Laboratory of Neuromodulation of Experimental Pain, Department of Anatomy, Insitute of Biomedical Sciences, University of São Paulo, Av. Professor Lineu Prestes 2415, ICB III, Cidade Universitária, Sao Paulo, 05508-900, Brazil.
University City of São Paulo, Campus of Pinheiros, Rua Butantan, Sao Paulo, 05425-140, Brazil.
Lasers Med Sci. 2019 Dec;34(9):1841-1847. doi: 10.1007/s10103-019-02785-6. Epub 2019 Apr 10.
Temporomandibular disorder (TMD) is a collective term that encompasses a set of clinical problems that affect the masticatory muscles, the temporomandibular joint, and associated structures. Despite their high clinical prevalence, the mechanisms of chronic craniofacial muscle pain are not yet well understood. Treatments for TMD pain relief and control should be minimally invasive, reversible, and conservative. Photobiomodulation (PBM) is a promising option once it is known to inhibit inflammatory response and to relief painful symptoms. Herein, the effects of PBM (660 nm, 30 mW, 16 J/cm, 0.2 cm, 15 s in a continuous frequency) on the pain sensitivity of rats submitted to an experimental model of TMD induced by CFA was evaluated. Experimental TMD was induced in rats by the injection of complete Freund's adjuvant (CFA) injection into the masseter muscle. Nociceptive behavior was evaluated by electronic von Frey before CFA and after 1 h, 3 h, 6 h, and 24 h and 7, 14, and 21 days after PBM treatment. Inflammatory infiltrate was evaluated by histology of the masseter muscle and fractalkine expression was evaluated by immunohistochemistry of the trigeminal ganglia. PBM reversed the mechanical hypersensitivity of the animals by inhibiting the local inflammatory response, observed by the decrease of the inflammatory infiltrate in the masseter muscle of rats and by a central inhibition of fractalkine observed in the trigeminal ganglion. These data provide new insights into the mechanisms involved in the effects of photobiomodulation therapy emphasizing its therapeutic potential in the treatment of TMD.
颞下颌关节紊乱症（TMD）是一个包含一组影响咀嚼肌、颞下颌关节和相关结构的临床问题的术语。尽管它们在临床上很常见，但慢性颅面肌肉疼痛的机制还不是很清楚。TMD 疼痛缓解和控制的治疗方法应该是微创的、可逆的和保守的。光生物调节（PBM）是一种很有前途的选择，因为它被证明可以抑制炎症反应和缓解疼痛症状。在此，评估了 PBM（660nm，30mW，16J/cm，0.2cm，15s 连续频率）对 CFA 诱导的 TMD 实验模型大鼠疼痛敏感性的影响。通过向咀嚼肌注射完全弗氏佐剂（CFA）诱导实验性 TMD。在 CFA 注射前和注射后 1h、3h、6h、24h 以及 PBM 治疗后 7d、14d 和 21d，通过电子 von Frey 评估痛觉行为。通过咀嚼肌的组织学评估炎症浸润，通过三叉神经节的免疫组织化学评估 fractalkine 表达。PBM 通过抑制局部炎症反应逆转了动物的机械性超敏反应，这可以通过减少大鼠咀嚼肌中的炎症浸润和观察到三叉神经节中 fractalkine 的中枢抑制来观察到。这些数据为光生物调节治疗作用的机制提供了新的见解，强调了其在 TMD 治疗中的治疗潜力。
