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Questions and Answers
What is the primary role of cytokines in periodontitis?
What is the primary role of cytokines in periodontitis?
Which bacterial virulence factor in P.gingivallis helps resist host defenses?
Which bacterial virulence factor in P.gingivallis helps resist host defenses?
How do matrix metalloproteinases (MMPs) contribute to periodontal disease?
How do matrix metalloproteinases (MMPs) contribute to periodontal disease?
What is the effect of leukotoxin produced by A.actinomycemcomitans?
What is the effect of leukotoxin produced by A.actinomycemcomitans?
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What initiates the initial lesion of periodontal disease?
What initiates the initial lesion of periodontal disease?
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Which type of white blood cell is primarily involved in the body's first line of defense against periodontitis?
Which type of white blood cell is primarily involved in the body's first line of defense against periodontitis?
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What happens to junctional epithelial cells during the immune response to periodontal pathogens?
What happens to junctional epithelial cells during the immune response to periodontal pathogens?
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Which factor is NOT a component of the inflammatory response in periodontitis?
Which factor is NOT a component of the inflammatory response in periodontitis?
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Which of the following statements accurately describes the role of matrix metalloproteinases (MMPs) in periodontal tissue destruction?
Which of the following statements accurately describes the role of matrix metalloproteinases (MMPs) in periodontal tissue destruction?
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What is the primary outcome of the immune system response in periodontal disease?
What is the primary outcome of the immune system response in periodontal disease?
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Which factor is NOT associated with an increased risk of infection in periodontal disease?
Which factor is NOT associated with an increased risk of infection in periodontal disease?
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Which clinical feature is indicative of periodontal disease progression?
Which clinical feature is indicative of periodontal disease progression?
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How does chronic inflammation affect periodontal tissues?
How does chronic inflammation affect periodontal tissues?
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What occurs within 4-7 days of plaque biofilm accumulation?
What occurs within 4-7 days of plaque biofilm accumulation?
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Which cell type is primarily responsible for phagocytosing bacteria in the sulcus?
Which cell type is primarily responsible for phagocytosing bacteria in the sulcus?
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What is a consequence of cytokine release by PMNs during inflammation?
What is a consequence of cytokine release by PMNs during inflammation?
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Which clinical feature indicates inflammation in the gingival marginal tissue?
Which clinical feature indicates inflammation in the gingival marginal tissue?
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What happens if the host response fails to control bacterial infections?
What happens if the host response fails to control bacterial infections?
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What characterizes the tissue level changes in response to inflammation?
What characterizes the tissue level changes in response to inflammation?
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How does good oral hygiene influence plaque biofilm and gingival health?
How does good oral hygiene influence plaque biofilm and gingival health?
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What is the primary role of macrophages in connective tissues during inflammation?
What is the primary role of macrophages in connective tissues during inflammation?
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What is primarily responsible for the production of antibodies in the affected connective tissue during an established lesion?
What is primarily responsible for the production of antibodies in the affected connective tissue during an established lesion?
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During an established lesion, what structural change occurs to the junctional epithelium?
During an established lesion, what structural change occurs to the junctional epithelium?
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What is the primary consequence of increased secretion of cytokines by epithelial cells in response to subgingival bacteria?
What is the primary consequence of increased secretion of cytokines by epithelial cells in response to subgingival bacteria?
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Which of the following best describes the host response during an advanced lesion of periodontitis?
Which of the following best describes the host response during an advanced lesion of periodontitis?
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What occurs to collagen in the connective tissue as the inflammation persists?
What occurs to collagen in the connective tissue as the inflammation persists?
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Which feature is NOT characteristic of an established lesion compared to initial gingivitis?
Which feature is NOT characteristic of an established lesion compared to initial gingivitis?
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What is the main consequence of unmanaged bacterial infection in the established lesion phase?
What is the main consequence of unmanaged bacterial infection in the established lesion phase?
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Which immune cells are key players in producing cytokines that contribute to the destruction of gingival connective tissue?
Which immune cells are key players in producing cytokines that contribute to the destruction of gingival connective tissue?
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Study Notes
Pathogenesis of Periodontitis
- Chemical Mediators: Cytokines, prostaglandins, matrix metalloproteinases.
- Cytokines: Small proteins controlling immune cell growth and activity, signaling the immune system.
- Action of Cytokines in Periodontitis: Release pro-inflammatory cytokines in response to pathogens, accelerating periodontal tissue destruction.
