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Questions and Answers

What determines whether the acute inflammatory response is beneficial or harmful to the periodontium?

  • The type of microbial challenge present
  • The presence of lipid mediators
  • The extent of the inflammatory response
  • The resolution effectiveness of the acute inflammation (correct)

Which statement about the resolution of inflammation is true?

  • It is an actively regulated biological process. (correct)
  • It is a purely passive process.
  • It happens regardless of microbial challenge removal.
  • It primarily occurs without any mediators.

What is the term used to describe the return to a noninflammatory state after inflammation?

  • Reconstitution
  • Homeostasis
  • Resolution
  • Catabasis (correct)

Which type of mediators are known to regulate the resolution of inflammation?

<p>Specialized pro-resolving lipid mediators (D)</p> Signup and view all the answers

Which of the following is true regarding unresolved inflammation?

<p>It is linked to periodontitis. (A)</p> Signup and view all the answers

What is the primary consequence of overactivity of polymorphonuclear leukocytes (PMNs) during inflammation?

<p>Destruction of connective tissue matrix (C)</p> Signup and view all the answers

Which of the following lipid mediators is NOT typically associated with inflammation?

<p>Antiinflammatory cytokines (B)</p> Signup and view all the answers

What is the role of catabasis in relation to inflammation?

<p>To facilitate a return to homeostasis (A)</p> Signup and view all the answers

What is one of the roles of cytokines in the context of periodontitis?

<p>Enhancing vascular permeability for immune cell migration (C)</p> Signup and view all the answers

Which cytokines are specifically associated with the pathogenesis of periodontitis?

<p>IL-1, IL-6, IL-8, and TNF-α (A)</p> Signup and view all the answers

What is the primary source of prostaglandin E (PGE) in inflamed periodontal tissues?

<p>Macrophages (A)</p> Signup and view all the answers

How do prostaglandins influence the work of osteoclasts in periodontal disease?

<p>They trigger osteoclasts to destroy alveolar bone (B)</p> Signup and view all the answers

What is the role of MMPs in maintaining periodontal health?

<p>Facilitating normal turnover of the connective tissue matrix (C)</p> Signup and view all the answers

Which cells are primarily responsible for producing MMPs in the context of periodontitis?

<p>PMNs and gingival fibroblasts (C)</p> Signup and view all the answers

What can the imbalance of the MMP-TIMP relationship lead to in periodontal health?

<p>Uncontrolled breakdown of the connective tissue matrix (D)</p> Signup and view all the answers

Which biological effects are associated with prostaglandins during inflammation?

<p>Increasing blood vessel permeability and dilation (C)</p> Signup and view all the answers

What initiates the host immune response in the initial lesion of periodontal disease?

<p>Presence of gram-negative bacteria and their metabolic products (D)</p> Signup and view all the answers

Which component plays a critical role in recruiting polymorphonuclear leukocytes (PMNs) to the site of bacterial infection?

<p>Biochemical mediators like cytokines (A)</p> Signup and view all the answers

What consequence results from the cytokines released by PMNs during the immune response?

<p>Destruction of healthy gingival connective tissue (C)</p> Signup and view all the answers

How does the inflammatory process evolve from gingivitis to periodontitis according to current theories?

<p>The host response is modified by cytokines and genetic factors. (A)</p> Signup and view all the answers

What is the primary goal of PMNs infiltrating the gingival connective tissue during the initial lesion phase?

<p>Reach and destroy bacterial pathogens (D)</p> Signup and view all the answers

Which histologic stage of periodontal disease follows the early lesion stage?

<p>Established lesion (B)</p> Signup and view all the answers

Which of the following accurately describes a finding at the advanced lesion stage of periodontal disease?

<p>Significant tissue destruction and tooth mobility (D)</p> Signup and view all the answers

What role do mediators like PGE2 and MMPs play in the pathogenesis of periodontal disease?

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

What is the primary biochemical mediator responsible for recruiting additional immune cells to an infection site?

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

Which statement accurately describes a feature of the early lesion phase of gingivitis?

<p>Epithelial ridges begin to form in the sulcular epithelium. (C)</p> Signup and view all the answers

What is the expected collagen loss at the tissue level during the early lesion of gingivitis?

