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.

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.

Bone grafting is a critical procedure in periodontal and dental surgery, aimed at restoring lost bone and supporting the regeneration of periodontal tissues. Various materials can be used for bone grafting, each with unique properties and applications.

A. Osseous Coagulum

• Composition: Osseous coagulum is a mixture of bone dust and blood. It is created using small particles ground from cortical bone.
• Sources: Bone dust can be obtained from various anatomical sites, including:
  • Lingual ridge of the mandible
  • Exostoses
  • Edentulous ridges
  • Bone distal to terminal teeth
• Application: This material is used in periodontal surgery to promote healing and regeneration of bone in areas affected by periodontal disease.

B. Bioactive Glass

• Composition: Bioactive glass consists of sodium and calcium salts, phosphates, and silicon dioxide.
• Function: It promotes bone regeneration by forming a bond with surrounding bone and stimulating cellular activity.

C. HTR Polymer

• Composition: HTR Polymer is a non-resorbable, microporous, biocompatible composite made from polymethyl methacrylate (PMMA) and polyhydroxymethacrylate.
• Application: This material is used in various dental and periodontal applications due to its biocompatibility and structural properties.

D. Other Bone Graft Materials

• Sclera: Used as a graft material due to its collagen content and biocompatibility.
• Cartilage: Can be used in certain grafting procedures, particularly in reconstructive surgery.
• Plaster of Paris: Occasionally used in bone grafting, though less common due to its non-biological nature.
• Calcium Phosphate Biomaterials: These materials are osteoconductive and promote bone healing.
• Coral-Derived Materials: Natural coral can be processed to create a scaffold for bone regeneration.

 Naber’s Probe and Furcation Involvement

Furcation involvement is a critical aspect of periodontal disease that affects the prognosis of teeth with multiple roots. Naber’s probe is a specialized instrument designed to assess furcation areas, allowing clinicians to determine the extent of periodontal attachment loss and the condition of the furcation. This lecture will cover the use of Naber’s probe, the classification of furcation involvement, and the clinical significance of these classifications.

Naber’s Probe

• Description: Naber’s probe is a curved, blunt-ended instrument specifically designed for probing furcation areas. Its unique shape allows for horizontal probing, which is essential for accurately assessing the anatomy of multi-rooted teeth.

• Usage: The probe is inserted horizontally into the furcation area to evaluate the extent of periodontal involvement. The clinician can feel the anatomical fluting between the roots, which aids in determining the classification of furcation involvement.

Classification of Furcation Involvement

Furcation involvement is classified into four main classes using Naber’s probe:

1. Class I:

   • Description: The furcation can be probed to a depth of 3 mm.
   • Clinical Findings: The probe can feel the anatomical fluting between the roots, but it cannot engage the roof of the furcation.
   • Significance: Indicates early furcation involvement with minimal attachment loss.

2. Class II:

   • Description: The furcation can be probed to a depth greater than 3 mm, but not through and through.
   • Clinical Findings: This class represents a range between Class I and Class III, where there is partial loss of attachment but not complete penetration through the furcation.
   • Significance: Indicates moderate furcation involvement that may require intervention.

3. Class III:

   • Description: The furcation can be completely probed through and through.
   • Clinical Findings: The probe passes from one furcation to the other, indicating significant loss of periodontal support.
   • Significance: Represents advanced furcation involvement, often associated with a poor prognosis for the affected tooth.

4. Class III+:

   • Description: The probe can go halfway across the tooth.
   • Clinical Findings: Similar to Class III, but with partial obstruction or remaining tissue.
   • Significance: Indicates severe furcation involvement with a significant loss of attachment.

5. Class IV:

   • Description: Clinically, the examiner can see through the furcation.
   • Clinical Findings: There is complete loss of tissue covering the furcation, making it visible upon examination.
   • Significance: Indicates the most severe form of furcation involvement, often leading to tooth mobility and extraction.

Measurement Technique

• Measurement Reference: Measurements are taken from an imaginary tangent connecting the prominences of the root surfaces of both roots. This provides a consistent reference point for assessing the depth of furcation involvement.

