Relationship of surface epithelium concentrations of IL-1 alpha and IL-1 beta to clinical inflammation during experimental gingivitis

Experimental evidence has clearly demonstrated that IL-1 cytokine levels increase in experimental gingivitis (EG) models in response to plaque accumulation following the cessation of oral hygiene. These changes in cytokine production are reported to occur prior to visible signs of clinical inflammation, and as such may represent early markers of gingival inflammation. This clinical study used a novel dermal sampling tape as a method to collect cytokines from gingival epithelium, as opposed to the more commonly sampled gingival crevicular fluid. The primary objective of the study was to examine the relationship between changes in cytokine levels and clinical inflammation. Ten subjects participated in a 14-day EG model, where 5 days following a dental prophylaxis subjects refrained from all oral hygiene measures for 14-days. Clinical measures including the Löe-Silness Gingival Index (GI), a bleeding index derived from the GI, and the inflammation index (II) were made at baseline prior to the initiation of the EG period and following 14 days of EG. Dermal tape samples were collected from the right posterior buccal quadrant of each subject at both baseline and day 14. The tapes were extracted and the extracts analyzed for both IL-1 alpha and IL-1 beta by ELISA. Results of this study indicate that over a 14-day EG period statistically significant (p < 0.05) increases in GI, gingival bleeding, II, and IL-1 alpha were observed (tested by matched-pairs t test and Wilcoxon signed ranks test). A directional increase in IL-1 beta was also observed. Linear regression analyses demonstrated a strong positive correlation between the number of gingival bleeding sites from the region of gingiva sampled with Sebutape and IL-1 alpha (r = 0.93), as well as IL-1 beta (r = 0.90). In addition, linear regression analyses also demonstrated a strong positive correlation between the mean II score from the region of gingiva sampled with Sebutape and IL-1 alpha (r = 0.93), as well as IL-1 beta (r = 0.86). Similar correlations were observed for whole mouth scores of the number of gingival bleeding sites and mean II with respect to IL-1 alpha and IL-1 beta levels. Collectively, these data confirm the utility of the dermal tape for sampling epithelium cytokine levels from the gingiva and demonstrate a strong positive correlation between IL-1 alpha and IL-1 beta concentrations and gingival inflammation.