title: Indicators of periodontal disease activity: an evaluation.
abstract: It is becoming increasingly apparent that the traditional clinical criteria are inadequate for: determining active disease sites in periodontitis, monitoring quantitatively the response to therapy or measuring the degree of susceptibility to future breakdown. In an attempt to develop objective measures, a wide variety of studies have been undertaken using saliva, blood, plaque and gingival crevicular fluid (GCF) as the specimen source. Examination has included: specific bacteria and their products; host cells and their products (enzymatic and antibacterial, both immunologic and non-immunologic); products of tissue injury derived from local epithelial and connective tissues and bone. Although most of the work to date has failed to provide reliable aids to the clinician, refinements in techniques for sampling and the availability of more sophisticated analytic techniques give cause for optimism. Methods proposed for detection of disease-associated bacteria in subgingival plaque vary in their sensitivity and specificity. Dark field microscopy shows some correlation with existing disease; however, the limited specificity of this method imposes severe restrictions on its usefulness. Highly specific polyclonal and monoclonal antisera to suspected pathogens Bacteroides gingivalis and Actinobacillus actinomycetemcomitans have been developed and improved methods of identification of these microbes in plaque by ELISA immunofluorescence and flow cytometry are under development. With respect to the host response, a strong correlation between antibody patterns to specific bacteria and periodontal disease categories appears to be emerging. Although most studies have focused on serum antibody derived from peripheral blood, a shift to detection of local antibody response appears to be likely. Techniques of measurement that are exquisitely sensitive have been developed for detection of major immune recognition proteins such as antibody and complement in crevicular fluid. Research efforts attempting to correlate local antibody response to local disease activity are underway. Measurement of GCF flow rate, endotoxin, H2S, butyrate and a variety of enzymes (e.g., collagenase, arylsulfatase, B-glucuronidase) show good correlation with levels of gingivitis. In periodontitis, the most promising markers of tissue breakdown are prostaglandins of the E series, the enzymes collagenase and aspartate aminotransferase, sulfated glycosaminoglycans, osteoclastic activating factor and bone resorptive capacity of crevicular cells. Assay of the migration of crevicular leucocytes in vivo can serve as an indicator of a defect in host resistance.(ABSTRACT TRUNCATED AT 400 WORDS)
mesh_terms: D000818:Animals; D000907:Antibodies, Bacterial / Q000032:analysis; D001419:Bacteria / Q000201:enzymology / Q000302:isolation & purification / Q000378:metabolism; D001431:Bacteriological Techniques; D001862:Bone Resorption / Q000473:pathology; D002087:Butyrates / Q000378:metabolism; D020148:Butyric Acid; D003165:Complement System Proteins / Q000276:immunology; D003773:Dental Plaque / Q000378:metabolism / Q000382:microbiology; D004573:Electrolytes / Q000032:analysis; D004731:Endotoxins / Q000378:metabolism; D005069:Evaluation Studies as Topic; D006801:Humans; D006862:Hydrogen Sulfide / Q000378:metabolism; D007424:Intracellular Fluid / Q000201:enzymology; D007781:Lactoferrin / Q000378:metabolism; D007962:Leukocytes / Q000378:metabolism; D009113:Muramidase / Q000378:metabolism; D010510:Periodontal Diseases / Q000175:diagnosis* / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology; D011073:Polyamines / Q000378:metabolism; D011422:Propionates / Q000378:metabolism
chemical_list: D000907:Antibodies, Bacterial; D002087:Butyrates; D004573:Electrolytes; D004731:Endotoxins; D011073:Polyamines; D011422:Propionates; D020148:Butyric Acid; D003165:Complement System Proteins; D009113:Muramidase; D007781:Lactoferrin; C029658:propionic acid; D006862:Hydrogen Sulfide