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

What role do plasma cells play in the established gingivitis stage?

<p>They produce large quantities of antibodies. (A)</p> Signup and view all the answers

What happens if the host immune response fails during the early lesion phase?

<p>The early lesion progresses to established gingivitis. (B)</p> Signup and view all the answers

Which cellular feature predominates during the established lesion phase of gingivitis?

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

Which of the following is NOT a characteristic of the gingival tissue during the early lesion phase?

<p>Predominance of B-lymphocytes. (B)</p> Signup and view all the answers

What initiates the inflammatory changes observed in the early lesion of gingivitis?

<p>Accumulation of plaque biofilm. (D)</p> Signup and view all the answers

What is the primary role of MMPs in periodontal tissue destruction?

<p>They mediate the destruction of the extracellular matrix. (A)</p> Signup and view all the answers

What effect does PGE2 have in the context of periodontal disease?

<p>It stimulates osteoclasts to resorb alveolar bone. (D)</p> Signup and view all the answers

Which of the following statements is true regarding the immune response in periodontitis?

<p>It can cause irreversible tissue damage. (C)</p> Signup and view all the answers

What is a key characteristic of the advanced lesion phase of periodontal disease?

<p>Destruction of alveolar bone. (C)</p> Signup and view all the answers

What primarily causes the migration of the junctional epithelium apically on the root surface?

<p>Destruction of the gingival connective tissue. (C)</p> Signup and view all the answers

Which factor does NOT contribute to the host's inability to control bacterial challenges in periodontal disease?

<p>Overactive macrophage function. (B)</p> Signup and view all the answers

What is a common clinical feature associated with advanced periodontal disease?

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

What is the hallmark of periodontitis due to chronic infection?

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

What is a consequence of increased permeability of blood vessels during an immune response in gingival tissue?

<p>Increased movement of PMNs into the gingival connective tissue (A)</p> Signup and view all the answers

How does the host response to bacterial infections affect tissue repair?

<p>Successful host responses allow for eventual tissue repair (D)</p> Signup and view all the answers

What role do cytokines play during the migration of PMNs in response to bacterial challenge?

<p>They attract additional cellular defenders to the site (A)</p> Signup and view all the answers

What changes occur in the initial phase of gingivitis following plaque accumulation?

<p>Development of initial lesions within 2 to 4 days (C)</p> Signup and view all the answers

What happens to the junctional epithelium during the early gingivitis process?

<p>It allows the penetration of bacterial toxins (A)</p> Signup and view all the answers

What is the initial location of plaque biofilm in a healthy body?

<p>Supragingival surfaces (D)</p> Signup and view all the answers

What is the role of macrophages during the early gingivitis process?

<p>They are attracted to the site and release biochemical mediators (B)</p> Signup and view all the answers

What occurs when bacterial pathogens are not controlled during the gingival response?

<p>The development of early gingivitis takes place (B)</p> Signup and view all the answers

Flashcards

Acute Inflammation Resolution

The process of shutting down the initial inflammatory response after a microbial challenge has been resolved. It's crucial for tissue health and repair.

Catabasis

The return to homeostasis (normal state) after inflammation, an actively regulated process.

Unresolved Inflammation

Inflammation that persists after the initial trigger is gone and does not return to a normal state; linked to many diseases.

Pro-inflammation Mediators

Substances (e.g., prostaglandins, leukotrienes) that cause or worsen inflammation and damage cells. Often overactive in periodontitis.

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Specialized Pro-resolving Lipid Mediators

Substances the body produces to actively reduce inflammation and promote healing.

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Periodontitis

A disease of the gums that involves unresolved inflammation, leading to bone loss and damage.

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Periodontal Disease Pathogenesis

The complex series of events leading from healthy gums to gingivitis to periodontitis, involving microbial infection, host response, and genetic/environmental factors.

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Cytokines in Periodontal Tissue

Cytokines increase vascular permeability, allowing immune cells to enter infected tissues. However, chronic cytokine activity can cause tissue damage, like in periodontitis.

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Key Cytokine in Periodontitis

IL-1, IL-6, IL-8, and TNF-α are important cytokines in the development of periodontitis.

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Initial Lesion (Periodontal Disease)

The first stage of periodontal disease, characterized by bacterial colonization of tooth surfaces near the gum line.

