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Questions and Answers
What primarily characterizes the established lesion in connective tissue?
What primarily characterizes the established lesion in connective tissue?
Which immune cells are involved in combating bacteria in the sulcus?
Which immune cells are involved in combating bacteria in the sulcus?
What role do cytokines play in the immune response during established gingivitis?
What role do cytokines play in the immune response during established gingivitis?
How does the junctional epithelium change during the progression of gingivitis?
How does the junctional epithelium change during the progression of gingivitis?
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What initiates the host immune response during the bacterial accumulation phase?
What initiates the host immune response during the bacterial accumulation phase?
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After how many days is established gingivitis generally observed following plaque biofilm accumulation?
After how many days is established gingivitis generally observed following plaque biofilm accumulation?
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What is the potential outcome if established gingivitis is not controlled in susceptible individuals?
What is the potential outcome if established gingivitis is not controlled in susceptible individuals?
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What is the primary role of PMNs during the bacterial accumulation phase?
What is the primary role of PMNs during the bacterial accumulation phase?
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What clinical feature is indicative of the initial lesion phase?
What clinical feature is indicative of the initial lesion phase?
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What additional substances are produced by macrophages exposed to gram-negative bacteria?
What additional substances are produced by macrophages exposed to gram-negative bacteria?
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Which feature is indicative of gingivitis as it progresses into an established lesion?
Which feature is indicative of gingivitis as it progresses into an established lesion?
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Which of the following statements about PMNs in early gingivitis is correct?
Which of the following statements about PMNs in early gingivitis is correct?
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How does the complement system relate to the host immune response during bacterial accumulation?
How does the complement system relate to the host immune response during bacterial accumulation?
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What role do macrophages play in the immune response during tissue destruction?
What role do macrophages play in the immune response during tissue destruction?
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During the early phase of gingivitis, what percentage of collagen loss is typically observed?
During the early phase of gingivitis, what percentage of collagen loss is typically observed?
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What occurs if the bacterial infection is not controlled after the initial lesion phase?
What occurs if the bacterial infection is not controlled after the initial lesion phase?
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What effect does increased permeability of blood vessels have during early gingivitis?
What effect does increased permeability of blood vessels have during early gingivitis?
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Which cellular feature predominantly characterizes an early lesion phase of gingivitis?
Which cellular feature predominantly characterizes an early lesion phase of gingivitis?
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What is the primary consequence of cytokine release by junctional epithelial cells in early gingivitis?
What is the primary consequence of cytokine release by junctional epithelial cells in early gingivitis?
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What is the primary consequence if the host immune response fails during the early lesions of gingivitis?
What is the primary consequence if the host immune response fails during the early lesions of gingivitis?
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What triggers the epithelial cells to secrete more cytokines during the gingivitis process?
What triggers the epithelial cells to secrete more cytokines during the gingivitis process?
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Which feature is a clinical observation of early gingivitis?
Which feature is a clinical observation of early gingivitis?
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What is the result of effective plaque biofilm control in response to gingivitis?
What is the result of effective plaque biofilm control in response to gingivitis?
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What primarily characterizes the established lesions of gingivitis?
What primarily characterizes the established lesions of 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 bacteria has the ability to invade host tissues in periodontal disease?
Which bacteria has the ability to invade host tissues in periodontal disease?
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What impact does smoking have on the host immune response.
What impact does smoking have on the host immune response.
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How do genetic factors contribute to periodontal disease?
How do genetic factors contribute to periodontal disease?
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Which of the following is a consequence of diabetes mellitus on the host immune response in periodontal disease?
Which of the following is a consequence of diabetes mellitus on the host immune response in periodontal disease?
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What is the effect of enzymes produced by periodontal bacteria?
What is the effect of enzymes produced by periodontal bacteria?
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Which acquired factor is a known risk for periodontal diseases?
Which acquired factor is a known risk for periodontal diseases?
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What is a notable effect of genetic variations in periodontal disease susceptibility?
What is a notable effect of genetic variations in periodontal disease susceptibility?
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What occurs as a result of the chronic immune response to periodontal infection?
What occurs as a result of the chronic immune response to periodontal infection?
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Which cellular component is primarily responsible for the destruction of the extracellular matrix of the gingiva?
Which cellular component is primarily responsible for the destruction of the extracellular matrix of the gingiva?
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What is the main outcome of the host's immune response during advanced periodontal disease?
What is the main outcome of the host's immune response during advanced periodontal disease?
