Percutaneous Cement-Augmented Screws Short Fixation for the Treatment of Severe Osteoporotic Vertebral Burst Fractures.

OBJECTIVE: This study aims to evaluate the therapeutic reliability of posterior percutaneous cement-augmented screws short fixation (PASF) in patients with severe osteoporotic vertebral burst fractures (OVBFs). METHODS: Single-level OVBFs with an anterior vertebral body height reduction ≥60% were included. A Frailty Index was used for preoperative frailty assessment. Back pain and related disability were assessed through the visual analog scale (VAS) and Oswestry Low Back Pain Disability Index (ODI), administered at injury time, preoperatively, postoperatively, at 12 months and at last patient follow-up evaluation. The main radiologic outcomes were represented by Cobb angle (CA) and anterior vertebral body compression percentage, measured at injury time, preoperative, postoperatively and at 12-month examination. In addition, the incidence of cement leakages and hardware failures was assessed. RESULTS: Thirty-three patients met the inclusion criteria. All patients were frail (76%) or semi-frail (24%). Significant vertebral body height restoration and segmental kyphosis improvement after PASF were documented (anterior vertebral body compression percentage, -40 [-43 to -37] vs. -67 [-70 to -65], P = 0.0001; CA, 10 [8-12] vs. 24 [23-26], P = 0.0001). The mean VAS and ODI scores documented optimal and long-enduring pain relief and related disability reduction after PASF (VAS score, 2 [2-3] vs. 8 [7-8], P = 0.0001; ODI, 22 [17-26] vs. 64 [60-69], P = 0.0001). Only 1 cement leakage (3%), asymptomatic, occurred. After a mean follow-up of 33 months, no early/late hardware failures were reported. CONCLUSIONS: The clinical and radiologic results of this study suggest that PASF could be a safe and effective treatment option for severe OVBFs when conservative treatments have failed.

Inflammatory mediators and signalling pathways controlling intervertebral disc degeneration.

Intervertebral disc (IVD) degeneration (IDD) is one of the major causes of back pain, a condition that represents a serious socio-economic burden. Deeper knowledge of the complex and fine relationship between IVD degeneration, tissue inflammation and pain, appears to be critical to improve the current therapies, which have so far proven themselves ineffective. Upon degeneration, IVD tissues become inflamed, and this inflammatory microenvironment is associated with a cascade of degenerative events that may eventually cause discogenic pain. In particular, several studies have highlighted the major role of a number of proinflammatory mediators not only in the onset of the inflammatory condition, but also in the development of IDD in general. In this review, we will present the main pathological events that occur during disc degeneration, focusing on the relationship between the abnormal inflammatory milieu of the degenerating IVD, IDD and the generation of pain. Finally, we will present the current therapies for the treatment of IDD and low back pain, and the perspectives of future, more effective therapies.