PERIOTEST Device in Periodontal Assessment

The PERIOTEST device is a valuable tool used in dentistry to assess the mobility of teeth and the reaction of the periodontium to applied forces. This lecture covers the principles of the PERIOTEST device, its measurement scale, and its clinical significance in evaluating periodontal health.

Function: The PERIOTEST device measures the reaction of the periodontium to a defined percussion force applied to the tooth. This is done using a tapping instrument that delivers a controlled force to the tooth.

Contact Time: The contact time between the tapping head and the tooth varies between 0.3 and 2 milliseconds. This duration is typically shorter for stable teeth compared to mobile teeth, allowing for a quick assessment of tooth stability.

PERIOTEST Scale

The PERIOTEST scale ranges from -8 to +50, with specific ranges indicating different levels of tooth mobility:

Clinical Significance

Assessment of Tooth Mobility:
The PERIOTEST device provides a quantitative measure of tooth mobility, which is essential for diagnosing periodontal disease and assessing the stability of teeth.

Correlation with Other Measurements:
The PERIOTEST values correlate well with:

• Tooth Mobility Assessed with a Metric System: This allows for a standardized approach to measuring mobility, enhancing the reliability of assessments.

• Degree of Periodontal Disease and Alveolar Bone Loss: Higher mobility readings often indicate more severe periodontal disease and greater loss of supporting bone, making the PERIOTEST a useful tool in monitoring disease progression.

Treatment Planning:
Understanding the mobility of teeth can aid in treatment planning, including decisions regarding periodontal therapy, splinting of mobile teeth, or extraction in cases of severe mobility.

Connective Tissue of the Gingiva and Related Cellular Components

The connective tissue of the gingiva, known as the lamina propria, plays a crucial role in supporting the gingival epithelium and maintaining periodontal health. This lecture will cover the structure of the lamina propria, the types of connective tissue fibers present, the role of Langerhans cells, and the changes observed in the periodontal ligament (PDL) with aging.

Structure of the Lamina Propria

1. Layers of the Lamina Propria:

   • The lamina propria consists of two distinct layers:
     1. Papillary Layer:
        • The upper layer that interdigitates with the epithelium, containing finger-like projections that increase the surface area for exchange of nutrients and waste.
     2. Reticular Layer:
        • The deeper layer that provides structural support and contains larger blood vessels and nerves.

2. Types of Connective Tissue Fibers:

   • The lamina propria contains three main types of connective tissue fibers:

     1. Collagen Fibers:
        • Type I Collagen: Forms the bulk of the lamina propria and provides tensile strength to the gingival fibers, essential for maintaining the integrity of the gingiva.
     2. Reticular Fibers:
        • These fibers provide a supportive network within the connective tissue.
     3. Elastic Fibers:
        • Contribute to the elasticity and flexibility of the gingival tissue.

   • Type IV Collagen:

     • Found branching between the Type I collagen bundles, it is continuous with the fibers of the basement membrane and the walls of blood vessels.

Langerhans Cells

1. Description:

   • Langerhans cells are dendritic cells located among keratinocytes at all suprabasal levels of the gingival epithelium.
   • They belong to the mononuclear phagocyte system and play a critical role in immune responses.

2. Function:

   • Act as antigen-presenting cells for lymphocytes, facilitating the immune reaction.
   • Contain specific granules known as Birbeck’s granules and exhibit marked ATP activity.

3. Location:

   • Found in the oral epithelium of normal gingiva and in small amounts in the sulcular epithelium.
   • Absent from the junctional epithelium of normal gingiva.

Changes in the Periodontal Ligament (PDL) with Aging

1. Aging Effects:
   • With aging, several changes have been reported in the periodontal ligament:
     • Decreased Numbers of Fibroblasts: This reduction can lead to impaired healing and regeneration of the PDL.
     • Irregular Structure: The PDL may exhibit a more irregular structure, paralleling changes in the gingival connective tissues.
     • Decreased Organic Matrix Production: This can affect the overall health and function of the PDL.
     • Epithelial Cell Rests: There may be a decrease in the number of epithelial cell rests, which are remnants of the Hertwig's epithelial root sheath.
     • Increased Amounts of Elastic Fibers: This change may contribute to the altered mechanical properties of the PDL.

