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Periodontics - NEETMDS- courses
NEET MDS Lessons
Periodontology

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.

  • 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

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. 

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.


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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.

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.

Gingival Crevicular Fluid (GCF)

Gingival crevicular fluid is an inflammatory exudate found in the gingival sulcus. It plays a significant role in periodontal health and disease.

A. Characteristics of GCF

  • Glucose Concentration: The glucose concentration in GCF is 3-4 times greater than that in serum, indicating increased metabolic activity in inflamed tissues.
  • Protein Content: The total protein content of GCF is much less than that of serum, reflecting its role as an inflammatory exudate.
  • Inflammatory Nature: GCF is present in clinically normal sulci due to the constant low-grade inflammation of the gingiva.

B. Drugs Excreted Through GCF

  • Tetracyclines and Metronidazole: These antibiotics are known to be excreted through GCF, making them effective for localized periodontal therapy.

C. Collection Methods for GCF

GCF can be collected using various techniques, including:

  1. Absorbing Paper Strips/Blotter/Periopaper: These strips absorb fluid from the sulcus and are commonly used for GCF collection.
  2. Twisted Threads: Placing twisted threads around and into the sulcus can help collect GCF.
  3. Micropipettes: These can be used for precise collection of GCF in research settings.
  4. Intra-Crevicular Washings: Flushing the sulcus with a saline solution can help collect GCF for analysis.

Feature Details
First valvular lesion Mitral regurgitation
Commonest valve Mitral (especially in children)
Minor criteria Fever (Modified Jones Criteria)
Subcutaneous nodules Non-tender, extensor surfaces
Erythema marginatum Associated with carditis
Diagnostic marker Aschoff's nodule
McCallum's patch Rheumatic endocarditis indicator

Dental Plaque

Dental plaque is a biofilm that forms on the surfaces of teeth and is composed of a diverse community of microorganisms. The development of dental plaque occurs in stages, beginning with primary colonizers and progressing to secondary colonization and plaque maturation.

Primary Colonizers

  • Timeframe:
    • Acquired within a few hours after tooth cleaning or exposure.
  • Characteristics:
    • Predominantly gram-positive facultative microbes.
  • Key Species:
    • Actinomyces viscosus
    • Streptococcus sanguis
  • Adhesion Mechanism:
    • Primary colonizers adhere to the tooth surface through specific adhesins.
    • For example, A. viscosus possesses fimbriae that bind to proline-rich proteins in the dental pellicle, facilitating initial attachment.

Secondary Colonization and Plaque Maturation

  • Microbial Composition:
    • As plaque matures, it becomes predominantly populated by gram-negative anaerobic microorganisms.
  • Key Species:
    • Prevotella intermedia
    • Prevotella loescheii
    • Capnocytophaga spp.
    • Fusobacterium nucleatum
    • Porphyromonas gingivalis
  • Coaggregation:
    • Coaggregation refers to the ability of different species and genera of plaque microorganisms to adhere to one another.
    • This process occurs primarily through highly specific stereochemical interactions of protein and carbohydrate molecules on cell surfaces, along with hydrophobic, electrostatic, and van der Waals forces.

Plaque Hypotheses

  1. Specific Plaque Hypothesis:

    • This hypothesis posits that only certain types of plaque are pathogenic.
    • The pathogenicity of plaque depends on the presence or increase of specific microorganisms.
    • It predicts that plaque harboring specific bacterial pathogens leads to periodontal disease due to the production of substances that mediate the destruction of host tissues.
  2. Nonspecific Plaque Hypothesis:

    • This hypothesis maintains that periodontal disease results from the overall activity of the entire plaque microflora.
    • It suggests that the elaboration of noxious products by the entire microbial community contributes to periodontal disease, rather than specific pathogens alone.

Iodine Effects

  • High dose, short period → Inhibits T4 synthesis (Wolff-Chaikoff effect)
  • Low dose, long period → Increases T4 synthesis (Jod-Basedow effect)

Drugs Inhibiting T4→T3 Conversion

Propranolol, Dexamethasone, Propylthiouracil, High-dose iodine, Radiographic contrast

Hypothyroidism

  • Best test: Raised TSH (primary hypothyroidism)
  • Causes: Amyloidosis, Sarcoidosis, Hemochromatosis, Scleroderma, Cystinosis
  • Drugs: Amiodarone, Lithium
  • Hashimoto thyroiditis

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