Host Response in Periodontitis

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Questions and Answers

In the context of periodontal disease, what is the primary role of host defense mechanisms?

  • To directly attack and eliminate bacterial pathogens.
  • To stimulate the production of bacterial biofilms.
  • To suppress the inflammatory response and promote bacterial colonization.
  • To protect the host tissues from damage caused by the host's own inflammatory and immune responses to periodontopathogens. (correct)

Which statement accurately describes the relationship between the oral microbiome and the host in periodontal disease?

  • Bacteria directly cause tissue damage without involvement of the host response.
  • The host response is triggered by bacteria, but the resulting inflammation largely mediates tissue damage in periodontitis. (correct)
  • The host response and the oral microbiome operate independently without influencing each other.
  • The host response is solely determined by the specific bacterial species present.

In the context of periodontal disease, what role do neutrophils play after being activated?

  • They become more specialized and carry out more complex functions, including shaping adaptive immune responses. (correct)
  • They undergo apoptosis within 24 hours of activation.
  • They revert to their original state after completing their primary function.
  • Their primary function is to suppress the humoral immune response.

What is the importance of the junctional epithelium (JE) in maintaining periodontal health?

<p>It facilitates the passage of immune cells and GCF, allowing for immune surveillance and defense. (B)</p>
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How does the composition and structure of the sulcular epithelium (SE) and junctional epithelium (JE) differ from the oral epithelium (OE) in terms of barrier function?

<p>The SE and JE have fewer cell layers and larger intercellular spaces, allowing for the passage of GCF and immune cells, unlike the OE. (B)</p>
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How do proteoglycans and glycosaminoglycans (GAGs) contribute to the functional integrity of the junction between the junctional epithelium (JE) and the tooth surface?

<p>They help maintain tissue turgidity, reinforcing the relatively weak hemidesmosomal attachment. (B)</p>
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What changes occur in the connective tissue structure as biofilm extends apically and inflammation progresses in periodontal disease?

<p>The highly organized fiber structure is disrupted and replaced by a dense concentration of immune cells. (A)</p>
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What is the role of complement components C3a and C5a in the context of the host immune response to bacterial infection?

<p>They increase vascular permeability and act as chemoattractants for PMNs. (B)</p>
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What is the primary function of the membrane-attack complex (MAC) formed by the complement system?

<p>To create pores in the cell membrane of pathogens, leading to their lysis. (B)</p>
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How does transcellular transmigration differ from paracellular transmigration in the context of neutrophil migration?

<p>Transcellular transmigration involves movement through a single endothelial cell, while paracellular transmigration involves movement between adjacent endothelial cells. (D)</p>
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What are the key functions of macrophages in the context of innate immunity?

<p>Phagocytosis, activation of bactericidal mechanisms, and antigen presentation. (A)</p>
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How do Toll-like receptors (TLRs) contribute to the innate immune response?

<p>By recognizing specific microbial components and initiating intracellular signaling cascades. (D)</p>
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How does sIgA protect the gingival mucosal surfaces?

<p>By preventing bacterial adherence and neutralizing bacterial toxins. (A)</p>
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What is the significance of antigen processing in T cell activation?

<p>It breaks down antigens into peptide fragments that can bind to MHC molecules for T cell recognition. (A)</p>
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How do Th1 cells promote inflammation?

<p>By releasing cytokines that activate macrophages. (D)</p>
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How does the nature of the antigen-presenting cell (APC) influence the type of immune response?

<p>If the APC is a macrophage, it tends to promote a pro-inflammatory Th1 type response, whereas if it is a B cell, it skews towards a humoral response. (B)</p>
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What is the role of sIgA in the context of periodontal disease?

<p>It prevents bacterial adherence and neutralizes bacterial toxins on mucosal surfaces. (A)</p>
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How do IgG and IgM antibodies contribute to the control of bacterial infection in periodontal tissues?

<p>They activate complement and promote phagocytosis. (C)</p>
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What is the role of IL-1 and TNF-alpha in the context of the host immune response to periodontal pathogens?

<p>They are important pro-inflammatory cytokines that promote bone resorption. (C)</p>
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Which statement best describes the interplay between innate and adaptive immunity in response to periodontal pathogens?

