## 4 Discussion  
Our findings confirm that PBMT effectively reduces pain intensity in Fibromyalgiagia, with both localized and whole-body applications demonstrating significant analgesic effects. Localized PBMT specifically targets hyperalgesia at tender points, resulting in significant reductions in pain scores [47; 53]. In contrast, whole-body PBMT provides systemic and sustained pain relief [54], with studies reporting prolonged reductions in VAS scores during follow-ups [36]. These findings align with evidence supporting PBMT's role in modulating central sensitization [55] and reducing neurogenic inflammation [56; 57]. The analgesic mechanisms of PBMT in patients with Fibromyalgiagia are multifactorial. They are primarily attributed to its ability to downregulate key pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-\(\alpha\)), interleukin-6 (IL-6), and interleukin-1 beta (IL-1\(\beta\)) [58; 59], which play a central role in the maintenance of chronic pain and systemic inflammation. Additionally, PBMT has been shown to enhance local microcirculation,thereby promoting oxygen and nutrient delivery to damaged tissues and facilitating tissue repair and recovery [60]. Moreover, recent evidence suggests that PBMT can modulate the activity of glial cells in the central nervous system, which are involved in the amplification and persistence of pain through neuroinflammatory pathways [61; 62]. By attenuating glial activation, PBMT may help reduce central sensitization and mitigate neuroinflammatory. Beyond its analgesic effects, PBMT has also shown promise in regard to reducing fatigue, particularly through its impact on mitochondrial function and cellular metabolism. This effect is mediated by the absorption of photons by specific intracellular chromophores, such as CCO, which are located within the mitochondrial respiratory chain [63; 64; 65]. Upon photon absorption, these chromophores facilitate the conversion of light energy into biochemical energy, triggering a cascade of events that lead to increased mitochondrial membrane potential, enhanced ATP production, and improved cellular respiration [66; 67; 68]. As a result, PBMT can enhance bioenergetic efficiency, which may help alleviate fatigue symptoms commonly reported by these patients. Additionally, PBMT has been shown to modulate mitochondrial membrane potential and regulate the production of reactive oxygen species (ROS), thereby promoting the redox balance and reducing oxidative stress [69; 70]. Rather than suppressing ROS entirely, PBMT induces a transient and controlled increase in ROS levels, which function as secondary messengers in essential cellular signaling pathways. This mild oxidative stimulus activates protective mechanisms and contributes to long-term reductions in oxidative damage, underscoring the importance of dose-dependent effects. Furthermore, PBMT increases membrane permeability, enhancing ion transport across the cytoplasmic membrane and supporting cellular homeostasis [71; 72]. It also stimulates oxidative enzymes, particularly CCO, thereby improving mitochondrial respiration and ATP synthesis [73; 74]. Importantly, concerns regarding potential neurotoxicity due to ROS accumulation are not supported by current preclinical or clinical evidence. On the contrary, at therapeutic dosages, PBMT promotes mitochondrial function without inducing structural or functional damage to sensory neurons. Clinical trials consistently report significant pain relief without any signs of neuropathic complications, suggesting that ROS production under PBMT acts as a beneficial signaling mechanism rather than a cytotoxic insult [69; 70]. Nevertheless, given the biphasic nature of PBMT responses, careful parameter selection remains essential to ensure efficacy and safety. Furthermore, PBMT modulates mitochondrial dynamics, particularly the processes of fission and fusion, which are essential for preserving mitochondrial integrity, optimizing ATP production, and adapting to cellular stress.