NEET MDS Lessons
Periodontology
Significant Immune Findings in Periodontal Diseases
Periodontal diseases are associated with various immune responses that can influence disease progression and severity. Understanding these immune findings is crucial for diagnosing and managing different forms of periodontal disease.
Immune Findings in Specific Periodontal Diseases
-
Acute Necrotizing Ulcerative Gingivitis (ANUG):
- Findings:
- PMN (Polymorphonuclear neutrophil) chemotactic defect: This defect impairs the ability of neutrophils to migrate to the site of infection, compromising the immune response.
- Elevated antibody titres to Prevotella intermedia and intermediate-sized spirochetes: Indicates an immune response to specific pathogens associated with the disease.
- Findings:
-
Pregnancy Gingivitis:
- Findings:
- No significant immune findings reported: While pregnancy gingivitis is common, it does not show distinct immune abnormalities compared to other forms of periodontal disease.
- Findings:
-
Adult Periodontitis:
- Findings:
- Elevated antibody titres to Porphyromonas gingivalis and other periodontopathogens: Suggests a heightened immune response to these specific bacteria.
- Occurrence of immune complexes in tissues: Indicates an immune reaction that may contribute to tissue damage.
- Immediate hypersensitivity to gingival bacteria: Reflects an exaggerated immune response to bacterial antigens.
- Cell-mediated immunity to gingival bacteria: Suggests involvement of T-cells in the immune response against periodontal pathogens.
- Findings:
-
Juvenile Periodontitis:
- Localized Juvenile Periodontitis (LJP):
- Findings:
- PMN chemotactic defect and depressed phagocytosis: Impairs the ability of neutrophils to respond effectively to bacterial invasion.
- Elevated antibody titres to Actinobacillus actinomycetemcomitans: Indicates an immune response to this specific pathogen.
- Findings:
- Generalized Juvenile Periodontitis (GJP):
- Findings:
- PMN chemotactic defect and depressed phagocytosis: Similar to LJP, indicating a compromised immune response.
- Elevated antibody titres to Porphyromonas gingivalis: Suggests an immune response to this pathogen.
- Findings:
- Localized Juvenile Periodontitis (LJP):
-
Prepubertal Periodontitis:
- Findings:
- PMN chemotactic defect and depressed phagocytosis: Indicates impaired neutrophil function.
- Elevated antibody titres to Actinobacillus actinomycetemcomitans: Suggests an immune response to this pathogen.
- Findings:
-
Rapid Periodontitis:
- Findings:
- Suppressed or enhanced PMN or monocyte chemotaxis: Indicates variability in immune response among individuals.
- Elevated antibody titres to several gram-negative bacteria: Reflects an immune response to multiple pathogens.
- Findings:
-
Refractory Periodontitis:
- Findings:
- Reduced PMN chemotaxis: Indicates impaired neutrophil migration, which may contribute to disease persistence despite treatment.
- Findings:
-
Desquamative Gingivitis:
- Findings:
- Diagnostic or characteristic immunopathology in two-thirds of cases: Suggests an underlying immune mechanism.
- Autoimmune etiology in cases resulting from pemphigus and pemphigoid: Indicates that some cases may be due to autoimmune processes affecting the gingival tissue.
- Findings:
Ecological Succession of Biofilm in Dental Plaque
Overview of Biofilm Formation
Biofilm formation on tooth surfaces is a dynamic process characterized by ecological succession, where microbial communities evolve over time. This process transitions from an early aerobic environment dominated by gram-positive facultative species to a later stage characterized by a highly oxygen-deprived environment where gram-negative anaerobic microorganisms predominate.
Stages of Biofilm Development
-
Initial Colonization:
- Environment: The initial phase occurs in an aerobic environment.
- Primary Colonizers:
- The first bacteria to colonize the pellicle-coated tooth surface are predominantly gram-positive facultative microorganisms.
- Key Species:
- Actinomyces viscosus
- Streptococcus sanguis
- Characteristics:
- These bacteria can thrive in the presence of oxygen and play a crucial role in the establishment of the biofilm.
-
Secondary Colonization:
- Environment: As the biofilm matures, the environment becomes increasingly anaerobic due to the metabolic activities of the initial colonizers.
- Secondary Colonizers:
- These microorganisms do not initially colonize clean tooth surfaces but adhere to the existing bacterial cells in the plaque mass.
- Key Species:
- Prevotella intermedia
- Prevotella loescheii
- Capnocytophaga spp.
