregnancy and puberty (hormonal changes, ­ blood vessel permeability), stress, poor diet

iii.Medications: often -> tissue overgrowth; e.g., oral contraceptives, antidepressants, heart medicines, transplant anti-rejection drugs

iv.Systemic diseases: e.g., diabetes, immunosuppression

B. Gingivitis: inflammation of gingiva; ­ with age; generally reversible

C. Periodontitis: inflammation of supporting tissues of teeth, characterized by loss of attachment (PDL) and bone; generally irreversible

D.       Periodontal disease as risk factor for systemic diseases:

1.        Causes difficulty for diabetics to control blood sugar

2.        Pregnant women with periodontal disease ~ 7 times more likely to have premature and/or underweight baby

3.        Periodontal diseased patients may be at risk for heart disease

Plaque Formation

Dental plaque is a biofilm that forms on the surfaces of teeth and is a key factor in the development of dental caries and periodontal disease. The process of plaque formation can be divided into three major phases:

1. Formation of Pellicle on the Tooth Surface

• Definition: The pellicle is a thin, acellular film that forms on the tooth surface shortly after cleaning.
• Composition: It is primarily composed of salivary glycoproteins and other proteins that are adsorbed onto the enamel surface.
• Function:
  • The pellicle serves as a protective barrier for the tooth surface.
  • It provides a substrate for bacterial adhesion, facilitating the subsequent stages of plaque formation.

2. Initial Adhesion & Attachment of Bacteria

• Mechanism:
  • Bacteria in the oral cavity begin to adhere to the pellicle-coated tooth surface.
  • This initial adhesion is mediated by specific interactions between bacterial adhesins (surface proteins) and the components of the pellicle.
• Key Bacterial Species:
  • Primary colonizers, such as Streptococcus sanguis and Actinomyces viscosus, are among the first to attach.
• Importance:
  • Successful adhesion is crucial for the establishment of plaque, as it allows for the accumulation of additional bacteria.

3. Colonization & Plaque Maturation

• Colonization:
  • Once initial bacteria have adhered, they proliferate and create a more complex community.
  • Secondary colonizers, including gram-negative anaerobic bacteria, begin to join the biofilm.
• Plaque Maturation:
  • As the plaque matures, it develops a three-dimensional structure, with different bacterial species occupying specific niches within the biofilm.
  • The matrix of extracellular polysaccharides and salivary glycoproteins becomes more pronounced, providing structural integrity to the plaque.
• Coaggregation:
  • Different bacterial species can adhere to one another through coaggregation, enhancing the complexity of the plaque community.

Composition of Plaque

• Matrix Composition:
  • Plaque is primarily composed of bacteria embedded in a matrix of salivary glycoproteins and extracellular polysaccharides.
• Implications for Removal:
  • The dense and cohesive nature of this matrix makes it difficult to remove plaque through simple rinsing or the use of sprays.
  • Effective plaque removal typically requires mechanical means, such as brushing and flossing, to disrupt the biofilm structure.

Ecological Succession of Biofilm in Dental Plaque

Overview of Biofilm Formation

Biofilm formation on tooth surfaces is a dynamic process characterized by ecological succession, where microbial communities evolve over time. This process transitions from an early aerobic environment dominated by gram-positive facultative species to a later stage characterized by a highly oxygen-deprived environment where gram-negative anaerobic microorganisms predominate.

Stages of Biofilm Development

1. Initial Colonization:

   • Environment: The initial phase occurs in an aerobic environment.
   • Primary Colonizers:
     • The first bacteria to colonize the pellicle-coated tooth surface are predominantly gram-positive facultative microorganisms.
     • Key Species:
       • Actinomyces viscosus
       • Streptococcus sanguis
   • Characteristics:
     • These bacteria can thrive in the presence of oxygen and play a crucial role in the establishment of the biofilm.

2. Secondary Colonization:

   • Environment: As the biofilm matures, the environment becomes increasingly anaerobic due to the metabolic activities of the initial colonizers.
   • Secondary Colonizers:
     • These microorganisms do not initially colonize clean tooth surfaces but adhere to the existing bacterial cells in the plaque mass.
     • Key Species:
       • Prevotella intermedia
       • Prevotella loescheii
       • Capnocytophaga spp.
       • Fusobacterium nucleatum
       • Porphyromonas gingivalis
   • Coaggregation:
     • Secondary colonizers adhere to primary colonizers through a process known as coaggregation, which involves specific interactions between bacterial cells.

