Host Immune Response to Plaque Biofilm
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Questions and Answers

What is a significant effect of lipopolysaccharide (LPS) in periodontal disease?

  • LPS initiates inflammation in periodontal tissues. (correct)
  • LPS enhances collagen synthesis.
  • LPS neutralizes bacterial enzymes.
  • LPS promotes tissue repair.

Which periodontal bacteria are known to invade host tissues?

  • Escherichia coli and Staphylococcus aureus.
  • Streptococcus mutans and Lactobacillus spp.
  • Prevotella intermedia and Fusobacterium nucleatum.
  • Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans. (correct)

How do certain periodontal bacteria hinder the host immune response?

  • By enhancing immune cell proliferation.
  • By synthesizing antibiotics.
  • By reducing bacterial colonization.
  • By producing enzymes that degrade host proteins. (correct)

What genetic factor is associated with aggressive types of periodontal diseases?

<p>Papillon-Lefèvre syndrome. (B)</p> Signup and view all the answers

What impact does tobacco smoking have on periodontal disease?

<p>It decreases PMN phagocytic capacity. (D)</p> Signup and view all the answers

How does diabetes mellitus affect the host response in periodontal disease?

<p>It reduces PMN function and increases inflammatory mediators. (C)</p> Signup and view all the answers

Which of the following factors does NOT affect the host immune response to plaque biofilm?

<p>Dietary habits. (B)</p> Signup and view all the answers

What role do enzymes produced by periodontal bacteria play in disease progression?

<p>They contribute to the breakdown of periodontium structure. (B)</p> Signup and view all the answers

Which of the following is NOT a consequence of smoking on periodontal health?

<p>Enhanced immune cell activity. (B)</p> Signup and view all the answers

What is the primary outcome of the host immune response in the context of periodontal disease?

<p>Irreversible tissue damage (B)</p> Signup and view all the answers

What role do macrophages play in periodontal disease?

<p>Producing high concentrations of cytokines and MMPs (C)</p> Signup and view all the answers

Which of the following describes a significant tissue-level change observed in advanced periodontal disease?

<p>Apical migration of junctional epithelium (C)</p> Signup and view all the answers

What mediates the destruction of alveolar bone in periodontal disease?

<p>PGE2 stimulating osteoclasts (C)</p> Signup and view all the answers

Which clinical feature is commonly associated with advanced periodontal disease?

<p>Tooth mobility (D)</p> Signup and view all the answers

What triggers the shift of gingival fibroblasts toward tissue destruction in periodontal disease?

<p>Host immune response intensity (D)</p> Signup and view all the answers

What initiates the host immune response during the bacterial accumulation phase?

<p>Metabolic products of gram-negative bacteria (A)</p> Signup and view all the answers

What is the primary goal of polymorphonuclear leukocytes (PMNs) in the initial lesion phase?

<p>To reach and destroy bacterial infections (B)</p> Signup and view all the answers

Which cytokines are important for stimulating the immune response in the initial lesion stage?

<p>Those released by junctional epithelial cells (C)</p> Signup and view all the answers

What clinical feature is observed during the initial lesion phase of periodontal disease?

<p>Healthy-looking gingiva (C)</p> Signup and view all the answers

What occurs if the bacterial infection is effectively controlled in the initial lesion stage?

<p>Repair of tissue destruction (C)</p> Signup and view all the answers

During early gingivitis, what changes occur in the composition of PMNs?

<p>Formation of a wall of cells around bacteria (B)</p> Signup and view all the answers

What effect does increased permeability of blood vessels have during the early lesion phase of gingivitis?

<p>Facilitation of PMN movement into the infection site (D)</p> Signup and view all the answers

What role do bacterial toxins play in early gingivitis?

<p>They penetrate the junctional epithelium causing damage (D)</p> Signup and view all the answers

What is a likely consequence of uncontrolled bacterial pathogens during the initial phase?

<p>Progression to early gingivitis (C)</p> Signup and view all the answers

How long does it typically take for the initial lesion phase to develop following plaque accumulation?

<p>2 to 4 days (B)</p> Signup and view all the answers

What role do macrophages play in the immune response during the early lesion phase?

<p>They release biochemical mediators that recruit additional immune cells. (D)</p> Signup and view all the answers

During the early lesion phase, what percentage of collagen loss is observed in the connective tissue?

<p>60% to 70% (C)</p> Signup and view all the answers

What initiates the inflammatory changes in gingival marginal tissue?

<p>Formation of subgingival plaque biofilm (C)</p> Signup and view all the answers

What happens to the sulcular epithelium during the early lesion phase?

<p>It proliferates to form epithelial extensions. (A)</p> Signup and view all the answers

What is a consequence if the host immune response fails to control the bacterial infection?

<p>The early lesion may progress to established gingivitis. (C)</p> Signup and view all the answers

What is the primary cell type predominating in established lesions?

<p>Plasma cells (C)</p> Signup and view all the answers

What is primarily responsible for the excessive loss of collagen in the affected connective tissue zone?

