perio quiz 10/12
|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)
|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|
-activate the complement system
|five major classes of antibodies|| -IgM (GCF)|
-IgE (mast cells)
-IgD (in all)
|function of T lymphocytes (T cells)|| -Intensify response of B lymphocytes and macrophages to bacterial infection.|
|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|
-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|
-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|
-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|
-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