The pathogenesis of periodontal tissue destruction involves the orches
trated sequential activation of several components of the host respons
e, each of which have the potential for providing diagnostic informati
on regarding the health or disease status of the periodontium. These e
vents include the bacterial triggering of serum components, the releas
e of vasoactive compounds, the recruitment of inflammatory cells, the
activation of phagocytes, the local secretion of immunoglobulins and i
nflammatory mediators, as well as connective tissue remodeling. For pu
rposes of diagnosis, much attention has been directed toward the measu
rement of local levels of specific byproducts of the pathogenic proces
s either within the tissues or in the adjacent crevicular fluid. These
are site-directed assessments of the local concentration of these byp
roducts, 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-b
ased, there is an increasing need to identify patients at risk for int
ervention strategies. Furthermore, there are substantial data that per
iodontal diseases are specific infections that occur in an appropriate
ly susceptible host. The expression of periodontal disease has a stron
g genetic component, which presumably defines the host's response ther
eby affecting susceptibility. For this reason, there is increased inte
rest in defining those elements of the host response which result in s
usceptibility to disease. The ultimate objective of a diagnostic strat
egy is to identify patients who are potentially at risk for acquiring
disease to enable preventive measures.