Host Response - Pathogenesis
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Questions and Answers

What primarily characterizes the established lesion in connective tissue?

  • Presence of plasma cells (correct)
  • High levels of neutrophils
  • Thick epithelial ridges
  • Lymphocyte dominance

Which immune cells are involved in combating bacteria in the sulcus?

  • B cells exclusively
  • Only lymphocytes
  • Macrophages and PMNs (correct)
  • Only plasma cells

What role do cytokines play in the immune response during established gingivitis?

  • They reduce inflammation
  • They promote healing of tissue
  • They recruit additional immune cells (correct)
  • They cause osteoclast activation

How does the junctional epithelium change during the progression of gingivitis?

<p>It loosens its attachment and transforms into pocket epithelium (A)</p> Signup and view all the answers

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

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

After how many days is established gingivitis generally observed following plaque biofilm accumulation?

<p>21 days (D)</p> Signup and view all the answers

What is the potential outcome if established gingivitis is not controlled in susceptible individuals?

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

What is the primary role of PMNs during the bacterial accumulation phase?

<p>To pass from blood vessels into the gingival connective tissue (A)</p> Signup and view all the answers

What clinical feature is indicative of the initial lesion phase?

<p>Healthy appearance of the gingiva (D)</p> Signup and view all the answers

What additional substances are produced by macrophages exposed to gram-negative bacteria?

<p>Cytokines, PGE2, and MMPs (C)</p> Signup and view all the answers

Which feature is indicative of gingivitis as it progresses into an established lesion?

<p>Decreased collagen production (B)</p> Signup and view all the answers

Which of the following statements about PMNs in early gingivitis is correct?

<p>They form a wall of cells to defend against the biofilm. (B)</p> Signup and view all the answers

How does the complement system relate to the host immune response during bacterial accumulation?

<p>It enhances the recognition of bacteria by immune cells. (B)</p> Signup and view all the answers

What role do macrophages play in the immune response during tissue destruction?

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

During the early phase of gingivitis, what percentage of collagen loss is typically observed?

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

What occurs if the bacterial infection is not controlled after the initial lesion phase?

<p>Development of early gingivitis (A)</p> Signup and view all the answers

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

<p>Increased movement of PMNs to the infection site (B)</p> Signup and view all the answers

Which cellular feature predominantly characterizes an early lesion phase of gingivitis?

<p>Presence of epithelial ridges (B)</p> Signup and view all the answers

What is the primary consequence of cytokine release by junctional epithelial cells in early gingivitis?

<p>Attraction of additional PMNs to the site of infection (A)</p> Signup and view all the answers

What is the primary consequence if the host immune response fails during the early lesions of gingivitis?

<p>Progression to established gingivitis (D)</p> Signup and view all the answers

What triggers the epithelial cells to secrete more cytokines during the gingivitis process?

<p>Presence of high subgingival bacterial numbers (C)</p> Signup and view all the answers

Which feature is a clinical observation of early gingivitis?

<p>Edema and redness of gingival marginal tissue (A)</p> Signup and view all the answers

What is the result of effective plaque biofilm control in response to gingivitis?

<p>Restoration of health through tissue repair (C)</p> Signup and view all the answers

What primarily characterizes the established lesions of gingivitis?

<p>Subgingival plaque biofilm extension and bacterial infiltration (D)</p> Signup and view all the answers

What role does lipopolysaccharide (LPS) play in periodontal disease?

<p>It initiates inflammation in periodontal tissues. (D)</p> Signup and view all the answers

Which bacteria has the ability to invade host tissues in periodontal disease?

<p>Porphyromonas gingivalis (B)</p> Signup and view all the answers

What impact does smoking have on the host immune response.

<p>It negatively affects T- and B-lymphocyte responses. (D)</p> Signup and view all the answers

How do genetic factors contribute to periodontal disease?

<p>They are associated with aggressive forms of the disease. (C)</p> Signup and view all the answers

Which of the following is a consequence of diabetes mellitus on the host immune response in periodontal disease?

<p>Increased levels of tumor necrosis factor-α. (B)</p> Signup and view all the answers

What is the effect of enzymes produced by periodontal bacteria?

<p>They degrade host proteins integral to the periodontium. (A)</p> Signup and view all the answers

Which acquired factor is a known risk for periodontal diseases?

<p>Diabetes mellitus (D)</p> Signup and view all the answers

What is a notable effect of genetic variations in periodontal disease susceptibility?

<p>They can modify the immune response to plaque biofilm. (D)</p> Signup and view all the answers

What occurs as a result of the chronic immune response to periodontal infection?

<p>Destruction of periodontal tissues (B)</p> Signup and view all the answers

Which cellular component is primarily responsible for the destruction of the extracellular matrix of the gingiva?

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

What is the main outcome of the host's immune response during advanced periodontal disease?

<p>Tissue destruction (D)</p> Signup and view all the answers

Which cells migrate apically on the root surface leading to the formation of a periodontal pocket?

<p>Cells of the junctional epithelium (B)</p> Signup and view all the answers

What characterizes the advanced lesion phase of periodontitis?

<p>Periodontal pocket formation and tooth mobility (C)</p> Signup and view all the answers

What role do osteoclasts play in periodontal disease progression?

<p>Resorbing the crest of the alveolar bone (B)</p> Signup and view all the answers

Which of the following statements about chronic inflammation in periodontitis is true?

