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Periodontology

Influence of Host Response on Periodontal Disease

The host response plays a critical role in the progression and management of periodontal disease. Various host factors influence bacterial colonization, invasion, tissue destruction, and healing processes. Understanding these interactions is essential for developing effective treatment strategies.

Aspects of Periodontal Disease and Host Factors

  1. Bacterial Colonization:

    • Host Factor: Antibody C in crevicular fluid.
    • Mechanism:
      • Antibody C inhibits the adherence and coaggregation of bacteria in the subgingival environment.
      • This action potentially reduces bacterial numbers by promoting lysis (destruction of bacterial cells).
    • Implication: A robust antibody response can help control the initial colonization of pathogenic bacteria, thereby influencing the onset of periodontal disease.
  2. Bacterial Invasion:

    • Host Factor: Antibody C-mediated lysis and neutrophil activity.
    • Mechanism:
      • Antibody C-mediated lysis reduces bacterial counts in the periodontal tissues.
      • Neutrophils, through processes such as chemotaxis (movement towards chemical signals), phagocytosis (engulfing and digesting bacteria), and lysis, further reduce bacterial counts.
    • Implication: An effective neutrophil response is crucial for controlling bacterial invasion and preventing the progression of periodontal disease.
  3. Tissue Destruction:

    • Host Factors: Antibody-mediated hypersensitivity and cell-mediated immune responses.
    • Mechanism:
      • Activation of tissue factors, such as collagenase, leads to the breakdown of connective tissue and periodontal structures.
      • The immune response can inadvertently contribute to tissue destruction, as inflammatory mediators can damage host tissues.
    • Implication: While the immune response is essential for fighting infection, it can also lead to collateral damage in periodontal tissues, exacerbating disease progression.
  4. Healing and Fibrosis:

    • Host Factors: Lymphocytes and macrophage-produced chemotactic factors.
    • Mechanism:
      • Lymphocytes and macrophages release chemotactic factors that attract fibroblasts to the site of injury.
      • Fibroblasts are activated by specific factors, promoting tissue repair and fibrosis (the formation of excess connective tissue).
    • Implication: A balanced immune response is necessary for effective healing and regeneration of periodontal tissues following inflammation.

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.

Epithelial Turnover Rates in Oral Tissues

Epithelial turnover is a critical process in maintaining the health and integrity of oral tissues. Understanding the turnover rates of different epithelial types in the oral cavity can provide insights into their regenerative capabilities and responses to injury or disease.

Turnover Rates of Oral Epithelial Tissues

  1. Junctional Epithelium:

    • Turnover Rate1-6 days
    • Description:
      • The junctional epithelium is a specialized epithelial tissue that forms the attachment between the gingiva and the tooth surface.
      • Its rapid turnover rate is essential for maintaining a healthy seal around the tooth and for responding quickly to inflammatory changes or injury.
  2. Palate, Tongue, and Cheeks:

    • Turnover Rate5-6 days
    • Description:
      • The epithelial tissues of the hard palate, tongue, and buccal mucosa (cheeks) have a moderate turnover rate.
      • This relatively quick turnover helps maintain the integrity of these surfaces, which are subject to mechanical stress and potential injury from food and other environmental factors.
  3. Gingiva:

    • Turnover Rate10-12 days
    • Description:
      • The gingival epithelium has a slower turnover rate compared to the junctional epithelium and the epithelium of the palate, tongue, and cheeks.
      • This slower rate reflects the need for stability in the gingival tissue, which plays a crucial role in supporting the teeth and maintaining periodontal health.

Clinical Significance

  • Wound Healing:

    • The rapid turnover of the junctional epithelium is particularly important in the context of periodontal health, as it allows for quick healing of any disruptions caused by inflammation or mechanical trauma.
  • Response to Disease:

    • Understanding the turnover rates can help clinicians anticipate how quickly tissues may respond to treatment or how they may regenerate after surgical procedures.
  • Oral Health Maintenance:

    • The varying turnover rates highlight the importance of maintaining good oral hygiene practices to support the health of these tissues, especially in areas with slower turnover rates like the gingiva.

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.

Assessing New Attachment in Periodontal Therapy

Assessing new attachment following periodontal therapy is crucial for evaluating treatment outcomes and understanding the healing process. However, various methods of assessment have limitations that must be considered. This lecture will discuss the reliability of different assessment methods for new attachment, including periodontal probing, radiographic analysis, and histologic methods.

1. Periodontal Probing

  • Assessment Method: Periodontal probing is commonly used to measure probing depth and attachment levels before and after therapy.

