pathogen p2 Flashcards
What is the role of sulcular epithelium in innate immunity?
Acts as a physical barrier to prevent microbial invasion.
How does saliva contribute to immune defense?
Saliva contains antimicrobial agents and flushes away pathogens.
What is the function of normal oral flora in immunity?
It competes with pathogens, reducing the chance of invasion.
What role do acute phase proteins play in immune defense?
They are secreted by the liver to aid in inflammatory response.
What are Toll-like receptors (TLRs)?
They recognize pathogens and activate immune responses.
What is the role of the complement system in immunity?
It aids in pathogen destruction through opsonization and lysis.
What do natural killer (NK) cells do in immunity?
They target and destroy infected or abnormal cells directly.
What are T-lymphocytes responsible for?
Cell-mediated immunity and coordinating immune responses.
What is the role of B-lymphocytes?
They produce antibodies for humoral immunity.
What are antigen-presenting cells (APCs)?
Cells that present antigens to T-cells, initiating an immune response.
What is the complement system’s classical pathway?
Activation occurs via an antigen-antibody complex starting with C1.
How does the alternative pathway of the complement system work?
Triggered by pathogen surfaces, activating complement directly.
What is the lectin pathway in the complement system?
Activated by mannose-binding lectin binding to pathogen surfaces.
What is the role of PMNs in epithelium?
They combat bacteria at the gingival sulcus through phagocytosis.
What do Langerhans cells do in the immune system?
They act as APCs, presenting antigens to initiate immune responses.
What inflammatory cells are in connective tissue?
Macrophages, plasma cells, lymphocytes, and PMNs.
What is the role of mast cells in connective tissue?
They release mediators like histamine, causing vasodilation.
Why are plasma cells important in immunity?
They produce antibodies that target specific pathogens.
What is the main function of the complement system?
To assist immune cells in identifying and destroying pathogens.
How do complement proteins trigger inflammation?
Anaphylatoxins like C3a and C5a activate mast cells and inflammation.
What is opsonization in the immune system?
The marking of pathogens for easier phagocytosis by immune cells.
How does complement mediate cell lysis?
Through the membrane attack complex, forming pores in pathogen cells.
What is chemotaxis in the context of the complement system?
Attraction of immune cells to the infection site by chemokines.
How does complement enhance phagocytosis?
It binds to pathogens, facilitating their uptake by phagocytes.
What are the primary phagocytic cells in periodontal tissues?
PMNs, monocytes, and macrophages.
What is the first step of phagocytosis?
Migration toward the bacteria, guided by chemotactic factors.
How do phagocytes adhere to bacteria?
Via surface receptors binding to the bacterial cell wall.
What happens to bacteria after phagocytosis?
They are engulfed in a phagosome that merges with lysosomes.
What mechanisms do phagocytes use to kill bacteria?
Oxidative (ROS) and non-oxidative mechanisms in lysosomes.
What are cytokines?
Proteins that enable immune cells to communicate and coordinate.
What is the role of pro-inflammatory cytokines?
They mediate inflammation, promoting immune responses.
What are reparative cytokines?
Growth factors like TGF-beta that aid in tissue repair.
What are chemokines?
A type of cytokine that directs the movement of immune cells.
Which cytokines act as anaphylatoxins?
C3a and C5a, triggering mast cell activation and inflammation.
How do cytokines impact periodontal disease?
They regulate inflammation, immune cell recruitment, and tissue changes.
What are MMPs?
Proteolytic enzymes that break down extracellular matrix components.
Which cells secrete MMPs in periodontal disease?
Primarily PMNs, macrophages, and fibroblasts.
How do MMPs contribute to periodontal tissue destruction?
Excessive MMP release degrades connective tissue, causing damage.
What are examples of MMPs in periodontal tissue?
MMP-1 (collagenase) and MMP-9 (gelatinase) involved in ECM breakdown.
What is the role of RANK in bone resorption?
It’s a receptor on osteoclast precursors that binds RANKL to form osteoclasts.
How does RANKL contribute to bone destruction?
It binds RANK, stimulating osteoclast formation and activity.
What is OPG’s role in bone preservation?
It binds RANKL, preventing RANK binding and reducing osteoclast activity.
How does dysregulation of RANK/RANKL/OPG lead to periodontitis?
Excess RANKL leads to more bone resorption than deposition.
What cytokines influence RANKL expression?
IL-1, IL-6, and TNF-alpha, promoting bone resorption in periodontitis.
What characterizes the initial lesion stage?
Acute inflammation with no visible signs, increased GCF flow.
What immune cells dominate the initial lesion?
PMNs, initiating the inflammatory response.
What histopathological changes occur in the initial lesion?
10% CT inflammation, vasodilation, and early tissue breakdown.
What defines the early lesion stage?
Mild gingivitis with redness, edema, and bleeding on probing.
What immune cells predominate in early lesions?
Mainly lymphocytes and macrophages.
What vascular changes occur in the early lesion?
Increased GCF, vasodilation, and formation of new blood vessels.
What defines an established lesion?
Chronic gingivitis with maximum inflammation and possible remission phases.
What cell types are prominent in established lesions?
Lymphocytes, plasma cells, PMNs, and mast cells.
How does connective tissue change in an established lesion?
Further destruction of connective tissue, deeper inflammatory cell migration.
What characterizes an advanced lesion?
Chronic periodontitis with bone loss and clinical attachment loss.
What is the primary immune cell in advanced lesions?
Plasma cells, predominant with IgG production.
What clinical signs indicate advanced lesions?
Deep periodontal pockets, bone loss, and tissue attachment loss.
What factors contribute to periodontitis?
Bacterial infection, host immune response, and environmental factors.
How does the host immune response influence periodontitis?
Excessive or imbalanced immune responses can cause tissue damage.
