Periodontal Medicaments

Periodontal diseases often require adjunctive therapies to traditional mechanical treatments such as scaling and root planing. Various medicaments have been developed to enhance the healing process and control infection in periodontal tissues.

1. Elyzol

• Composition:
  • Elyzol is an oil-based gel containing 25% metronidazole. It is formulated with glyceryl mono-oleate and sesame oil.
• Clinical Use:
  • Elyzol has been found to be equivalent to scaling and root planing in terms of effectiveness for treating periodontal disease.
  • However, no adjunctive effects beyond those achieved with mechanical debridement have been demonstrated.

2. Actisite

• Composition:

  • Actisite consists of tetracycline-containing fibers.
  • Each fiber has a diameter of 0.5 mm and contains 12.7 mg of tetracycline per 9 inches of fiber.

• Clinical Use:

  • The fibers are placed directly into periodontal pockets, where they release tetracycline over time, helping to reduce bacterial load and promote healing.

3. Arestin

• Composition:

  • Arestin contains minocycline, which is delivered as a biodegradable powder in a syringe.

• Clinical Use:

  • Arestin is indicated for the treatment of periodontal disease and is applied directly into periodontal pockets, where it provides localized antibiotic therapy.

4. Atridox

• Composition:

  • Atridox contains 10% doxycycline in a syringeable gel system that is biodegradable.

• Clinical Use:

  • The gel is injected into periodontal pockets, where it solidifies and releases doxycycline over time, aiding in the management of periodontal disease.

5. Dentamycin and Periocline

• Composition:

  • Both Dentamycin and Periocline contain 2% minocycline hydrochloride.

• Clinical Use:

  • These products are used similarly to other local delivery systems, providing localized antibiotic therapy to reduce bacterial infection in periodontal pockets.

6. Periochip

• Composition:

  • Periochip is a biodegradable chip that contains chlorhexidine.

• Clinical Use:

  • The chip is placed in the gingival crevice, where it releases chlorhexidine over time, providing antimicrobial action and helping to control periodontal disease.

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.

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

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.

🫁 Respiratory Physiology & Pathology

🧬 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