The microenvironmental mechanism of postoperative recurrence in cervical spondylotic myelopathy: regulation by the glial scar–inflammation axis

Cervical spondylotic myelopathy (CSM) is a severe degenerative spinal disorder caused by cervical spinal stenosis due to cervical degeneration, which compresses the spinal cord. Patients in the mid-to late-stages of the disease frequently undergo surgical treatment; however, some may still suffer from persistent sensorimotor dysfunction, inadequate pain relief, and surgery-related complications. Although substantial progress has been achieved in comprehending the pathology of CSM in recent years, the postoperative pathological mechanisms remain poorly understood, particularly the specific molecular mechanisms influencing the development of complications. Traditional research has focused on mechanical compression caused by herniated material, neglecting the potential adverse effects of postoperative immune microenvironment imbalance in the spinal cord. Current studies suggest that the glial scar–inflammation axis, which is triggered by abnormal activation of neural immune cells (glia) and peripheral immune cells (e.g., Th17 cells and neutrophils) and their interactions—may serve as a key factor contributing to poor postoperative outcomes and disease recurrence. This review summarizes the recent advances in the biology and pathology of the glial scar–inflammation axis following conventional surgical treatment for CSM, as well as innovative therapeutic strategies, such as stem cell transplantation. It aims to provide new insights and directions for future research on postoperative complications and their treatment in CSM.