Gingival Anatomy

• Attached Gingiva Width: Greatest in maxillary incisors (3.5 – 4.5mm) and mandibular incisors (3.3 – 3.9mm)
• Least Width: Maxillary 1st premolars (1.9mm) and mandibular premolars (1.8mm)
• Biological Width: Connective tissue attachment (1.07mm) + Epithelial attachment (0.97mm) = ~2mm
• Oral Epithelium: 0.2 – 0.3mm thick, can be keratinized/parakeratinized

Junctional Epithelium (JE)

• Attached to enamel by hemidesmosomes
• Keratinocytes attached by desmosomes
• Internal basal lamina → tooth surface
• External basal lamina → gingival connective tissue

Cementum

• Maximum thickness: Apical third & furcation (150 – 200μm)
• Coronal half: 16 – 60μm
• Acellular cementum: First formed, covers cervical third
• Cellular cementum: Forms when tooth reaches occlusal plane

PERIODONTAL LIGAMENT (PDL) FIBERS

Principal Fibers (Type I Collagen)

1. Oblique fibers: Largest group, bear vertical forces
2. Alveolar crest fibers: Prevent tooth extrusion
3. Transseptal fibers: Only fibers reconstructed after bone destruction (considered gingival fibers)

Key Point

• Reticular fibers: Type III collagen

• Angulation vs Adaptation:
  • Angulation: Angle between blade face and tooth surface.
  • Adaptation: Relationship of blade’s working end to tooth surface.
• Curettes:
  • Gracey: Blade offset at 60°.
  • Universal: Blade angle at 90°.
  • After Five: Extended shank by 3 mm; available in all Gracey numbers except 9 – 10.
  • Mini Five: Blade half the length of conventional curette.
  • Langer Curette: Gracey curette modified with universal blade angle.
• Scaling & Sharpening:
  • Blade angulation for scaling: 45 – 90°; for curettage: >90°.
  • Sharpening angle: 100 – 110°.
  • Chisel scaler: Push motion; Hoe scaler: Blade bent at 99°.
  • Sickle scaler blade-to-shank angle: 70°.
• Microsurgery:
  • Instrument weight: 15 – 20 g.
  • Principles: Butt joint approximation, enhanced motor skills, minimal trauma.
• Suturing:
  • Needle entry: Right angle, 2 – 3 mm from incision.

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.

Hormonal Effects on Periodontal Tissues

Optimal Treatment Timing

• Safest Period: Early second trimester (weeks 14-20)
• Rationale: Organogenesis complete, uterine size manageable

Clinical Manifestations

• Most Striking Feature: Pronounced ease of bleeding (pregnancy gingivitis)
• Mechanism: Increased vascular permeability due to hormonal changes

Microbial Changes

• Bacterial Shift: Increased Prevotella intermedia
• Hormonal Influence: Estrogen and progesterone serve as growth factors for certain bacteria

🧬 Blood Disorders

• Polycythemia vera: Common cause of Budd – Chiari
• PNH: Rare cause of Budd – Chiari
• Thalassemia & Hemolytic anemia: Lead to unconjugated hyperbilirubinemia
• Anemia: Can cause high-output heart failure
• Hemophilia A: Deficiency of Factor VIII
• ITP vs TTP: ITP = isolated thrombocytopenia; TTP = microangiopathy