背景:Bertolotti综合征(BS)的特征是与腰骶移行椎骨(LSTV)相关的慢性疼痛和功能障碍。该研究旨在研究Castellvi2aLSTV中可见的横突和the骨之间的假关节的组织学特征,并探讨神经组织参与疼痛产生。
方法:使用S100蛋白染色进行免疫组织化学分析以评估神经组织的存在。
结果:这些变化包括纤颤,软骨细胞克隆,蛋白聚糖基质的改变,和局灶性软骨细胞坏死。值得注意的是,在任何标本中都没有观察到神经组织,如通过阴性S100蛋白染色证实的。
结论:研究结果表明,神经组织不参与BS疼痛的伤害性机制。假关节和骨关节炎关节之间的组织学相似性表明,假关节本身可能是BS疼痛的重要来源。这些见解有助于我们了解BS的病理生理学,并支持在考虑手术干预之前优先使用NSAIDs等药物控制疼痛的治疗范式。未来的研究需要更大的样本量和体内模型来进一步验证这些发现,并探索LSTV中生物力学力下关节组织学的变化。
BACKGROUND: Bertolotti syndrome (BS) is characterized by chronic pain and functional impairment associated with lumbosacral transitional vertebrae (LSTVs). The study aimed to investigate the histologic characteristics of the pseudoarticulation between the enlarged transverse process and sacrum seen in Castellvi 2a LSTV and explore the involvement of nervous tissue in pain generation.
METHODS: Immunohistochemical analysis using S100 protein staining was performed to assess the presence of nerve tissue.
RESULTS: These changes included fibrillation, chondrocyte cloning, alterations in the proteoglycan matrix, and focal chondrocyte necrosis. Notably, no nerve tissue was observed in any of the specimens, as confirmed by negative S100 protein staining.
CONCLUSIONS: The study findings suggest that nerve tissue is not involved in the nociceptive mechanisms underlying pain in BS. The histologic similarities between the pseudoarticulation and osteoarthritic joints indicate that pseudoarticulation itself may be a significant source of pain in BS. These insights contribute to our understanding of the pathophysiology of BS and support treatment paradigms prioritizing pain control with medications such as NSAIDs before considering surgical intervention. Future studies with larger sample sizes and in vivo models are needed to further validate these findings and explore the changes in joint histology under biomechanical forces in LSTVs.