Clinical Significance

• Prognosis: The classification of furcation involvement is crucial for determining the prognosis of multi-rooted teeth. Higher classes of furcation involvement generally indicate a poorer prognosis and may necessitate more aggressive treatment strategies.

• Treatment Planning: Understanding the extent of furcation involvement helps clinicians develop appropriate treatment plans, which may include scaling and root planing, surgical intervention, or extraction.

• Monitoring: Regular assessment of furcation involvement using Naber’s probe can help monitor disease progression and the effectiveness of periodontal therapy.

Aggressive periodontitis (AP) is a multifactorial, severe, and rapidly progressive form of periodontitis that primarily affects younger patients. It is characterized by a unique set of clinical and microbiological features that distinguish it from other forms of periodontal disease.

Key Characteristics

• Rapid Progression: AP is marked by a swift deterioration of periodontal tissues.
• Age Group: Primarily affects adolescents and young adults, but can occur at any age.
• Multifactorial Etiology: Involves a combination of microbiological, immunological, genetic, and environmental factors.

Other Findings

• Presence of Aggregatibacter actinomycetemcomitans (A.a.) in diseased sites.
• Abnormal host responses, including impaired phagocytosis and chemotaxis.
• Hyperresponsive macrophages leading to exaggerated inflammatory responses.
• The disease may exhibit self-arresting tendencies in some cases.

Classification

Aggressive periodontitis can be classified into two main types:

1. Localized Aggressive Periodontitis (LAP): Typically affects the permanent molars and incisors, often with localized attachment loss.
2. Generalized Aggressive Periodontitis (GAP): Involves more widespread periodontal tissue destruction.

Risk Factors

Microbiological Factors

• Aggregatibacter actinomycetemcomitans: A primary pathogen associated with LAP, producing a potent leukotoxin that kills neutrophils.
• Different strains of A.a. produce varying levels of leukotoxin, with highly toxic strains more prevalent in affected individuals.

Immunological Factors

• Human Leukocyte Antigens (HLAs): HLA-A9 and B-15 are candidate markers for aggressive periodontitis.
• Defective neutrophil function leads to impaired chemotaxis and phagocytosis.
• Hyper-responsive macrophage phenotype, characterized by elevated levels of PGE2 and IL-1β, may contribute to connective tissue breakdown and bone loss.

Genetic Factors

• Familial clustering of neutrophil abnormalities suggests a genetic predisposition.
• Genetic control of antibody responses to A.a., with variations in the ability to produce protective IgG2 antibodies.

Environmental Factors

• Smoking is a significant risk factor, with smokers experiencing more severe periodontal destruction compared to non-smokers.

Treatment Approaches

General Considerations

• Treatment strategies depend on the type and extent of periodontal destruction.
• GAP typically has a poorer prognosis compared to LAP, as it is less likely to enter spontaneous remission.

Conventional Periodontal Therapy

• Patient Education: Informing patients about the disease and its implications.
• Oral Hygiene Instructions: Reinforcing proper oral hygiene practices.
• Scaling and Root Planing: Removal of plaque and calculus to control local factors.

Surgical Resection Therapy

• Aimed at reducing or eliminating pocket depth.
• Contraindicated in cases of severe horizontal bone loss due to the risk of increased tooth mobility.

Regenerative Therapy

• Potential for regeneration is promising in AP cases.
• Techniques include open flap surgical debridement, root surface conditioning with tetracycline, and the use of allogenic bone grafts.
• Recent advances involve the use of enamel matrix proteins to promote cementum regeneration and new attachment.

Antimicrobial Therapy

• Often required as adjunctive treatment to eliminate A.a. from periodontal tissues.
• Tetracycline: Administered in various regimens to concentrate in periodontal tissues and inhibit A.a. growth.
• Combination Therapy: Metronidazole combined with amoxicillin has shown efficacy alongside periodontal therapy.
• Doxycycline: Used at a dose of 100 mg/day.
• Chlorhexidine (CHX): Irrigation and home rinsing to control bacterial load.

Host Modulation

• Involves the use of sub-antimicrobial dose doxycycline (SDD) to prevent periodontal attachment loss by modulating the activity of matrix metalloproteinases (MMPs), particularly collagenase and gelatinase.

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.