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Ch15 Host Immune
Periodontology DENT-230
| Question | Answer |
|---|---|
| Host response | the body's response to bacteria |
| Virulence Factor | the mechanisms that enable biofilm bacteria to colonize and damage the tissues of the periodontium. Either structural characteristics or substances produced by the bacteria |
| Primary virulence factors of the periodontium | Presence of lipopolysaccharide, Ability to invade tissues, Ability to produce enzymes |
| Catabasis | actively regulated biologic process of inflammation resolution to noninflammatory state |
| Lipid proinflammatory mediators include | prostaglandins, thromboxanes, prostacyclins and leukotrienes. Associated with the recruitment of PMNs and tissue destruction |
| Pro-resolving lipid mediators | chemical mediators that regulate the activity of inflammation. 1) terminate PMN recruitment, 2) stimulate macrophages to remove dead cells 3)promote antibacterial activities 4)promote repair, regeneration and homeostasis |
| biochemical mediators | "middlemen" sent by host cells to activate inflammation. Cytokines, prostaglandins, matrix metalloproteinases (MMPs) |
| Cytokines | powerful regulatory proteins released by host immune cells that influence the behavior of other cells. Signaling proteins. Bond to site receptors on target cells. IL-1, IL-6, IL-8 and TNF-a |
| Prostaglandins | powerful biochemical mediators derived from fatty acids expressed on the surface of most cells , D, E, F, G, H , I . Primarily produced by macrophages |
| Prostaglandin E series | play important role in bone destruction. Prostaglandins initiate most of the bone destruction seen in periodontitis |
| MMP | Matrix metalloproteinases, a family of at least 12 different proteolytic enzymes that acto together to break down the connective tissue matrix. Produced by PMNs and gingival fibroblasts |
| TIMPs | tissue inhibitors of matrix metalloproteinases, work to inhibit function of MMPs, which are a part of tissue turnover in health. |
| Pathogenesis | chain of events in a disease process Activate host response, Genetic , Environmental and Acquired factors alter pathways, Inflammatory response and termination |
| Bone remodeling | breakdown of old bone and subsequent re-creation (deposition) of new bone |
| Osteoblasts | Bone building cells |
| Osteoclasts | bone-resorbing cells |
| RANKL | Receptor Activator of nuclear factor k-B A cell-membrane bound protein that regulates osteoclast differentiation (maturation) and activation |
| OPG | Osteoprotogerin Secreted byosteoblasts and protects bone from excessive resorption by binding to RANKL. OPG suppresses resorption of alveolar bone, keeping bone levels stable |
| Homeostatic condition | When the body is able to maintain stable bone levels. Thought to exist when levels of RANKL and OPG are in balance in the periodontal tissues. |
| Bone resorption | occurs when osteoclasts are stimulated by RANKL to resorb alveolar bone. When Periodontium is inflamed, levels of OPG decrease |
Created by:
SonyaP
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