ANUG symptoms: Metallic taste, Pasty saliva, Punched – out papilla

Red complex: Porphyromonas, Treponema denticola, Tannerella forsythia

Drug enlargement: Phenytoin = Fibrotic, Cyclosporine = Vascular

Healing times: 2 – 7 (epithelialization), 21 (collagen), 1 week (flap attachment)

Bone graft memory: FDBA = Conductive, DFDBA = Inductive

Diagnosis Criteria

• FBS ≥ 126 mg/dL
• HbA1C > 6.5%
• eAG based on HbA1C
• Oral GTT 2-hr post-load: 140–199 mg/dL → Impaired Glucose Tolerance
• HbA1C 5.7–6.4% → Pre-diabetic range

Zones of Periodontal Disease

Listgarten described four distinct zones that can be observed in periodontal lesions. These zones may blend with each other and may not be present in every case.

Zones of Periodontal Disease

1. Zone 1: Bacterial Zone

   • Description: This is the most superficial zone, consisting of a diverse array of bacteria.
   • Characteristics:
     • The bacterial zone is primarily composed of various microbial species, including both pathogenic and non-pathogenic bacteria.
     • This zone is critical in the initiation and progression of periodontal disease, as the presence of specific bacteria can trigger inflammatory responses in the host.

2. Zone 2: Neutrophil Rich Zone

   • Description: This zone contains numerous leukocytes, predominantly neutrophils.
   • Characteristics:
     • The neutrophil-rich zone is indicative of the body’s immune response to the bacterial invasion.
     • Neutrophils are the first line of defense and play a crucial role in phagocytosing bacteria and releasing inflammatory mediators.
     • The presence of a high number of neutrophils suggests an acute inflammatory response, which is common in active periodontal disease.

3. Zone 3: Necrotic Zone

   • Description: This zone consists of disintegrated tissue cells, fibrillar material, remnants of collagen fibers, and spirochetes.
   • Characteristics:
     • The necrotic zone reflects tissue destruction and is characterized by the presence of dead or dying cells.
     • Fibrillar material and remnants of collagen fibers indicate the breakdown of the extracellular matrix, which is essential for maintaining periodontal tissue integrity.
     • Spirochetes, which are associated with more aggressive forms of periodontal disease, can also be found in this zone, contributing to the necrotic process.

4. Zone 4: Zone of Spirochetal Infiltration

   • Description: This zone consists of well-preserved tissue that is infiltrated with large and medium spirochetes.
   • Characteristics:
     • The zone of spirochetal infiltration indicates a more chronic phase of periodontal disease, where spirochetes invade the connective tissue.
     • The presence of well-preserved tissue suggests that while spirochetes are present, the tissue has not yet undergone extensive necrosis.
     • This zone is significant as it highlights the role of spirochetes in the pathogenesis of periodontal disease, particularly in cases of necrotizing periodontal diseases.

Gingivitis

Gingivitis is an inflammatory condition of the gingiva that can progress through several distinct stages. Understanding these stages is crucial for dental professionals in diagnosing and managing periodontal disease effectively. This lecture will outline the four stages of gingivitis, highlighting the key pathological changes that occur at each stage.

I. Initial Lesion

• Characteristics:
  • Increased Permeability: The microvascular bed in the gingival tissues becomes more permeable, allowing for the passage of fluids and immune cells.
  • Increased GCF Flow: There is an increase in the flow of gingival crevicular fluid (GCF), which is indicative of inflammation and immune response.
  • PMN Cell Migration: The migration of polymorphonuclear leukocytes (PMNs) is facilitated by various adhesion molecules, including:
    • Intercellular Cell Adhesion Molecule 1 (ICAM-1)
    • E-selectin (ELAM-1) in the dentogingival vasculature.
• Clinical Implications: This stage marks the beginning of the inflammatory response, where the body attempts to combat the initial bacterial insult.

II. Early Lesion

• Characteristics:

  • Leukocyte Infiltration: There is significant infiltration of leukocytes, particularly lymphocytes, into the connective tissue of the junctional epithelium.
  • Fibroblast Degeneration: Several fibroblasts within the lesion exhibit signs of degeneration, indicating tissue damage.
  • Proliferation of Basal Cells: The basal cells of the junctional and sulcular epithelium begin to proliferate, which may be a response to the inflammatory process.

• Clinical Implications: This stage represents a transition from initial inflammation to more pronounced tissue changes, with the potential for further progression if not managed.

III. Established Lesion

• Characteristics:

  • Predominance of Plasma Cells and B Lymphocytes: There is a marked increase in plasma cells and B lymphocytes, indicating a more advanced immune response.
  • Increased Collagenolytic Activity: The activity of collagen-degrading enzymes increases, leading to the breakdown of collagen fibers in the connective tissue.
  • B Cell Subclasses: The B cells present in the established lesion are predominantly of the IgG1 and IgG3 subclasses, which are important for the immune response.

• Clinical Implications: This stage is characterized by chronic inflammation, and if left untreated, it can lead to further tissue destruction and the transition to advanced lesions.

IV. Advanced Lesion

• Characteristics:

  • Loss of Connective Tissue Attachment: There is significant loss of connective tissue attachment to the teeth, which can lead to periodontal pocket formation.
  • Alveolar Bone Loss: Extensive damage occurs to the alveolar bone, contributing to the overall loss of periodontal support.
  • Extensive Damage to Collagen Fibers: The collagen fibers in the gingival tissues are extensively damaged, further compromising the structural integrity of the gingiva.
  • Predominance of Plasma Cells: Plasma cells remain predominant, indicating ongoing immune activity and inflammation.

• Clinical Implications: This stage represents the transition from gingivitis to periodontitis, where irreversible damage can occur. Early intervention is critical to prevent further progression and loss of periodontal support.

Aggressive Periodontitis (formerly Juvenile Periodontitis)

• Historical Names: Previously referred to as periodontosis, deep cementopathia, diseases of eruption, Gottleib’s diseases, and periodontitis marginalis progressive.
• Risk Factors:
  • High frequency of Actinobacillus actinomycetemcomitans.
  • Immune defects (functional defects of PMNs and monocytes).
  • Autoimmunity and genetic factors.
  • Environmental factors, including smoking.
• Clinical Features:
  • Vertical loss of alveolar bone around the first molars and incisors, typically beginning around puberty.
  • Bone loss patterns often described as "target" or "bull" shaped lesions.