3. Coaggregation Examples:

   • Coaggregation is a critical mechanism that facilitates the establishment of complex microbial communities within the biofilm.
   • Well-Known Examples:
     • Fusobacterium nucleatum with Streptococcus sanguis
     • Prevotella loescheii with Actinomyces viscosus
     • Capnocytophaga ochracea with Actinomyces viscosus

Implications of Ecological Succession

• Microbial Diversity: The transition from gram-positive to gram-negative organisms reflects an increase in microbial diversity and complexity within the biofilm.
• Pathogenic Potential: The accumulation of anaerobic gram-negative bacteria is associated with the development of periodontal diseases, as these organisms can produce virulence factors that contribute to tissue destruction and inflammation.
• Biofilm Stability: The interactions between different bacterial species through coaggregation enhance the stability and resilience of the biofilm, making it more challenging to remove through mechanical cleaning.

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Subgingival and Supragingival Calculus

Overview of Calculus Formation

Calculus, or tartar, is a hardened form of dental plaque that can form on both supragingival (above the gum line) and subgingival (below the gum line) surfaces. Understanding the differences between these two types of calculus is essential for effective periodontal disease management.

Subgingival Calculus

1. Color and Composition:

   • Appearance: Subgingival calculus is typically dark green or dark brown in color.
   • Causes of Color:
     • The dark color is likely due to the presence of matrix components that differ from those found in supragingival calculus.
     • It is influenced by iron heme pigments that are associated with the bleeding of inflamed gingiva, reflecting the inflammatory state of the periodontal tissues.

2. Formation Factors:

   • Matrix Components: The subgingival calculus matrix contains blood products, which contribute to its darker coloration.
   • Bacterial Environment: The subgingival environment is typically more anaerobic and harbors different bacterial species compared to supragingival calculus.

Supragingival Calculus

1. Formation Factors:

   • Dependence on Plaque and Saliva:
     • The degree of supragingival calculus formation is primarily influenced by the amount of bacterial plaque present and the secretion of salivary glands.
     • Increased plaque accumulation leads to greater calculus formation.

2. Inorganic Components:

   • Source: The inorganic components of supragingival calculus are mainly derived from saliva.
   • Composition: These components include minerals such as calcium and phosphate, which contribute to the calcification process of plaque.

Comparison of Inorganic Components

• Supragingival Calculus:

  • Inorganic components are primarily sourced from saliva, which contains minerals that facilitate the formation of calculus on the tooth surface.

• Subgingival Calculus:

  • In contrast, the inorganic components of subgingival calculus are derived mainly from crevicular fluid (serum transudate), which seeps into the gingival sulcus and contains various proteins and minerals from the bloodstream.

Bacterial Properties Involved in Evasion of Host Defense Mechanisms

Bacteria have evolved various strategies to evade the host's immune defenses, allowing them to persist and cause disease. Understanding these mechanisms is crucial for developing effective treatments and preventive measures against bacterial infections, particularly in the context of periodontal disease. This lecture will explore the bacterial species involved, their properties, and the biological effects of these properties on host defense mechanisms.

Host Defense Mechanisms and Bacterial Evasion Strategies

1. Specific Antibody Evasion

   • Bacterial Species:
     • Porphyromonas gingivalis
     • Prevotella intermedia
     • Prevotella melaninogenica
     • Capnocytophaga spp.
   • Bacterial Property:
     • IgA- and IgG-degrading proteases
   • Biologic Effect:
     • Degradation of specific antibodies, which impairs the host's ability to mount an effective immune response against these bacteria.

2. Evasion of Polymorphonuclear Leukocytes (PMNs)

   • Bacterial Species:
     • Aggregatibacter actinomycetemcomitans
     • Fusobacterium nucleatum
     • Porphyromonas gingivalis
     • Treponema denticola
   • Bacterial Properties:
     • Leukotoxin: A toxin that can induce apoptosis in PMNs.
     • Heat-sensitive surface protein: May interfere with immune recognition.
     • Capsule: A protective layer that inhibits phagocytosis.
     • Inhibition of superoxide production: Reduces the oxidative burst necessary for bacterial killing.
   • Biologic Effects:
     • Inhibition of PMN function, leading to decreased bacterial killing.
     • Induction of apoptosis (programmed cell death) in PMNs, reducing the number of immune cells available to fight infection.
     • Inhibition of phagocytosis, allowing bacteria to evade clearance.

