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What initiates the host immune response in the bacterial accumulation stage of periodontal disease?
What initiates the host immune response in the bacterial accumulation stage of periodontal disease?
During the initial lesion phase, what is the primary clinical appearance of the gingiva?
During the initial lesion phase, what is the primary clinical appearance of the gingiva?
What happens if the bacterial infection is controlled during the bacterial accumulation stage?
What happens if the bacterial infection is controlled during the bacterial accumulation stage?
What occurs during the transition from bacterial accumulation to early gingivitis?
What occurs during the transition from bacterial accumulation to early gingivitis?
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What is the role of PMNs in the periodontal disease development stages?
What is the role of PMNs in the periodontal disease development stages?
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What outcome results from an unsuccessful host response to bacterial infection?
What outcome results from an unsuccessful host response to bacterial infection?
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What happens to gingival crevicular fluid volume during the initial lesion phase?
What happens to gingival crevicular fluid volume during the initial lesion phase?
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What cellular feature is characteristic of the early gingivitis stage?
What cellular feature is characteristic of the early gingivitis stage?
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What is the primary function of PMNs in the early lesion stage of gingivitis?
What is the primary function of PMNs in the early lesion stage of gingivitis?
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Which immune cells are predominantly present in the early lesion phase of gingivitis?
Which immune cells are predominantly present in the early lesion phase of gingivitis?
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What biochemical mediators are released by macrophages in response to gingival infection?
What biochemical mediators are released by macrophages in response to gingival infection?
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What notable tissue alteration occurs in the sulcular epithelium during early gingivitis?
What notable tissue alteration occurs in the sulcular epithelium during early gingivitis?
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What is the consequence of the host immune response failing to control the infection in gingivitis?
What is the consequence of the host immune response failing to control the infection in gingivitis?
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What is the percentage of collagen loss observed in the connective tissue during the early lesion of gingivitis?
What is the percentage of collagen loss observed in the connective tissue during the early lesion of gingivitis?
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Which of the following changes is NOT typically observed during the early stages of gingivitis?
Which of the following changes is NOT typically observed during the early stages of gingivitis?
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What triggers the increased secretion of cytokines by epithelial cells during gingivitis?
What triggers the increased secretion of cytokines by epithelial cells during gingivitis?
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What role does lipopolysaccharide (LPS) play in periodontal disease?
What role does lipopolysaccharide (LPS) play in periodontal disease?
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Which of the following bacteria is known to invade host tissues?
Which of the following bacteria is known to invade host tissues?
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Which factor is recognized as a significant environmental risk for periodontal disease?
Which factor is recognized as a significant environmental risk for periodontal disease?
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How do genetic factors influence periodontal disease susceptibility?
How do genetic factors influence periodontal disease susceptibility?
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What effect does diabetes mellitus have on the host immune response to periodontal pathogens?
What effect does diabetes mellitus have on the host immune response to periodontal pathogens?
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What is the impact of collagenases and proteases produced by periodontal bacteria?
What is the impact of collagenases and proteases produced by periodontal bacteria?
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What is a known consequence of tobacco smoking on the immune response in periodontal disease?
What is a known consequence of tobacco smoking on the immune response in periodontal disease?
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Which condition is directly associated with aggressive types of periodontal diseases?
Which condition is directly associated with aggressive types of periodontal diseases?
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What characterizes the established lesion in periodontal disease?
What characterizes the established lesion in periodontal disease?
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How do plasma cells contribute to fighting bacterial infections in periodontal disease?
How do plasma cells contribute to fighting bacterial infections in periodontal disease?
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What is one of the effects of cytokines released during the immune response in periodontal disease?
What is one of the effects of cytokines released during the immune response in periodontal disease?
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What change occurs to the junctional epithelium in the established lesion phase?
What change occurs to the junctional epithelium in the established lesion phase?
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Which clinical feature is characteristic of established gingivitis?
Which clinical feature is characteristic of established gingivitis?
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Which of the following actions can help control the bacterial challenge during established gingivitis?
Which of the following actions can help control the bacterial challenge during established gingivitis?
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What can happen if established gingivitis is not controlled in certain individuals?
What can happen if established gingivitis is not controlled in certain individuals?
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What primary feature characterizes the plaque biofilm in periodontitis?
What primary feature characterizes the plaque biofilm in periodontitis?
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What primarily mediates the destruction of the extracellular matrix in the periodontium?
What primarily mediates the destruction of the extracellular matrix in the periodontium?
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Which cells are responsible for bone resorption in response to periodontal disease?
Which cells are responsible for bone resorption in response to periodontal disease?
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What is the outcome of the host immune response in chronic periodontal disease?
What is the outcome of the host immune response in chronic periodontal disease?
