Anatomy and Histology of the Periodontium

Gingiva (normal clinical appearance): no muscles, no glands; keratinized

• Color: coral pink but does vary with individuals and races due to cutaneous pigmentation
• Papillary contour: pyramidal shape with one F and one L papilla and the col filling interproximal space to the contact area (col the starting place gingivitis)
• Marginal contour: knife-edged and scalloped
• Texture: stippled (orange-peel texture); blow air to dry out and see where stippling ends to see end of gingiva
• Consistency: firm and resilient (push against it and won’t move); bound to underlying bone
• Sulcus depth: 0-3mm
• Exudate: no exudates (blood, pus, water)

  Anatomic and histological structures

Gingival unit: includes periodontium above alveolar crest of bone

a. Alveolar mucosa: histology- non-keratinized, stratified, squamous epithelium, submucosa with glands, loose connective tissue with collagen and elastin, muscles.  No epithelial ridges, no stratum granulosum (flattened cells below keratin layer)

b. Mucogingival junction: clinical demarcation between alveolar mucosa and attached gingiva

c. Attached gingiva: histology- keratinized, stratified, squamous epithelium with epithelial ridges (basal cell layer, prickle cell layer, granular cell layer (stratum granulosum), keratin layer); no submucosa

• Dense connective tissue: predominantly collagen, bound to periosteum of bone by Sharpey fibers
• Reticular fibers between collagen fibers and are continuous with reticulin in blood vessels

d. Free gingival groove: demarcation between attached and free gingiva; denotes base of gingival sulcus in normal gingiva; not always seen

e. Free gingival margin: area from free gingival groove to epithelial attachment (up and over ® inside)

• Oral surface: stratified, squamous epithelium with epithelial ridges
• Tooth side surface (sulcular epithelium): non-keratinized, stratified, squamous epithelium with no epithelial ridges (basal cell and prickle cell layers)

f. Gingival sulcus: space bounded by tooth surface, sulcular epithelium, and junctional epithelium; 0-3mm depth; space between epithelium and tooth

g. Dento-gingival junction: combination of epithelial and fibrous attachment

• Junctional epithelium (epithelial attachment): attachment of epithelial cells by hemi-desmosomes and sticky substances (basal lamina- 800-1200 A, DAS-acid mucopolysaccharides, hyaluronic acid, chondroitin sulfate A, C, and B), to enamel, enamel and cementum, or cementum depending on stage of passive eruption.  Length ranges from 0.25-1.35mm.
• Fibrous attachment: attachment of collagen fibers (Sharpey’s fibers) into cementum just beneath epithelial attachment; ~ 1mm thick

h. Nerve fibers: myelinated and non-myelinated (for pain) in connective tissue.  Both free and specialized endings for pain, touch pressure, and temperature -> proprioception.  If dentures, rely on TMJ.

i.Mesh of terminal argyophilic fibers (stain silver), some extending into epithelium

ii  Meissner-type corpuscles: pressure sensitive sensory nerve encased in CT

iii.Krause-type corpuscles: temperature receptors

iv. Encapsulated spindles

i. Gingival fibers:

i.  Gingivodental group:

• Group I (A): from cementum to free gingival margin
• Group II (B): from cementum to attached gingiva
• Group III (C): from cementum over alveolar crest to periosteum on buccal and lingual plates

ii.  Circular (ligamentum circularis): encircles tooth in free gingiva

iii. Transeptal fibers: connects cementum of adjacent teeth, runs over interdental septum of alveolar bone.  Separates gingival unit from attachment apparatus.

Transeptal and Group III fibers the major defense against stuff getting into bone and ligament.

2.  Attachment apparatus: periodontium below alveolar crest of bone

Periodontal ligament: Sharpey’s fibers (collagen) connecting cementum to bone (bundle bone).  Few elastic and oxytalan fibers associated with blood vessels and embedded in cementum in cervical third of tooth.  Components divided as follows:

i. Alveolar crest fibers: from cementum just below CEJ apical to alveolar crest of bone

ii.Horizontal fibers: just apical to alveolar crest group, run at right angles to long axis of tooth from cementum horizontally to alveolar bone proper

iii.Oblique fibers: most numerous, from cementum run coronally to alveolar bone proper

iv. Apical fibers: radiate from cementum around apex of root apically to alveolar bone proper, form socket base

v. Interradicular fibers: found only between roots of multi-rooted teeth from cementum to alveolar bone proper

vi. Intermediate plexus: fibers which splice Sharpey’s fibers from bone and cementum

vii. Epithelial Rests of Malassez: cluster and individual epithelial cells close to cementum which are remnants of Hertwig’s epithelial root sheath; potential source of periodontal cysts.

viii. Nerve fibers: myelinated and non-myelinated; abundant supply of sensory free nerve endings capable of transmitting tactile pressure and pain sensation by trigeminal pathway and elongated spindle-like nerve fiber for proprioceptive impulses

Cementum: 45-50% inorganic; 50-55% organic (enamel is 97% inorganic; dentin 70% inorganic)

i.  Acellular cementum: no cementocytes; covers dentin (older) in coronal ½ to 2/3 of root, 16-60 mm thick

ii. Cellular cementum: cementocytes; covers dentin in apical ½ to 1/3 of root; also may cover acellular cementum areas in repair areas, 15-200 mm thick

iii. Precementum (cementoid): meshwork of irregularly arranged collagen in surface of cementum where formation starts

iv. Cemento-enamel junction (CEJ): 60-65% of time cementum overlaps enamel; 30% meet end-to-end; 5-10% space between

v. Cementum slower healing than bone or PDL.  If expose dentinotubules ® root sensitivity.