  • Limitations:

    • Coronal Positioning of Probe Tip: After therapy, when the inflammatory lesion is resolved, the probe tip may stop coronal to the apical termination of the epithelium. This can lead to misleading interpretations of attachment gain.
    • Infrabony Defects: Following treatment of infrabony defects, new bone may form so close to the tooth surface that the probe cannot penetrate. This can result in a false impression of improved attachment levels.
    • Interpretation of Results: A gain in probing attachment level does not necessarily indicate a true gain of connective tissue attachment. Instead, it may reflect improved health of the surrounding tissues, which increases resistance to probe penetration.

2. Radiographic Analysis and Reentry Operations

  • Assessment Method: Radiographic analysis involves comparing radiographs taken before and after therapy to evaluate changes in bone levels. Reentry operations allow for direct inspection of the treated area.

  • Limitations:

    • Bone Fill vs. New Attachment: While radiographs can provide evidence of new bone formation (bone fill), they do not document the formation of new root cementum or a new periodontal ligament. Therefore, radiographic evidence alone cannot confirm the establishment of new attachment.

3. Histologic Methods

  • Assessment Method: Histologic analysis involves examining tissue samples under a microscope to assess the formation of new attachment, including new cementum and periodontal ligament.

  • Advantages:

    • Validity: Histologic methods are considered the only valid approach to assess the formation of new attachment accurately.
  • Limitations:

    • Pre-Therapy Assessment: Accurate assessment of the attachment level prior to therapy is essential for histologic analysis. If the initial attachment level cannot be determined with certainty, it may compromise the validity of the findings.

Gingivitis

Gingivitis is an inflammatory condition of the gingiva that can progress through several distinct stages. Understanding these stages is crucial for dental professionals in diagnosing and managing periodontal disease effectively. This lecture will outline the four stages of gingivitis, highlighting the key pathological changes that occur at each stage.

I. Initial Lesion

  • Characteristics:
    • Increased Permeability: The microvascular bed in the gingival tissues becomes more permeable, allowing for the passage of fluids and immune cells.
    • Increased GCF Flow: There is an increase in the flow of gingival crevicular fluid (GCF), which is indicative of inflammation and immune response.
    • PMN Cell Migration: The migration of polymorphonuclear leukocytes (PMNs) is facilitated by various adhesion molecules, including:
      • Intercellular Cell Adhesion Molecule 1 (ICAM-1)
      • E-selectin (ELAM-1) in the dentogingival vasculature.
  • Clinical Implications: This stage marks the beginning of the inflammatory response, where the body attempts to combat the initial bacterial insult.

II. Early Lesion

  • Characteristics:

    • Leukocyte Infiltration: There is significant infiltration of leukocytes, particularly lymphocytes, into the connective tissue of the junctional epithelium.
    • Fibroblast Degeneration: Several fibroblasts within the lesion exhibit signs of degeneration, indicating tissue damage.
    • Proliferation of Basal Cells: The basal cells of the junctional and sulcular epithelium begin to proliferate, which may be a response to the inflammatory process.
  • Clinical Implications: This stage represents a transition from initial inflammation to more pronounced tissue changes, with the potential for further progression if not managed.

III. Established Lesion

  • Characteristics:

    • Predominance of Plasma Cells and B Lymphocytes: There is a marked increase in plasma cells and B lymphocytes, indicating a more advanced immune response.
    • Increased Collagenolytic Activity: The activity of collagen-degrading enzymes increases, leading to the breakdown of collagen fibers in the connective tissue.
    • B Cell Subclasses: The B cells present in the established lesion are predominantly of the IgG1 and IgG3 subclasses, which are important for the immune response.
  • Clinical Implications: This stage is characterized by chronic inflammation, and if left untreated, it can lead to further tissue destruction and the transition to advanced lesions.

IV. Advanced Lesion

  • Characteristics:

    • Loss of Connective Tissue Attachment: There is significant loss of connective tissue attachment to the teeth, which can lead to periodontal pocket formation.
    • Alveolar Bone Loss: Extensive damage occurs to the alveolar bone, contributing to the overall loss of periodontal support.
    • Extensive Damage to Collagen Fibers: The collagen fibers in the gingival tissues are extensively damaged, further compromising the structural integrity of the gingiva.
    • Predominance of Plasma Cells: Plasma cells remain predominant, indicating ongoing immune activity and inflammation.
  • Clinical Implications: This stage represents the transition from gingivitis to periodontitis, where irreversible damage can occur. Early intervention is critical to prevent further progression and loss of periodontal support.

Some important points about the periodontal pocket :
·Soft tissue of pocket wall shows both proliferative & degenerative changes
·Most severe degenerative changes are seen on the lateral wall of pocket
·Plasma cells are the predominant infiltrate (80%). Others include lymphocytes & a scattering of PMNs
·Height of junctional epithelium shortened to only 50-100µm
·Severity of degenerative changes is not linked to pocket depth
·Junctional epithelium starts to lose attachment to tooth when PMN infiltration in junctional epithelium increases above 60%.

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