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Periodontics - NEETMDS- courses
NEET MDS Lessons
Periodontology

  • Mobility Tests: Perio test, Fremitus test.
  • Bone Evaluation: Transgingival probing.
  • Halitosis Detection: Gold standard = Organoleptic analysis.
  • Indices:
    • PMA Index: Gingival disease.
    • Ramfjord Index Teeth: 16, 21, 24, 36, 41, 44.
    • Merin’s Classification: Patient recall.
    • Surrogate Endpoint: Reduction in probing depth.

Aggressive Periodontitis (formerly Juvenile Periodontitis)

  • Historical Names: Previously referred to as periodontosis, deep cementopathia, diseases of eruption, Gottleib’s diseases, and periodontitis marginalis progressive.
  • Risk Factors:
    • High frequency of Actinobacillus actinomycetemcomitans.
    • Immune defects (functional defects of PMNs and monocytes).
    • Autoimmunity and genetic factors.
    • Environmental factors, including smoking.
  • Clinical Features:
    • Vertical loss of alveolar bone around the first molars and incisors, typically beginning around puberty.
    • Bone loss patterns often described as "target" or "bull" shaped lesions.

  • Angulation vs Adaptation:
    • Angulation: Angle between blade face and tooth surface.
    • Adaptation: Relationship of blade’s working end to tooth surface.
  • Curettes:
    • Gracey: Blade offset at 60°.
    • Universal: Blade angle at 90°.
    • After Five: Extended shank by 3 mm; available in all Gracey numbers except 9 – 10.
    • Mini Five: Blade half the length of conventional curette.
    • Langer Curette: Gracey curette modified with universal blade angle.
  • Scaling & Sharpening:
    • Blade angulation for scaling: 45 – 90°; for curettage: >90°.
    • Sharpening angle: 100 – 110°.
    • Chisel scaler: Push motion; Hoe scaler: Blade bent at 99°.
    • Sickle scaler blade-to-shank angle: 70°.
  • Microsurgery:
    • Instrument weight: 15 – 20 g.
    • Principles: Butt joint approximation, enhanced motor skills, minimal trauma.
  • Suturing:
    • Needle entry: Right angle, 2 – 3 mm from incision.

Periodontal Bone Grafts

Bone grafting is a critical procedure in periodontal surgery, aimed at restoring lost bone and supporting the regeneration of periodontal tissues.

1. Bone Blend

 Bone blend is a mixture of cortical or cancellous bone that is procured using a trephine or rongeurs, placed in an amalgam capsule, and triturated to achieve a slushy osseous mass. This technique allows for the creation of smaller particle sizes, which enhances resorption and replacement with host bone.

Particle Size: The ideal particle size for bone blend is approximately 210 x 105 micrometers.

Rationale: Smaller particle sizes improve the chances of resorption and integration with the host bone, making the graft more effective.

2. Types of Periodontal Bone Grafts

A. Autogenous Grafts

Autogenous grafts are harvested from the patient’s own body, providing the best compatibility and healing potential.

  1. Cortical Bone Chips

    • History: First used by Nabers and O'Leary in 1965.
    • Characteristics: Composed of shavings of cortical bone removed during osteoplasty and ostectomy from intraoral sites.
    • Challenges: Larger particle sizes can complicate placement and handling, and there is a potential for sequestration. This method has largely been replaced by autogenous osseous coagulum and bone blend.
  2. Osseous Coagulum and Bone Blend

    • Technique: Intraoral bone is obtained using high- or low-speed round burs and mixed with blood to form an osseous coagulum (Robinson, 1969).
    • Advantages: Overcomes disadvantages of cortical bone chips, such as inability to aspirate during collection and variability in quality and quantity of collected bone.
    • Applications: Used in various periodontal procedures to enhance healing and regeneration.
  3. Intraoral Cancellous Bone and Marrow

    • Sources: Healing bony wounds, extraction sockets, edentulous ridges, mandibular retromolar areas, and maxillary tuberosity.
    • Applications: Provides a rich source of osteogenic cells and growth factors for bone regeneration.
  4. Extraoral Cancellous Bone and Marrow

    • Sources: Obtained from the anterior or posterior iliac crest.
    • Advantages: Generally offers the greatest potential for new bone growth due to the abundance of cancellous bone and marrow.

