肌肉骨骼疾病(MSD)与疼痛有关,并导致患者的活动能力和生活质量降低。氡疗法被用作药物治疗的替代或补充。根据以前的报道,氡水疗导致镇痛和抗炎作用,但是细胞和分子机制是未知的。先前的一项研究(RAD-ON01)显示,骨侵蚀标志物如胶原蛋白片段(C末端端肽,退行性MSD患者血清中的ctxspa治疗后,ctx)降低。在未来的范围内,这里介绍的安慰剂对照RAD-ON02试验,我们分析了氡和热spa治疗对破骨细胞生成的影响。从病人的血液中,我们分离单核细胞,将它们接种在骨片上,并在存在生长因子的情况下将它们分化为成熟的破骨细胞(mOC)。随后的分析显示,两种处理后的mOC比例较小,在氡水疗治疗后更小。骨切片上显著减少的再吸收面积反映了该结果。只有在氡水疗治疗后,我们在患者血清中检测到NF-κB受体活化因子配体(RANKL)的显著降低,这表明OC的分化降低。然而,骨吸收(CTX)和骨形成的其他标志物(OPG,OCN)在两种治疗后均未改变。脂肪因子,例如内脂素和瘦素,通过影响破骨细胞生成在某些MSD类型中起作用,两种治疗后都没有改变。Further,免疫细胞也对破骨细胞生成有影响,通过抑制和促进OCs的终末分化和活化,分别。氡处理后,Treg细胞的比例显著增加,而Th17细胞没有改变。总的来说,我们观察到两种治疗方法对破骨细胞生成和骨吸收均有影响.此外,氡spa处理影响了Treg细胞群以及Th17/Treg比值受到影响,指向氡水疗后免疫系统的贡献。这些来自RAD-ON02试验的患者的数据表明,氡并不单独对骨骼代谢产生影响,尽管与热水疗治疗相比,氡后它们更明显。
Musculoskeletal disorders (MSDs) are associated with pain and lead to reduced mobility and quality of life for patients. Radon therapy is used as alternative or complementary to pharmaceutical treatments. According to previous reports, radon spa leads to analgesic and anti-inflammatory effects, but the cellular and molecular mechanisms are widely unknown. A previous
study (RAD-ON01) revealed, that bone erosion markers like collagen fragments (C-terminal telopeptide, CTX) are reduced after radon spa treatment in serum of patients with degenerative MSDs. Within the scope of the prospective, placebo-controlled RAD-ON02
trial presented here, we analyzed the influence of radon and thermal spa treatment on
osteoclastogenesis. From patient blood, we isolate monocytes, seeded them on bone slices and differentiated them in the presence of growth factors into mature osteoclasts (mOCs). Subsequent analysis showed a smaller fraction of mOCs after both treatments, which was even smaller after radon spa treatment. A significantly reduced resorbed area on bone slices reflects this result. Only after radon spa treatment, we detected in the serum of patients a significant decrease of receptor activator of NF-κB ligand (RANKL), which indicates reduced differentiation of OCs. However, other markers for bone resorption (CTX) and bone formation (OPG, OCN) were not altered after both treatments. Adipokines, such as visfatin and leptin that play a role in some MSD-types by affecting osteoclastogenesis, were not changed after both treatments. Further, also immune cells have an influence on osteoclastogenesis, by inhibiting and promoting terminal differentiation and activation of OCs, respectively. After radon treatment, the fraction of Treg cells was significantly increased, whereas Th17 cells were not altered. Overall, we observed that both treatments had an influence on
osteoclastogenesis and bone resorption. Moreover, radon spa treatment affected the Treg cell population as well as the Th17/Treg ratio were affected, pointing toward a contribution of the immune system after radon spa. These data obtained from patients enrolled in the RAD-ON02
trial indicate that radon is not alone responsible for the effects on bone metabolism, even though they are more pronounced after radon compared to thermal spa treatment.