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Periodontology - NEETMDS- courses
NEET MDS Lessons
Periodontology

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.

Effects of Smoking on the Etiology and Pathogenesis of Periodontal Disease

Smoking is a significant risk factor for the development and progression of periodontal disease. It affects various aspects of periodontal health, including microbiology, immunology, and physiology. Understanding these effects is crucial for dental professionals in managing patients with periodontal disease, particularly those who smoke.

Etiologic Factors and the Impact of Smoking

  1. Microbiology

    • Plaque Accumulation:
      • Smoking does not affect the rate of plaque accumulation on teeth. This means that smokers may have similar levels of plaque as non-smokers.
    • Colonization of Periodontal Pathogens:
      • Smoking increases the colonization of shallow periodontal pockets by periodontal pathogens. This can lead to an increased risk of periodontal disease.
      • There are higher levels of periodontal pathogens found in deep periodontal pockets among smokers, contributing to the severity of periodontal disease.
  2. Immunology

    • Neutrophil Function:
      • Smoking alters neutrophil chemotaxis (the movement of neutrophils towards infection), phagocytosis (the process by which neutrophils engulf and destroy pathogens), and the oxidative burst (the rapid release of reactive oxygen species to kill bacteria).
    • Cytokine Levels:
      • Increased levels of pro-inflammatory cytokines such as Tumor Necrosis Factor-alpha (TNF-α) and Prostaglandin E2 (PGE2) are found in the gingival crevicular fluid (GCF) of smokers. These cytokines play a role in inflammation and tissue destruction.
    • Collagenase and Elastase Production:
      • There is an increase in neutrophil collagenase and elastase in GCF, which can contribute to the breakdown of connective tissue and exacerbate periodontal tissue destruction.
    • Monocyte Response:
      • Smoking enhances the production of PGE2 by monocytes in response to lipopolysaccharides (LPS), further promoting inflammation and tissue damage.
  3. Physiology

    • Gingival Blood Vessels:
      • Smoking leads to a decrease in gingival blood vessels, which can impair the delivery of immune cells and nutrients to the periodontal tissues, exacerbating inflammation.
    • Gingival Crevicular Fluid (GCF) Flow:
      • There is a reduction in GCF flow and bleeding on probing, even in the presence of increased inflammation. This can mask the clinical signs of periodontal disease, making diagnosis more challenging.
    • Subgingival Temperature:
      • Smoking is associated with a decrease in subgingival temperature, which may affect the metabolic activity of periodontal pathogens.
    • Recovery from Local Anesthesia:
      • Smokers may require a longer time to recover from local anesthesia, which can complicate dental procedures and patient management.

Clinical Implications

  1. Increased Risk of Periodontal Disease:

    • Smokers are at a higher risk for developing periodontal disease due to the combined effects of altered microbial colonization, impaired immune response, and physiological changes in the gingival tissues.
  2. Challenges in Diagnosis:

    • The reduced bleeding on probing and altered GCF flow in smokers can lead to underdiagnosis or misdiagnosis of periodontal disease. Dental professionals must be vigilant in assessing periodontal health in smokers.
  3. Treatment Considerations:

    • Smoking cessation should be a key component of periodontal treatment plans. Educating patients about the effects of smoking on periodontal health can motivate them to quit.
    • Treatment may need to be more aggressive in smokers due to the increased severity of periodontal disease and the altered healing response.
  4. Monitoring and Maintenance:

    • Regular monitoring of periodontal health is essential for smokers, as they may experience more rapid disease progression. Tailored maintenance programs should be implemented to address their specific needs.

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.

Connective Tissue of the Gingiva and Related Cellular Components

The connective tissue of the gingiva, known as the lamina propria, plays a crucial role in supporting the gingival epithelium and maintaining periodontal health. This lecture will cover the structure of the lamina propria, the types of connective tissue fibers present, the role of Langerhans cells, and the changes observed in the periodontal ligament (PDL) with aging.