<p>Matrix metalloproteinases (MMPs) (D)</p> Signup and view all the answers

What role do cytokines play in the immune response to bacterial infection?

<p>They recruit additional immune cells. (D)</p> Signup and view all the answers

What additional cellular defenders are recruited by the presence of subgingival bacteria?

<p>PMNs, macrophages, and lymphocytes (B)</p> Signup and view all the answers

What happens to the junctional epithelium during the established gingivitis phase?

<p>It begins to transform into pocket epithelium. (D)</p> Signup and view all the answers

How does good patient self-care affect plaque biofilm in the context of gingivitis?

<p>It can disrupt plaque biofilm and lead to a return to health. (B)</p> Signup and view all the answers

What is indicated by the presence of inflammatory changes such as edema and redness in gingival tissue?

<p>Early stage of periodontal disease (D)</p> Signup and view all the answers

What is a significant outcome of the host response during established gingivitis?

<p>The response often successfully controls the bacterial challenge. (D)</p> Signup and view all the answers

What is the expected duration for the development of the early lesion phase following plaque accumulation?

<p>4 to 7 days (A)</p> Signup and view all the answers

Which of the following features is NOT associated with established gingivitis?

<p>Clinical features are less noticeable than early stages (C)</p> Signup and view all the answers

What stimulates gingival fibroblasts to produce additional PGE2 and MMPs?

<p>Bacterial presence (C)</p> Signup and view all the answers

What is the role of PMNs in the established lesion?

<p>They continue to assist in fighting bacteria. (B)</p> Signup and view all the answers

What is a common consequence if established gingivitis is not controlled?

<p>It may progress to periodontitis. (B)</p> Signup and view all the answers

What happens to the connective tissue during the established lesion phase?

<p>It is characterized by destruction of healthy tissue. (B)</p> Signup and view all the answers

What occurs at the tissue level features in the established lesion phase?

<p>Epithelial ridges extend deeper into connective tissue. (B)</p> Signup and view all the answers

Flashcards

LPS in Plaque Biofilm

Lipopolysaccharide (LPS) is an endotoxin found on the outer membrane of gram-negative bacteria in mature plaque biofilm. It triggers inflammation in periodontal tissues.

Bacterial Tissue Invasion

Certain periodontal bacteria, like Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, can penetrate host tissues, evading some host defenses.

Bacterial Enzymes in Periodontal Disease

Periodontal bacteria produce enzymes like collagenases and proteases that break down host tissue proteins in the periodontium.

Genetic Factors in Periodontal Disease

Genetic factors play a role in periodontal disease susceptibility. Variations in genes affect the immune response, making some more prone to the diseases.

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Environmental Risk Factor for Periodontal Disease

Smoking decreases neutrophil function, reduces gingival blood flow, and affects immune responses, increasing periodontal disease risk.

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Diabetes Impact on Host Response

Diabetes impairs neutrophil function, and increases inflammatory mediators, negatively impacting periodontal ligament and osteoblast functions.

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Bacterial Accumulation (Initial Lesion)

Bacteria first colonize tooth surfaces near the gum line, triggering the body's immune response.

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PMNs in Initial Lesion

White blood cells (PMNs) move from blood vessels into the gum tissue to fight bacteria.

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Complement System Activation

A part of the immune system is activated during the initial bacterial invasion.

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Early Gingivitis (Early Lesion)

Bacterial biofilm matures, producing toxins that penetrate the junctional epithelium, leading to inflammation.

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Migration of PMNs

White blood cells travel through the junctional epithelium to reach bacteria in the periodontal pockets.

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Cytokines' Role in Early Gingivitis

Cytokines released by the immune cells attract more defenders and cause tissue damage.

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PMN Migration

Polymorphonuclear neutrophils (PMNs) move through connective tissue towards the gum sulcus to combat bacteria.

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Macrophage Recruitment

Macrophages are drawn to the infection site and release mediators (like cytokines, PGE2, and MMPs) to call for more immune cells.

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T-Lymphocyte Role

T-lymphocytes travel to the affected tissue, producing cytokines and antibodies to help with the immune response.

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Sulcular Epithelial Changes

The sulcular epithelium and surrounding connective tissue experience collagen loss (60-70%) and form ridges during the early lesion.

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Junctional Epithelium Proliferation

Junctional epithelial cells multiply due to inflammation.

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Early Lesion Duration

The early gingivitis phase, from plaque development, lasts 4-7 days and varies between individuals.

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Host Response Control

The large number of PMNs, macrophages, and T-lymphocytes are effective in containing bacterial pathogens.

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Established Gingivitis

If the immune response fails in early stage gingivitis, it progresses to established gingivitis, a more advanced stage of progressing disease.

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Subgingival Plaque

Subgingival plaque extends into the gingival sulcus, detaching the junctional epithelium from the tooth.

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Cytokine Stimulation

High subgingival bacterial levels stimulate epithelial cells to secrete more cytokines, increasing immune cell recruitment.

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Established Gingivitis

A stage of gingivitis characterized by plasma cells dominating the inflamed connective tissue and intensified symptoms compared to initial stages.

