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)

Immunological Profile

• T4:T8 Ratio: 1:1 in healthy periodontitis patients
• HIV Association: Altered ratio of 0.6:1 indicates immunocompromise

Radiographic Changes

• First Sign: Fuzziness or break in lamina dura at alveolar crest
• Progression: Loss of cortical outline, trabecular pattern changes
• Most Severe Changes: Occur along the lateral wall of the periodontal pocket

Effects of Smoking on the Etiology and Pathogenesis of Periodontal Disease

Smoking is a significant risk factor for the development and progression of periodontal disease. It affects various aspects of periodontal health, including microbiology, immunology, and physiology. Understanding these effects is crucial for dental professionals in managing patients with periodontal disease, particularly those who smoke.

Etiologic Factors and the Impact of Smoking

1. Microbiology

   • Plaque Accumulation:
     • Smoking does not affect the rate of plaque accumulation on teeth. This means that smokers may have similar levels of plaque as non-smokers.
   • Colonization of Periodontal Pathogens:
     • Smoking increases the colonization of shallow periodontal pockets by periodontal pathogens. This can lead to an increased risk of periodontal disease.
     • There are higher levels of periodontal pathogens found in deep periodontal pockets among smokers, contributing to the severity of periodontal disease.

2. Immunology

   • Neutrophil Function:
     • Smoking alters neutrophil chemotaxis (the movement of neutrophils towards infection), phagocytosis (the process by which neutrophils engulf and destroy pathogens), and the oxidative burst (the rapid release of reactive oxygen species to kill bacteria).
   • Cytokine Levels:
     • Increased levels of pro-inflammatory cytokines such as Tumor Necrosis Factor-alpha (TNF-α) and Prostaglandin E2 (PGE2) are found in the gingival crevicular fluid (GCF) of smokers. These cytokines play a role in inflammation and tissue destruction.
   • Collagenase and Elastase Production:
     • There is an increase in neutrophil collagenase and elastase in GCF, which can contribute to the breakdown of connective tissue and exacerbate periodontal tissue destruction.
   • Monocyte Response:
     • Smoking enhances the production of PGE2 by monocytes in response to lipopolysaccharides (LPS), further promoting inflammation and tissue damage.

3. Physiology

   • Gingival Blood Vessels:
     • Smoking leads to a decrease in gingival blood vessels, which can impair the delivery of immune cells and nutrients to the periodontal tissues, exacerbating inflammation.
   • Gingival Crevicular Fluid (GCF) Flow:
     • There is a reduction in GCF flow and bleeding on probing, even in the presence of increased inflammation. This can mask the clinical signs of periodontal disease, making diagnosis more challenging.
   • Subgingival Temperature:
     • Smoking is associated with a decrease in subgingival temperature, which may affect the metabolic activity of periodontal pathogens.
   • Recovery from Local Anesthesia:
     • Smokers may require a longer time to recover from local anesthesia, which can complicate dental procedures and patient management.

Clinical Implications

1. Increased Risk of Periodontal Disease:

   • Smokers are at a higher risk for developing periodontal disease due to the combined effects of altered microbial colonization, impaired immune response, and physiological changes in the gingival tissues.

2. Challenges in Diagnosis:

   • The reduced bleeding on probing and altered GCF flow in smokers can lead to underdiagnosis or misdiagnosis of periodontal disease. Dental professionals must be vigilant in assessing periodontal health in smokers.

3. Treatment Considerations:

   • Smoking cessation should be a key component of periodontal treatment plans. Educating patients about the effects of smoking on periodontal health can motivate them to quit.
   • Treatment may need to be more aggressive in smokers due to the increased severity of periodontal disease and the altered healing response.

4. Monitoring and Maintenance:

   • Regular monitoring of periodontal health is essential for smokers, as they may experience more rapid disease progression. Tailored maintenance programs should be implemented to address their specific needs.

Keratinized Gingiva and Attached Gingiva

The gingiva is an essential component of the periodontal tissues, providing support and protection for the teeth. Understanding the characteristics of keratinized gingiva, particularly attached gingiva, is crucial for assessing periodontal health.

Keratinized Gingiva

1. Definition:

   • Keratinized gingiva refers to the gingival tissue that is covered by a layer of keratinized epithelium, providing a protective barrier against mechanical and microbial insults.

2. Areas of Keratinized Gingiva:

   • Attached Gingiva:
     • Extends from the gingival groove to the mucogingival junction.
   • Marginal Gingiva:
     • The free gingival margin that surrounds the teeth.
   • Hard Palate:
     • The roof of the mouth, which is also covered by keratinized tissue.

Attached Gingiva

1. Location:

   • The attached gingiva is the portion of the gingiva that is firmly bound to the underlying alveolar bone.

2. Width of Attached Gingiva:

   • The width of attached gingiva varies based on location and can increase with age and in cases of supraerupted teeth.

3. Measurements:

   • Greatest Width:
     • Found in the incisor region:
       • Maxilla: 3.5 mm - 4.5 mm
       • Mandible: 3.3 mm - 3.9 mm
   • Narrowest Width:
     • Found in the posterior region:
       • Maxillary First Premolar: 1.9 mm
       • Mandibular First Premolar: 1.8 mm

Clinical Significance

• Importance of Attached Gingiva:

  • The width of attached gingiva is important for periodontal health, as it provides a buffer zone against mechanical forces and helps maintain the integrity of the periodontal attachment.
  • Insufficient attached gingiva may lead to increased susceptibility to periodontal disease and gingival recession.

• Assessment:

  • Regular assessment of the width of attached gingiva is essential during periodontal examinations to identify potential areas of concern and to plan appropriate treatment strategies.

🧬 Risk Factors

• Increased homocysteine levels
• Raised lipoprotein(a)
• Nephrotic syndrome increases CAD risk
• Unsaturated fatty acid intake: Protective
• Best probability predictor in elderly: LDL/HDL ratio

⚕️ Diagnosis & Presentation

🧪 Enzymes & Drugs

• Enzyme ↑ at 4 – 6 hrs, ↓ in 3 – 4 days: CPK
• Stress ECHO agent: Dobutamine
• Intervention of choice: Streptokinase + Heparin
• Thrombolytics window: Within 12 hrs of MI

🚨 Prognosis & Complications

• Day 1: Maximum MI mortality
• Post-MI valvular lesion: Mitral regurgitation
• Best predictor of morbidity: LVEF
• Fatal thrombolysis complication: Intracranial hemorrhage
• LAD artery nicknamed: Widow’s artery

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.