Structure of the Lamina Propria

  1. Layers of the Lamina Propria:

    • The lamina propria consists of two distinct layers:
      1. Papillary Layer:
        • The upper layer that interdigitates with the epithelium, containing finger-like projections that increase the surface area for exchange of nutrients and waste.
      2. Reticular Layer:
        • The deeper layer that provides structural support and contains larger blood vessels and nerves.
  2. Types of Connective Tissue Fibers:

    • The lamina propria contains three main types of connective tissue fibers:

      1. Collagen Fibers:
        • Type I Collagen: Forms the bulk of the lamina propria and provides tensile strength to the gingival fibers, essential for maintaining the integrity of the gingiva.
      2. Reticular Fibers:
        • These fibers provide a supportive network within the connective tissue.
      3. Elastic Fibers:
        • Contribute to the elasticity and flexibility of the gingival tissue.
    • Type IV Collagen:

      • Found branching between the Type I collagen bundles, it is continuous with the fibers of the basement membrane and the walls of blood vessels.

Langerhans Cells

  1. Description:

    • Langerhans cells are dendritic cells located among keratinocytes at all suprabasal levels of the gingival epithelium.
    • They belong to the mononuclear phagocyte system and play a critical role in immune responses.
  2. Function:

    • Act as antigen-presenting cells for lymphocytes, facilitating the immune reaction.
    • Contain specific granules known as Birbeck’s granules and exhibit marked ATP activity.
  3. Location:

    • Found in the oral epithelium of normal gingiva and in small amounts in the sulcular epithelium.
    • Absent from the junctional epithelium of normal gingiva.

Changes in the Periodontal Ligament (PDL) with Aging

  1. Aging Effects:
    • With aging, several changes have been reported in the periodontal ligament:
      • Decreased Numbers of Fibroblasts: This reduction can lead to impaired healing and regeneration of the PDL.
      • Irregular Structure: The PDL may exhibit a more irregular structure, paralleling changes in the gingival connective tissues.
      • Decreased Organic Matrix Production: This can affect the overall health and function of the PDL.
      • Epithelial Cell Rests: There may be a decrease in the number of epithelial cell rests, which are remnants of the Hertwig's epithelial root sheath.
      • Increased Amounts of Elastic Fibers: This change may contribute to the altered mechanical properties of the PDL.

Classification of Cementum According to Schroeder

Cementum is a specialized calcified tissue that covers the roots of teeth and plays a crucial role in periodontal health. According to Schroeder, cementum can be classified into several distinct types based on its cellular composition and structural characteristics. Understanding these classifications is essential for dental professionals in diagnosing and treating periodontal conditions.

Classification of Cementum

  1. Acellular Afibrillar Cementum:

    • Characteristics:
      • Contains neither cells nor collagen fibers.
      • Present in the coronal region of the tooth.
      • Thickness ranges from 1 µm to 15 µm.
    • Function:
      • This type of cementum is thought to play a role in the attachment of the gingiva to the tooth surface.
  2. Acellular Extrinsic Fiber Cementum:

    • Characteristics:
      • Lacks cells but contains closely packed bundles of Sharpey’s fibers, which are collagen fibers that anchor the cementum to the periodontal ligament.
      • Typically found in the cervical third of the roots.
      • Thickness ranges from 30 µm to 230 µm.
    • Function:
      • Provides strong attachment of the periodontal ligament to the tooth, contributing to the stability of the tooth in its socket.
  3. Cellular Mixed Stratified Cementum:

    • Characteristics:
      • Contains both extrinsic and intrinsic fibers and may contain cells.
      • Found in the apical third of the roots, at the apices, and in furcation areas.
      • Thickness ranges from 100 µm to 1000 µm.
    • Function:
      • This type of cementum is involved in the repair and adaptation of the tooth root, especially in response to functional demands and periodontal disease.
  4. Cellular Intrinsic Fiber Cementum:

    • Characteristics:
      • Contains cells but no extrinsic collagen fibers.
      • Primarily fills resorption lacunae, which are areas where cementum has been resorbed.
    • Function:
      • Plays a role in the repair of cementum and may be involved in the response to periodontal disease.
  5. Intermediate Cementum:

    • Characteristics:
      • A poorly defined zone located near the cementoenamel junction (CEJ) of certain teeth.
      • Appears to contain cellular remnants of the Hertwig's epithelial root sheath (HERS) embedded in a calcified ground substance.
    • Function:
      • Its exact role is not fully understood, but it may be involved in the transition between enamel and cementum.