- Fusobacterium nucleatum
- Porphyromonas gingivalis
- Coaggregation:
- Secondary colonizers adhere to primary colonizers through a process known as coaggregation, which involves specific interactions between bacterial cells.
-
Coaggregation Examples:
- Coaggregation is a critical mechanism that facilitates the establishment of complex microbial communities within the biofilm.
- Well-Known Examples:
- Fusobacterium nucleatum with Streptococcus sanguis
- Prevotella loescheii with Actinomyces viscosus
- Capnocytophaga ochracea with Actinomyces viscosus
Implications of Ecological Succession
- Microbial Diversity: The transition from gram-positive to gram-negative organisms reflects an increase in microbial diversity and complexity within the biofilm.
- Pathogenic Potential: The accumulation of anaerobic gram-negative bacteria is associated with the development of periodontal diseases, as these organisms can produce virulence factors that contribute to tissue destruction and inflammation.
- Biofilm Stability: The interactions between different bacterial species through coaggregation enhance the stability and resilience of the biofilm, making it more challenging to remove through mechanical cleaning.
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Subgingival and Supragingival Calculus
Overview of Calculus Formation
Calculus, or tartar, is a hardened form of dental plaque that can form on both supragingival (above the gum line) and subgingival (below the gum line) surfaces. Understanding the differences between these two types of calculus is essential for effective periodontal disease management.
Subgingival Calculus
-
Color and Composition:
- Appearance: Subgingival calculus is typically dark green or dark brown in color.
- Causes of Color:
- The dark color is likely due to the presence of matrix components that differ from those found in supragingival calculus.
- It is influenced by iron heme pigments that are associated with the bleeding of inflamed gingiva, reflecting the inflammatory state of the periodontal tissues.
-
Formation Factors:
- Matrix Components: The subgingival calculus matrix contains blood products, which contribute to its darker coloration.
- Bacterial Environment: The subgingival environment is typically more anaerobic and harbors different bacterial species compared to supragingival calculus.
Supragingival Calculus
-
Formation Factors:
- Dependence on Plaque and Saliva:
- The degree of supragingival calculus formation is primarily influenced by the amount of bacterial plaque present and the secretion of salivary glands.
- Increased plaque accumulation leads to greater calculus formation.
- Dependence on Plaque and Saliva:
-
Inorganic Components:
- Source: The inorganic components of supragingival calculus are mainly derived from saliva.
- Composition: These components include minerals such as calcium and phosphate, which contribute to the calcification process of plaque.
Comparison of Inorganic Components
-
Supragingival Calculus:
- Inorganic components are primarily sourced from saliva, which contains minerals that facilitate the formation of calculus on the tooth surface.
-
Subgingival Calculus:
- In contrast, the inorganic components of subgingival calculus are derived mainly from crevicular fluid (serum transudate), which seeps into the gingival sulcus and contains various proteins and minerals from the bloodstream.
Sutures for Periodontal Flaps
Suturing is a critical aspect of periodontal surgery, particularly when managing periodontal flaps. The choice of suture material can significantly influence healing, tissue adaptation, and overall surgical outcomes.
1. Nonabsorbable Sutures
Nonabsorbable sutures are designed to remain in the tissue until they are manually removed. They are often used in situations where long-term support is needed.
A. Types of Nonabsorbable Sutures
-
Silk (Braided)
- Characteristics:
- Excellent handling properties and knot security.
- Provides good tissue approximation.
- Applications: Commonly used in periodontal surgeries due to its ease of use and reliability.
- Characteristics:
-
Nylon (Monofilament) (Ethilon)
- Characteristics:
- Strong and resistant to stretching.
- Less tissue reactivity compared to silk.
- Applications: Ideal for delicate tissues and areas requiring minimal tissue trauma.
- Characteristics:
-
ePTFE (Monofilament) (Gore-Tex)
- Characteristics:
- Biocompatible and non-reactive.
- Excellent tensile strength and flexibility.
- Applications: Often used in guided tissue regeneration procedures and in areas where long-term support is needed.
- Characteristics:
-
Polyester (Braided) (Ethibond)
- Characteristics:
- High tensile strength and good knot security.
- Less pliable than silk.
- Applications: Used in situations requiring strong sutures, such as in flap stabilization.
- Characteristics:
2. Absorbable Sutures
Absorbable sutures are designed to be broken down by the body over time, eliminating the need for removal. They are often used in periodontal surgeries where temporary support is sufficient.
A. Types of Absorbable Sutures
-
Surgical Gut
-
Plain Gut (Monofilament)
- Absorption Time: Approximately 30 days.
