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.

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.

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.

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.

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)

ANUG (Acute Necrotizing Ulcerative Gingivitis)

• Signs: Punched – out crater depressions of interdental papilla
• Symptoms: Metallic foul taste, pasty saliva
• Treatment: 3 visits (2nd visit: 1 – 2 days after 1st; 3rd visit: 5 days after 2nd)

NUG/NUP

• No pocket formation (destroys junctional epithelium)

Primary Herpetic Gingivostomatitis

• Cellular change: Ballooning degeneration → Tzanck cells
• Treatment:
  • Within 3 days: Acyclovir 15 mg/kg × 5 times × 7 days
  • After 3 days: Supportive care with NSAIDs

Leukemic Gingivitis

• Most common in acute monocytic leukemia

Lead Intoxication

• Steel gray linear pigmentation (Burton's line)

• MS (Mitral Stenosis): No LVH
• Aortic Stenosis (AS):
  • Edward Sapiens valve used
  • Gallavardin sign present
  • Can cause sudden death
  • Classical triad: Exertional dyspnea, angina, syncope (no palpitations)
• MVP (Mitral Valve Prolapse):
  • Most common lesion in India
  • Autosomal dominant
• AR (Aortic Regurgitation):
  • Austin Flint murmur
  • Palpitations common
• TR (Tricuspid Regurgitation):
  • Most common cause: Cor pulmonale
• Williams syndrome: Associated with AS