Clinical Significance

  • Importance of Cementum:

    • Understanding the different types of cementum is crucial for diagnosing periodontal diseases and planning treatment strategies.
    • The presence of various types of cementum can influence the response of periodontal tissues to disease and trauma.
  • Cementum in Periodontal Disease:

    • Changes in the thickness and composition of cementum can occur in response to periodontal disease, affecting tooth stability and attachment.

Aggressive Periodontitis (formerly Juvenile Periodontitis)

  • Historical Names: Previously referred to as periodontosis, deep cementopathia, diseases of eruption, Gottleib’s diseases, and periodontitis marginalis progressive.
  • Risk Factors:
    • High frequency of Actinobacillus actinomycetemcomitans.
    • Immune defects (functional defects of PMNs and monocytes).
    • Autoimmunity and genetic factors.
    • Environmental factors, including smoking.
  • Clinical Features:
    • Vertical loss of alveolar bone around the first molars and incisors, typically beginning around puberty.
    • Bone loss patterns often described as "target" or "bull" shaped lesions.

Gracey Curettes

Gracey curettes are specialized instruments designed for periodontal therapy, particularly for subgingival scaling and root planing. Their unique design allows for optimal adaptation to the complex anatomy of the teeth and surrounding tissues. This lecture will cover the characteristics, specific uses, and advantages of Gracey curettes in periodontal practice.

  • Gracey curettes are area-specific curettes that come in a set of instruments, each designed and angled to adapt to specific anatomical areas of the dentition.

  • Purpose: They are considered some of the best instruments for subgingival scaling and root planing due to their ability to provide excellent adaptation to complex root anatomy.

Specific Gracey Curette Designs and Uses

  1. Gracey 1/2 and 3/4:

    • Indication: Designed for use on anterior teeth.
    • Application: Effective for scaling and root planing in the anterior region, allowing for precise access to the root surfaces.
  2. Gracey 5/6:

    • Indication: Suitable for anterior teeth and premolars.
    • Application: Versatile for both anterior and premolar areas, providing effective scaling in these regions.
  3. Gracey 7/8 and 9/10:

    • Indication: Designed for posterior teeth, specifically for facial and lingual surfaces.
    • Application: Ideal for accessing the buccal and lingual surfaces of posterior teeth, ensuring thorough cleaning.
  4. Gracey 11/12:

    • Indication: Specifically designed for the mesial surfaces of posterior teeth.
    • Application: Allows for effective scaling of the mesial aspects of molars and premolars.
  5. Gracey 13/14:

    • Indication: Designed for the distal surfaces of posterior teeth.
    • Application: Facilitates access to the distal surfaces of molars and premolars, ensuring comprehensive treatment.

Key Features of Gracey Curettes

  • Area-Specific Design: Each Gracey curette is tailored for specific areas of the dentition, allowing for better access and adaptation to the unique contours of the teeth.

  • Offset Blade: Unlike universal curettes, the blade of a Gracey curette is not positioned at a 90-degree angle to the lower shank. Instead, the blade is angled approximately 60 to 70 degrees from the lower shank, which is referred to as an "offset blade." This design enhances the instrument's ability to adapt to the tooth surface and root anatomy.

Advantages of Gracey Curettes

  1. Optimal Adaptation: The area-specific design and offset blade allow for better adaptation to the complex anatomy of the roots, making them highly effective for subgingival scaling and root planing.

  2. Improved Access: The angled blades enable clinicians to access difficult-to-reach areas, such as furcations and concavities, which are often challenging with standard instruments.

  3. Enhanced Efficiency: The design of Gracey curettes allows for more efficient removal of calculus and biofilm from root surfaces, contributing to improved periodontal health.

  4. Reduced Tissue Trauma: The precise design minimizes trauma to the surrounding soft tissues, promoting better healing and patient comfort.

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