B. Bone Allografts

Bone allografts are harvested from donors and can be classified into three main types:

  1. Undermineralized Freeze-Dried Bone Allograft (FDBA)

    • Introduction: Introduced in 1976 by Mellonig et al.
    • Process: Freeze drying removes approximately 95% of the water from bone, preserving morphology, solubility, and chemical integrity while reducing antigenicity.
    • Efficacy: FDBA combined with autogenous bone is more effective than FDBA alone, particularly in treating furcation involvements.
  2. Demineralized (Decalcified) FDBA

    • Mechanism: Demineralization enhances osteogenic potential by exposing bone morphogenetic proteins (BMPs) in the bone matrix.
    • Osteoinduction vs. Osteoconduction: Demineralized grafts induce new bone formation (osteoinduction), while undermineralized allografts facilitate bone growth by providing a scaffold (osteoconduction).
  3. Frozen Iliac Cancellous Bone and Marrow

    • Usage: Used sparingly due to variability in outcomes and potential complications.

Comparison of Allografts and Alloplasts

  • Clinical Outcomes: Both FDBA and DFDBA have been compared to porous particulate hydroxyapatite, showing little difference in post-treatment clinical parameters.
  • Histological Healing: Grafts of DFDBA typically heal with regeneration of the periodontium, while synthetic bone grafts (alloplasts) heal by repair, which may not restore the original periodontal architecture.

Influence of Host Response on Periodontal Disease

The host response plays a critical role in the progression and management of periodontal disease. Various host factors influence bacterial colonization, invasion, tissue destruction, and healing processes. Understanding these interactions is essential for developing effective treatment strategies.

Aspects of Periodontal Disease and Host Factors

  1. Bacterial Colonization:

    • Host Factor: Antibody C in crevicular fluid.
    • Mechanism:
      • Antibody C inhibits the adherence and coaggregation of bacteria in the subgingival environment.
      • This action potentially reduces bacterial numbers by promoting lysis (destruction of bacterial cells).
    • Implication: A robust antibody response can help control the initial colonization of pathogenic bacteria, thereby influencing the onset of periodontal disease.
  2. Bacterial Invasion:

    • Host Factor: Antibody C-mediated lysis and neutrophil activity.
    • Mechanism:
      • Antibody C-mediated lysis reduces bacterial counts in the periodontal tissues.
      • Neutrophils, through processes such as chemotaxis (movement towards chemical signals), phagocytosis (engulfing and digesting bacteria), and lysis, further reduce bacterial counts.
    • Implication: An effective neutrophil response is crucial for controlling bacterial invasion and preventing the progression of periodontal disease.
  3. Tissue Destruction:

    • Host Factors: Antibody-mediated hypersensitivity and cell-mediated immune responses.
    • Mechanism:
      • Activation of tissue factors, such as collagenase, leads to the breakdown of connective tissue and periodontal structures.
      • The immune response can inadvertently contribute to tissue destruction, as inflammatory mediators can damage host tissues.
    • Implication: While the immune response is essential for fighting infection, it can also lead to collateral damage in periodontal tissues, exacerbating disease progression.
  4. Healing and Fibrosis:

    • Host Factors: Lymphocytes and macrophage-produced chemotactic factors.
    • Mechanism:
      • Lymphocytes and macrophages release chemotactic factors that attract fibroblasts to the site of injury.
      • Fibroblasts are activated by specific factors, promoting tissue repair and fibrosis (the formation of excess connective tissue).
    • Implication: A balanced immune response is necessary for effective healing and regeneration of periodontal tissues following inflammation.

🔬 Key Features & Forms

  • Most infective form: Cavitary lesion
  • Primary TB Presentation: Unilateral hilar lymphadenopathy
  • Rich focus: Meninges (associated with TB meningitis)
  • Cavitation: Absent in HIV-associated or primary TB

💡 Special Manifestations

  • Hypersensitivity to Mycobacteria: Phlyctenular conjunctivitis
  • Poncet’s disease: Joint pains without active arthritis
  • Miliary TB: Mantoux test negative
  • Recurrent hemoptysis source: Bronchial artery

💊 Drug Details

  • Streptomycin: Not used in TB meningitis
  • Bedaquiline: New drug for MDR-TB

Classification by Extent

  • Generalized: >30% sites affected

Classification by Severity

  • Moderate: 3 – 4 mm bone loss
  • Severe: >5 mm bone loss

Aggressive Periodontitis

  • Rate: 3 – 4 times faster bone loss than chronic
  • Classic sign: Arc – shaped bone loss (distal 2nd premolar to mesial 2nd molar)
  • Associated: HLA A9 and B15 antigens
  • Receptor defect: Poorly functional monocyte FcγR2

Pain Characteristics

  • Periodontal pocket pain: "Deep in bone" feeling

Bone Loss Patterns

  • Radius of action: 1.5 – 2.5 mm (Page & Schroeder)
  • Reverse architecture: Facial/lingual plates lost, radicular bone preserved
  • TFO signs: Increased mobility (first clinical sign)

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