title: New clinical diagnostic strategies based on pathogenesis of disease.
abstract: The pathogenesis of periodontal tissue destruction involves the orchestrated sequential activation of several components of the host response, each of which have the potential for providing diagnostic information regarding the health or disease status of the periodontium. These events include the bacterial triggering of serum components, the release of vasoactive compounds, the recruitment of inflammatory cells, the activation of phagocytes, the local secretion of immunoglobulins and inflammatory mediators, as well as connective tissue remodeling. For purposes of diagnosis, much attention has been directed toward the measurement of local levels of specific byproducts of the pathogenic process either within the tissues or in the adjacent crevicular fluid. These are site-directed assessments of the local concentration of these byproducts, and with the important exception of antibody levels, very few byproducts of the periodontal pathogenic process have been studied on a systemic level. However, since the risk associated with periodontal disease progression is primarily patient-based and secondarily site-based, there is an increasing need to identify patients at risk for intervention strategies. Furthermore, there are substantial data that periodontal diseases are specific infections that occur in an appropriately susceptible host. The expression of periodontal disease has a strong genetic component, which presumably defines the host's response thereby affecting susceptibility. For this reason, there is increased interest in defining those elements of the host response which result in susceptibility to disease. The ultimate objective of a diagnostic strategy is to identify patients who are potentially at risk for acquiring disease to enable preventive measures.
authors.affiliation: University of North Carolina at Chapel Hill Dental Research Center 27599-7455.
authors.forename: S
authors.initials: S
authors.lastname: Offenbacher
authors.forename: J G
authors.initials: JG
authors.lastname: Collins
authors.forename: R R
authors.initials: RR
authors.lastname: Arnold
mesh_terms: D000907:Antibodies, Bacterial / Q000097:blood; D001421:Bacteria, Anaerobic / Q000472:pathogenicity; D004796:Clinical Enzyme Tests; D016207:Cytokines / Q000502:physiology; D004198:Disease Susceptibility; D005883:Gingival Crevicular Fluid / Q000201:enzymology; D006801:Humans; D009000:Monocytes / Q000276:immunology; D009504:Neutrophils / Q000201:enzymology / Q000276:immunology; D010510:Periodontal Diseases / Q000175:diagnosis* / Q000209:etiology* / Q000276:immunology; D011237:Predictive Value of Tests; D012307:Risk Factors; D013601:T-Lymphocytes / Q000276:immunology; D014774:Virulence
chemical_list: D000907:Antibodies, Bacterial; D016207:Cytokines