Minimally Invasive Anterior Decompression Technique without Instrumented Fusion for Huge Ossification of the Posterior Longitudinal Ligament in the Thoracic Spine : Technical Note And Literature Review

Yu, Jae Won; Yun, Sang-O; Hsieh, Chang-Sheng; Lee, Sang-Ho

doi:10.3340/jkns.2017.0404.017.r1

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“…It is considered one of the most challenging spinal surgeries, mainly owing to its unique anatomy and pathophysiological factors. The main disadvantages of this operation can be summarized as follows: i) The incidence of thoracic natural kyphosis may limit the positive effect of spinal cord retreat following posterior decompression; ii) the thoracic spinal cord is characterized by relatively low blood supply, leading to spinal cord ischemia and consequently spinal cord injury; and iii) OPLL with tight adhesion to the dural sac increases the difficulty of removing the ossified ligament and increases the risk of intraoperative spinal cord injury (3)(4)(5)(6)(7)(8). Therefore, patients with T-OPLL that proceed to surgical treatment often result in unsatisfactory prognosis (9,10).…”

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confidence: 99%

The COL6A1 rs201153092 single nucleotide polymorphism, associates with thoracic ossification of the posterior longitudinal ligament

et al. 2019

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Thoracic ossification of the posterior longitudinal ligament (T-OPLL) is one of the most common factors that causes thoracic spinal stenosis, resulting in intractable myelopathy and radiculopathy. Our previous study reported that the rs201153092 polymorphism present in the collagen 6A1 (COL6A1) gene was a potentially pathogenic locus for the development of T-OPLL. The present study aimed to determine whether the rs201153092 mutation causes abnormal expression of COL6A1 in Han Chinese patients with T-OPLL, and to examine the effects of this mutation on osteogenesis by establishing a model of osteogenic differentiation. COL6A1 gene mutant and wild-type mouse 3T3-E1 embryonic osteoblast models were constructed to induce the differentiation of these cells into osteoblasts. The potential of the mutation site to induce abnormal expression of the COL6A1 gene and osteogenic markers was assessed via reverse transcription-quantitative PCR and western blot analyses. The results demonstrated that the rs201153092A mutation site resulted in significantly increased COL6A1 gene expression levels in the OPLL tissues obtained following clinical surgery. This mutation was shown to play an important role in the development of T-OPLL by regulating the overexpression of the COL6A1 gene and significantly increasing the expression levels of osteogenic markers. The findings of the present study suggested that the rs201153092A mutant variant could increase the expression levels of COL6A1 and consequently play a role in the pathogenesis of T-OPLL.

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