Talk to us?

- NEETMDS- courses
NEET MDS Lessons
Periodontology

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.

Some important points about the periodontal pocket :
·Soft tissue of pocket wall shows both proliferative & degenerative changes
·Most severe degenerative changes are seen on the lateral wall of pocket
·Plasma cells are the predominant infiltrate (80%). Others include lymphocytes & a scattering of PMNs
·Height of junctional epithelium shortened to only 50-100µm
·Severity of degenerative changes is not linked to pocket depth
·Junctional epithelium starts to lose attachment to tooth when PMN infiltration in junctional epithelium increases above 60%.

Dimensions of Toothbrushes

Toothbrushes play a crucial role in maintaining oral hygiene, and their design can significantly impact their effectiveness. The American Dental Association (ADA) has established guidelines for the dimensions and characteristics of acceptable toothbrushes. This lecture will outline these specifications and discuss their implications for dental health.

Acceptable Dimensions of Toothbrushes

  1. Brushing Surface Dimensions:

    • Length:
      • Acceptable brushing surfaces should measure between 1 to 1.25 inches (25.4 to 31.8 mm) long.
    • Width:
      • The width of the brushing surface should range from 5/16 to 3/8 inch (7.9 to 9.5 mm).
    • Rows of Bristles:
      • Toothbrushes should have 2 to 4 rows of bristles to effectively clean the teeth and gums.
    • Tufts per Row:
      • Each row should contain 5 to 12 tufts of bristles, allowing for adequate coverage and cleaning ability.
  2. Filament Diameter:

    • The diameter of the bristles can vary, affecting the stiffness and cleaning effectiveness:
      • Soft Filaments:
        • Diameter of 0.2 mm (0.007 inches). Ideal for sensitive gums and children.
      • Medium Filaments:
        • Diameter of 0.3 mm (0.012 inches). Suitable for most adults.
      • Hard Filaments:
        • Diameter of 0.4 mm (0.014 inches). Generally not recommended for daily use as they can be abrasive to the gums and enamel.
  3. Filament Stiffness:

    • The stiffness of the bristles is determined by the diameter relative to the length of the filament. Thicker filaments tend to be stiffer, which can affect the brushing technique and comfort.

Special Considerations for Children's Toothbrushes

  • Size:
    • Children's toothbrushes are designed to be smaller to accommodate their smaller mouths and teeth.
  • Bristle Thickness:
    • The bristles are thinner, measuring 0.005 inches (0.1 mm) in diameter, making them gentler on sensitive gums.
  • Bristle Length:
    • The bristles are shorter, typically around 0.344 inches (8.7 mm), to ensure effective cleaning without causing discomfort.

Clinical Implications

  1. Choosing the Right Toothbrush:

    • Dental professionals should guide patients in selecting toothbrushes that meet ADA specifications to ensure effective plaque removal and gum protection.
    • Emphasizing the importance of using soft or medium bristles can help prevent gum recession and enamel wear.
  2. Education on Brushing Technique:

    • Proper brushing technique is as important as the toothbrush itself. Patients should be educated on how to use their toothbrush effectively, regardless of the type they choose.
  3. Regular Replacement:

    • Patients should be advised to replace their toothbrush every 3 to 4 months or sooner if the bristles become frayed. This ensures optimal cleaning effectiveness.
  4. Special Considerations for Children:

    • Parents should be encouraged to choose appropriately sized toothbrushes for their children and to supervise brushing to ensure proper technique and effectiveness.

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.

Modified Widman Flap Procedure

The modified Widman flap procedure is a surgical technique used in periodontal therapy to treat periodontal pockets while preserving the surrounding tissues and promoting healing. This lecture will discuss the advantages and disadvantages of the modified Widman flap, its indications, and the procedural steps involved.

Advantages of the Modified Widman Flap Procedure

  1. Intimate Postoperative Adaptation:

    • The main advantage of the modified Widman flap procedure is the ability to establish a close adaptation of healthy collagenous connective tissues and normal epithelium to all tooth surfaces. This promotes better healing and integration of tissues post-surgery
  2. Feasibility for Bone Implantation:

    • The modified Widman flap procedure is advantageous over curettage, particularly when the implantation of bone and other substances is planned. This allows for better access and preparation of the surgical site for grafting .
  3. Conservation of Bone and Optimal Coverage:

    • Compared to conventional reverse bevel flap surgery, the modified Widman flap conserves bone and provides optimal coverage of root surfaces by soft tissues. This results in:
      • A more aesthetically pleasing outcome.
      • A favorable environment for oral hygiene.
      • Potentially less root sensitivity and reduced risk of root caries.
      • More effective pocket closure compared to pocket elimination procedures .
  4. Minimized Gingival Recession:

    • When reattachment or minimal gingival recession is desired, the modified Widman flap is preferred over subgingival curettage, making it a suitable choice for treating deeper pockets (greater than 5 mm) and other complex periodontal conditions.

Disadvantages of the Modified Widman Flap Procedure

  1. Interproximal Architecture:
    • One apparent disadvantage is the potential for flat or concave interproximal architecture immediately following the removal of the surgical dressing, particularly in areas with interproximal bony craters. This can affect the aesthetic outcome and may require further management .

