Stage 1: Initial Lesion

• 2 – 4 days after plaque accumulation

Stage 2: Early Lesion

• Timeline: 4 – 7 days after plaque accumulation
• T – lymphocyte dominance

Stage 3: Established Lesion

• Characteristic: Plasma cells and B – lymphocytes dominance

Bleeding on Probing (BOP)

• Appears earlier than visual signs
• Absence = good negative predictor of attachment loss

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.

🧪 GERD & Barrett’s Esophagus

🧫 Peptic Ulcer

• Commonest site: Duodenal bulb (1st part)
• Most frequent complication: Hemorrhage
• Best residual H. pylori test: Urea breath test
• Treatment for Zollinger – Ellison syndrome: PPI

• Bone Defects:
  • Most common: Osseous craters.
  • Best graft success: Three-walled defects.
  • Bone graft types:
    • Autogenous cancellous: Most osteogenic.
    • Xenograft: From different species.
  • Osteoplasty: Recontouring without removing supporting bone.
  • Osteotomy: Removes supporting bone.
• Implants:
  • Minimum 5 mm from mental foramen.
  • Blade implants: Linkow; Cylindrical: Schroeder.
  • Micro-movement >150 µm: Fibrous tissue formation.
  • Connective tissue near implant: No blood vessels, many fibroblasts.
  • Probing: Use plastic probes; max force = 25 N.
  • Florida probe tip: 0.4 mm.

Morphological Classification

Three-Wall Defect (Intrabony Defect)

• Description: Defect contained by three bony walls
• Prognosis: Best regenerative potential
• Treatment: Ideal candidate for GTR procedures

Two-Wall Defect (Crater)

• Description: Defect between two adjacent teeth
• Characteristics: Interdental bone loss
• Prevalence: Most common osseous defect in chronic periodontitis

One-Wall Defect (Hemiseptum)

• Description: Defect with only one remaining bony wall
• Prognosis: Poorest regenerative potential
• Treatment: Often requires resective therapy

Bone Loss Patterns

Horizontal Bone Loss

• Associated Pocket Type: Suprabony pocket
• Pattern: Uniform reduction in alveolar bone height
• Radiographic Appearance: Horizontal radiolucency

Vertical/Angular Bone Loss

• Associated Pocket Type: Infrabony pocket
• Pattern: Uneven bone destruction
• Clinical Significance: More complex treatment requirements

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.