Perio Quiz 4
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55 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 a disease. |
| "Calculus Theory" | before 1960, everyone was equally susceptible to periodontal disease; calculus was responsible for disease. Treatment- prophylaxis every 6 months and quantity not the quality of plaque was responsible for disease; patients told to brush 3x/day. |
| "Non-specific Plaque Theory" | 1965-1975, bacteria in plaque caused disease. All plaque essentially the same; too much plaque caused disease. Treatment- prophylaxis 2-3x/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 w/ 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, & systemic etiologic factors for disease. focus on patient self care & frequent professional care |
| Continuous model theory | periodontal destruction is slow and constant until tooth loss; the severity of the disease increases w/age. |
| 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 |
| Gingivitis | most common form of periodontal disease found in individuals of all ages. |
| Periodontal disease | has been found to be leading cause of tooth loss in adults older than 45 yr of age |
| Primary Risk Factor of Periodontitis | Dental Plaque Biofilm (bacterial infection -local & systemic contribution factors -*Host response to biofilm bacteria |
| Factors in order to infect the tissues & cause disease | -Bacteria must be pathogenic & reach a critical mass -Bacteria must be highly organized into complex communities -Susceptible host that reacts to the bacteria -Periodontal pathogens are communicable (can be passed between parent & child or spouse through saliva) |
| Risk Indicators | factors that modify or amplify the likelihood of developing periodontal disease |
| Major Risk Factors for periodontitis | -specific bacterial pathogens (calculus) -cigarette smoking -diabetes mellitus (systemic) |
| 3 species of Dental plaque Biofilm | 1. Aggregatibacter actinomycetemcomitans 2. Porphyromonas gingivialis 3. Tannerella forsythia |
| Immune System | a collection of responses that protects the body against infections by bacteria, viruses, fungi, toxins, and parasites & determines which cells/molecules it encounters are self or foreign substances. |
| Function (prime purpose) of immune system | to defend life of the host (yourself) by identifiying foreign substances in the body & respond by sending certain types of cells to the infection site & produce biochemical substances to counteract the foreign invaders |
| Overzealous Immune Response (by host) | if response by host is confused or too intense it begins to harm the body that it is trying to protect. |
| Leukocytes (WBC)/Host Cells participating in the immune response | 1. Neutrophils (PMNs) 2. Macrophages 3. Lymphocytes (B & T cells) 4. Mast Cells |
| Mast Cells | cells found in the gingival connective tissue that contain granules and release substances such as heparin & histamine. |
| Host tissue changes seen in the inflammatory response | ~microcirculation changes -vasodilation -increase vascular permeabilit -fluid exudate ~response of various host defense cells |
| Primary Components of the immune system | -Phagocytes -Lymphocytes -Complement System |
| Phagocytes | large WBCs that engulf and digest bacteria -Neutrophils (PMN) -Macrophages |
| Process of Phagocytosis | 1. External wall of phagocytic cell sticks to the bacteria 2. Phagosome surrounds bacteria & brings it into the cell 3. Phagolysosome digests bacteria 4. Phagocyte releases the phagolysosome contents into surrounding tissue **Phagocytosis is more effective if opsonins are present! |
| Opsonins | antibodies or complement binding to the surface of the bacteria, coating the bacteria so they are easier to be identified by PMNs and the "swallowed" |
| Chemotaxis* | *Signaling process that stimulates cells to go to areas of tissue damage; both neutrophils & macrophages are attracted to sites of injury by chemotaxis |
| Neutrophils (PMNs) | *Major Function: phagocytic cells *First ling of defense in acute inflammation -largest group of WBCs present during first 24-48 hrs of inflammation response by hose -short-lived cells (1 day) |
| Function of Neutrophils | -migrate to JE/gingival sulcus & engulf and destroy periodontal disease bacteria -cyctoplasm filled w/many granules (Lysosomes) which containt enzymes that allow PMNs to kill/digest bacteria but also cause death of host tissue in the process! |
