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Periodontology

Periodontal Bone Grafts

Bone grafting is a critical procedure in periodontal surgery, aimed at restoring lost bone and supporting the regeneration of periodontal tissues.

1. Bone Blend

 Bone blend is a mixture of cortical or cancellous bone that is procured using a trephine or rongeurs, placed in an amalgam capsule, and triturated to achieve a slushy osseous mass. This technique allows for the creation of smaller particle sizes, which enhances resorption and replacement with host bone.

Particle Size: The ideal particle size for bone blend is approximately 210 x 105 micrometers.

Rationale: Smaller particle sizes improve the chances of resorption and integration with the host bone, making the graft more effective.

2. Types of Periodontal Bone Grafts

A. Autogenous Grafts

Autogenous grafts are harvested from the patient’s own body, providing the best compatibility and healing potential.

  1. Cortical Bone Chips

    • History: First used by Nabers and O'Leary in 1965.
    • Characteristics: Composed of shavings of cortical bone removed during osteoplasty and ostectomy from intraoral sites.
    • Challenges: Larger particle sizes can complicate placement and handling, and there is a potential for sequestration. This method has largely been replaced by autogenous osseous coagulum and bone blend.
  2. Osseous Coagulum and Bone Blend

    • Technique: Intraoral bone is obtained using high- or low-speed round burs and mixed with blood to form an osseous coagulum (Robinson, 1969).
    • Advantages: Overcomes disadvantages of cortical bone chips, such as inability to aspirate during collection and variability in quality and quantity of collected bone.
    • Applications: Used in various periodontal procedures to enhance healing and regeneration.
  3. Intraoral Cancellous Bone and Marrow

    • Sources: Healing bony wounds, extraction sockets, edentulous ridges, mandibular retromolar areas, and maxillary tuberosity.
    • Applications: Provides a rich source of osteogenic cells and growth factors for bone regeneration.
  4. Extraoral Cancellous Bone and Marrow

    • Sources: Obtained from the anterior or posterior iliac crest.
    • Advantages: Generally offers the greatest potential for new bone growth due to the abundance of cancellous bone and marrow.

B. Bone Allografts

Bone allografts are harvested from donors and can be classified into three main types:

  1. Undermineralized Freeze-Dried Bone Allograft (FDBA)

    • Introduction: Introduced in 1976 by Mellonig et al.
    • Process: Freeze drying removes approximately 95% of the water from bone, preserving morphology, solubility, and chemical integrity while reducing antigenicity.
    • Efficacy: FDBA combined with autogenous bone is more effective than FDBA alone, particularly in treating furcation involvements.
  2. Demineralized (Decalcified) FDBA

    • Mechanism: Demineralization enhances osteogenic potential by exposing bone morphogenetic proteins (BMPs) in the bone matrix.
    • Osteoinduction vs. Osteoconduction: Demineralized grafts induce new bone formation (osteoinduction), while undermineralized allografts facilitate bone growth by providing a scaffold (osteoconduction).
  3. Frozen Iliac Cancellous Bone and Marrow

    • Usage: Used sparingly due to variability in outcomes and potential complications.

Comparison of Allografts and Alloplasts

  • Clinical Outcomes: Both FDBA and DFDBA have been compared to porous particulate hydroxyapatite, showing little difference in post-treatment clinical parameters.
  • Histological Healing: Grafts of DFDBA typically heal with regeneration of the periodontium, while synthetic bone grafts (alloplasts) heal by repair, which may not restore the original periodontal architecture.

Alveolar Process

The alveolar process is a critical component of the dental anatomy, providing support for the teeth and playing a vital role in periodontal health. Understanding its structure and composition is essential for dental professionals in diagnosing and treating various dental conditions.

Components of the Alveolar Process

  1. External Plate of Cortical Bone:

    • Description: The outer layer of the alveolar process is composed of cortical bone, which is dense and forms a protective outer shell.
    • Composition:
      • Formed by Haversian bone, which consists of organized structures called osteons.
      • Compacted bone lamellae contribute to the strength and stability of the alveolar process.
  2. Alveolar Bone Proper:

    • Description: The inner socket wall of the alveolar process is known as the alveolar bone proper.
    • Radiographic Appearance:
      • It is seen as the lamina dura on radiographs, appearing as a radiopaque line surrounding the tooth roots.
    • Histological Features:
      • Contains a series of openings known as the cribriform plate.
      • These openings allow neurovascular bundles to connect the periodontal ligament with the central component of the alveolar bone, which is the cancellous bone.
  3. Cancellous Bone:

    • Description: Located between the external cortical bone and the alveolar bone proper, cancellous bone consists of trabecular structures.
    • Function:
      • Acts as supporting alveolar bone, providing strength and flexibility to the alveolar process.
    • Interdental Septum:
      • The interdental septum consists of cancellous supporting bone enclosed within a compact border, providing stability between adjacent teeth.