Indications for the Modified Widman Flap Procedure

  • Deep Pockets: Pockets greater than 5 mm, especially in the anterior and buccal maxillary posterior regions.
  • Intrabony Pockets and Craters: Effective for treating pockets with vertical bone loss.
  • Furcation Involvement: Suitable for managing periodontal disease in multi-rooted teeth.
  • Bone Grafts: Facilitates the placement of bone grafts during surgery.
  • Severe Root Sensitivity: Indicated when root sensitivity is a significant concern.

Procedure Overview

  1. Incisions and Flap Reflection:

    • Vertical Incisions: Made to access the periodontal pocket.
    • Crevicular Incision: A horizontal incision along the gingival margin.
    • Horizontal Incision: Undermines and removes the collar of tissue around the teeth.
  2. Conservative Debridement:

    • Flap is reflected just beyond the alveolar crest.
    • Careful removal of all plaque and calculus while preserving the root surface.
    • Frequent sterile saline irrigation is used to maintain a clean surgical field.
  3. Preservation of Proximal Bone Surface:

    • The proximal bone surface is preserved and not curetted, allowing for better healing and adaptation of the flap.
    • Exact flap adaptation is achieved with full coverage of the bone.
  4. Suturing:

    • Suturing is aimed at achieving primary union of the proximal flap projections, ensuring proper healing and tissue integration.

Postoperative Care

  • Antibiotic Ointment and Periodontal Dressing: Traditionally, antibiotic ointment was applied over sutures, and a periodontal dressing was placed. However, these practices are often omitted today.
  • Current Recommendations: Patients are advised not to disturb the surgical area and to use a chlorhexidine mouth rinse every 12 hours for effective plaque control and to promote healing.


--------------

 

 

Neutrophil Disorders Associated with Periodontal Diseases

Neutrophils play a crucial role in the immune response, particularly in combating infections, including those associated with periodontal diseases. Various neutrophil disorders can significantly impact periodontal health, leading to increased susceptibility to periodontal diseases. This lecture will explore the relationship between neutrophil disorders and specific periodontal diseases.

Neutrophil Disorders

  1. Diabetes Mellitus

    • Description: A metabolic disorder characterized by high blood sugar levels due to insulin resistance or deficiency.
    • Impact on Neutrophils: Diabetes can impair neutrophil function, including chemotaxis, phagocytosis, and the oxidative burst, leading to an increased risk of periodontal infections.
  2. Papillon-Lefevre Syndrome

    • Description: A rare genetic disorder characterized by palmoplantar keratoderma and severe periodontitis.
    • Impact on Neutrophils: Patients exhibit neutrophil dysfunction, leading to early onset and rapid progression of periodontal disease.
  3. Down’s Syndrome

    • Description: A genetic disorder caused by the presence of an extra chromosome 21, leading to various developmental and health issues.
    • Impact on Neutrophils: Individuals with Down’s syndrome often have impaired neutrophil function, which contributes to an increased prevalence of periodontal disease.
  4. Chediak-Higashi Syndrome

    • Description: A rare genetic disorder characterized by immunodeficiency, partial oculocutaneous albinism, and neurological problems.
    • Impact on Neutrophils: This syndrome results in defective neutrophil chemotaxis and phagocytosis, leading to increased susceptibility to infections, including periodontal diseases.
  5. Drug-Induced Agranulocytosis

    • Description: A condition characterized by a dangerously low level of neutrophils due to certain medications.
    • Impact on Neutrophils: The reduction in neutrophil count compromises the immune response, increasing the risk of periodontal infections.
  6. Cyclic Neutropenia

    • Description: A rare genetic disorder characterized by recurrent episodes of neutropenia (low neutrophil count) occurring every 21 days.
    • Impact on Neutrophils: During neutropenic episodes, patients are at a heightened risk for infections, including periodontal disease.

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.

Classification of Embrasures

  1. Type I Embrasures:

    • Description: These are characterized by the presence of interdental papillae that completely fill the embrasure space, with no gingival recession.
    • Recommended Cleaning Device:
      • Dental Floss: Dental floss is most effective in cleaning Type I embrasures. It can effectively remove plaque and debris from the tight spaces between teeth.
  2. Type II Embrasures:

    • Description: These embrasures have larger spaces due to some loss of attachment, but the interdental papillae are still present.
    • Recommended Cleaning Device:
      • Interproximal Brush: For Type II embrasures, interproximal brushes are recommended. These brushes have bristles that can effectively clean around the exposed root surfaces and between teeth, providing better plaque removal than dental floss in these larger spaces.
  3. Type III Embrasures:

    • Description: These spaces occur when there is significant loss of attachment, resulting in the absence of interdental papillae.
    • Recommended Cleaning Device:
      • Single Tufted Brushes: Single tufted brushes (also known as end-tuft brushes) are ideal for cleaning Type III embrasures. They can reach areas that are difficult to access with traditional floss or brushes, effectively cleaning the exposed root surfaces and the surrounding areas.

Explore by Exams