The relationship of β‐glucuronidase activity in crevicular fluid to clinical parameters of periodontal disease: Findings from a multicenter study

Abstract Previous reports have suggested that persistently elevated levels of the acidic glycohydrolase β‐glucuronidase (βG) in gingival crevicular fluid (GCF) can identify patients with chronic adult periodontitis who are at risk for future probing attachment loss (PAL). To comprehensively study βG activity in GCF, a multicenter trial examining the relationship of the enzyme in GCF to traditional clinical parameters of periodontal disease and PAL was conducted. In this report, the baseline data was used to evaluate the relationship of βG activity in GCF to traditional parameters of periodontal disease. The study group included 130 patients who had been treated for periodontal disease and were on a regular recall schedule, and 10 patients with chronic adult 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 teeth. As a control, GCF samples and clinical data were collected from 62 patients with a healthy periodontium or mild inflammatory gingivitis without loss of probing attachment. At baseline, βG activity for the periodontitis patients ranged from 0 to 1704 Units (U), with a median of 32 U. βG could not be detected in 0.2% of samples (activity ≤2.0 U). The 90% cumulative relative frequency was 139 U. For the healthy/gingivitis subjects βG 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. βG activity in GCF was not related to gender or age. For the periodontitis patients, elevated enzyme activity (140 U) was most often associated with molar teeth, followed by maxillary bicuspids. Maxillary central incisors, and mandibular central and lateral incisors displayed the lowest frequency of elevated enzyme activity. The relationship of βG 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 samples contained low enzyme activity (90% of sampies ≤U). Descriptive indicators demonstrated a trend of increased βG activity with increased probing depth. The median βG activity shifted from 15 U for 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 rather than representing a shift in the distribution profile. The relationship of bleeding on probing to βG activity was assessed on a tooth basis (bleeding at 0 to 6 sites). Teeth with no bleeding sites demonstrated a median βG activity of 22 U, while teeth with 5–6 bleeding sites had a median βG activity of 86 U. Again, this was the result of a broadening and flattening of the distribution observed with increased occurrence of bleeding on probing. These data suggest that while sites and teeth with increased severity of periodontal disease demonstrate greater βG activity, quantitative assessment of this enzyme in GCF provides a different measure of periodontal pathology than traditional clinical parameters of disease.