Structural Characteristics

  • Facial and Lingual Portions:
    • Most of the facial and lingual portions of the tooth socket are formed by compact bone alone, providing robust support for the teeth.
  • Cancellous Bone Distribution:
    • Cancellous bone surrounds the lamina dura in specific areas:
      • Apical Areas: The region at the tip of the tooth root.
      • Apicolingual Areas: The area where the root meets the lingual surface.
      • Interradicular Areas: The space between the roots of multi-rooted teeth.

Pathogens Implicated in Periodontal Diseases

Periodontal diseases are associated with a variety of pathogenic microorganisms. Below is a list of key pathogens implicated in different forms of periodontal disease, along with their associations:

General Pathogens Associated with Periodontal Diseases

  • Actinobacillus actinomycetemcomitans:

    • Strongly associated with destructive periodontal disease.
  • Porphyromonas gingivalis:

    • A member of the "black pigmented Bacteroides group" and a significant contributor to periodontal disease.
  • Bacteroides forsythus:

    • Associated with chronic periodontitis.
  • Spirochetes (Treponema denticola):

    • Implicated in various periodontal conditions.
  • Prevotella intermedia/nigrescens:

    • Also belongs to the "black pigmented Bacteroides group" and is associated with several forms of periodontal disease.
  • Fusobacterium nucleatum:

    • Plays a role in the progression of periodontal disease.
  • Campylobacter rectus:

    • These organisms include members of the new genus Wolinella and are associated with periodontal disease.

Principal Bacteria Associated with Specific Periodontal Diseases

  1. Adult Periodontitis:

    • Porphyromonas gingivalis
    • Prevotella intermedia
    • Bacteroides forsythus
    • Campylobacter rectus
  2. Refractory Periodontitis:

    • Bacteroides forsythus
    • Porphyromonas gingivalis
    • Campylobacter rectus
    • Prevotella intermedia
  3. Localized Juvenile Periodontitis (LJP):

    • Actinobacillus actinomycetemcomitans
    • Capnocytophaga
  4. Periodontitis in Juvenile Diabetes:

    • Capnocytophaga
    • Actinobacillus actinomycetemcomitans
  5. Pregnancy Gingivitis:

    • Prevotella intermedia
  6. Acute Necrotizing Ulcerative Gingivitis (ANUG):

    • Prevotella intermedia
    • Intermediate-sized spirochetes

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.

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.

Modified Gingival Index (MGI)

The Modified Gingival Index (MGI) is a clinical tool used to assess the severity of gingival inflammation. It provides a standardized method for evaluating the health of the gingival tissues, which is essential for diagnosing periodontal conditions and monitoring treatment outcomes. Understanding the scoring criteria of the MGI is crucial for dental professionals in their assessments.

Scoring Criteria for the Modified Gingival Index (MGI)

The MGI uses a scale from 0 to 4 to classify the degree of gingival inflammation. Each score corresponds to specific clinical findings:

  1. Score 0: Absence of Inflammation

    • Description: No signs of inflammation are present in the gingival tissues.
    • Clinical Significance: Indicates healthy gingiva with no bleeding or other pathological changes.
  2. Score 1: Mild Inflammation

    • Description:
      • Slight change in color (e.g., slight redness).
      • Little change in texture of any portion of the marginal or papillary gingival unit, but not affecting the entire unit.
    • Clinical Significance: Suggests early signs of gingival inflammation, which may require monitoring and preventive measures.
  3. Score 2: Mild Inflammation (Widespread)

    • Description:
      • Similar criteria as Score 1, but involving the entire marginal or papillary gingival unit.
    • Clinical Significance: Indicates a more widespread mild inflammation that may necessitate intervention to prevent progression.
  4. Score 3: Moderate Inflammation

    • Description:
      • Glazing of the gingiva.
      • Redness, edema, and/or hypertrophy of the marginal or papillary gingival unit.
    • Clinical Significance: Reflects a moderate level of inflammation that may require active treatment to reduce inflammation and restore gingival health.
  5. Score 4: Severe Inflammation

    • Description:
      • Marked redness, edema, and/or hypertrophy of the marginal or papillary gingival unit.
      • Presence of spontaneous bleeding, congestion, or ulceration.
    • Clinical Significance: Indicates severe gingival disease that requires immediate intervention and may be associated with periodontal disease.

Clinical Application of the MGI

  1. Assessment of Gingival Health:

    • The MGI provides a systematic approach to evaluate gingival health, allowing for consistent documentation of inflammation levels.
  2. Monitoring Treatment Outcomes:

    • Regular use of the MGI can help track changes in gingival health over time, assessing the effectiveness of periodontal treatments and preventive measures.
  3. Patient Education:

    • The MGI can be used to educate patients about their gingival health status, helping them understand the importance of oral hygiene and regular dental visits.
  4. Research and Epidemiological Studies:

    • The MGI is often used in clinical research to evaluate the prevalence and severity of gingival disease in populations.

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).

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