THE RELATIONSHIP OF BETA-GLUCURONIDASE ACTIVITY IN CREVICULAR FLUID TO CLINICAL-PARAMETERS OF PERIODONTAL-DISEASE - FINDINGS FROM A MULTICENTER STUDY

Previous reports have suggested that persistently elevated levels of t he acidic glycohydrolase beta-glucuronidase (beta G) in gingival crevi cular fluid (GCF) can identify patients with chronic adult periodontit is who are at risk for future probing attachment loss (PAL). To compre hensively study beta G activity in GCF, a multicenter trial examining the relationship of the enzyme in GCF to traditional clinical paramete rs of periodontal disease and PAL was conducted. In this report, the b aseline data was used to evaluate the relationship of beta G activity in GCF to traditional parameters of periodontal disease. The study gro up included 130 patients who had been treated for periodontal disease and were on a regular recall schedule, and 10 patients with chronic ad ult periodontitis who had never received treatment. Upon entering the longitudinal trial, the patients were examined, and a standardized 30- s GCF sample was collected from the mesiobuccal crevice of all study t eeth. As a control, GCF samples and clinical data were collected from 62 patients with a healthy periodontium or mild inflammatory gingiviti s without loss of probing attachment. At baseline, beta G activity for the periodontitis patients ranged from 0 to 1704 Units (U), with a me dian of 32 U. beta G could not be detected in 0.2% of samples (activit y less than or equal to 2.0 U). The 90% cumulative relative frequency was 139 U. For the healthy/gingivitis subjects beta G activity ranged from 0 to 504 U, with a median of 22 U. Enzyme was not detectable in 0 .4% of samples. Only 0.9% of samples contained greater than 139 U. bet a G activity in GCF was not related to gender or age. For the periodon titis patients, elevated enzyme activity(greater than or equal to 140 U) was most often associated with molar teeth, followed by maxillary b icuspids. Maxillary central incisors, and mandibular central and later al incisors displayed the lowest frequency of elevated enzyme activity . The relationship of beta G activity to the traditional parameters of probing depth and bleeding on probing was assessed. For shallow sites (1.0-1.5 mm, 2.0-2.5 mm probing depth), the large majority of GCF sam ples contained low enzyme activity (90% of samples < 50 U). Descriptiv e indicators demonstrated a trend of increased beta G activity with in creased probing depth. The median beta G activity shifted from 15 U fo r the shallowest sites (1.0-1.5 mm) to 127 U for the deepest sites (5- 8 mm). However, this was due to a broadening of the distribution rathe r than representing a shift in the distribution profile. The relations hip of bleeding on probing to beta G activity was assessed on a tooth basis (bleeding at 0 to 6 sites). Teeth with no bleeding sites demonst rated a median beta G activity of 22 U, while teeth with 5-6 bleeding sites had a median beta G activity of 86 U. Again, this was the result of a broadening and flattening of the distribution observed with incr eased occurrence of bleeding on probing. These data suggest that while sites and teeth with increased severity of periodontal disease demons trate greater beta G activity, quantitative assessment of this enzyme in GCF provides a different measure of periodontal pathology than trad itional clinical parameters of disease.