Stippling of the Gingiva

• Stippling refers to the textured surface of the gingiva that resembles the skin of an orange. This characteristic is best observed when the gingiva is dried.

• Characteristics:

  • Location:
    • The attached gingiva is typically stippled, while the marginal gingiva is not.
    • The central portion of the interdental gingiva may exhibit stippling, but its marginal borders are usually smooth.
  • Surface Variation:
    • Stippling is generally less prominent on the lingual surfaces compared to the facial surfaces and may be absent in some individuals.
  • Age-Related Changes:
    • Stippling is absent in infancy, begins to appear around 5 years of age, increases until adulthood, and may start to disappear in old age.

Attached Gingiva

• Definition: The attached gingiva is the portion of the gingiva that is firmly bound to the underlying alveolar bone and extends from the free gingival groove to the mucogingival junction, where it meets the alveolar mucosa.

• Characteristics:

  • Structure:
    • The attached gingiva is classified as a mucoperiosteum, tightly bound to the underlying alveolar bone.
  • Width:
    • The width of the attached gingiva is greatest in the incisor region, measuring approximately:
      • 3.5 – 4.5 mm in the maxilla
      • 3.3 – 3.9 mm in the mandible
    • It is narrower in the posterior segments, measuring about:
      • 1.9 mm in the maxillary first premolars
      • 1.8 mm in the mandibular first premolars.
  • Histological Features:
    • The attached gingiva is thick and keratinized (or parakeratinized) and is classified as masticatory mucosa.
    • Masticatory mucosa is characterized by a keratinized epithelium and a thick lamina propria, providing resistance to mechanical forces.

Masticatory vs. Lining Mucosa

• Masticatory Mucosa:

  • Found in areas subject to high compression and friction, such as the gingiva and hard palate.
  • Characterized by keratinized epithelium and a thick lamina propria, making it resistant to masticatory forces.

• Lining Mucosa:

  • Mobile, distensible, and non-keratinized.
  • Found in areas such as the lips, cheeks, alveolus, floor of the mouth, ventral surface of the tongue, and soft palate.

• Specialized Mucosa:

  • Found on the dorsum of the tongue, adapted for specific functions such as taste.

Aggressive periodontitis (AP) is a multifactorial, severe, and rapidly progressive form of periodontitis that primarily affects younger patients. It is characterized by a unique set of clinical and microbiological features that distinguish it from other forms of periodontal disease.

Key Characteristics

• Rapid Progression: AP is marked by a swift deterioration of periodontal tissues.
• Age Group: Primarily affects adolescents and young adults, but can occur at any age.
• Multifactorial Etiology: Involves a combination of microbiological, immunological, genetic, and environmental factors.

Other Findings

• Presence of Aggregatibacter actinomycetemcomitans (A.a.) in diseased sites.
• Abnormal host responses, including impaired phagocytosis and chemotaxis.
• Hyperresponsive macrophages leading to exaggerated inflammatory responses.
• The disease may exhibit self-arresting tendencies in some cases.

Classification

Aggressive periodontitis can be classified into two main types:

1. Localized Aggressive Periodontitis (LAP): Typically affects the permanent molars and incisors, often with localized attachment loss.
2. Generalized Aggressive Periodontitis (GAP): Involves more widespread periodontal tissue destruction.

Risk Factors

Microbiological Factors

• Aggregatibacter actinomycetemcomitans: A primary pathogen associated with LAP, producing a potent leukotoxin that kills neutrophils.
• Different strains of A.a. produce varying levels of leukotoxin, with highly toxic strains more prevalent in affected individuals.

Immunological Factors

• Human Leukocyte Antigens (HLAs): HLA-A9 and B-15 are candidate markers for aggressive periodontitis.
• Defective neutrophil function leads to impaired chemotaxis and phagocytosis.
• Hyper-responsive macrophage phenotype, characterized by elevated levels of PGE2 and IL-1β, may contribute to connective tissue breakdown and bone loss.

Genetic Factors

• Familial clustering of neutrophil abnormalities suggests a genetic predisposition.
• Genetic control of antibody responses to A.a., with variations in the ability to produce protective IgG2 antibodies.

Environmental Factors

• Smoking is a significant risk factor, with smokers experiencing more severe periodontal destruction compared to non-smokers.

Treatment Approaches

General Considerations

• Treatment strategies depend on the type and extent of periodontal destruction.
• GAP typically has a poorer prognosis compared to LAP, as it is less likely to enter spontaneous remission.