<p>It causes more damage than the bacterial infection itself. (C)</p> Signup and view all the answers

What is a hallmark of periodontitis?

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

Flashcards

Lipopolysaccharide (LPS)

A toxic component of gram-negative bacteria found on their outer membrane, responsible for initiating inflammation in periodontal tissues.

Ability of Bacteria to Invade Tissues

The ability of certain bacteria to invade and penetrate host tissues, allowing them to evade immune defenses.

Enzymes Produced by Periodontal Bacteria

Enzymes produced by some periodontal bacteria that can directly break down crucial proteins in the periodontium, contributing to tissue damage.

Genetic Factors in Periodontal Disease

Genetic factors can make individuals more susceptible to periodontal disease.

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Smoking and Periodontal Disease

Smoking can significantly impact the immune system, making individuals more vulnerable to periodontal disease.

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Diabetes and Periodontal Disease

Diabetes mellitus can worsen periodontal disease by impairing the immune response and increasing inflammatory markers.

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Genetic Variations in Immune Mediator Formation

Variations in genes that control the production of immune signaling molecules can influence the body's response to plaque biofilm.

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Environmental factors and Periodontal Disease

Environmental factors, specifically smoking, can have a strong impact on the host immune response to plaque biofilm.

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Bacterial Accumulation (Initial Lesion)

The first stage of periodontal disease begins when bacteria gather near the gum line. This creates a biofilm, a sticky layer of germs, and the immune system is activated.

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Cellular Features of Initial Lesion

Gram-negative bacteria and their products trigger the host immune response. This response involves releasing cytokines that draw neutrophils (PMNs) to the site.

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Cytokines in Initial Lesion

Cytokines are small proteins released by cells that act as signals to communicate with other cells. In the case of periodontal disease, cytokines tell PMNs to join the battle against bacteria.

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Polymorphonuclear Leukocytes (PMNs)

Polymorphonuclear leukocytes (PMNs) are white blood cells that are the first line of defense against infection. They move from the blood vessels into the gum tissue to reach the bacteria in the sulcus.

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Complement System in Initial Lesion

The complement system is a group of proteins in the immune system that work together to destroy bacteria. These proteins activate the immune response and are crucial in fighting infection.

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Tissue Level Features in Initial Lesion

The initial biofilm forms above the gum line (supragingivally). Changes in blood flow occur in the gum tissues. Additionally, the fluid in the gum pocket increases.

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Clinical Features of Initial Lesion

The gingiva may appear healthy despite bacteria accumulating. This stage occurs within 2 to 4 days after plaque biofilm formation. The immune response can often control the infection and restore tissue.

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Outcome of Host Response in Initial Lesion

If the immune response successfully eliminates the bacteria, the tissue repairs itself, and the body is restored to its healthy state. However, if the bacteria are not controlled, the disease progresses to early gingivitis.

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Early Gingivitis

The initial stage of gingivitis, characterized by inflammation and tissue damage.

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PMNs (Polymorphonuclear Neutrophils)

Immune cells that engulf and destroy bacteria.

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Macrophage

A type of white blood cell that plays a crucial role in long-term immune responses.

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T-lymphocytes

A type of white blood cell responsible for targeted immune responses.

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Sulcular Epithelium

A small, thin tissue that lines the gingival sulcus.

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MMP (Matrix Metalloproteinase)

A type of protein that breaks down collagen, contributing to tissue damage.

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Epithelial Ridges

Outgrowths of the sulcular epithelium that extend into the connective tissue.

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Subgingival Plaque Biofilm Formation

The process of plaque biofilm accumulating on the tooth surface and extending subgingivally into the sulcus.

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Established Gingivitis

The stage of gingivitis characterized by a dominant presence of plasma cells in the connective tissue.

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Plasma Cells

White blood cells that produce antibodies to fight infections, particularly prevalent in established gingivitis.

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Initial Gingivitis

The initial stage of gingivitis, characterized by a less prominent immune response.

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Collagen Destruction

The breakdown of collagen, a protein that provides support and strength to tissues, in gingivitis.

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Pocket Epithelium

A type of tissue that lines the pocket formed by the loosened attachment of the gingiva to the tooth.

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Cytokines

A chemical signal produced by macrophages, helping to recruit and activate other immune cells.

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PGE2 (Prostaglandin E2)

A hormone-like substance that promotes inflammation and collagen degradation in gingivitis.

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Periodontal pocket

A deep pocket in the gum tissue formed by the apical migration of the junctional epithelium, creating a protected environment for bacteria.

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Host response to periodontal bacteria

The body's immune response to chronic bacterial infection in the periodontal pocket.

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Cellular Defenders

White blood cells, primarily neutrophils, macrophages, and epithelial cells, that are involved in the fight against bacteria.

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Matrix Metalloproteinases (MMPs)

An enzyme produced by macrophages that breaks down collagen and other connective tissues.

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Prostaglandin E2 (PGE2)

A prostaglandin that stimulates bone resorption by osteoclasts.

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Tissue Destruction in Periodontitis

The process of irreversible tissue destruction that occurs as a consequence of the chronic inflammatory response in periodontitis.

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Advanced Periodontal Lesions

The final stage of periodontal disease characterized by significant tissue destruction, including pocket formation, bone loss, and tooth mobility.

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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

  • 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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