<p>Innate and adaptive immune responses collaborate and promote each other to eliminate the pathogen effectively. (A)</p>
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Flashcards

Host Defense Goals

Local anatomy, inflammation, and immune mechanisms protect the host from damage by putative periodontopathogens.

Gingivitis/Periodontitis

Plaque-induced gingivitis and periodontitis are chronic inflammatory conditions with inflammation and healing attempts.

Host Response

The host's response to bacteria triggers most of the damage in periodontitis.

Innate Immunity Factors

Intact epithelial barrier, Saliva, Lysozyme, Peroxidase, Inflammation, sIgA, GCF, Complement factors, PMNs, Macrophages.

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Adaptive Immunity Factors

slgA (Humoral immunity), Humoral immunity in GCF and periodontium,IgG, IgM, IgA, Cell-mediated immunity in periodontium and GCF, T cell help and Cytotoxicity, γδ T cells

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Junctional Epithelium (JE)

Less organized with fewer desmosomal junctions but more cells.

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Rete Pegs' Function

Oral epithelium and connective tissue interface created by presence of numerous rete pegs, increasing surface area for contact between epithelium and connective tissue.

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JE and Fiber System

Functional integrity of junction between JE and tooth is reinforced by functional integrity of fiber system within gingiva.

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JE Attachment

Enables JE to attach to tooth surface via hemi-desmosomes, functionality believed to be connected with relative immaturity of JE cells; immaturity maintained by relatively high cell turnover

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Complement System

Group of ~20 proteins that function in a cascading process.

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Transition to Advanced Lesion

Factors responsible for transition unknown; host response may have changed or change in nature of the bacterial plaque.

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Neutrophil Function

Phagocytosis and activation of bactericidal mechanisms.

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Neutrophil Granules

Cytosol of neutrophil packed full of electron dense granules which contain a numb of potent components capable of lysing bacteria.

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Class II MHC Function

Bacterial fragments bound by MHC class II in vesicles.

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Lymphocyte Activation

Effector cells eliminate antigen.

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Helper T cells

Promotes B cell proliferation and subsequent differentiation into plasma cells

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Phagocytes

Important in the battle against extracellular bacterial infections; important functions are phagocytosis during which reactive oxygen (RO) and reactive nitrogen (RN) species are produced.

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sIgA Function

sIgA is concentrated on and protects gingival mucosal surfaces by preventing bacterial adherence and neutralising bacterial toxins

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IgM and IgG

Whether it is IgM or IgG, both classes can activate complement and bring about bacterial cell death, attract further inflammatory cells.

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Study Notes

  • Host response is a protective mechanism essential to prevent systemic infection

  • Periodontitis' tissue damage is mainly due to host responses activated by microbes.

  • Innate and adaptive immunity operate together to defend the host

  • Periodontitis and gingivitis are chronic inflammatory conditions where destruction and repair occur.

  • Inflammation involves a complex network of responses and processes being both pro-inflammatory and anti-inflammatory

Phagocytes

  • Phagocytes perform phagocytosis to combat extracellular bacterial infections,
  • They produce reactive oxygen (RO) and reactive nitrogen (RN) species.
  • Immune cells communicate using protein messengers called cytokines.

Neutrophils

  • Neutrophils' lifespan is longer than previously thought, and they promote humoral responses and suppress T cell function.
  • IL-1 and TNF-alpha are significant pro-inflammatory cytokines.

Pathogen Recognition

  • Recognition of pathogens and antigens is mediated by lymphocytes, B and T cells.
  • Plasma cells, Th, and Tc are effector cells

Antigen Presenting Cells

  • Antigen Presenting cells (APCs) are vital for antigen recognition by T cells
  • T helper cells promote inflammation by activating macrophages
  • T helper cells release cytokines to promote antibody production

Immunoglobulin

  • Immunoglobulin classes impart different properties
  • Secretory IgA protects mucosal surfaces by preventing bacteria and neutralizing bacterial toxins

Immunoglobulin G and M

  • IgG and IgM present in Gingival Crevicular Fluid, activate complement for bacterial cell death and recruitment of inflammatory cells
  • Both promote phagocytosis either directly or with complement activation.

Complement

  • Complement is a group of proteins in serum and periodontal tissues.
  • Immune complexes or microbial surfaces activate them, leading to the construction of MAC that disrupts cell membranes and promotes inflammation.

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