| Lysosomal Enzymes include... | -collagenase -B-glucuronidase -alkaline phosphatase |
| Enzymes | __________detectable in GCF during periodontitis |
| Macrophages | large phagocytes w/ kidney-shapes nucleus & few granules *called this when present in tissues -*Highly phagocytic cells -found mainly in CT, few migrate to gingival sulcus -slower to arrive to site & long living cells (months) |
| monocytes | macrophages are called ______ when in blood |
| Function of Macrophages | *secrete enzymes- prostaglandins & cytokines -present antigen to Tcells and together play important role in chronic inflammation |
| Lymphocytes | small WBCs that recognize and control foreign invaders |
| 2 main types* of lymphocytes | 1. B-lymphocytes 2. T-lymphocytes |
| B-Lymphocytes (b-cells) | specialized b-cells called Plasma Cells* -primary functin to produce/secrete *antibodies (protein molecules) into the bloodstream |
| *functions of antibodies or immunoglobins | -neutralize bacteria or their toxins -coat bacteria -activate the complement system |
| 5 Major Classes* of antibodies/immunoglobins | IgM & IgG (GCF) both primarily in periodontal tissues IgA (saliva) IgE (on mast cells) IgD (does not have a prevalent place) |
| T-Lymphocytes (t-cells) | -function: intensify reponse of B-lymphocytes and macrophages to bacterial infection -*Produce Cytokines (a protein secreted by a cell) such as interleukins |
| Complement system | series of circulating proteins found in blood -second line of defense |
| 4 Principle Functions of complement system | 1. *Opsonization of pathogens- coat the bacterial surface making them more easily recognized by phagocytes 2. *Recruits additional phagocytic cells to the infection 3. forms pores in certain bacteria by creating a protein unit which punctures bacteria's cell memembrane (called a **membrane attack complex) 4. *Immune Clearance- "housekeeping" function, removal of immune complexes from circulation |
| Inflammatory Mediators | Biologically active compounds secreted by immune cells that activates the inflammatory response |
| 3 Important inflammatory mediators | -Cytokins -Prostaglandins (PGE) -Matrix Metalloproteinases (MMPs) |
| Cytokins | powerful periodontal mediators (Interleukin-1,6,8, tumor necrosis factor) that influence the behavior of other cells -transmit signals from cell to cell, signals immune system to send more phagocytes -*Produced by: nuetrophils, macrophages, b-cells, epithelial cells, gingival fibroblasts, and osteoblasts in response to injury or microorganisms |
| Chemokines | major subgroup of Cytokins; cause additional immune cells to be attracted to site |
| Cytokine Functions | -Recruit cells (PMNs & Macrophages) to infection site -increases vessel permeability (increased movement of immune cells and complement into tissue) -can initiate tissue destruction and bone loss in chronic inflammatory disease |
| Prostaglandins (PGE) | PGE2 most important e-series: important role in periodontal bone destructions -Important sources: Neutrophils, Macrophages (major in inflamed tissues) |
| Functions of Prostaglandins (PGE) | -increase vascular permeability and vasodilatation (redness & edema) -trigger increases osteoclastic activity (resorption of bone) -promote overproduction of MMP enzymes -major initiators of alveolar bone loss in periodontitis |
| Matrix Metalloproteinases (MMPs) | -family of 12 different enzymes produced by cells of the body -act together to break down connective tissue matrix -*Sources: produced by cells activated by bacteial LPS (endotoxin-part of bacterial cell wall) ~Macrophages, gingival fibroblasts(major source), JE 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 |
| Acute Inflammation | -rapid onset (2 weeks or less) -PMNs play main role in phagocytose microbes, releasing cytokins -C-reactive protein (CRP) produce during this stage due to being triggered by oral bacteria byproducts in bloodstream -results in inflamed arteries and promotes blood clot formation |
| Chronic Inflammation | -long lived (2-3 weeks) -sings of inflammation may be absent -permanent damage to body's tissues results -Accumulation of Macrophages characterizes chronic inflammation releasing IL-1, TNF-alpha and prostaglandins. -Periods of remission and exacerbation |
| 5 classic signs of acute inflammation | 1. redness 2. heat 3. swelling 4. pain 5. loss of function |
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