A Comparative Evaluation of Interleukin 1 Beta and Prostaglandin E2 with and without Low-level Laser Therapy during En masse Retraction

Contemp Clin Dent. 2018 Apr-Jun;9(2):267-275. doi: 10.4103/ccd.ccd_859_17.

Abstract

Background and objectives: Orthodontic forces are known to produce mechanical damage and inflammatory mediators such as prostaglandins (PGs) and interleukin (IL)-1, in the periodontium and dental pulp. Low-level laser therapy (LLLT) is a stimulator of the on-going biological process in tissue and found to be effective in modulating cell activity, which is involved in orthodontic tooth movement. Here, a humble effort has been made to study two such cytokines, namely IL-1 β and PG E2 (PGE2) which are partially responsible for bone turnover. The purpose of this study was to compare the changes occurring in the values of IL-1 β and PGE2 in the gingival crevicular fluid (GCF) during en masse retraction with and without LLLT.

Methodology: GCF was collected using micropipettes from the distal ends of upper canines. The experimental side was exposed to biostimulation using 810 nm gallium-aluminum-arsenide diode laser and the contralateral side taken as control. A total of 10 irradiations for 10 s per site were given, five on the buccal side and five on the palatal side, to cover the entire periodontal fibers and the alveolar process around the tooth. After 7 days and 21 days of retraction, GCF sample was collected. Quantitative analysis of IL-1 β and PGE2 in the GCF samples was assessed using a commercially available Raybiotech® IL-1 β and Human PGE2.

Results: (1) IL-1 β and PGE2 levels showed significant results from baseline to 21 days after LLLT irradiation. (2) LLLT-assisted retraction was significantly faster than conventional retraction.

Interpretation and conclusion: It was concluded from the study that IL-1 β and PGE2 levels peaked after LLLT. The difference in the levels of both cytokines was statistically significant.

Keywords: Cytokine; interleukin 1 beta; low-level laser therapy; prostaglandin E2.