[Effect of Chinese medicine "gu chi wan" on chemotaxis and phagocytosis of polymorphonuclear leukocytes from peripheral blood in juvenile periodontitis patients].
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With the recent description of 12 different forms and sub-forms of periodontitis by the World Workshop in Clinical Periodontics (1989), increased emphasis has been placed on diagnosis. Dr. Ranney's review addressed the specificity and sensitivity of current diagnostic tests with respect to their ability to differentiate between health and disease and between the individual disease states. Although considerable microbiologic and immunologic data have been accumulated in the past decade, very little of this information has proved to be sufficiently sensitive to be of use in differential diagnosis. Clinical measurements provide us with an insensitive, retrospective analysis of what has already occurred but allow us to diagnose disease based on its natural history. Measures of attachment levels, by use of conventional probes, are only sufficiently sensitive indicators of periodontitis when as much as 20-30% of attachment has already been lost. Current technological improvements in probing measurements and radiographic assessment may increase sensitivity in this area. Future improvements in diagnostic techniques will occur with the advent of sensitive biochemical analyses of gingival crevicular fluid. These assays will provide a more objective analysis of inflammation and, in time, will provide sufficient sensitivity to allow for differentiation between and among the various forms of periodontal disease. Future directions in diagnosis will focus on the identification of disease-susceptible individuals and the prediction of future periodontal breakdown.
Considerable evidence suggests that there is some genetic basis for the early onset forms of disease. The molecular abnormality and its genetic inheritance has been established in some cases of generalized prepubertal periodontitis. Family studies of juvenile periodontitis indicate that this disorder is transmitted by autosomal recessive genes, although additional data indicate genetic heterogeneity in this clinically defined disease. Recent evidence also suggests that susceptibility to periodontal disease may be related in part to genetically determined immune responsiveness to bacterial lipopolysaccharides. Although specific genetic risk factors have not been identified for the more common adult chronic periodontitis, recent studies indicate that there is significant genetic variance in the population for clinical and radiographic measures of disease. More precise definitions of disease phenotypes will facilitate future genetic epidemiologic studies of the periodontal diseases.
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