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Prostaglandins (PGE)

Prostaglandins are cell signaling molecules. Specifically, PGE plays a key role in bone loss during periodontitis, promoting blood vessel dilation and osteoclast activity.

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Host Immune Response (Periodontal Disease)

The body's reaction to bacterial infection in the gums, involving cells releasing mediators like cytokines and antibodies.

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Prostaglandin Source (Periodontitis)

Macrophages are the primary source of prostaglandins in inflamed periodontal tissues, although other cells also contribute.

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Bacterial Features (Initial Lesion)

Gram-negative bacteria and their byproducts in the early stages of gum disease that initiate the body's immune response.

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Cellular Features (Initial Lesion)

Junctional epithelial cells release mediators (like cytokines, PGE2, MMPs, TNFα) stimulating immune response in the gums.

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Prostaglandin Function: Blood Vessels

Prostaglandins increase blood vessel permeability and dilation, allowing immune cells to enter the affected periodontal tissue.

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Polymorphonuclear Leukocytes(PMNs)

Immune cells (white blood cells) that travel to the infected area to fight bacteria in the gums.

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Prostaglandin Function: Bone Destruction

Prostaglandins activate osteoclasts, leading to alveolar bone breakdown in periodontitis.

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Prostaglandin Function: MMP Production

Prostaglandins stimulate the production of destructive enzymes called Matrix Metalloproteinases (MMPs).

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MMPs (Matrix Metalloproteinases)

MMPs are a family of enzymes that break down connective tissue. Their overproduction leads to tissue damage.

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MMP Sources (Periodontitis)

Polymorphonuclear leukocytes (PMNs), macrophages, and gingival fibroblasts are the main cells that produce MMPs in periodontitis.

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MMP Role: Health vs. Disease

MMPs are normally involved in healthy tissue turnover, but their overproduction is usually regulated by TIMPs. Disruption of this balance leads to excess breakdown in chronic infections, like in periodontitis.

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Early Gingivitis (Early Lesion) Initial Stage

The early stage of gum disease, characterized by plaque biofilm accumulation, increasing gingival crevicular fluid, and vascular dilatation. Clinically the gingiva appears healthy but is vulnerable to further development of disease if not treated.

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Plaque Biofilm Accumulation

The buildup of bacteria and their byproducts (toxins) on teeth and gums.

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Gingival Crevicular Fluid Increase

The rise in fluid in the gingival crevice (the space between the tooth and gum) during early inflammation.

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Vascular Dilatation

Widening of blood vessels around the teeth and gums.

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PMN Migration

The movement of neutrophils (PMNs) into the gum tissue to fight bacteria.

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Phagocytosis by PMNs

Neutrophils engulfing and destroying bacteria.

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Cytokine Release

Immune signals released by cells to attract and activate more immune cells.

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Bacterial Toxins

Harmful substances produced by bacteria that damage tissues.

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Host Response

Body's defenses fighting against the bacterial infection.

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Cytokine Production

PMNs, macrophages, and epithelial cells create cytokines that harm periodontal tissues.

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Macrophage Activity

Macrophages make a lot of cytokines, PGE2, and MMPs to destroy connective tissue and bone.

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MMP Action

MMPs destroy the extracellular matrix, collagen, and periodontal ligament.

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PGE2 Role

PGE2 stimulates osteoclasts to destroy alveolar bone.

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Periodontal Pocket Formation

The junctional epithelium migrates, creating a pocket.

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Fibroblast Shift

Fibroblasts change and promote tissue breakdown, not repair.

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Osteoclast Activity

Osteoclasts break down the alveolar bone.

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Periodontal Pocket Characteristics

Bleeding, ligament damage, bone loss, and tooth movement are key signs.

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Irreversible Tissue Damage

Periodontal tissue destruction is not recoverable.

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Chronic Inflammation (Perio)

A long-lasting infection that overwhelms tissue repair.

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Factors Influencing Periodontitis

PMN dysfunction, bacterial virulence, smoking, stress, and diabetes contribute to the failure to control the infection.

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Biochemical mediators

Molecules that attract more immune cells to an infection site.