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Which cells migrate apically on the root surface leading to the formation of a periodontal pocket?
Which cells migrate apically on the root surface leading to the formation of a periodontal pocket?
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What characterizes the advanced lesion phase of periodontitis?
What characterizes the advanced lesion phase of periodontitis?
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What role do osteoclasts play in periodontal disease progression?
What role do osteoclasts play in periodontal disease progression?
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Which of the following statements about chronic inflammation in periodontitis is true?
Which of the following statements about chronic inflammation in periodontitis is true?
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What is a hallmark of periodontitis?
What is a hallmark of periodontitis?
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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, although essential, are not alone responsible for tissue destruction. The body's response to bacteria in plaque biofilm is the main cause of damage.
- The host response aims to defend against bacteria in plaque biofilm, but doesn't prioritize preserving the tooth itself.
Factors Enhancing Microbial Challenge
- Bacteria are essential for periodontal disease initiation and progression.
- Virulence factors enable biofilm bacteria to colonize and harm tissues. These can be structural or produced substances.
- LPS (lipopolysaccharide): A component of gram-negative bacteria, can initiate inflammation.
- Tissue invasion: Some bacteria can invade epithelial cells.
- Enzyme production: Collagenases and proteases directly degrade host proteins.
Factors Affecting the Host Immune Response
- Genetic, environmental, and acquired factors affect host susceptibility to periodontal disease. They influence response or tissue metabolism.
- Genetic factors: Link to periodontal disease, studied in twins and families. Conditions like Papillon-Lefèvre syndrome and LAD are associated with aggressive periodontal disease.
- Environmental factors: Smoking significantly impacts the immune and inflammatory systems, decreasing PMN phagocytic capacity, altering blood vessel health, & affecting lymphocyte response.
- Acquired Factors: Diabetes mellitus affects host response by reducing PMN function and increasing inflammation markers like IL-1, TNF-α, and PGE2, reducing fibroblasts' proliferation.
Inflammation: A Protective, Potentially Harmful Host Response
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Acute inflammation: The body's immediate defense against microbial invasion.
- Involves immune cells (PMNs, macrophages, T/B lymphocytes, fibroblasts, epithelial cells) and biochemical mediators.
- Serves as a first line of defense, removing stimuli, repairing tissues, and creating a favorable environment for repair.
- Resolution (catabasis) is essential: successful resolution prevents harmful effects. Issues with resolution can lead to chronic inflammation.
Inflammatory Biochemical Mediators
- Cytokines (released by immune cells): Crucial regulators of cell behaviour. Can be both tissue-protective or -destructive and critical to periodontitis. Key examples include IL-1, IL-6, IL-8, and TNF-α
- Prostaglandins (PGE2): Important inflammatory mediators derived from fatty acids, play a role in bone destruction in periodontitis, affect blood vessel permeability, and trigger osteoclast activity.
- Matrix Metalloproteinases (MMPs): A family of proteolytic enzymes that break down connective tissue matrix. Their role in periodontitis is substantial and tissue destructive when their control is impaired.
- The balance between MMPs and their inhibitors (TIMPs) is crucial for healthy connective tissue. Disruption leads to pathologic breakdown.
Tissue Destruction by Biochemical Mediators
- Each mediator plays a specific role in the local damage to tissues during periodontitis. The table directly correlates the inflammatory mediators with the type of local tissue affects observed in the inflammation/infection response. This demonstrates the multifactoral impact of these events, as these factors impact more than a single tissue.
Current Theory of Pathogenesis
- Periodontal disease development is complex and multifactorial.
- Microbial challenge activates the host response.
- Genetic, environmental, and acquired factors impact the immunoinflammatory response.
- Inflammatory mediators contribute to tissue destruction.
- Resolution of inflammation and returning to homeostasis is also crucial to preventing the negative effects of inflammation.
Histologic Stages of Periodontal Disease
- Bacterial accumulation (initial lesion): Early bacterial colonization, initiating host immune response.
- Early gingivitis (early lesion): Increasing bacterial challenge, escalating PMN and macrophage activity affecting the gingival connective tissue, early tissue changes are apparent.
- Established gingivitis (established lesion): Deeper bacterial penetration, more severe tissue inflammation and destruction (including collagen loss), and visible clinical changes.
- Periodontitis (advanced lesion): Severe tissue damage, formation of pockets, irreversible bone loss, as well as clinical signs. Factors like genetic and environmental conditions and ineffective immune responses potentially contribute to disease progression.
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