The Host Response in Gingival Crevicular Fluid: Potential Applications in Periodontitis Clinical Trials

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Abstract
Traditional clinical variables of periodontal pathology have only limited value as indicators for future disease progression in patients with adult periodontitis. Consequently, other aspects of the periodontal lesion are being examined for their diagnostic utility. Analysis of the host response in gingival crevicular fluid (GCF) is among the most intensely studied of these new diagnostic approaches. Specific indicators of the humoral immune response, cellular immune response, and acute inflammatory response have been identified in GCF. The relationship of indicators of the humoral immune response to active periodontal disease is equivocal. Specific indicators of the cellular immune response in GCF may ultimately prove to be important diagnostically, but the relationship of any specific marker to active periodontal disease has not been reported. In contrast, the acute inflammatory response in GCF has been extensively studied and a number of factors appear to be associated with an increased risk for future disease progression. Indicators of enhanced polymorphonuclear leukocyte activity, (lysosomal β-glucuronidase, lysosomal collagenase), Prostaglandin E2, and an indicator of acute tissue destruction (the cytoplasmic enzymes aspartate aminotransferase) have been associated with the occurrence of clinical attachment loss. An example of the application of a GCF marker in a periodontitis clinical trial is provided by describing the relationship of lysosomal βglucuronidase in GCF at baseline and 2 weeks following root planing and scaling to the occurrence of disease activity during the following 6 months. Persistently elevated levels of this enzyme were related to clinical attachment loss. The positive, negative, and total predictive values for β-glucuronidase as an identifier of clinical attachment loss were 86%, 71%, and 76%, respectively. The accumulated evidence suggests that inclusion of a GCF-based determination of the acute inflammatory response in periodontitis clinical trials is justified. The information obtained may provide both a quantitative assessment of the host response and a measure of how effective the therapy is in reducing the risk of future clinical attachment loss. J Periodontol 1992; 63:1117–1123.