perio quiz 10/12
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44 terms
Terms | Definitions |
|---|---|
 etiology | The study of all factors that may be involved in the development of a disease. |
| epidemiology | The study of prevalence, incidence and etiology of a disease within the total population (rather than an individual patient). |
| prevalence | Number of cases of a disease that can be identified within a specified population at a given point of time. |
| incidence | Number of new disease cases of a disease that occur in a given interval of time. |
| measuring the disease prevalence | Determined by clinical examinations on cross section of groups using indices. Indices measure the amount and severity of disease. |
| calculus theory | -Before 1960. Everyone was equally susceptible to periodontal disease; calculus was responsible for disease. -Treatment- Professional prophylaxis every 6 months and quanitity not the quality of plaque was responsible for disease; patients told to brush 3x a day to remove food particles. |
| non specific plaque theory | -1965-1975. Bacteria in plaque caused disease. All plaque essentially the same; too much plaque caused disease. -Treatment- Professional prophylaxis 2-3x a year, meticulous plaque control by patient and if patient did not respond to treatment, it was their fault. |
| host bacterial interaction theory | -Current. Bacterial infection alone not enough; interaction of the host with pathogenic bacteria controls whether disease occurs or not. Not everyone is equally susceptible but rather some individuals are more "at risk for disease." -Treatment- Manage the bacterial, local and systemic etiologic factors for disease. -Focus- Patient self care and frequent professional use. |
| models of periodontal disease activity/ progression | -Continuous model theory -Intermittent disease progression |
| continuous model theory | Periodontal destruction is slow and constant until tooth loss; the severity of the disease increases with age. Original theory. |
| intermittent disease progression | Periods of sporadic periodontal disease activity occurs during a limited time period followed by remission. period of remission may last for months or for a much longer period of time. |
| etiologic factors of periodontitis | -primary risk factor: biofilm (bacterial infection) -local contributing factors -systematic contributing risk factors -host response to biofilm bacteria |
| to infect tissues and cause disease | -Bacteria must be pathogenic and reach a critical mass. -Bacteria must be highly organized into complex communities. -Susceptible host that reacts to the bacteria -Periodontal pathogens are communicable |
| risk factors for developing periodontal disease | -Dental plaque biofilm -Local oral conditions (calculus, faulty restorations) -Cigarette smoking -Diabetes |
| immune system | A collection of responses that protects the body against infections by bacteria, viruses, fungi, toxins, and parasites and determines which cells/molecules it encounters are self or foreign substances. |
| neutrophils PMN's (Major function: phagocytic cells) | -First line of defense in acute inflammation; arrive at injury site w/in mins -Make up largest group (70%) of circulating WBC's present during the first 24-48 hours -Short lived cells (1 days) die when filled with phagocytized bacteria. -Migrate to JE/gingival sulcus aand engulf and destroy periodontal disease bacteria. -Neutrophil cytoplasm filled w/many graunles (lysosomes) which contain enzymes that allow PMNs to kill/digest bacteria but also cause death of host tissue in the process. -Lysomsomal enzymes include collagenase, B-glucuronidase, alkaline phosphatase -enzymes detectable in GCF during periodontisits. |
| macrophages | -Large phogcyes w/kidney shaped nucleus and few granules -Called monocytes in blood, macrophages in tissues -Highly phagocytic cells; found mainly in CT, few migrate to gingival sulcus. -Slower to arrive at site of infection and long living cells (months)in CT -Secrete prostoglandins and cytokines -Present antigen to T cells and together play imp role in chronic inflammation |
| lymphocytes | -Small WBCs that recognize and control foreign invaders. -2 main types- B lymphocytes and T lymphocytes |
| B lymphocytes (B cells) | -Specialized B cells are plasma cells |
| primary function of B cells | -Produce/secrete antibodies (protein molecules) into bloodstream. |
| function of anitbodies or immunoglobulins | -Neutralize bacteria or their toxins -coat bacteria -activate the complement system |
| five major classes of antibodies | -IgM (GCF) -IgG (GCF) -IgA (saliva) -IgE (mast cells) -IgD (in all) |
| function of T lymphocytes (T cells) | -Intensify response of B lymphocytes and macrophages to bacterial infection. -Produce cytokines |
| cytokines | A protein secreted by a cell, such as interleukins. A cell that produces a cell. |
| complement system | Series of circulating proteins found in blood; the second line of defense. |
| functions of complement system | -Opsonization of pathogens; coat bacterial surface making them more easily recognized by phagocytes. -Recruits additional phagocytic cells to the infection. -Forms pores in certain bacteria by creating a protein unit which punctures bacteria's cell membrane. (called a membrane attack complex) -Immune Clearance- housekeeping function, removal of immune complexes from circulation |
| inflammatory mediators | Biologically active compounds secreted by immune cells that activates the inflammatory response. |
| important inflammatory mediators in periodontal disease | -Cytokines -Prostoglandins (PGE) -Matrix metalloproteinases (MMPs) |
| cytokines | Powerful periodontal mediators that influence the behavior of other cells. |
| chemokines | Major subgroup of cytokines, cause additional immune cells to be attracted to site. -Transmit signals from cell to cell, signals immune system to send more phagocytes |
| cytokines are produced by | -Neutrophils -macrophages -B lymphocytes -epithelial cells -gingival fibroblasts -osteoblasts in response to injury or microorganisms |
| cytokine functions | -Recruit cells (PMNs and macrophages) to infection site -Increases vessel permeabilility- increased movement of immune cells and complement into tissues -Can initiate tissue destruction and bone loss in chronic inflammatory diseases |
| prostoglandins | Most important E series; imp role in periodontal bone destruction. |
| important sources of prostoglandins | -Neutrophils -Macrophages; major source in inflamed periodontal tissues. |
| functions of prostoglandins | -Increase vascular permeability and vasodialation -Trigger increased osteoclastic activity -Promote overproduction of MMP enzymes -Major initiators of alveolar bone loss in periodonitits |
| matrix/metalloproteinases MMPs | -Family of 12 different enzymes produced by cells of the body. -Act together to break down connective tissue matrix |
| sources of MMPs | -Produced by cells activated by bacterial LPS -Macrophages -Gingival fibroblasts (major source) -Junctional Epithelial cells -Neutrophils (major source) |
| functions of MMPs | -In health: facilitate normal turnover of periodontal connective tissue matrix -In infection: large amounts are released to attempt to kill bacteria -Overproduction-breakdown of connective tissue in periodontium -Results in gingival recession, pocket formation and tooth mobility |
| stages of inflammation | -Acute inflammation -C-Reactive Protein (CRP) |
| acute inflammation | -Rapid onset/short term (2 weeks or less), normal process that protects and heals the body following physical injury or infection. -PMNs play main role in phagocytose microbes, releasing cytokines -If body eliminates all microogranisms the tissue heals and inflammation ceases |
| C-reactive protein (CRP) | Produced by liver during this stage due to being triggered by oral bacteria byproducts in bloodstream. Results in inflamed arteries and promotes blood clot formation. |
| classic signs of acute inflammation | -Redness -Heat -Swelling -Pain -Loss of Function |
| chronic inflammation | Long lived, out of control inflammatory response (over 2-3 weeks) |
| characteristics of chronic inflammation | -Signs of inflammation may be absent -Host is unable to eliminate microorganisms -Accumulaton of macrophages characterizes chronic inflammation releasing IL-1, TNF-alpha and prostaglandins -Periods of remission -Exacerbation |
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