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Periodontology

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.

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.

Gingival Crevicular Fluid (GCF)

Gingival crevicular fluid is an inflammatory exudate found in the gingival sulcus. It plays a significant role in periodontal health and disease.

A. Characteristics of GCF

  • Glucose Concentration: The glucose concentration in GCF is 3-4 times greater than that in serum, indicating increased metabolic activity in inflamed tissues.
  • Protein Content: The total protein content of GCF is much less than that of serum, reflecting its role as an inflammatory exudate.
  • Inflammatory Nature: GCF is present in clinically normal sulci due to the constant low-grade inflammation of the gingiva.

B. Drugs Excreted Through GCF

  • Tetracyclines and Metronidazole: These antibiotics are known to be excreted through GCF, making them effective for localized periodontal therapy.

C. Collection Methods for GCF

GCF can be collected using various techniques, including:

  1. Absorbing Paper Strips/Blotter/Periopaper: These strips absorb fluid from the sulcus and are commonly used for GCF collection.
  2. Twisted Threads: Placing twisted threads around and into the sulcus can help collect GCF.
  3. Micropipettes: These can be used for precise collection of GCF in research settings.
  4. Intra-Crevicular Washings: Flushing the sulcus with a saline solution can help collect GCF for analysis.

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.

Desquamative Gingivitis

  • Characteristics: Desquamative gingivitis is characterized by intense erythema, desquamation, and ulceration of both free and attached gingiva.
  • Associated Diseases:
    • Lichen Planus
    • Pemphigus
    • Pemphigoid
    • Linear IgA Disease
    • Chronic Ulcerative Stomatitis
    • Epidermolysis Bullosa
    • Systemic Lupus Erythematosus (SLE)
    • Dermatitis Herpetiformis

Classification of Cementum According to Schroeder

Cementum is a specialized calcified tissue that covers the roots of teeth and plays a crucial role in periodontal health. According to Schroeder, cementum can be classified into several distinct types based on its cellular composition and structural characteristics. Understanding these classifications is essential for dental professionals in diagnosing and treating periodontal conditions.

Classification of Cementum

  1. Acellular Afibrillar Cementum:

    • Characteristics:
      • Contains neither cells nor collagen fibers.
      • Present in the coronal region of the tooth.
      • Thickness ranges from 1 µm to 15 µm.
    • Function:
      • This type of cementum is thought to play a role in the attachment of the gingiva to the tooth surface.
  2. Acellular Extrinsic Fiber Cementum:

    • Characteristics:
      • Lacks cells but contains closely packed bundles of Sharpey’s fibers, which are collagen fibers that anchor the cementum to the periodontal ligament.
      • Typically found in the cervical third of the roots.
      • Thickness ranges from 30 µm to 230 µm.
    • Function:
      • Provides strong attachment of the periodontal ligament to the tooth, contributing to the stability of the tooth in its socket.
  3. Cellular Mixed Stratified Cementum:

    • Characteristics:
      • Contains both extrinsic and intrinsic fibers and may contain cells.
      • Found in the apical third of the roots, at the apices, and in furcation areas.
      • Thickness ranges from 100 µm to 1000 µm.
    • Function:
      • This type of cementum is involved in the repair and adaptation of the tooth root, especially in response to functional demands and periodontal disease.
  4. Cellular Intrinsic Fiber Cementum:

    • Characteristics:
      • Contains cells but no extrinsic collagen fibers.
      • Primarily fills resorption lacunae, which are areas where cementum has been resorbed.
    • Function:
      • Plays a role in the repair of cementum and may be involved in the response to periodontal disease.
  5. Intermediate Cementum:

    • Characteristics:
      • A poorly defined zone located near the cementoenamel junction (CEJ) of certain teeth.
      • Appears to contain cellular remnants of the Hertwig's epithelial root sheath (HERS) embedded in a calcified ground substance.
    • Function:
      • Its exact role is not fully understood, but it may be involved in the transition between enamel and cementum.

Clinical Significance

  • Importance of Cementum:

    • Understanding the different types of cementum is crucial for diagnosing periodontal diseases and planning treatment strategies.
    • The presence of various types of cementum can influence the response of periodontal tissues to disease and trauma.
  • Cementum in Periodontal Disease:

    • Changes in the thickness and composition of cementum can occur in response to periodontal disease, affecting tooth stability and attachment.

Plaque Formation

Dental plaque is a biofilm that forms on the surfaces of teeth and is a key factor in the development of dental caries and periodontal disease. The process of plaque formation can be divided into three major phases:

1. Formation of Pellicle on the Tooth Surface

  • Definition: The pellicle is a thin, acellular film that forms on the tooth surface shortly after cleaning.
  • Composition: It is primarily composed of salivary glycoproteins and other proteins that are adsorbed onto the enamel surface.
  • Function:
    • The pellicle serves as a protective barrier for the tooth surface.
    • It provides a substrate for bacterial adhesion, facilitating the subsequent stages of plaque formation.

2. Initial Adhesion & Attachment of Bacteria

  • Mechanism:
    • Bacteria in the oral cavity begin to adhere to the pellicle-coated tooth surface.
    • This initial adhesion is mediated by specific interactions between bacterial adhesins (surface proteins) and the components of the pellicle.
  • Key Bacterial Species:
    • Primary colonizers, such as Streptococcus sanguis and Actinomyces viscosus, are among the first to attach.
  • Importance:
    • Successful adhesion is crucial for the establishment of plaque, as it allows for the accumulation of additional bacteria.

3. Colonization & Plaque Maturation

  • Colonization:
    • Once initial bacteria have adhered, they proliferate and create a more complex community.
    • Secondary colonizers, including gram-negative anaerobic bacteria, begin to join the biofilm.
  • Plaque Maturation:
    • As the plaque matures, it develops a three-dimensional structure, with different bacterial species occupying specific niches within the biofilm.
    • The matrix of extracellular polysaccharides and salivary glycoproteins becomes more pronounced, providing structural integrity to the plaque.
  • Coaggregation:
    • Different bacterial species can adhere to one another through coaggregation, enhancing the complexity of the plaque community.

Composition of Plaque

  • Matrix Composition:
    • Plaque is primarily composed of bacteria embedded in a matrix of salivary glycoproteins and extracellular polysaccharides.
  • Implications for Removal:
    • The dense and cohesive nature of this matrix makes it difficult to remove plaque through simple rinsing or the use of sprays.
    • Effective plaque removal typically requires mechanical means, such as brushing and flossing, to disrupt the biofilm structure.

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