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首页> 外文期刊>Osteoarthritis and cartilage >Effect of interval-training exercise on subchondral bone in a chemically-induced osteoarthritis model
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Effect of interval-training exercise on subchondral bone in a chemically-induced osteoarthritis model

机译：间歇训练对化学性骨关节炎模型中软骨下骨的影响

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Objectives: The role of subchondral bone in osteoarthritis (OA) development is well admitted. Cross-talk between subchondral bone and cartilage may be disrupted in OA, leading to altered subchondral bone remodeling. Osteocytes are involved in bone remodeling control and could play a key role in OA progression. Our purpose of this study was to evaluate the preventive effect of interval-training exercise on subchondral bone and osteocyte in monosodium iodoacetate (MIA) model of experimental OA. Methods: At baseline, 48 male Wistar rats (8 weeks old) were separated into two groups: interval-training exercise or no exercise for 10 weeks. After this training period, each group was divided into two subgroups: MIA-injected knee (1 mg/100 μl saline) and saline-injected knee. Four weeks later, rats were sacrificed and carefully dissected. Evaluated parameters were: cartilage degeneration by OA scoring, bone mineral density (BMD) by Dual energy X-ray Absorptiometry (DXA), trabecular subchondral bone microarchitecture by micro-computed tomography (μCT), cortical subchondral bone lacunar osteocyte occupancy (by Toluidine Blue staining) and cleaved caspase-3 positive apoptosis (by epifluorescence). Results: Our results showed deleterious effects of MIA on cartilage. OA induced a decrease in proximal tibia (PT) BMD which was prevented by exercise. Exercise induced increase in full osteocyte lacunae surface and osteocyte occupancy (+60%) of cortical subchondral bone independently of OA. Osteocyte apoptosis (<1%) in cortical subchondral bone was not different whatever the group at sacrifice. Conclusion: Our results suggest that preliminary interval-training improved BMD and osteocytes lacunar occupancy in subchondral bone. Our interval-training did not prevent MIA-induced cartilage degeneration.
机译：目的：软骨下骨在骨关节炎（OA）发展中的作用已被公认。骨软骨下骨与软骨之间的串扰在OA中可能会中断，从而导致软骨下骨重塑改变。骨细胞参与骨重塑控制，并可能在OA进展中发挥关键作用。我们本研究的目的是评估碘伏乙酸单钠（MIA）模型中的间隔训练运动对软骨下骨和骨细胞的预防作用。方法：在基线时，将48只雄性Wistar大鼠（8周龄）分为两组：间歇训练或不运动10周。在此训练期后，将每组分为两个亚组：注射MIA的膝盖（1 mg / 100μl生理盐水）和注射盐水的膝盖。四周后，处死大鼠并仔细解剖。评估的参数包括：OA评分导致的软骨变性，双能X线骨密度仪（DXA）评估的骨矿物质密度（BMD），微计算机断层摄影术（μCT）的小梁软骨下骨微体系结构，皮质软骨下骨腔隙性骨细胞占用（甲苯胺蓝）染色）和切割的caspase-3阳性凋亡（通过落射荧光）。结果：我们的结果显示MIA对软骨具有有害作用。 OA导致胫骨近端（PT）BMD降低，可通过运动来预防。运动导致骨皮质软骨下陷的完整骨细胞表面增加和皮质软骨下骨的骨细胞占有率（+ 60％）独立于OA。无论处死哪个组，皮质软骨下骨中的骨细胞凋亡（<1％）都没有差异。结论：我们的结果表明，初步的间歇训练可以改善软骨下骨的骨密度和骨细胞腔隙占用。我们的间歇训练并未阻止MIA诱导的软骨变性。

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