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Periodontics > pathogen p2 > Flashcards

pathogen p2 Flashcards

1
Q

What is the role of sulcular epithelium in innate immunity?

A

Acts as a physical barrier to prevent microbial invasion.

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2
Q

How does saliva contribute to immune defense?

A

Saliva contains antimicrobial agents and flushes away pathogens.

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3
Q

What is the function of normal oral flora in immunity?

A

It competes with pathogens, reducing the chance of invasion.

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4
Q

What role do acute phase proteins play in immune defense?

A

They are secreted by the liver to aid in inflammatory response.

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5
Q

What are Toll-like receptors (TLRs)?

A

They recognize pathogens and activate immune responses.

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6
Q

What is the role of the complement system in immunity?

A

It aids in pathogen destruction through opsonization and lysis.

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7
Q

What do natural killer (NK) cells do in immunity?

A

They target and destroy infected or abnormal cells directly.

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8
Q

What are T-lymphocytes responsible for?

A

Cell-mediated immunity and coordinating immune responses.

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9
Q

What is the role of B-lymphocytes?

A

They produce antibodies for humoral immunity.

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10
Q

What are antigen-presenting cells (APCs)?

A

Cells that present antigens to T-cells, initiating an immune response.

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11
Q

What is the complement system’s classical pathway?

A

Activation occurs via an antigen-antibody complex starting with C1.

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12
Q

How does the alternative pathway of the complement system work?

A

Triggered by pathogen surfaces, activating complement directly.

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13
Q

What is the lectin pathway in the complement system?

A

Activated by mannose-binding lectin binding to pathogen surfaces.

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14
Q

What is the role of PMNs in epithelium?

A

They combat bacteria at the gingival sulcus through phagocytosis.

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15
Q

What do Langerhans cells do in the immune system?

A

They act as APCs, presenting antigens to initiate immune responses.

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16
Q

What inflammatory cells are in connective tissue?

A

Macrophages, plasma cells, lymphocytes, and PMNs.

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17
Q

What is the role of mast cells in connective tissue?

A

They release mediators like histamine, causing vasodilation.

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18
Q

Why are plasma cells important in immunity?

A

They produce antibodies that target specific pathogens.

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19
Q

What is the main function of the complement system?

A

To assist immune cells in identifying and destroying pathogens.

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20
Q

How do complement proteins trigger inflammation?

A

Anaphylatoxins like C3a and C5a activate mast cells and inflammation.

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21
Q

What is opsonization in the immune system?

A

The marking of pathogens for easier phagocytosis by immune cells.

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22
Q

How does complement mediate cell lysis?

A

Through the membrane attack complex, forming pores in pathogen cells.

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23
Q

What is chemotaxis in the context of the complement system?

A

Attraction of immune cells to the infection site by chemokines.

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24
Q

How does complement enhance phagocytosis?

A

It binds to pathogens, facilitating their uptake by phagocytes.

25
Q

What are the primary phagocytic cells in periodontal tissues?

A

PMNs, monocytes, and macrophages.

26
Q

What is the first step of phagocytosis?

A

Migration toward the bacteria, guided by chemotactic factors.

27
Q

How do phagocytes adhere to bacteria?

A

Via surface receptors binding to the bacterial cell wall.

28
Q

What happens to bacteria after phagocytosis?

A

They are engulfed in a phagosome that merges with lysosomes.

29
Q

What mechanisms do phagocytes use to kill bacteria?

A

Oxidative (ROS) and non-oxidative mechanisms in lysosomes.

30
Q

What are cytokines?

A

Proteins that enable immune cells to communicate and coordinate.

31
Q

What is the role of pro-inflammatory cytokines?

A

They mediate inflammation, promoting immune responses.

32
Q

What are reparative cytokines?

A

Growth factors like TGF-beta that aid in tissue repair.

33
Q

What are chemokines?

A

A type of cytokine that directs the movement of immune cells.

34
Q

Which cytokines act as anaphylatoxins?

A

C3a and C5a, triggering mast cell activation and inflammation.

35
Q

How do cytokines impact periodontal disease?

A

They regulate inflammation, immune cell recruitment, and tissue changes.

36
Q

What are MMPs?

A

Proteolytic enzymes that break down extracellular matrix components.

37
Q

Which cells secrete MMPs in periodontal disease?

A

Primarily PMNs, macrophages, and fibroblasts.

38
Q

How do MMPs contribute to periodontal tissue destruction?

A

Excessive MMP release degrades connective tissue, causing damage.

39
Q

What are examples of MMPs in periodontal tissue?

A

MMP-1 (collagenase) and MMP-9 (gelatinase) involved in ECM breakdown.

40
Q

What is the role of RANK in bone resorption?

A

It’s a receptor on osteoclast precursors that binds RANKL to form osteoclasts.

41
Q

How does RANKL contribute to bone destruction?

A

It binds RANK, stimulating osteoclast formation and activity.

42
Q

What is OPG’s role in bone preservation?

A

It binds RANKL, preventing RANK binding and reducing osteoclast activity.

43
Q

How does dysregulation of RANK/RANKL/OPG lead to periodontitis?

A

Excess RANKL leads to more bone resorption than deposition.

44
Q

What cytokines influence RANKL expression?

A

IL-1, IL-6, and TNF-alpha, promoting bone resorption in periodontitis.

45
Q

What characterizes the initial lesion stage?

A

Acute inflammation with no visible signs, increased GCF flow.

46
Q

What immune cells dominate the initial lesion?

A

PMNs, initiating the inflammatory response.

47
Q

What histopathological changes occur in the initial lesion?

A

10% CT inflammation, vasodilation, and early tissue breakdown.

48
Q

What defines the early lesion stage?

A

Mild gingivitis with redness, edema, and bleeding on probing.

49
Q

What immune cells predominate in early lesions?

A

Mainly lymphocytes and macrophages.

50
Q

What vascular changes occur in the early lesion?

A

Increased GCF, vasodilation, and formation of new blood vessels.

51
Q

What defines an established lesion?

A

Chronic gingivitis with maximum inflammation and possible remission phases.

52
Q

What cell types are prominent in established lesions?

A

Lymphocytes, plasma cells, PMNs, and mast cells.

53
Q

How does connective tissue change in an established lesion?

A

Further destruction of connective tissue, deeper inflammatory cell migration.

54
Q

What characterizes an advanced lesion?

A

Chronic periodontitis with bone loss and clinical attachment loss.

55
Q

What is the primary immune cell in advanced lesions?

A

Plasma cells, predominant with IgG production.

56
Q

What clinical signs indicate advanced lesions?

A

Deep periodontal pockets, bone loss, and tissue attachment loss.

57
Q

What factors contribute to periodontitis?

A

Bacterial infection, host immune response, and environmental factors.

58
Q

How does the host immune response influence periodontitis?

A

Excessive or imbalanced immune responses can cause tissue damage.

Periodontics (5 decks)

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