Alveolar bone: 65% inorganic, 35% organic

i. Alveolar bone proper (cribriform plate): lamina dura on x-ray; bundle bone receive Sharpey fibers from PDL

ii. Supporting bone: cancellous, trabecular (vascularized) and F and L plates of compact bone

Blood supply to periodontium

i. Alveolar blood vessels (inferior and superior)

A) Interalveolar: actually runs through bone then exits, main supply to alveolar bone and PDL

B) Supraperiosteal: just outside bone, to gingiva and alveolar bone

C) Dental (pulpal): to pulp and periapical area

D) Terminal vessels (supracrestal): anastomose of A and B above beneath the sulcular epithelium

E) PDL gets blood from: most from branches of interalveolar blood vessels from alveolar bone marrow spaces, supraperiosteal vessels when interalveolar vessels not present, pulpal (apical) vessels, supracrestal gingival vessels

ii. Lymphatic drainage: accompany blood vessels to regional lymph nodes (esp. submaxillary group)

Assessing New Attachment in Periodontal Therapy

Assessing new attachment following periodontal therapy is crucial for evaluating treatment outcomes and understanding the healing process. However, various methods of assessment have limitations that must be considered. This lecture will discuss the reliability of different assessment methods for new attachment, including periodontal probing, radiographic analysis, and histologic methods.

1. Periodontal Probing

• Assessment Method: Periodontal probing is commonly used to measure probing depth and attachment levels before and after therapy.

• Limitations:

  • Coronal Positioning of Probe Tip: After therapy, when the inflammatory lesion is resolved, the probe tip may stop coronal to the apical termination of the epithelium. This can lead to misleading interpretations of attachment gain.
  • Infrabony Defects: Following treatment of infrabony defects, new bone may form so close to the tooth surface that the probe cannot penetrate. This can result in a false impression of improved attachment levels.
  • Interpretation of Results: A gain in probing attachment level does not necessarily indicate a true gain of connective tissue attachment. Instead, it may reflect improved health of the surrounding tissues, which increases resistance to probe penetration.

2. Radiographic Analysis and Reentry Operations

• Assessment Method: Radiographic analysis involves comparing radiographs taken before and after therapy to evaluate changes in bone levels. Reentry operations allow for direct inspection of the treated area.

• Limitations:

  • Bone Fill vs. New Attachment: While radiographs can provide evidence of new bone formation (bone fill), they do not document the formation of new root cementum or a new periodontal ligament. Therefore, radiographic evidence alone cannot confirm the establishment of new attachment.

3. Histologic Methods

• Assessment Method: Histologic analysis involves examining tissue samples under a microscope to assess the formation of new attachment, including new cementum and periodontal ligament.

• Advantages:

  • Validity: Histologic methods are considered the only valid approach to assess the formation of new attachment accurately.

• Limitations:

  • Pre-Therapy Assessment: Accurate assessment of the attachment level prior to therapy is essential for histologic analysis. If the initial attachment level cannot be determined with certainty, it may compromise the validity of the findings.

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.

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.

Automated Probing Systems

Automated probing systems have become increasingly important in periodontal assessments, providing enhanced accuracy and efficiency in measuring pocket depths and clinical attachment levels. This lecture will focus on the Florida Probe System, the Foster-Miller Probe, and the Toronto Automated Probe, discussing their features, advantages, and limitations.

1. Florida Probe System

• Overview: The Florida Probe System is an automated probing system designed to facilitate accurate periodontal assessments. It consists of several components:

  • Probe Handpiece: The instrument used to measure pocket depths.
  • Digital Readout: Displays measurements in real-time.
  • Foot Switch: Allows for hands-free operation.
  • Computer Interface: Connects the probe to a computer for data management.

• Specifications:

  • Probe Diameter: The end of the probe is 0.4 mm in diameter, allowing for precise measurements in periodontal pockets.

• Advantages:

  • Constant Probing Force: The system applies a consistent force during probing, reducing variability in measurements.
  • Precise Electronic Measurement: Provides accurate and reproducible measurements of pocket depths.
  • Computer Storage of Data: Enables easy storage, retrieval, and analysis of patient data, facilitating better record-keeping and tracking of periodontal health over time.

• Disadvantages:

  • Lack of Tactile Sensitivity: The automated nature of the probe means that clinicians do not receive tactile feedback, which can be important for assessing tissue health.
  • Fixed Force Setting: The use of a fixed force setting throughout the mouth may not account for variations in tissue condition, potentially leading to inaccurate measurements or patient discomfort.

2. Foster-Miller Probe

• Overview: The Foster-Miller Probe is another automated probing system that offers unique features for periodontal assessment.

• Capabilities:

  • Pocket Depth Measurement: This probe can measure pocket depths effectively.
  • Detection of the Cemento-Enamel Junction (CEJ): It is capable of coupling pocket depth measurements with the detection of the CEJ, providing valuable information about clinical attachment levels.

3. Toronto Automated Probe

• Overview: The Toronto Automated Probe is designed to enhance the accuracy of probing in periodontal assessments.

• Specifications:

  • Probing Mechanism: The sulcus is probed with a 0.5 mm nickel titanium wire that is extended under air pressure, allowing for gentle probing.
  • Angular Control: The system controls angular discrepancies using a mercury tilt sensor, which limits angulation within ±30 degrees. This feature helps maintain consistent probing angles.

• Limitations:

  • Reproducible Positioning: The probe requires reproducible positioning of the patient’s head, which can be challenging in some clinical settings.
  • Limited Access: The design may not easily accommodate measurements of second or third molars, potentially limiting its use in comprehensive periodontal assessments.

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.