- Characteristics: Made from sheep or cow intestines; provides good tensile strength initially but loses strength quickly.
- Applications: Suitable for soft tissue approximation where rapid absorption is desired.
-
Chromic Gut (Monofilament)
- Absorption Time: Approximately 45 to 60 days.
- Characteristics: Treated with chromium salts to delay absorption; retains strength longer than plain gut.
- Applications: Used in areas where a longer healing time is expected.
-
-
Synthetic Absorbable Sutures
-
Polyglycolic Acid (Braided) (Vicryl, Ethicon)
- Absorption Time: Approximately 16 to 20 days.
- Characteristics: Provides good tensile strength and is absorbed predictably.
- Applications: Commonly used in periodontal and oral surgeries due to its handling properties.
-
Dexon (Davis & Geck)
- Characteristics: Similar to Vicryl; made from polyglycolic acid.
- Applications: Used in soft tissue approximation and ligation.
-
Polyglycaprone (Monofilament) (Maxon)
- Absorption Time: Similar to Vicryl.
- Characteristics: Offers excellent tensile strength and is absorbed more slowly than other synthetic options.
- Applications: Ideal for areas requiring longer support during healing.
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Connective Tissue of the Gingiva and Related Cellular Components
The connective tissue of the gingiva, known as the lamina propria, plays a crucial role in supporting the gingival epithelium and maintaining periodontal health. This lecture will cover the structure of the lamina propria, the types of connective tissue fibers present, the role of Langerhans cells, and the changes observed in the periodontal ligament (PDL) with aging.
Structure of the Lamina Propria
-
Layers of the Lamina Propria:
- The lamina propria consists of two distinct layers:
- Papillary Layer:
- The upper layer that interdigitates with the epithelium, containing finger-like projections that increase the surface area for exchange of nutrients and waste.
- Reticular Layer:
- The deeper layer that provides structural support and contains larger blood vessels and nerves.
- Papillary Layer:
- The lamina propria consists of two distinct layers:
-
Types of Connective Tissue Fibers:
-
The lamina propria contains three main types of connective tissue fibers:
- Collagen Fibers:
- Type I Collagen: Forms the bulk of the lamina propria and provides tensile strength to the gingival fibers, essential for maintaining the integrity of the gingiva.
- Reticular Fibers:
- These fibers provide a supportive network within the connective tissue.
- Elastic Fibers:
- Contribute to the elasticity and flexibility of the gingival tissue.
- Collagen Fibers:
-
Type IV Collagen:
- Found branching between the Type I collagen bundles, it is continuous with the fibers of the basement membrane and the walls of blood vessels.
-
Langerhans Cells
-
Description:
- Langerhans cells are dendritic cells located among keratinocytes at all suprabasal levels of the gingival epithelium.
- They belong to the mononuclear phagocyte system and play a critical role in immune responses.
-
Function:
- Act as antigen-presenting cells for lymphocytes, facilitating the immune reaction.
- Contain specific granules known as Birbeck’s granules and exhibit marked ATP activity.
-
Location:
- Found in the oral epithelium of normal gingiva and in small amounts in the sulcular epithelium.
- Absent from the junctional epithelium of normal gingiva.
Changes in the Periodontal Ligament (PDL) with Aging
- Aging Effects:
- With aging, several changes have been reported in the periodontal
ligament:
- Decreased Numbers of Fibroblasts: This reduction can lead to impaired healing and regeneration of the PDL.
- Irregular Structure: The PDL may exhibit a more irregular structure, paralleling changes in the gingival connective tissues.
- Decreased Organic Matrix Production: This can affect the overall health and function of the PDL.
- Epithelial Cell Rests: There may be a decrease in the number of epithelial cell rests, which are remnants of the Hertwig's epithelial root sheath.
- Increased Amounts of Elastic Fibers: This change may contribute to the altered mechanical properties of the PDL.
- With aging, several changes have been reported in the periodontal
ligament:
Zones of Periodontal Disease
Listgarten described four distinct zones that can be observed in periodontal lesions. These zones may blend with each other and may not be present in every case.
Zones of Periodontal Disease
-
Zone 1: Bacterial Zone
- Description: This is the most superficial zone, consisting of a diverse array of bacteria.
- Characteristics:
- The bacterial zone is primarily composed of various microbial species, including both pathogenic and non-pathogenic bacteria.
- This zone is critical in the initiation and progression of periodontal disease, as the presence of specific bacteria can trigger inflammatory responses in the host.