Conventional Periodontal Therapy

• Patient Education: Informing patients about the disease and its implications.
• Oral Hygiene Instructions: Reinforcing proper oral hygiene practices.
• Scaling and Root Planing: Removal of plaque and calculus to control local factors.

Surgical Resection Therapy

• Aimed at reducing or eliminating pocket depth.
• Contraindicated in cases of severe horizontal bone loss due to the risk of increased tooth mobility.

Regenerative Therapy

• Potential for regeneration is promising in AP cases.
• Techniques include open flap surgical debridement, root surface conditioning with tetracycline, and the use of allogenic bone grafts.
• Recent advances involve the use of enamel matrix proteins to promote cementum regeneration and new attachment.

Antimicrobial Therapy

• Often required as adjunctive treatment to eliminate A.a. from periodontal tissues.
• Tetracycline: Administered in various regimens to concentrate in periodontal tissues and inhibit A.a. growth.
• Combination Therapy: Metronidazole combined with amoxicillin has shown efficacy alongside periodontal therapy.
• Doxycycline: Used at a dose of 100 mg/day.
• Chlorhexidine (CHX): Irrigation and home rinsing to control bacterial load.

Host Modulation

• Involves the use of sub-antimicrobial dose doxycycline (SDD) to prevent periodontal attachment loss by modulating the activity of matrix metalloproteinases (MMPs), particularly collagenase and gelatinase.

Changes in Plaque pH After Sucrose Rinse

The pH of dental plaque is a critical factor in the development of dental caries and periodontal disease. Key findings from various studies that investigated the changes in plaque pH following carbohydrate rinses, particularly focusing on sucrose and glucose.

Key Findings from Studies

1. Monitoring Plaque pH Changes:

   • A study reported that changes in plaque pH after a sucrose rinse were monitored using plaque sampling, antimony and glass electrodes, and telemetry.
   • Results:
     • The minimum pH at approximal sites (areas between teeth) was approximately 0.7 pH units lower than that on buccal surfaces (outer surfaces of the teeth).
     • The pH at the approximal site remained below resting levels for over 120 minutes.
     • The area under the pH response curves from approximal sites was five times greater than that from buccal surfaces, indicating a more significant and prolonged acidogenic response in interproximal areas.

2. Stephan's Early Studies (1935):

   • Method: Colorimetric measurement of plaque pH suspended in water.
   • Findings:
     • The pH of 211 plaque samples ranged from 4.6 to 7.0.
     • The mean pH value was found to be 5.9, indicating a generally acidic environment in dental plaque.

3. Stephan's Follow-Up Studies (1940):

   • Method: Use of an antimony electrode to measure in situ plaque pH after rinsing with sugar solutions.
   • Findings:
     • A 10% solution of glucose or sucrose caused a rapid drop in plaque pH by about 2 units within 2 to 5 minutes, reaching values between 4.5 and 5.0.
     • A 1% lactose solution lowered the pH by 0.3 units, while a 1% glucose solution caused a drop of 1.5 units.
     • A 1% boiled starch solution resulted in a reduction of 1.5 pH units over 51 minutes.
     • In all cases, the pH tended to return to initial values within approximately 2 hours.

4. Investigation of Proximal Cavities:

   • Studies of actual proximal cavities opened mechanically showed that the lowest pH values ranged from 4.6 to 4.1.
   • After rinsing with a 10% glucose or sucrose solution, the pH in the plaque dropped to between 4.5 and 5.0 within 2 to 5 minutes and gradually returned to baseline levels within 1 to 2 hours.

Implications

• The studies highlight the significant impact of carbohydrate exposure, particularly sucrose and glucose, on the pH of dental plaque.
• The rapid drop in pH following carbohydrate rinses indicates an acidogenic response from plaque microorganisms, which can contribute to enamel demineralization and caries development.
• The prolonged acidic environment in approximal sites suggests that these areas may be more susceptible to caries due to the slower recovery of pH levels.

Localized Aggressive Periodontitis and Necrotizing Ulcerative Gingivitis

Localized Aggressive Periodontitis (LAP)

Localized aggressive periodontitis, previously known as localized juvenile periodontitis, is characterized by specific microbial profiles and clinical features.

