Recent findings illustrate LDRT's ability to modulate significant immunological and molecular processes involved in OA pathogenesis, such as suppressing pro-inflammatory cytokines (e.g. TNF-α, IL-1β, IL-6), increasing anti-inflammatory mediators (e.g. IL-10, TGF-β), suppressing matrix-degrading enzymes (e.g. MMP-13), and restoring mitochondrial activity through modulation of oxidative stress. Additionally, LDRT influences inflammatory cell activity within the local joint microenvironment without inducing systemic immunosuppression. While available data suggest a favorable safety profile, standardized protocols and long-term outcomes are still lacking, necessitating further high-quality randomized controlled trials.
Khakshour et al. (Thu,) studied this question.
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