• MAP formula: Diastolic + 1/3 Pulse Pressure
• Pulse Pressure: Systolic – Diastolic
• Sphygmomanometer readings: Slightly higher than intra-arterial
• J Curve Phenomenon: Excessive BP lowering → adverse cardiac events
• Best drug for angina with HTN: Metoprolol
• Contraindicated in diabetic HTN: Thiazides
• ACEI side effect: Hyperkalemia
• Aliskiren: Direct renin antagonist

• Plaque Biofilm:
  • Quorum sensing: bacterial communication
  • Co-aggregation: Gram-negative adherence
• Microbial Shift (Health → Disease):
  • Facultative → Obligate anaerobes
  • Fermenting → Proteolytic
  • Cocci → Rods
  • Non-motile → Motile
• Immunoglobulins:
  • Saliva: IgA
  • GCF: IgG
• Interleukins & MMPs:
  • IL-1β: Most potent bone-destructive cytokine
  • MMP-8 & MMP-1: Collagenases
  • MMP-2 & MMP-9: Gelatinases
  • Activated by neutrophil proteases (e.g., cathepsin G)

Stage I: Initial Lesion

• Cellular Infiltrate: Polymorphonuclear neutrophils (PMNs) present
• Timeframe: Develops within 2-4 days of plaque accumulation
• Characteristics: Subclinical changes, increased vascular permeability

Stage III: Established Lesion

• Duration: Develops after 2-3 weeks of continuous plaque exposure
• Cellular Changes: Plasma cell dominance, collagen destruction
• Clinical Features: Frank gingivitis with erythema, edema, and bleeding on probing

ANUG (Acute Necrotizing Ulcerative Gingivitis)

Microbiology

• Primary Organisms: Spirochetes and Prevotella species
• Pathogenesis: Opportunistic infection in compromised host defense

Demographics

• Primary Population: Young adults (20-30 years)
• Risk Factors: Stress, smoking, malnutrition, immunocompromise

Clinical Presentation

• Pathognomonic Sign: Crater-like depressions on interdental papilla
• Additional Features: Spontaneous bleeding, halitosis, lymphadenopathy
• Pain: Severe, spontaneous gingival pain

Staging System (7 Stages)

1. Stages 1-2: Necrotizing Ulcerative Gingivitis (NUG)
2. Stages 3-4: Necrotizing Ulcerative Periodontitis (NUP)
3. Stages 5-6: Necrotizing Stomatitis
4. Stage 7: Noma (cancrum oris) - life-threatening condition

Hypercementosis

Hypercementosis is a dental condition characterized by the excessive deposition of cementum on the roots of teeth. This condition can have various clinical implications and is associated with several underlying factors. Understanding hypercementosis is essential for dental professionals in diagnosing and managing related conditions.

Characteristics of Hypercementosis

1. Definition:

   • Hypercementosis is defined as a generalized thickening of the cementum, often accompanied by nodular enlargement of the apical third of the root. It can also manifest as spike-like excrescences known as cemental spikes.

2. Forms of Hypercementosis:

   • Generalized Type: Involves a uniform thickening of cementum across multiple teeth.
   • Localized Type: Characterized by nodular enlargements or cemental spikes, which may result from:
     • Coalescence of cementicles adhering to the root.
     • Calcification of periodontal fibers at their insertion points into the cementum.

Radiographic Appearance

• Radiographic Features:
  • On radiographs, hypercementosis is identified by the presence of a radiolucent shadow of the periodontal ligament and a radiopaque lamina dura surrounding the area of hypercementosis, similar to normal cementum.
  • Differentiation:
    • Hypercementosis can be differentiated from other conditions such as periapical cemental dysplasia, condensing osteitis, and focal periapical osteopetrosis, as these entities are located outside the shadow of the periodontal ligament and lamina dura.

Etiology of Hypercementosis

• Varied Etiology:

  • The exact cause of hypercementosis is not completely understood, but several factors have been identified:
    • Spike-like Hypercementosis: Often results from excessive tension due to orthodontic appliances or occlusal forces.
    • Generalized Hypercementosis: Can occur in various circumstances, including:
      • Teeth Without Antagonists: In cases where teeth lack opposing teeth, hypercementosis may develop as a compensatory mechanism to keep pace with excessive tooth eruption.
      • Low-Grade Periapical Irritation: Associated with pulp disease, where hypercementosis serves as compensation for the loss of fibrous attachment to the tooth.

• Systemic Associations:

  • Hypercementosis may also be observed in systemic conditions, including:
    • Paget’s Disease: Characterized by hypercementosis of the entire dentition.
    • Other Conditions: Acromegaly, arthritis, calcinosis, rheumatic fever, and thyroid goiter have also been linked to hypercementosis.

Clinical Implications

1. Diagnosis:

   • Recognizing hypercementosis is important for accurate diagnosis and treatment planning. Radiographic evaluation is essential for distinguishing hypercementosis from other dental pathologies.

2. Management:

   • While hypercementosis itself may not require treatment, it can complicate dental procedures such as extractions or endodontic treatments. Understanding the condition can help clinicians anticipate potential challenges.

3. Monitoring:

   • Regular monitoring of patients with known systemic conditions associated with hypercementosis is important to manage any potential complications.

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