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What effect does PGE2 have in the context of periodontal disease?
What effect does PGE2 have in the context of periodontal disease?
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Which of the following is a clinical feature of advanced periodontal disease?
Which of the following is a clinical feature of advanced periodontal disease?
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How does the immune response contribute to tissue destruction in periodontitis?
How does the immune response contribute to tissue destruction in periodontitis?
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What happens to the junctional epithelium in response to periodontal infection?
What happens to the junctional epithelium in response to periodontal infection?
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What characterizes the transition from a gingival pocket to a periodontal pocket?
What characterizes the transition from a gingival pocket to a periodontal pocket?
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Study Notes
Host Immune Response to Plaque Biofilm
- Periodontal disease is a bacterial infection that triggers an inflammatory response in periodontal tissues.
- Bacteria are essential for the disease, but the body's response to the bacteria, in plaque biofilm, is the primary cause of tissue destruction.
- Host response refers to the body's response to bacteria.
- The immune system attempts to eliminate pathogens and limit infection spread, not specifically preserve the tooth or its tissues.
- Virulence factors enable biofilm bacteria to colonize and damage periodontal tissues. These factors can be structural characteristics or substances produced by the bacteria.
- Lipopolysaccharide (LPS) is a component of mature plaque biofilm. Gram-negative bacteria with LPS are virulent.
- Certain bacteria can invade host tissues, avoiding host defenses.
- Certain bacterial enzymes degrade host proteins, contributing to periodontal damage.
- Factors affecting host response include:
- Genetics: Genetic factors can increase susceptibility to periodontal disease.
- Environmental: Tobacco smoking negatively impacts the immune system and inflammatory responses.
- Acquired: Conditions like diabetes mellitus can affect the host response due to irregular blood sugar.
Inflammation: A Protective Host Response
- Acute inflammation is the body's first line of defense against invasion, eliminating harmful agents, replacing damaged cells, and initiating tissue repair.
- Inflammation resolution (catabasis) is a regulated process that re-establishes normal tissue health following removal of a microbial challenge.
- Inflammation can be favorable or detrimental, depending on its resolution process; uncontrolled or unresolved inflammation is damaging.
- Pro-inflammatory mediators (like prostaglandins, thromboxanes, prostacyclins, and leukotrienes) are associated with periodontitis. These mediators contribute to the destructive process by attracting neutrophils (PMNs).
- Inflammation-resolving mediators help dampen the acute response and stimulate tissue repair.
- Unresolved chronic inflammation can damage host tissues if the host response cannot contain the infection quickly.
Inflammatory Biochemical Mediators
- Cytokines, prostaglandins, and matrix metalloproteinases (MMPs) are important biochemical mediators in periodontitis.
- Cytokines are proteins that regulate cell behavior; their production is stimulated during an infection/tissue injury. Some play tissue-protective roles whereas others have potential to harm.
- Prostaglandins increase blood vessel permeability, allowing immune cells influx, and trigger osteoclast activity, destroying bone.
- MMPs (a class of proteases) break down the connective tissue matrix and promote tissue destruction.
- Imbalances or excessive production of these mediators frequently contribute to damage in periodontitis.
Histological Stages of Periodontal Disease
- Histological stages of periodontal disease (initial, early, established, advanced) depict progressive tissue changes in response to plaque.
- Initial lesion: Characterized by bacterial accumulation near the gingival margin, resulting in inflammatory responses by the host (increased vascular dilation and PMN migration)
- Early lesion: Increased inflammation is evident; cytokines, prostaglandins, and MMPs are produced. Sulcular epithelial ridges also appear during this phase.
- Established lesion: Plasma cells are prevalent, tissue changes are more pronounced, and collagen loss is notable.
- Advanced lesion (periodontitis): Characterized by periodontal pocket formation, alveolar bone destruction, and tooth mobility. Significant tissue damage during this stage is considered irreversible.
Current Theory of Pathogenesis
- The interplay between microbial challenges and the host response is a multilayered process affecting periodontal disease progression.
- Risk factors like genetic predisposition, environmental factors (like smoking), and acquired factors (like diabetes) affect the host response and tissue metabolism; making an individual susceptible to developing periodontitis.
- Bacteria produce virulence factors for initiation of periodontal disease while host immune cells release and produce inflammatory mediators to try to fight the bacteria.
- If microbial infection and host inflammatory response are not controlled, damage to connective tissue/alveolar bone occurs leading to periodontitis.
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Description
This quiz explores the host immune response to plaque biofilm associated with periodontal disease. It highlights the role of bacterial infection, virulence factors, and the body's inflammatory response in tissue destruction. Test your knowledge about the complex interactions between bacteria and the immune system in periodontal health.
