Risk Markers for Changes in Periodontal Pathology in the Third Molar and Non-Third Molar Regions

Abstract

Identify risk markers at baseline associated with changes in periodontal probing depth (PD) over time for the 3rd molar region and non-3rd molars in young adults. The data were from healthy subjects with four asymptomatic 3rd molars, enrolled in an IRB-approved longitudinal trial. Demographic and oral health data were collected at baseline. Gingival crevicular fluid (GCF) samples were taken from the mesial of all 1st molars and distal of all 2nd molars. GCF samples were independently analyzed by ELISA for levels of IL-1β and PGE2 as a measure of oral inflammation. A pooled patient mediator level was then calculated as the mean of the eight site values. Subgingival biofilm samples were taken from the distal of all 2nd molars prior to periodontal probing. The presence and levels of periodontal pathogens were determined using whole chromosomal DNA probes and checkerboard DNA-DNA hybridization. Baseline subject levels of periodontal pathogens were chosen to determine the level of periodontal pathogens in subjects’ biofilm. Gingival crevicular fluid (GCF) inflammatory mediators were chosen to assess subjects’ immune response to the pathogens. Full mouth PD, six sites per tooth, was conducted to determine periodontal status at baseline and at longest follow-up. The 3rd molar region was defined as the PD for 6 sites around the 3rd molars and the 2 sites on the distal of the 2nd molars. The non-3rd molar region was defined as the remainder of the PD sites in the mouth. A PD >4mm was considered indicative of periodontal pathology. The primary outcome measures for this study were the occurrence at longest follow-up of a PD in the 3rd molar region and in non-3rd molars in study subjects, dichotomized by PD<, >4mm. Predictor variables at baseline were subjects: 3rd molar region PD, levels of “orange cluster” and “red cluster” periodontal pathogens, and levels of GCF IL-1β and PGE2. Changes from enrollment to longest follow-up were compared by the McNemar’s Test. Level of significance was 0.05. Data from 195 subjects were available with a median follow-up of 5.9 years (IQ 4.6-6.9y). Median age at enrollment was 26.2 years (IQ 22-34y); 52% were female, 84% Caucasian and 10% African American. If at least one PD >4mm was detected in the 3rd molar region at baseline, 64% subjects had at least one PD >4mm in the 3rd molar region at follow-up and 18% at least four PD >4mm compared to baseline PD <4mm, 15% and 5%, respectively. Non-3rd molar region PD >4mm was also significantly more likely. The extent of 3rd molar periodontal pathology at baseline predicted the extent of 3rd molar and non-3rd molar periodontal pathology at longest follow-up. If at least four PD >4mm were detected in the 3rd molar region at follow-up, median number PD >4mm was 7 (IQ 5-12). If subjects had at least four PD >4mm in non-3rd molars at follow-up, median number PD >4mm was 11 (IQ 7-18.5). Baseline subject levels of GCF IL-1β were significant predictors of periodontal pathology at follow-up in the 3rd molar region and non-3rd molar region. If baseline levels of GCF IL-1β were above the median 432.0 ng/m/L (IQ 196.5-869.7), 73% of subjects had at least one PD >4mm in the 3rd molar region at follow-up vs. 54% below the median, and 58% of subjects had at least one PD >4mm in the non-3rd molar region at follow-up vs. 39%. Baseline levels of “orange” or “red” cluster pathogens significantly predicted follow-up 3rd molar region PD >4mm, but not non-3rd molar PD >4mm. The presence of risk markers for oral inflammation were associated with worsening 3rd molar and non-3rd molar periodontal pathology.