3. Evasion of Lymphocytes

   • Bacterial Species:
     • Aggregatibacter actinomycetemcomitans
     • Fusobacterium nucleatum
     • Tannerella forsythia
     • Prevotella intermedia
   • Bacterial Properties:
     • Leukotoxin: Induces apoptosis in lymphocytes.
     • Cytolethal distending toxin: Affects cell cycle progression and induces cell death.
     • Heat-sensitive surface protein: May interfere with immune recognition.
     • Cytotoxin: Directly damages immune cells.
   • Biologic Effects:
     • Killing of mature B and T cells, leading to a weakened adaptive immune response.
     • Nonlethal suppression of lymphocyte activity, impairing the immune response.
     • Impairment of lymphocyte function by arresting the cell cycle, leading to decreased responses to antigens and mitogens.
     • Induction of apoptosis in mononuclear cells and lymphocytes, further reducing immune capacity.

4. Inhibition of Interleukin-8 (IL-8) Production

   • Bacterial Species:
     • Porphyromonas gingivalis
   • Bacterial Property:
     • Inhibition of IL-8 production by epithelial cells.
   • Biologic Effect:
     • Impairment of PMN response to bacteria, leading to reduced recruitment and activation of neutrophils at the site of infection.

Microbes in Periodontics

Bacteria Associated with Periodontal Health

• Primary Species:

  • Gram-Positive Facultative Bacteria:
    • Streptococcus:
      • S. sanguis
      • S. mitis
      • A. viscosus
      • A. naeslundii
    • Actinomyces:
      • Beneficial for maintaining periodontal health.

• Protective or Beneficial Bacteria:

  • Key Species:
    • S. sanguis
    • Veillonella parvula
    • Corynebacterium ochracea
  • Characteristics:
    • Found in higher numbers at inactive periodontal sites (no attachment loss).
    • Low numbers at sites with active periodontal destruction.
    • Prevent colonization of pathogenic microorganisms (e.g., S. sanguis produces peroxide).

• Clinical Relevance:

  • High levels of C. ochracea and S. sanguis are associated with greater attachment gain post-therapy.

Microbiology of Chronic Plaque-Induced Gingivitis

• Composition:

  • Roughly equal proportions of:
    • Gram-Positive: 56%
    • Gram-Negative: 44%
    • Facultative: 59%
    • Anaerobic: 41%

• Predominant Gram-Positive Species:

  • S. sanguis
  • S. mitis
  • S. intermedius
  • S. oralis
  • A. viscosus
  • A. naeslundii
  • Peptostreptococcus micros

• Predominant Gram-Negative Species:

  • Fusobacterium nucleatum
  • Porphyromonas intermedia
  • Veillonella parvula
  • Haemophilus spp.
  • Capnocytophaga spp.
  • Campylobacter spp.

• Pregnancy-Associated Gingivitis:

  • Increased levels of steroid hormones and P. intermedia.

Chronic Periodontitis

• Key Microbial Species:

  • High levels of:
    • Porphyromonas gingivalis
    • Bacteroides forsythus
    • Porphyromonas intermedia
    • Campylobacter rectus
    • Eikenella corrodens
    • Fusobacterium nucleatum
    • Actinobacillus actinomycetemcomitans
    • Peptostreptococcus micros
    • Treponema spp.
    • Eubacterium spp.

• Pathogenic Mechanisms:

  • P. gingivalis and A. actinomycetemcomitans can invade host tissue cells.
  • Viruses such as Epstein-Barr Virus-1 (EBV-1) and human cytomegalovirus (HCMV) may contribute to bone loss.

Localized Aggressive Periodontitis

• Microbiota Characteristics:
  • Predominantly gram-negative, capnophilic, and anaerobic rods.
  • Almost all localized juvenile periodontitis (LJP) sites harbor A. actinomycetemcomitans, which can comprise up to 90% of the total cultivable microbiota.

Erythema Multiforme

• Characteristics: Erythema multiforme presents with "target" or "bull's eye" lesions, often associated with:
  • Etiologic Factors:
    • Herpes simplex infection.
    • Mycoplasma infection.
    • Drug reactions (e.g., sulfonamides, penicillins, phenylbutazone, phenytoin).