-
Zone 2: Neutrophil Rich Zone
- Description: This zone contains numerous leukocytes, predominantly neutrophils.
- Characteristics:
- The neutrophil-rich zone is indicative of the body’s immune response to the bacterial invasion.
- Neutrophils are the first line of defense and play a crucial role in phagocytosing bacteria and releasing inflammatory mediators.
- The presence of a high number of neutrophils suggests an acute inflammatory response, which is common in active periodontal disease.
-
Zone 3: Necrotic Zone
- Description: This zone consists of disintegrated tissue cells, fibrillar material, remnants of collagen fibers, and spirochetes.
- Characteristics:
- The necrotic zone reflects tissue destruction and is characterized by the presence of dead or dying cells.
- Fibrillar material and remnants of collagen fibers indicate the breakdown of the extracellular matrix, which is essential for maintaining periodontal tissue integrity.
- Spirochetes, which are associated with more aggressive forms of periodontal disease, can also be found in this zone, contributing to the necrotic process.
-
Zone 4: Zone of Spirochetal Infiltration
- Description: This zone consists of well-preserved tissue that is infiltrated with large and medium spirochetes.
- Characteristics:
- The zone of spirochetal infiltration indicates a more chronic phase of periodontal disease, where spirochetes invade the connective tissue.
- The presence of well-preserved tissue suggests that while spirochetes are present, the tissue has not yet undergone extensive necrosis.
- This zone is significant as it highlights the role of spirochetes in the pathogenesis of periodontal disease, particularly in cases of necrotizing periodontal diseases.
Hypercementosis
Hypercementosis is a dental condition characterized by the excessive deposition of cementum on the roots of teeth. This condition can have various clinical implications and is associated with several underlying factors. Understanding hypercementosis is essential for dental professionals in diagnosing and managing related conditions.
Characteristics of Hypercementosis
-
Definition:
- Hypercementosis is defined as a generalized thickening of the cementum, often accompanied by nodular enlargement of the apical third of the root. It can also manifest as spike-like excrescences known as cemental spikes.
-
Forms of Hypercementosis:
- Generalized Type: Involves a uniform thickening of cementum across multiple teeth.
- Localized Type: Characterized by nodular
enlargements or cemental spikes, which may result from:
- Coalescence of cementicles adhering to the root.
- Calcification of periodontal fibers at their insertion points into the cementum.
Radiographic Appearance
- Radiographic Features:
- On radiographs, hypercementosis is identified by the presence of a radiolucent shadow of the periodontal ligament and a radiopaque lamina dura surrounding the area of hypercementosis, similar to normal cementum.
- Differentiation:
- Hypercementosis can be differentiated from other conditions such as periapical cemental dysplasia, condensing osteitis, and focal periapical osteopetrosis, as these entities are located outside the shadow of the periodontal ligament and lamina dura.
Etiology of Hypercementosis
-
Varied Etiology:
- The exact cause of hypercementosis is not completely understood, but
several factors have been identified:
- Spike-like Hypercementosis: Often results from excessive tension due to orthodontic appliances or occlusal forces.
- Generalized Hypercementosis: Can occur in
various circumstances, including:
- Teeth Without Antagonists: In cases where teeth lack opposing teeth, hypercementosis may develop as a compensatory mechanism to keep pace with excessive tooth eruption.
- Low-Grade Periapical Irritation: Associated with pulp disease, where hypercementosis serves as compensation for the loss of fibrous attachment to the tooth.
- The exact cause of hypercementosis is not completely understood, but
several factors have been identified:
-
Systemic Associations:
- Hypercementosis may also be observed in systemic conditions,
including:
- Paget’s Disease: Characterized by hypercementosis of the entire dentition.
- Other Conditions: Acromegaly, arthritis, calcinosis, rheumatic fever, and thyroid goiter have also been linked to hypercementosis.
- Hypercementosis may also be observed in systemic conditions,
including:
Clinical Implications
-
Diagnosis:
- Recognizing hypercementosis is important for accurate diagnosis and treatment planning. Radiographic evaluation is essential for distinguishing hypercementosis from other dental pathologies.
-
Management:
- While hypercementosis itself may not require treatment, it can complicate dental procedures such as extractions or endodontic treatments. Understanding the condition can help clinicians anticipate potential challenges.
-
Monitoring:
- Regular monitoring of patients with known systemic conditions associated with hypercementosis is important to manage any potential complications.
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
-
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.
-
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.
-
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.
-
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.