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.

Dental Calculus

Dental calculus, also known as tartar, is a hard deposit that forms on teeth due to the mineralization of dental plaque. Understanding the composition and crystal forms of calculus is essential for dental professionals in diagnosing and managing periodontal disease.

Crystal Forms in Dental Calculus

1. Common Crystal Forms:

   • Dental calculus typically contains two or more crystal forms. The most frequently detected forms include:
     • Hydroxyapatite:
       • This is the primary mineral component of both enamel and calculus, constituting a significant portion of the calculus sample.
       • Hydroxyapatite is a crystalline structure that provides strength and stability to the calculus.
     • Octacalcium Phosphate:
       • Detected in a high percentage of supragingival calculus samples (97% to 100%).
       • This form is also a significant contributor to the bulk of calculus.

2. Other Crystal Forms:

   • Brushite:
     • More commonly found in the mandibular anterior region of the mouth.
     • Brushite is a less stable form of calcium phosphate and may indicate a younger calculus deposit.
   • Magnesium Whitlockite:
     • Typically found in the posterior areas of the mouth.
     • This form may be associated with older calculus deposits and can indicate changes in the mineral composition over time.

3. Variation with Age:

   • The incidence and types of crystal forms present in calculus can vary with the age of the deposit.
   • Younger calculus deposits may have a higher proportion of brushite, while older deposits may show a predominance of hydroxyapatite and magnesium whitlockite.

Clinical Significance

1. Understanding Calculus Formation:

   • Knowledge of the crystal forms in calculus can help dental professionals understand the mineralization process and the conditions under which calculus forms.

2. Implications for Treatment:

   • The composition of calculus can influence treatment strategies. For example, older calculus deposits may be more difficult to remove due to their hardness and mineral content.

3. Assessment of Periodontal Health:

   • The presence and type of calculus can provide insights into a patient’s oral hygiene practices and periodontal health. Regular monitoring and removal of calculus are essential for preventing periodontal disease.

4. Research and Development:

   • Understanding the mineral composition of calculus can aid in the development of new dental materials and treatments aimed at preventing calculus formation and promoting oral health.

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)

Components of Gingival Crevicular Fluid (GCF) and Matrix Metalloproteinases (MMPs)

Gingival crevicular fluid (GCF) is a serum-like fluid found in the gingival sulcus that plays a significant role in periodontal health and disease. Understanding its composition, particularly glucose and protein content, as well as the role of matrix metalloproteinases (MMPs) in tissue remodeling, is essential for dental professionals.

Composition of Gingival Crevicular Fluid (GCF)

1. Glucose and Hexosamines:

   • GCF contains compounds such as glucose, hexosamines, and hexuronic acid.
   • Glucose Levels:
     • Blood glucose levels do not correlate with GCF glucose levels; in fact, glucose concentration in GCF is three to four times greater than that in serum.
     • This elevated glucose level is interpreted as a result of the metabolic activity of adjacent tissues and the influence of local microbial flora.

2. Protein Content:

   • The total protein content of GCF is significantly less than that of serum.
   • This difference in protein concentration reflects the unique environment of the gingival sulcus and the specific functions of GCF in periodontal health.

Matrix Metalloproteinases (MMPs)

1. Definition and Function:

   • MMPs are a family of proteolytic enzymes that degrade extracellular matrix molecules, including collagen, gelatin, and elastin.
   • They are produced by various cell types, including:
     • Neutrophils
     • Macrophages
     • Fibroblasts
     • Epithelial cells
     • Osteoblasts and osteoclasts

2. Classification:

   • MMPs are classified based on their substrate specificity, although it is now recognized that many MMPs can degrade multiple substrates. The classification includes:
     • Collagenases: e.g., MMP-1 and MMP-8 (break down collagen)
     • Gelatinases: Type IV collagenases
     • Stromelysins
     • Matrilysins
     • Membrane-type metalloproteinases
     • Others

3. Activation and Inhibition:

   • MMPs are secreted in an inactive form (latent) and require proteolytic cleavage for activation. This activation is facilitated by proteases such as cathepsin G produced by neutrophils.
   • Inhibitors: MMPs are regulated by proteinase inhibitors, which possess anti-inflammatory properties. Key inhibitors include:
     • Serum Inhibitors:
       • α1-antitrypsin
       • α2-macroglobulin (produced by the liver, inactivates various proteinases)
     • Tissue Inhibitors:
       • Tissue inhibitors of metalloproteinases (TIMPs), with TIMP-1 being particularly important in periodontal disease.
   • Antibiotic Inhibition: MMPs can also be inhibited by tetracycline antibiotics, leading to the development of sub-antimicrobial formulations of doxycycline as a systemic adjunctive treatment for periodontitis, exploiting its anti-MMP properties.

Merkel Cells

1. Location and Function:
   • Merkel cells are located in the deeper layers of the epithelium and are associated with nerve endings.
   • They are connected to adjacent cells by desmosomes and are identified as tactile receptors.
   • These cells play a role in the sensation of touch and pressure, contributing to the sensory functions of the oral mucosa.

Clinical Implications

1. GCF Analysis:

   • The composition of GCF, including glucose and protein levels, can provide insights into the inflammatory status of the periodontal tissues and the presence of periodontal disease.

2. Role of MMPs in Periodontal Disease:

   • MMPs are involved in the remodeling of periodontal tissues during inflammation and disease progression. Understanding their regulation and activity is crucial for developing therapeutic strategies.

