Host Response Tests for Diagnosing Periodontal Diseases

E xtensive data collected over the past decade demonstrate clearly that diseaseactive and disease‐inactive periodontal pockets exist, disease progression is infrequent and episodic, and most progression occurs in a small proportion of highly susceptible individuals. Furthermore, traditionally used diagnostic procedures do not identify susceptible individuals nor distinguish between disease‐active and disease‐inactive periodontal sites. New diagnostic tests based on host response factors that will aid in resolving these problems appear to be possible. Sources of material for use in such tests include gingival crevicular fluid (GCF), blood cells, and blood serum. Of these, components in GCF are most promising, at least in the immediate future. Although more than 40 GCF components have been studied, efforts that attempt to relate the presence and amount of a given component to an independent measure of active disease are very few in number. As a consequence, we do not yet know the potential for most GCF components as the basis of diagnostic tests. Those components that have been documented to associate with active disease as measured by attachment loss of 2 mm or greater include alkaline Phosphatase, β‐glucuronidase, prostaglandin‐E 2 , aspartate aminotransferase, and IgG 4 antibody subclass. Even in these cases, the data base is small and additional clinical studies are needed to document claims. At the present time, tests based on β‐glucuronidase, nonspecific neutral proteases, and aspartate aminotransferase are being commercialized. One test has received FDA approval. Tests based on blood cells have limited application for patients with adult periodontitis, but are useful for patients with earlyonset forms of periodontitis. An abnormality in the leukocyte adherence molecules on the surfaces of neutrophils is diagnostic for generalized prepubertal periodontitis, and defects in chemotactic receptor numbers and in a surface molecule designated as GP110 are found on the neutrophils of most but not all localized juvenile periodontitis patients. Recent data indicate that enhanced unstimulated or stimulated release of PGE 2 and Interleukin‐1 by peripheral blood monocytes may be an indicator of susceptibility to severe periodontitis. Assessment of the humoral immune response as reflected by serum antibodies to antigens of periodontopathic bacteria shows little promise as the basis for tests diagnostic of site‐specific disease activity. However, the capacity of an individual to mount an IgG 2 subclass response to carbohydrate antigens may have potential as an indicator of disease susceptibility. J Periodontol 1992; 63:356–366 .