Department of Spine Surgery, Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Key Laboratory of Organ Injury, Aging and Regenerative Medicine of Hunan Province, Changsha, People's Republic of China.
Spine (Phila Pa 1976). 2019 Aug 15;44(16):E930-E938. doi: 10.1097/BRS.0000000000003023.
The lumbar facet joint (LFJ) osteoarthritis (OA) model that highly mimics the clinical conditions was established and evaluated.
Here, we innovatively constructed and evaluated the aberrant mechanical loading-related LFJ OA model.
LFJ is the only true synovial joint in a functional spinal unit in mammals. The LFJ osteoarthritis is considered to contribute 15% to 45% of low back pain. The establish of animal models highly mimicking the clinical conditions is a useful tool for the investigation of LFJ OA. However, the previously established animal models damaged the LFJ structure directly, which did not demonstrate the effect of aberrant mechanical loading on the development of LFJ osteoarthritis.
In the present study, an animal model for LFJ degeneration was established by the unilateral osteotomy of LFJ (OLFJ) in L4/5 unit to induce the spine instability. Then, the change of contralateral LFJ was evaluated by morphological and molecular biological techniques.
We showed that the OLFJ induced instability accelerated the cartilage degeneration of the contralateral LFJ. Importantly, the SRμCT elucidated that the three-dimensional structure of the subchondral bone changed in contralateral LFJ, indicated as the abnormity of bone volume/total volume ratio (BV/TV), trabecular pattern factor (Tb. Pf), and the trabecular thickness (Tb. Th). Immunostaining further demonstrated the uncoupled osteoclastic bone resorption, and bone formation in the subchondral bone of contralateral LFJ, indicated as increased activity of osteoclast, osteoblast, and Type H vessels.
We develop a novel LFJ OA model demonstrating the effect of abnormal mechanical instability on the degeneration of LFJ. This LFJ degeneration model that highly mimics the clinical conditions is a valuable tool to investigate the LFJ osteoarthritis.
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建立并评估了高度模拟临床情况的腰椎小关节（LFJ）骨关节炎（OA）模型。
本研究创新性地构建并评估了与异常机械负荷相关的 LFJ OA 模型。
LFJ 是哺乳动物中唯一具有功能的脊柱单位中的真正滑膜关节。LFJ 骨关节炎被认为导致 15%至 45%的下腰痛。高度模拟临床情况的动物模型的建立是研究 LFJ OA 的有用工具。然而，之前建立的动物模型直接损伤了 LFJ 结构，并未显示异常机械负荷对 LFJ 骨关节炎发展的影响。
本研究通过 L4/5 节段单侧 LFJ 骨切开术（OLFJ）诱导脊柱不稳，建立了 LFJ 退变的动物模型。然后，通过形态学和分子生物学技术评估对侧 LFJ 的变化。
我们发现 OLFJ 诱导的不稳定加速了对侧 LFJ 的软骨退变。重要的是，三维重建分析（SRμCT）表明，对侧 LFJ 的软骨下骨三维结构发生改变，表现为骨体积/总体积比（BV/TV）、骨小梁模式因子（Tb. Pf）和骨小梁厚度（Tb. Th）的异常。免疫染色进一步证实了对侧 LFJ 软骨下骨中破骨细胞骨吸收和骨形成的解偶联，表现为破骨细胞、成骨细胞和 H 型血管活性增加。
我们开发了一种新的 LFJ OA 模型，证明了异常机械不稳定性对 LFJ 退变的影响。这种高度模拟临床情况的 LFJ 退变模型是研究 LFJ 骨关节炎的有价值工具。
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