Neuroscience Graduate Program, Universidade Federal do Rio Grande do Sul (UFRGS), Instituto de Ciências Básicas da Saúde, Porto Alegre, RS, Brazil.
Brain Institute, Universidade Federal do Rio Grande do Norte (UFRN), Natal, RN, Brazil.
Cartilage. 2021 Dec;13(2_suppl):1309S-1321S. doi: 10.1177/1947603519876338. Epub 2019 Sep 30.
Chronic pain associated with osteoarthritis (OA) often leads to reduced function and engagement in activities of daily living. Current pharmacological treatments remain relatively ineffective. This study investigated the efficacy of photobiomodulation therapy (PBMT) on cartilage integrity and central pain biomarkers in adult male Wistar rats.
We evaluated the cartilage degradation and spinal cord sensitization using the monoiodoacetate (MIA) model of OA following 2 weeks of delayed PBMT treatment (i.e., 15 days post-MIA). Multiple behavioral tests and knee joint histology were used to assess deficits related to OA. Immunohistochemistry was performed to assess chronic pain sensitization in spinal cord dorsal horn regions. Furthermore, we analyzed the principal components related to pain-like behavior and cartilage integrity.
MIA induced chronic pain-like behavior with respective cartilage degradation. PBMT had no effects on overall locomotor activity, but positive effects on weight support ( = 0.001; effect size [ES] = 1.01) and mechanical allodynia ( = 0.032; ES = 0.51). Greater optical densitometry of PBMT-treated cartilage was evident in superficial layers ( = 0.020; ES = 1.34), likely reflecting the increase of proteoglycan and chondrocyte contents. In addition, PBMT effects were associated to decreased contribution of spinal glial cells to pain-like behavior ( = 0.001; ES = 0.38).
PBMT during the chronic phase of MIA-induced OA promoted cartilage recovery and reduced the progression or maintenance of spinal cord sensitization. Our data suggest a potential role of PBMT in reducing cartilage degradation and long-term central sensitization associated with chronic OA.
与骨关节炎(OA)相关的慢性疼痛通常会导致功能下降和日常活动参与度降低。目前的药物治疗仍然相对无效。本研究旨在探讨光生物调节疗法(PBMT)对成年雄性 Wistar 大鼠软骨完整性和中枢疼痛生物标志物的影响。
我们使用 MIA 诱导的 OA 模型,在延迟 PBMT 治疗(即 MIA 后 15 天)后 2 周评估软骨降解和脊髓敏化情况。多项行为测试和膝关节组织学用于评估与 OA 相关的缺陷。免疫组织化学用于评估脊髓背角区域的慢性疼痛敏化情况。此外,我们分析了与疼痛样行为和软骨完整性相关的主要成分。
MIA 诱导了慢性疼痛样行为和相应的软骨降解。PBMT 对整体运动活动没有影响,但对体重支撑有积极影响( = 0.001;效应大小[ES] = 1.01)和机械性痛觉过敏( = 0.032;ES = 0.51)。在浅层,PBMT 治疗的软骨的光密度测量值更高( = 0.020;ES = 1.34),这可能反映了蛋白聚糖和软骨细胞含量的增加。此外,PBMT 的作用与脊髓胶质细胞对疼痛样行为的贡献减少有关( = 0.001;ES = 0.38)。
在 MIA 诱导的 OA 慢性期进行 PBMT 可促进软骨恢复,并减少脊髓敏化的进展或维持。我们的数据表明,PBMT 可能在减轻与慢性 OA 相关的软骨降解和长期中枢敏化方面发挥作用。