- Prostaglandins: Produced during inflammation, contributing to bone resorption, chemotaxis, and vascular changes.
- Matrix Metalloproteinases (MMPs): Enzymes degrading connective tissue and extracellular matrix components, part of the inflammatory response.
- Polymorphonuclear Leukocytes (PMNs): White blood cells, the body's first line of defense against pathogens, including neutrophils, eosinophils, basophils, and mast cells.
- Bacteria Involved in Periodontitis & Virulence Factors:
- P. gingivalis: Gingipains (for nutrient uptake); carbohydrate capsule (resists host defenses).
- T. denticola: Adherence mechanisms (bind to fibroblasts); degrades cytokines, disrupting host defense.
- T. forsythia: Proteases and apoptotic factors (cause cell death to immune cells).
- A. actinomycetemcomitans: Leukotoxin (destroys white blood cells, inhibits immune response); proteases and toxins (destroy and invade host epithelial cells).
Initial Lesion (2-4 Days After Plaque Biofilm Accumulation)
- Bacterial Features: Bacteria colonize tooth surfaces.
- Cellular Features: Junctional epithelial cells release inflammatory mediators; polymorphonuclear leukocytes (PMNs) are recruited to the area; PMNs migrate into the sulcus, phagocytosing bacteria, and releasing cytokines that can damage healthy gingival connective tissue.
- Tissue Level Features: Plaque biofilm localized supragingivally; vascular dilation in the dentogingival complex (junctional, sulcular, and oral epithelium, connective tissue); gingival crevicular fluid increases in volume, attracting inflammatory cells.
- Clinical Features: Clinically, gingiva appears healthy.
- Host Response: Successful host response if bacteria are effectively cleared and the damage is repairable. Body repair is possible if the bacteria and infection are controlled.
Early Lesion (4-7 Days After Plaque Biofilm Accumulation)
- Bacterial Features: Plaque biofilm accumulation continues and matures; toxins and byproducts penetrate junctional epithelium.
- Cellular Features: PMNs migrate toward the inflammation site, cytokines released by the junctional epithelium increase bacterial defenders; increased blood vessel permeability allows for more PMNs to migrate through tissue near the infection site.
- Tissue Level: Sulcular epithelium and surrounding connective tissue are affected, collagen loss occurs; junctional epithelium cells begin to proliferate, forming epithelial ridges; inflammation is present.
- Clinical Features: Edema (fluid build-up), inflammation, redness of the gingival marginal tissue are observed clinically.
Established Lesion (21 Days After Plaque Biofilm Accumulation)
- Bacterial Features: Plaque biofilm extends subgingivally; disrupts attachment of coronal portion of junctional epithelium from tooth surface.
- Cellular Features: Migration of additional cellular defenders to the site of infection (e.g., PMNs, macrophages, lymphocytes, plasma cells produce antibodies); immune cells increase to fight bacteria, and more toxic chemicals and collagen destruction occur.
- Tissue Level: Epithelial ridges extend deeper into gingival connective tissue; junctional epithelium loosens and transforms into pocket epithelium; more collagen degradation occurs.
- Clinical Features: All features of gingivitis are more evident at this point.
Advanced Lesion: Periodontitis
- Bacterial Features: Plaque biofilm grows laterally and apically along the root surface; periodontal pockets provide a great environment for continued subgingival bacterial growth.
- Cellular Features: Host response intensifies, with bacterial infection becoming chronic, and the inflammation in the periodontium (cementum, PDL, alveolar bone, and gingiva). Increased cellular defenders; immune system releases excessive chemicals that damage periodontal tissues.
- Tissue Level: Destruction of periodontal tissue continues; junctional epithelium cells migrate apically, forming a periodontal pocket; gingival fibroblasts are involved in this tissue degradation.
- Clinical Features: Periodontal pocketing, bleeding on probing, loss of alveolar bone, furcation involvement, and tooth mobility are observed.
- Host Response: Chronic inflammation damages periodontium more than the infection itself; abnormal PMN function, presence of bacterial virulence factors, and systemic factors (e.g., smoking, diabetes) can influence host response.
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Description
Explore the complex mechanisms behind periodontitis in this quiz. Learn about the roles of cytokines, prostaglandins, and matrix metalloproteinases in inflammatory responses. Test your knowledge on the bacteria involved and their virulence factors.
