The Effect of 630 nm Photobiomodulation on the Anti-Inflammatory Effect of Human Gingival Fibroblasts

Zeqing Chen,Xuwen Liu,Zhicheng Lu,Shijie Huang,Haokuan Qin,Muqing Liu

doi:10.3390/photonics8090360

Abstract

Periodontal disease is the most common oral chronic inflammatory disease in humans. Recent studies have indicated that red light Photobiomodulation (PBM) could inhibit cell inflammation effectively, but the effect of different doses of PBM on the treatment of inflammation has to be improved. Thus, this study was aimed to investigate the effects of various doses of PBM (630 ± 30 nm, (1) 5 mW/cm2, 1 J/cm2, 200 s; (2) 5 mW/cm2, 3 J/cm2, 600 s; (3) 5 mW/cm2, 9 J/cm2, 1800 s; (4) 5 mW/cm2, 18 J/cm2, 3600 s; (5) 5 mW/cm2,36 J/cm2, 7200 s) on the anti-inflammatory response of human gingival fibroblasts. Our results suggested that PBM (630 ± 30 nm) with doses of 18 J/cm2 and 36 J/cm2 could significantly inhibit the production of inflammatory cytokines such as Prostaglandin E2 (PGE2) and IL-8, presumably due to the fact that a high dose of PBM treatment could reduce intracellular Reactive oxygen species (ROS) in human gingival fibroblasts, thus reducing the expression of COX-2 enzyme. In addition, it was found that treatment with different doses of PBM (630 ± 30 nm) did not result in reduced mitochondrial membrane potential and mitochondrial dysfunction in human gingival fibroblasts. Our study provides a theoretical reference for the selection of PBM parameters and the application of PBM in the clinical treatment of periodontitis.

Highlights

Periodontal disease is the major cause of adult tooth loss and is commonly characterized by a chronic inflammation caused by infection of oral bacteria
Our findings demonstrated that a certain dose of 630 nm red light PBM could inhibit the inflammatory response in Human gingival fibroblasts (HGFs) induced by LPS, which was reflected in the inhibition of the production of Prostaglandin E2 (PGE2) and IL-8
The production of PGE2 regulated by PBM was more sensitive to light dose than that of IL-8

Summary

Introduction

Periodontal disease is the major cause of adult tooth loss and is commonly characterized by a chronic inflammation caused by infection of oral bacteria. The lipopolysaccharide of Porphyromonas gingivalis (Pg. LPS) is a key factor in the development of periodontitis. Human gingival fibroblasts (HGFs) are the major constituents of gingival connective tissue, and it may directly interact with bacteria and bacterial products (including LPS) in periodontitis lesions. It is suggested that HGFs play an important role in the host responses to LPS in periodontal disease [1]. LPS can enhance the production of inflammatory cytokines such as PGE2, interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-alpha) in HGFs. Inflammatory cytokines are involved in the development of periodontitis, which promotes the release of large amounts of inflammatory cytokines such as PGE2 and IL-8 [2,3]. Several experiments have shown that LPS promotes the release of PGE2 and IL-1β in HGFs [4,5]

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