Murphy Kieran, Elias Gavin, Steppan Jim, Boxley Chett, Balagurunathan Kuberan, Victor Xylophone, Meaders Thomas, Muto Mario
University of Toronto, Toronto, Ontario, Canada.
University of Toronto, Toronto, Ontario, Canada.
J Vasc Interv Radiol. 2016 Aug;27(8):1242-1250.e3. doi: 10.1016/j.jvir.2016.04.012. Epub 2016 Jun 28.
To elucidate the mechanism of action of intradiscal oxygen-ozone therapy for herniated intervertebral disc therapy.
Ozone's mechanism of action was investigated using 3 approaches: mathematical models of intervertebral disc space to explore the relationship between disc pressure and volume; ozonolysis experiments using glycosaminoglycans (GAGs) from a Chinese hamster ovary cell line that were similar in composition to GAGs found in human nucleus pulposus; and experiments in which live Yucatan miniature pigs received various concentrations of percutaneous, image-guided intradiscal oxygen-ozone treatment and were examined (after sacrifice) with histology and semiquantitative analysis of disc cytokine concentrations.
Engineering calculations support observations that a small (6%) disc volume reduction can result in considerable (9.84%) intradiscal pressure reduction. Porcine disc histology and Chinese hamster ovary GAG ozonolysis results showed that administered ozone reacted with and fragmented disc proteoglycans, reducing disc volume through disc dehydration. Cytokine analysis of porcine discs found that each of 4 cytokines measured (interleukin [IL]-1β, IL-6, IL-8, and tumor necrosis factor α) increased in concentration after 2 wt% ozone treatment.
Oxygen-ozone therapy breaks down proteoglycan GAGs that maintain disc osmotic pressure, dehydrating the nucleus pulposus and reducing intervertebral disc volume. This is likely a primary mechanism by which ozone relieves nerve root compression and alleviates herniated disc-related pain. Additionally, 2 wt% ozone appears to interact with intradiscal cytokines, generating an antiinflammatory response that may contribute to symptom improvement.
阐明椎间盘内氧 - 臭氧疗法治疗椎间盘突出症的作用机制。
采用三种方法研究臭氧的作用机制:椎间盘间隙数学模型,以探索椎间盘压力与体积之间的关系;使用来自中国仓鼠卵巢细胞系的糖胺聚糖(GAGs)进行臭氧分解实验,该细胞系的GAGs组成与人类髓核中的GAGs相似;以及对活的尤卡坦小型猪进行经皮、影像引导的椎间盘内不同浓度氧 - 臭氧治疗实验,并在处死动物后进行组织学检查和椎间盘细胞因子浓度的半定量分析。
工程计算支持以下观察结果,即椎间盘体积小幅减少(6%)可导致椎间盘内压力显著降低(9.84%)。猪椎间盘组织学和中国仓鼠卵巢GAG臭氧分解结果表明,注入的臭氧与椎间盘蛋白聚糖发生反应并使其碎片化,通过椎间盘脱水减少椎间盘体积。对猪椎间盘的细胞因子分析发现,在2 wt%臭氧治疗后,所检测的4种细胞因子(白细胞介素[IL]-1β、IL-6、IL-8和肿瘤坏死因子α)的浓度均升高。
氧 - 臭氧疗法分解维持椎间盘渗透压的蛋白聚糖GAGs,使髓核脱水并减少椎间盘体积。这可能是臭氧缓解神经根压迫和减轻椎间盘突出相关疼痛的主要机制。此外,2 wt%的臭氧似乎与椎间盘内细胞因子相互作用,产生抗炎反应,这可能有助于症状改善。