• Microbiota Composition:
  • The microbiota associated with LAP is predominantly composed of:
    • Gram-Negative, Capnophilic, and Anaerobic Rods.
  • Key Organisms:
    • Actinobacillus actinomycetemcomitans: The main organism involved in LAP.
    • Other significant organisms include:
      • Porphyromonas gingivalis
      • Eikenella corrodens
      • Campylobacter rectus
      • Bacteroides capillus
      • Spirochetes (various species).
  • Viral Associations:
    • Herpes viruses, including Epstein-Barr Virus-1 (EBV-1) and Human Cytomegalovirus (HCMV), have also been associated with LAP.

Necrotizing Ulcerative Gingivitis (NUG)

• Microbial Profile:
  • NUG is characterized by high levels of:
    • Prevotella intermedia
    • Spirochetes (various species).
• Clinical Features:
  • NUG presents with necrosis of the gingival tissue, pain, and ulceration, often accompanied by systemic symptoms.

Microbial Shifts in Periodontal Disease

When comparing the microbiota across different states of periodontal health, a distinct microbial shift can be identified as the disease progresses from health to gingivitis to periodontitis:

1. From Gram-Positive to Gram-Negative:

   • Healthy gingival sites are predominantly colonized by gram-positive bacteria, while diseased sites show an increase in gram-negative bacteria.

2. From Cocci to Rods (and Later to Spirochetes):

   • In health, cocci (spherical bacteria) are prevalent. As the disease progresses, there is a shift towards rod-shaped bacteria, and in advanced stages, spirochetes become more prominent.

3. From Non-Motile to Motile Organisms:

   • Healthy sites are often dominated by non-motile bacteria, while motile organisms increase in number as periodontal disease develops.

4. From Facultative Anaerobes to Obligate Anaerobes:

   • In health, facultative anaerobes (which can survive with or without oxygen) are common. In contrast, obligate anaerobes (which thrive in the absence of oxygen) become more prevalent in periodontal disease.

5. From Fermenting to Proteolytic Species:

   • The microbial community shifts from fermentative bacteria, which primarily metabolize carbohydrates, to proteolytic species that break down proteins, contributing to tissue destruction and inflammation.

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.

Classification of Periodontal Pockets

Periodontal pockets are an important aspect of periodontal disease, reflecting the health of the supporting structures of the teeth. Understanding the classification of these pockets is essential for diagnosis, treatment planning, and management of periodontal conditions.

Classification of Pockets

1. Gingival Pocket:

   • Also Known As: Pseudo-pocket.
   • Formation:
     • Formed by gingival enlargement without destruction of the underlying periodontal tissues.
     • The sulcus is deepened due to the increased bulk of the gingiva.
   • Characteristics:
     • There is no destruction of the supporting periodontal tissues.
     • Typically associated with conditions such as gingival hyperplasia or inflammation.

2. Periodontal Pocket:

   • Definition: A pocket that results in the destruction of the supporting periodontal tissues, leading to the loosening and potential exfoliation of teeth.
   • Classification Based on Location:
     • Suprabony Pocket:
       • The base of the pocket is coronal to the alveolar bone.
       • The pattern of bone destruction is horizontal.
       • The transseptal fibers are arranged horizontally in the space between the base of the pocket and the alveolar bone.
     • Infrabony Pocket:
       • The base of the pocket is apical to the alveolar bone, meaning the pocket wall lies between the bone and the tooth.
       • The pattern of bone destruction is vertical.
       • The transseptal fibers are oblique rather than horizontal.

Classification of Periodontal Pockets

1. Suprabony Pocket (Supracrestal or Supraalveolar):

   • Location: Base of the pocket is coronal to the alveolar bone.
   • Bone Destruction: Horizontal pattern of bone loss.
   • Transseptal Fibers: Arranged horizontally.

2. Infrabony Pocket (Intrabony, Subcrestal, or Intraalveolar):

   • Location: Base of the pocket is apical to the alveolar bone.
   • Bone Destruction: Vertical pattern of bone loss.
   • Transseptal Fibers: Arranged obliquely.

Classification of Pockets According to Involved Tooth Surfaces

1. Simple Pocket:

   • Definition: Involves only one tooth surface.
   • Example: A pocket that is present only on the buccal surface of a tooth.

2. Compound Pocket:

   • Definition: A pocket present on two or more surfaces of a tooth.
   • Example: A pocket that involves both the buccal and lingual surfaces.

3. Spiral Pocket:

   • Definition: Originates on one tooth surface and twists around the tooth to involve one or more additional surfaces.
   • Example: A pocket that starts on the mesial surface and wraps around to the distal surface.