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Review
. 2023 Sep 19;24(18):14293.
doi: 10.3390/ijms241814293.

The Mechanisms and Efficacy of Photobiomodulation Therapy for Arthritis: A Comprehensive Review

Affiliations
Review

The Mechanisms and Efficacy of Photobiomodulation Therapy for Arthritis: A Comprehensive Review

Renlong Zhang et al. Int J Mol Sci. .

Abstract

Rheumatoid arthritis (RA) and osteoarthritis (OA) have a significant impact on the quality of life of patients around the world, causing significant pain and disability. Furthermore, the drugs used to treat these conditions frequently have side effects that add to the patient's burden. Photobiomodulation (PBM) has emerged as a promising treatment approach in recent years. PBM effectively reduces inflammation by utilizing near-infrared light emitted by lasers or LEDs. In contrast to photothermal effects, PBM causes a photobiological response in cells, which regulates their functional response to light and reduces inflammation. PBM's anti-inflammatory properties and beneficial effects in arthritis treatment have been reported in numerous studies, including animal experiments and clinical trials. PBM's effectiveness in arthritis treatment has been extensively researched in arthritis-specific cells. Despite the positive results of PBM treatment, questions about specific parameters such as wavelength, dose, power density, irradiation time, and treatment site remain. The goal of this comprehensive review is to systematically summarize the mechanisms of PBM in arthritis treatment, the development of animal arthritis models, and the anti-inflammatory and joint function recovery effects seen in these models. The review also goes over the evaluation methods used in clinical trials. Overall, this review provides valuable insights for researchers investigating PBM treatment for arthritis, providing important references for parameters, model techniques, and evaluation methods in future studies.

Keywords: animal arthritis models; anti-inflammation; clinic trials; osteoarthritis; photobiomodulation; rheumatoid arthritis.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
PBM exerts its therapeutic effects on arthritis through five key mechanisms: regulation of angiogenesis, stimulation of ATP production in cells, modulation of arthritis-related genes, regulation of the secretion of joint-related enzymes, and modulation of the expression of cytokines, including both pro-inflammatory and anti-inflammatory factors. These mechanisms collectively contribute to the efficacy of PBM treatment for arthritis. The regulation of angiogenesis helps reduce the infiltration of inflammatory cells and promotes increased blood flow, aiding in the management of arthritis. Increased ATP production enhances the function and activity of cells involved in arthritis. Modulating gene expression can modify the production of enzymes and inflammatory factors, leading to a reduction in the production of enzymes that damage joint tissues. The overall result is a decrease in inflammation and improvement in arthritis symptoms.
Figure 2
Figure 2
The activation of innate immunity is the underlying mechanism that triggers RA. Dendritic cells (DCs), macrophages, and activated B and T cells express major histocompatibility complex, CD80/CD86, and other inflammatory stimulatory proteins, which contribute to the differentiation of T cells into T helper 1 (Th1) and Th17 cell phenotypes. Once activated, T and B cells secrete inflammatory cytokines and chemokines, further activating leukocytes, macrophages, fibroblasts, and endothelial cells. This complex network of molecular and cytokine-mediated interactions forms the basis of RA pathogenesis. Each cell involved in the pathogenesis of RA plays a significant role in mediating inflammation and joint destruction. Therefore, inhibiting the function and response of these cells has become a crucial objective in alleviating or potentially curing RA.

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