Ukrainian Dental Almanac
ДИНАМІКА ЕКСПРЕСІЇ ГЕНІВ ЕПІТЕЛІАЛЬНИХ АЛАРМІНІВ IL-25, IL-33 І TSLP У СЛИЗОВІЙ ОБОЛОНЦІ РОТА ПРИ ХРОНІЧНОМУ РЕЦИДИВУЮЧОМУ ГЕРПЕТИЧНОМУ СТОМАТИТІ
By S.M. Zadorozhna, A.V. Marchenko, O.A. Shlykova and 1 others.
Abstract
Introduction. Chronic recurrent herpetic stomatitis (CRHS), caused by HSV-1, is characterized by periodic viral reactivation accompanied by inflammatory and reparative changes. The alarmins TSLP, IL-33, and IL-25 are involved in these processes; however, their expression patterns in CRHS and the potential for their modulation by pathogenetically targeted therapy remain insufficiently studied. Photobiomodulation and zinc supplementation are promising adjuncts to standard antiviral therapy aimed at optimizing inflammatory and reparative processes. Aim. To evaluate the utility of IL25, IL33, and TSLP gene expression as molecular markers of oral mucosal repair in CRHS by comparatively analyzing their dynamics during standard and optimized treatment regimens. Methods. Twenty patients with CRHS during an exacerbation were examined and divided into two groups: standard therapy (n=10) and standard therapy supplemented with photobiomodulation and zinc (n=10). Clinical healing dynamics and the expression of IL25, IL33, and TSLP genes in scrapings obtained from the lesion site were assessed using quantitative real-time PCR before treatment and on day 10. Results. Baseline IL25 and IL33 expression levels did not differ significantly between the groups (p=0.186 and p=0.308, respectively). On day 10, IL25 expression decreased significantly in the standard-treatment group (p=0.037) but remained unchanged in the optimized-treatment group (p=0.492); the groups differed significantly in the fold change in IL25 expression (p=0.038). IL33 expression on day 10 was significantly higher in the optimized-treatment group (p=0.017), with no significant within-group changes in either group. TSLP was detected in only 7 of 40 samples: in the optimized-treatment group, it was detectable before therapy but not on day 10, whereas in the standard-treatment group, the opposite pattern was observed, with TSLP detected only on day 10. No association was found between IL25 or IL33 expression and time to epithelialization; however, on day 10, a significant positive correlation between IL25 and IL33 expression was observed in the optimized-treatment group (ρ=0.733; p=0.016). Conclusions. The alarmins IL25, IL33, and TSLP are expressed in the oral mucosa of patients with CRHS and show dynamic changes during treatment, supporting their potential use as molecular markers of epithelial status. Standard and optimized therapies have different effects on their expression, which may reflect differences in their effects on epithelial reparative processes. The differential dynamics of TSLP and the maintenance of IL25 and IL33 expression despite accelerated healing indicate that alarmin levels should be interpreted with consideration of the phase of the reparative process.






