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

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%.

Classification by Extent

• Generalized: >30% sites affected

Classification by Severity

• Moderate: 3 – 4 mm bone loss
• Severe: >5 mm bone loss

Aggressive Periodontitis

• Rate: 3 – 4 times faster bone loss than chronic
• Classic sign: Arc – shaped bone loss (distal 2nd premolar to mesial 2nd molar)
• Associated: HLA A9 and B15 antigens
• Receptor defect: Poorly functional monocyte FcγR2

Pain Characteristics

• Periodontal pocket pain: "Deep in bone" feeling

Bone Loss Patterns

• Radius of action: 1.5 – 2.5 mm (Page & Schroeder)
• Reverse architecture: Facial/lingual plates lost, radicular bone preserved
• TFO signs: Increased mobility (first clinical sign)

• Attached Gingiva Width:
  • Maxillary incisors: 3.5 – 4.5 mm
  • Mandibular incisors: 3.3 – 3.9 mm
  • Least in premolars (~1.8 – 1.9 mm)
• Cementum:
  • Thickest in apical third and furcation (150 – 200 µm)
  • Acellular cementum: cervical third
  • Cellular cementum: forms after occlusal contact
• PDL Fibres:
  • Principal: Type I collagen
  • Reticular: Type III collagen
  • Oblique fibres: Largest group, resist vertical forces
  • Transseptal fibres: Reconstructed post bone loss
  • Alveolar crest fibres: Prevent extrusion

• 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.

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.