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.

Trauma from Occlusion

Trauma from occlusion refers to the injury sustained by periodontal tissues when occlusal forces exceed their adaptive capacity.

1. Trauma from Occlusion

• This term describes the injury that occurs to periodontal tissues when the forces exerted during occlusion (the contact between opposing teeth) exceed the ability of those tissues to adapt.
• Traumatic Occlusion: An occlusion that produces such injury is referred to as a traumatic occlusion. This can result from various factors, including malocclusion, excessive occlusal forces, or parafunctional habits (e.g., bruxism).

2. Clinical Signs of Trauma to the Periodontium

The most common clinical sign of trauma to the periodontium is:

• Increased Tooth Mobility: As the periodontal tissues are subjected to excessive forces, they may become compromised, leading to increased mobility of the affected teeth. This is often one of the first observable signs of trauma from occlusion.

3. Radiographic Signs of Trauma from Occlusion

Radiographic examination can reveal several signs indicative of trauma from occlusion:

1. Increased Width of Periodontal Space:

   • The periodontal ligament space may appear wider on radiographs due to the increased forces acting on the tooth, leading to a loss of attachment and bone support.

2. Vertical Destruction of Inter-Dental Septum:

   • Trauma from occlusion can lead to vertical bone loss in the inter-dental septa, which may be visible on radiographs as a reduction in bone height between adjacent teeth.

3. Radiolucency and Condensation of the Alveolar Bone:

   • Areas of radiolucency may indicate bone loss, while areas of increased radiopacity (condensation) can suggest reactive changes in the bone due to the stress of occlusal forces.

4. Root Resorption:

   • In severe cases, trauma from occlusion can lead to root resorption, which may be observed as a loss of root structure on radiographs.

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.

Necrotizing Ulcerative Gingivitis (NUG)

Necrotizing Ulcerative Gingivitis (NUG), also known as Vincent's disease or trench mouth, is a severe form of periodontal disease characterized by the sudden onset of symptoms and specific clinical features.

Etiology and Predisposing Factors

• Sudden Onset: NUG is characterized by a rapid onset of symptoms, often following debilitating diseases or acute respiratory infections.
• Lifestyle Factors: Changes in living habits, such as prolonged work without adequate rest, poor nutrition, tobacco use, and psychological stress, are frequently noted in patient histories .
• Smoking: Smoking has been identified as a significant predisposing factor for NUG/NDP .
• Immune Compromise: Conditions that compromise the immune system, such as poor oral hygiene, smoking, and emotional stress, are major contributors to the development of NUG .

Clinical Presentation

• Symptoms: NUG presents with:
  • Punched-out, crater-like depressions at the crest of interdental papillae.
  • Marginal gingival involvement, with rare extension to attached gingiva and oral mucosa.
  • Grey, pseudomembranous slough covering the lesions.
  • Spontaneous bleeding upon slight stimulation of the gingiva.
  • Fetid odor and increased salivation.

Microbiology

• Mixed Bacterial Infection: NUG is caused by a complex of anaerobic bacteria, often referred to as the fusospirochetal complex, which includes:
  • Treponema vincentii
  • Treponema denticola
  • Treponema macrodentium
  • Fusobacterium nucleatum
  • Prevotella intermedia
  • Porphyromonas gingivalis

Treatment

1. Control of Acute Phase:

   • Clean the wound with an antibacterial agent.
   • Irrigate the lesion with warm water and 5% vol/vol hydrogen peroxide.
   • Prescribe oxygen-releasing mouthwash (e.g., hydrogen peroxide DPF, sodium perborate DPF) to be used thrice daily.
   • Administer oral metronidazole for 3 to 5 days. If sensitive to metronidazole, prescribe penicillin; if sensitive to both, consider erythromycin or clindamycin.
   • Use 2% chlorhexidine in select cases for a short duration.

2. Management of Residual Condition:

   • Remove predisposing local factors (e.g., overhangs).
   • Perform supra- and subgingival scaling.
   • Consider gingivoplasty to correct any residual gingival deformities.

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.

Significant Immune Findings in Periodontal Diseases

Periodontal diseases are associated with various immune responses that can influence disease progression and severity. Understanding these immune findings is crucial for diagnosing and managing different forms of periodontal disease.

Immune Findings in Specific Periodontal Diseases

1. Acute Necrotizing Ulcerative Gingivitis (ANUG):

   • Findings:
     • PMN (Polymorphonuclear neutrophil) chemotactic defect: This defect impairs the ability of neutrophils to migrate to the site of infection, compromising the immune response.
     • Elevated antibody titres to Prevotella intermedia and intermediate-sized spirochetes: Indicates an immune response to specific pathogens associated with the disease.

2. Pregnancy Gingivitis:

   • Findings:
     • No significant immune findings reported: While pregnancy gingivitis is common, it does not show distinct immune abnormalities compared to other forms of periodontal disease.

3. Adult Periodontitis:

   • Findings:
     • Elevated antibody titres to Porphyromonas gingivalis and other periodontopathogens: Suggests a heightened immune response to these specific bacteria.
     • Occurrence of immune complexes in tissues: Indicates an immune reaction that may contribute to tissue damage.
     • Immediate hypersensitivity to gingival bacteria: Reflects an exaggerated immune response to bacterial antigens.
     • Cell-mediated immunity to gingival bacteria: Suggests involvement of T-cells in the immune response against periodontal pathogens.

4. Juvenile Periodontitis:

   • Localized Juvenile Periodontitis (LJP):
     • Findings:
       • PMN chemotactic defect and depressed phagocytosis: Impairs the ability of neutrophils to respond effectively to bacterial invasion.
       • Elevated antibody titres to Actinobacillus actinomycetemcomitans: Indicates an immune response to this specific pathogen.
   • Generalized Juvenile Periodontitis (GJP):
     • Findings:
       • PMN chemotactic defect and depressed phagocytosis: Similar to LJP, indicating a compromised immune response.
       • Elevated antibody titres to Porphyromonas gingivalis: Suggests an immune response to this pathogen.

5. Prepubertal Periodontitis:

   • Findings:
     • PMN chemotactic defect and depressed phagocytosis: Indicates impaired neutrophil function.
     • Elevated antibody titres to Actinobacillus actinomycetemcomitans: Suggests an immune response to this pathogen.

6. Rapid Periodontitis:

   • Findings:
     • Suppressed or enhanced PMN or monocyte chemotaxis: Indicates variability in immune response among individuals.
     • Elevated antibody titres to several gram-negative bacteria: Reflects an immune response to multiple pathogens.

7. Refractory Periodontitis:

   • Findings:
     • Reduced PMN chemotaxis: Indicates impaired neutrophil migration, which may contribute to disease persistence despite treatment.

8. Desquamative Gingivitis:

   • Findings:
     • Diagnostic or characteristic immunopathology in two-thirds of cases: Suggests an underlying immune mechanism.
     • Autoimmune etiology in cases resulting from pemphigus and pemphigoid: Indicates that some cases may be due to autoimmune processes affecting the gingival tissue.