3. Therapeutic Applications:

   • The use of sub-antimicrobial doxycycline as an adjunctive treatment for periodontitis highlights the importance of MMP inhibition in managing periodontal disease.

4. Sensory Function:

   • The presence of Merkel cells in the gingival epithelium underscores the importance of sensory feedback in maintaining oral health and function.

Necrotizing Ulcerative Gingivitis (NUG)

Necrotizing Ulcerative Gingivitis (NUG), also known as Vincent's disease or trench mouth, is a severe form of periodontal disease characterized by the sudden onset of symptoms and specific clinical features.

Etiology and Predisposing Factors

• Sudden Onset: NUG is characterized by a rapid onset of symptoms, often following debilitating diseases or acute respiratory infections.
• Lifestyle Factors: Changes in living habits, such as prolonged work without adequate rest, poor nutrition, tobacco use, and psychological stress, are frequently noted in patient histories .
• Smoking: Smoking has been identified as a significant predisposing factor for NUG/NDP .
• Immune Compromise: Conditions that compromise the immune system, such as poor oral hygiene, smoking, and emotional stress, are major contributors to the development of NUG .

Clinical Presentation

• Symptoms: NUG presents with:
  • Punched-out, crater-like depressions at the crest of interdental papillae.
  • Marginal gingival involvement, with rare extension to attached gingiva and oral mucosa.
  • Grey, pseudomembranous slough covering the lesions.
  • Spontaneous bleeding upon slight stimulation of the gingiva.
  • Fetid odor and increased salivation.

Microbiology

• Mixed Bacterial Infection: NUG is caused by a complex of anaerobic bacteria, often referred to as the fusospirochetal complex, which includes:
  • Treponema vincentii
  • Treponema denticola
  • Treponema macrodentium
  • Fusobacterium nucleatum
  • Prevotella intermedia
  • Porphyromonas gingivalis

Treatment

1. Control of Acute Phase:

   • Clean the wound with an antibacterial agent.
   • Irrigate the lesion with warm water and 5% vol/vol hydrogen peroxide.
   • Prescribe oxygen-releasing mouthwash (e.g., hydrogen peroxide DPF, sodium perborate DPF) to be used thrice daily.
   • Administer oral metronidazole for 3 to 5 days. If sensitive to metronidazole, prescribe penicillin; if sensitive to both, consider erythromycin or clindamycin.
   • Use 2% chlorhexidine in select cases for a short duration.

2. Management of Residual Condition:

   • Remove predisposing local factors (e.g., overhangs).
   • Perform supra- and subgingival scaling.
   • Consider gingivoplasty to correct any residual gingival deformities.

 Naber’s Probe and Furcation Involvement

Furcation involvement is a critical aspect of periodontal disease that affects the prognosis of teeth with multiple roots. Naber’s probe is a specialized instrument designed to assess furcation areas, allowing clinicians to determine the extent of periodontal attachment loss and the condition of the furcation. This lecture will cover the use of Naber’s probe, the classification of furcation involvement, and the clinical significance of these classifications.

Naber’s Probe

• Description: Naber’s probe is a curved, blunt-ended instrument specifically designed for probing furcation areas. Its unique shape allows for horizontal probing, which is essential for accurately assessing the anatomy of multi-rooted teeth.

• Usage: The probe is inserted horizontally into the furcation area to evaluate the extent of periodontal involvement. The clinician can feel the anatomical fluting between the roots, which aids in determining the classification of furcation involvement.

Classification of Furcation Involvement

Furcation involvement is classified into four main classes using Naber’s probe:

1. Class I:

   • Description: The furcation can be probed to a depth of 3 mm.
   • Clinical Findings: The probe can feel the anatomical fluting between the roots, but it cannot engage the roof of the furcation.
   • Significance: Indicates early furcation involvement with minimal attachment loss.

2. Class II:

   • Description: The furcation can be probed to a depth greater than 3 mm, but not through and through.
   • Clinical Findings: This class represents a range between Class I and Class III, where there is partial loss of attachment but not complete penetration through the furcation.
   • Significance: Indicates moderate furcation involvement that may require intervention.

3. Class III:

   • Description: The furcation can be completely probed through and through.
   • Clinical Findings: The probe passes from one furcation to the other, indicating significant loss of periodontal support.
   • Significance: Represents advanced furcation involvement, often associated with a poor prognosis for the affected tooth.

4. Class III+:

   • Description: The probe can go halfway across the tooth.
   • Clinical Findings: Similar to Class III, but with partial obstruction or remaining tissue.
   • Significance: Indicates severe furcation involvement with a significant loss of attachment.

5. Class IV:

   • Description: Clinically, the examiner can see through the furcation.
   • Clinical Findings: There is complete loss of tissue covering the furcation, making it visible upon examination.
   • Significance: Indicates the most severe form of furcation involvement, often leading to tooth mobility and extraction.

Measurement Technique

• Measurement Reference: Measurements are taken from an imaginary tangent connecting the prominences of the root surfaces of both roots. This provides a consistent reference point for assessing the depth of furcation involvement.

Clinical Significance

• Prognosis: The classification of furcation involvement is crucial for determining the prognosis of multi-rooted teeth. Higher classes of furcation involvement generally indicate a poorer prognosis and may necessitate more aggressive treatment strategies.

• Treatment Planning: Understanding the extent of furcation involvement helps clinicians develop appropriate treatment plans, which may include scaling and root planing, surgical intervention, or extraction.

• Monitoring: Regular assessment of furcation involvement using Naber’s probe can help monitor disease progression and the effectiveness of periodontal therapy.