The study of all factors that may be involved in the development of a disease.
The study of prevalence, incidence and etiology of a disease within the total population (rather than an individual patient).
Number of cases of a disease that can be identified within a specified population at a given point of time.
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.
-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)
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.
-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
-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
-IgE (mast cells)
-IgD (in all)
function of T lymphocytes (T cells)
-Intensify response of B lymphocytes and macrophages to bacterial infection.
A protein secreted by a cell, such as interleukins. A cell that produces a cell.
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
Biologically active compounds secreted by immune cells that activates the inflammatory response.
important inflammatory mediators in periodontal disease
-Matrix metalloproteinases (MMPs)
Powerful periodontal mediators that influence the behavior of other cells.
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
-osteoblasts in response to injury or microorganisms
-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
Most important E series; imp role in periodontal bone destruction.
important sources of prostoglandins
-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
-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
-C-Reactive Protein (CRP)
-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
-Loss of Function
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