Progression from Gingivitis to Periodontitis

The transition from gingivitis to periodontitis is a critical process in periodontal disease progression. This lecture will outline the key stages involved in this progression, highlighting the changes in microbial composition, host response, and tissue alterations.

Pathway of Progression

1. Establishment and Maturation of Supragingival Plaque:

   • The process begins with the formation of supragingival plaque, which is evident in gingivitis.
   • As this plaque matures, it becomes more complex and can lead to changes in the surrounding tissues.

2. Migration of Periodontopathogenic Bacteria:

   • When the microbial load overwhelms the local host immune response, pathogenic bacteria migrate subgingivally (below the gum line).
   • This migration establishes a subgingival niche that is conducive to the growth of periodontopathogenic bacteria.

Initial Lesion

• Timeline:
  • The initial lesion, characterized by subclinical gingivitis, appears approximately 2 to 4 days after the colonization of the gingival sulcus by bacteria.
• Clinical Manifestations:
  • Vasculitis: Inflammation of blood vessels in the gingival tissue.
  • Exudation of Serous Fluid: Increased flow of gingival crevicular fluid (GCF) from the gingival sulcus.
  • Increased PMN Migration: Polymorphonuclear neutrophils (PMNs) migrate into the sulcus in response to the inflammatory process.
  • Alteration of Junctional Epithelium: Changes occur at the base of the pocket, affecting the integrity of the junctional epithelium.
  • Collagen Dissolution: Perivascular collagen begins to dissolve, contributing to tissue breakdown.

Early Lesion

• Timeline:
  • The early lesion forms within 4 to 7 days after the initial lesion due to the continued accumulation of bacterial plaque.
• Characteristics:
  • Leukocyte Accumulation: There is a significant increase in leukocytes at the site of acute inflammation, indicating an ongoing immune response.
  • Cytopathic Alterations: Resident fibroblasts undergo cytopathic changes, affecting their function and viability.
  • Collagen Loss: Increased collagen loss occurs within the marginal gingiva, contributing to tissue destruction.
  • Proliferation of Basal Cells: The basal cells of the junctional epithelium proliferate in response to the inflammatory environment.

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.

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.

Trauma from Occlusion

Trauma from occlusion refers to the injury sustained by periodontal tissues when occlusal forces exceed their adaptive capacity.

1. Trauma from Occlusion

• This term describes the injury that occurs to periodontal tissues when the forces exerted during occlusion (the contact between opposing teeth) exceed the ability of those tissues to adapt.
• Traumatic Occlusion: An occlusion that produces such injury is referred to as a traumatic occlusion. This can result from various factors, including malocclusion, excessive occlusal forces, or parafunctional habits (e.g., bruxism).

2. Clinical Signs of Trauma to the Periodontium

The most common clinical sign of trauma to the periodontium is:

• Increased Tooth Mobility: As the periodontal tissues are subjected to excessive forces, they may become compromised, leading to increased mobility of the affected teeth. This is often one of the first observable signs of trauma from occlusion.

3. Radiographic Signs of Trauma from Occlusion

Radiographic examination can reveal several signs indicative of trauma from occlusion:

1. Increased Width of Periodontal Space:

   • The periodontal ligament space may appear wider on radiographs due to the increased forces acting on the tooth, leading to a loss of attachment and bone support.

2. Vertical Destruction of Inter-Dental Septum:

   • Trauma from occlusion can lead to vertical bone loss in the inter-dental septa, which may be visible on radiographs as a reduction in bone height between adjacent teeth.

3. Radiolucency and Condensation of the Alveolar Bone:

   • Areas of radiolucency may indicate bone loss, while areas of increased radiopacity (condensation) can suggest reactive changes in the bone due to the stress of occlusal forces.

4. Root Resorption:

   • In severe cases, trauma from occlusion can lead to root resorption, which may be observed as a loss of root structure on radiographs.