Boudenot A, Presle N, Uzbekov R, Toumi H, Pallu S, Lespessailles E
EA 4708 I3MTO, University of Orléans, Orléans, France.
UMR 7365 CNRS, Universite de Lorraine, Vandoeuvre-les-Nancy, France.
Osteoarthritis Cartilage. 2014 Aug;22(8):1176-85. doi: 10.1016/j.joca.2014.05.020. Epub 2014 Jun 10.
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.
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).
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.
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.
软骨下骨在骨关节炎（OA）发展中的作用已得到广泛认可。在OA中，软骨下骨与软骨之间的相互作用可能被破坏，导致软骨下骨重塑改变。骨细胞参与骨重塑控制，可能在OA进展中起关键作用。本研究的目的是评估间歇训练运动对实验性OA碘乙酸钠（MIA）模型中软骨下骨和骨细胞的预防作用。
在基线时，将48只雄性Wistar大鼠（8周龄）分为两组：进行10周的间歇训练运动或不运动。在此训练期后，每组再分为两个亚组：注射MIA的膝关节（1mg/100μl生理盐水）和注射生理盐水的膝关节。四周后，处死大鼠并仔细解剖。评估的参数包括：通过OA评分评估软骨退变，通过双能X线吸收法（DXA）测量骨密度（BMD），通过微计算机断层扫描（μCT）评估小梁软骨下骨微结构，通过甲苯胺蓝染色评估皮质软骨下骨腔隙骨细胞占有率，以及通过落射荧光评估裂解的半胱天冬酶-3阳性凋亡。
我们的结果显示MIA对软骨有有害影响。OA导致胫骨近端（PT）骨密度降低，而运动可预防这种降低。运动导致皮质软骨下骨全骨细胞腔隙表面和骨细胞占有率增加（+60%），且与OA无关。无论处死时属于哪个组，皮质软骨下骨中的骨细胞凋亡（<1%）均无差异。
我们的结果表明，初步的间歇训练可改善软骨下骨的骨密度和骨细胞腔隙占有率。我们的间歇训练不能预防MIA诱导的软骨退变。