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Plasma Cells

Immune cells that produce antibodies to fight bacteria in gingivitis.

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Immune Response (Gingivitis)

Body's reaction to bacterial challenge, increasing inflammation and tissue damage in gingivitis.

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Cytokines, PGE2, and MMPs

Chemicals released by immune cells, initiating tissue damage and collagen destruction in gingivitis.

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Epithelial Ridges

Structures in the gum tissue that extend deeper into connective tissue, maintaining epithelial integrity.

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Junctional Epithelium Changes

The attachment of junctional epithelium to root surface in gingivitis weakens and transforms into pocket epithelium, which is more permeable.

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Collagen Loss

Continued breakdown of collagen in the connective tissue of the gums during gingivitis.

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Clinical Features (Established Gingivitis)

Stronger inflammation and other symptoms are seen in established gingivitis compared to initial stages.

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Timeframe of Established Gingivitis

Typically appears around 21 days after plaque biofilm buildup, showing a delay in noticeable symptoms.

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Outcome Control (Gingivitis)

Effective treatment (professional and self-care) can stop bacterial growth and restore gum health.

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Gingivitis to Periodontitis

In some people, uncontrolled gingivitis can progress to periodontitis, where the damage extends to deeper supporting structures.

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Periodontal Pocket Formation

The gingival pocket deepens due to the apical migration of the junctional epithelium, connective tissue destruction, and periodontal ligament breakdown in reaction to invading bacteria.

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Chronic Inflammation

Persistent immune response to bacterial infection, leading to tissue damage.

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Host Immune Response Damage

The intense immune response, while trying to fight infection, actually causes more tissue damage than the bacteria.

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Tissue Destruction Periodontal Disease

In periodontal disease, the damage to periodontal tissues due to immune responses now overwhelms the body's ability to repair these tissues.

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Alveolar Bone Loss

Destruction of the bone surrounding the teeth due to activities of osteoclasts stimulated by PGE2.

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Periodontal Pocket

A deepened gingival sulcus, forming a pocket where bacteria can thrive due to the apical migration of junctional epithelium, causing damage and inflammation.

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Cytokines and MMPs

Immune cells (like PMNs and macrophages) release these chemicals, leading to the destruction of periodontal tissues.

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PGE2 Role in Periodontal Disease

This molecule, a product of inflammation, signals to bone-resorbing cells (osteoclasts) and causes damage.

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Study Notes

Host Immune Response to Plaque Biofilm

  • Periodontal disease is a bacterial infection causing inflammation in periodontal tissues.
  • Bacteria are essential for periodontal disease, but the host response plays a significant role in tissue destruction.
  • The host response involves the immune system's attempt to defend against invading bacteria.
  • Bacteria that cause damage through virulence factors (structural properties or produced substances).
  • Factors that enhance microbial challenge include lipopolysaccharide (LPS), the ability to invade tissues, and the ability to produce enzymes.
  • Factors influencing the host response include genetics (Papillon-Lefèvre syndrome, leukocyte adhesion deficiency, etc.), environmental factors (e.g.,smoking), and acquired factors (e.g., diabetes mellitus)
  • Inflammation is a crucial part of the host response; it's initially protective but can become harmful in periodontitis.
  • Acute inflammation occurs as a first line of defense, but needs to be properly shut down for periodontal health.
  • The resolution of inflammation (catabasis) is equally important for tissue health
  • Chronic inflammation can lead to tissue damage if not resolved efficiently
  • Inflammatory biochemical mediators include cytokines (IL-1, IL-6, IL-8, and TNF-α), prostaglandins (PGE2), and matrix metalloproteinases (MMPs).
  • MMPs break down connective tissue, while TIMPs regulate their activity.
  • Cytokines: regulate other cells, can be protective or destructive. IL-1, IL-6, IL-8, and TNF-α are crucial in periodontitis.
  • Prostaglandins: regulate blood vessel dilation and influence osteoclast activity. PGE2 is important in bone destruction.

Histologic Stages in the Development of Periodontal Disease

  • Four stages: bacterial accumulation, early gingivitis, established gingivitis, and periodontitis.
  • Bacterial Accumulation (Initial Lesion): Bacteria colonize the tooth surface, initiate the host immune response, with PMN recruitment to the site. Gingival tissues appear healthy in this stage.
  • Early Gingivitis (Early Lesion): Increased bacterial challenge, PMNs migrate toward bacteria, gingival tissues show early inflammation. This stage typically develops 4-7 days after plaque accumulation.
  • Established Gingivitis (Established Lesion): Bacteria extends deeper into the gingival sulcus. Increased immune response, and cells like plasma cells are recruited. Epithelial ridges develop, as well as changes to connective tissue.
  • Periodontitis (Advanced Lesion): The host response is overwhelmed, leading to irreversible tissue damage (pocket formation, bone loss).

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Description

This quiz explores the complex interaction between the host immune response and plaque biofilm in periodontal disease. It covers how bacterial infections trigger inflammation and the various factors influencing both microbial challenge and host defense mechanisms. Test your knowledge on the crucial elements that contribute to periodontal tissue destruction.

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