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MMPs in tissue

Enzymes that break down collagen, resulting in tissue loss. Implicated in gum disease.

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T-lymphocytes in gingiva

A type of white blood cell that migrates to the gums and produces immune response molecules (cytokines, antibodies).

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Early lesion composition

Predominantly consists of T-cells.

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Sulcular epithelium damage

Significant collagen loss (60-70%) in the sulcus region.

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Epithelial ridges

Extensions of epithelium protruding into connective tissue, inflammation-related.

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Junctional epithelial cells proliferation

Cells increase in number.

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Clinical signs of gingivitis

Inflammation in the gums, such as swelling and redness, can be seen clinically.

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Incubation period (gingivitis)

Takes 4-7 days after plaque buildup.

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Bacterial control (early gingivitis)

PMNs, macrophages, and T-lymphocytes are helpful in controlling infection. Proper care is important.

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Subgingival biofilm

Plaque that accumulates below the gumline.

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Established lesion cells

High number of plasma cells are associated with it.

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Plasma cells in periodontitis

Leukocytes that produce antibodies to fight bacteria.

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Antibody function

Proteins that help fight and control bacteria.

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Study Notes

Host Immune Response to Plaque Biofilm

  • Periodontal disease is a bacterial infection
  • Bacteria, alone are not enough to cause periodontal disease, the host response is crucial
  • Host response is the body's response to bacterial infection in the plaque biofilm, aiming to eliminate pathogens and limit infection spread
  • Virulence factors enhance microbial challenge:
    • Presence of lipopolysaccharide (LPS) from gram-negative bacteria
    • Ability to invade host tissues
    • Production of enzymes to degrade host proteins

Host Factors Affecting Immune Response

  • Genetic factors: Contribute to periodontal disease susceptibility
  • Environmental factors: Tobacco smoking negatively impacts immune/inflammatory system
  • Acquired factors: Diabetes mellitus impacts the host response (reduced PMN function, increased inflammatory mediators)

Inflammation as a Protective Host Response

  • Host responds to microbes by releasing biochemical mediators to fight bacteria
    • Cells involved: PMNs, antigen-presenting cells (macrophages, Langerhans cells), T- and B-lymphocytes, fibroblasts, and epithelial cells
  • Acute inflammation is protective, but must resolve efficiently
  • Unresolved, chronic inflammation can cause damage, like in periodontitis

Inflammatory Biochemical Mediators

  • Cytokines: Secreted by immune cells, influencing other cell behavior and potential tissue destruction
    • Key ones: IL-1, IL-6, IL-8, and TNF-α
  • Prostaglandins (primarily PGE2): Increase vascular permeability, impacting bone destruction by stimulating osteoclasts
  • Matrix Metalloproteinases (MMPs): Enzymes that break down connective tissue matrix
    • MMP overactivity is negatively regulated by TIMPs (tissue inhibitors of matrix metalloproteinases)

Histologic Stages of Periodontal Disease

  • Bacterial Accumulation (Initial):
    • Bacteria colonize the tooth surface, activating host immune response
    • PMNs are recruited, tissue looks healthy clinically
  • Early Gingivitis (Early Lesion):
    • Increased bacterial challenge leads to heightened inflammation
    • PMNs, macrophages, and other cells fight bacteria, also damaging healthy tissue
    • Sulcular epithelium changes, leading to epithelial ridges
  • Established Gingivitis (Established Lesion):
    • Biofilm extends subgingivally
    • Plasma cells (producing antibodies) and increased host response, leading to more tissue damage
  • Periodontitis (Advanced Lesion):
    • Chronic inflammation dominates, leading to periodontal pockets, alveolar bone loss, and tooth mobility
    • Tissue and cellular damage becomes irreversible

Current Theory of Pathogenesis

  • Periodontal disease development is complex, involving microbial challenge, host response, and modifying risk factors (e.g., genetics, environment, acquired factors)
  • Imbalance between microbial challenge and host response leads to tissue destruction

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Host Response Pathogenesis PDF

Description

This quiz explores the intricate relationship between host immune responses and plaque biofilm in periodontal disease. It covers the mechanisms of host response, the role of genetic and environmental factors, and how inflammation acts as a protective measure against bacterial infections. Test your understanding of how these factors contribute to periodontal health.

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