AI Article Synopsis
- The study involved analyzing CT scans of the lumbar spine in older adults to understand the relationship between intradiscal vacuum phenomenon (IDVP) and disc degeneration over time.
- Results showed that while most cases of IDVP stayed at a similar severity, some worsened, improved, or fused, with new cases developing in some patients during the study period.
- Interestingly, the presence of IDVP did not correlate with significantly worse back pain among participants, suggesting that back pain experiences vary despite degeneration severity.
Article Abstract
Study Design: Observational serial computed tomography (CT) analysis of the lumbar spine in a normal-aging population.
Objective: To assess the natural history of the intradiscal vacuum phenomenon (IDVP) and its role in disc degeneration.
Background: The natural history of disc degeneration is well described but our understanding of the end stage of pathogenesis remains incomplete. Magnetic resonance imaging loses accuracy with advanced degeneration, becoming hyporesonant and indistinct. Cadaveric specimens display adaptive changes in the disc with loss of the hydrostatic capacity of the nucleus, increased intradiscal clefts, and endplate impermeability. IDVP is associated with advanced disc degeneration and CT is the optimal modality to visualize this, yet these insights remain unreported.
Patients And Methods: Patients only included historic CT abdomen scans of those over 60 years of age without acute or relevant spinal pathology, with a diagnosis of at least one level with IDVP on the original CT scan, and all of whom had a similar scan >7 years later. A history of clinically significant back pain was also recorded.
Results: CT scans included 360 levels in 29 males and 31 females (mean: 68.9 y), displaying 82 levels of IDVP, with a second scan included after a mean of 10.3 years. Most levels displayed the same level of severity (persisted, 45) compared with where some progressed (26), regressed (8), and fused (3; P < 0.01). There was also an increased incidence, 37/60 (62%) of developing IDVP at another level. Disc heights were reduced with increased severity of IDVP. A record of back pain was evident in 31/60 patients, which was not significantly worse in those with worsening severity or additional level involvement over the study period.
Conclusion: As disc degeneration advances, the associated IDVP persists in most cases, displaying a plateauing of severity over long periods, but rarely with progression to autofusion.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1097/BRS.0000000000004945 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Gain-of-function ANXA11 mutation cause late-onset ALS with aberrant protein aggregation, neuroinflammation and autophagy impairment.
Acta Neuropathol Commun
January 2025
Department of Neurology, Peking Union Medical College Hospital, Peking Union Medical College (PUMC) and Chinese Academy of Medical Science (CAMS), Beijing, China.
Mutations in the ANXA11 gene, encoding an RNA-binding protein, have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS), but the underlying in vivo mechanisms remain unclear. This study examines the clinical features of ALS patients harboring the ANXA11 hotspot mutation p.P36R, characterized by late-onset motor neuron disease and occasional multi-system involvement.
View Article and Find Full Text PDFFerristatin II protects nucleus pulposus against degeneration through inhibiting ferroptosis and activating HIF-1α pathway mediated mitophagy.
Int Immunopharmacol
January 2025
Department of Spine Surgery, Shandong Provincial Hospital affiliated to Shandong First Medical University, Jinan, Shandong 250000, China; Department of Spine Surgery, Shandong Provincial Hospital, Shandong University, Jinan, Shandong 250000, China. Electronic address:
Background: Nucleus pulposus (NP) degeneration represents a significant contributing factor in the pathogenesis of intervertebral disc (IVD) degeneration (IVDD), and is a key underlying mechanism in several lumbar spine pathologies. Nevertheless, the precise mechanisms that govern NP degeneration remain unclear. A significant contributing factor to IVDD has been identified as ferroptosis.
View Article and Find Full Text PDFMARCHF8-mediated ubiquitination via TGFBI regulates NF-κB dependent inflammatory responses and ECM degradation in intervertebral disc degeneration.
PLoS One
January 2025
Department of Orthopedics, Shanghai Pudong New Area People's Hospital, Shanghai, China.
Article Synopsis
- The study investigates the role of TGFBI as a key gene in the development of intervertebral disc degeneration (IDD) and how it is regulated by MARCHF8.
- The researchers used advanced gene analysis techniques to identify significant gene modules related to IDD and found that changes in TGFBI levels affect cell behavior, inflammation, and extracellular matrix breakdown.
- Results indicated that MARCHF8 plays a crucial role in regulating TGFBI expression, which impacts NP cell apoptosis and inflammatory responses through the NF-κB signaling pathway.
'Disc degeneration in distal unfused segments: cause or consequence of adding-on after posterior fusion of lenke 3c, 5c, 6c adolescent idiopathic scoliosis?'.
Acta Neurochir (Wien)
January 2025
Department of Orthopaedics & Traumatology, Haydarpasa Numune Training and Research Hospital, Istanbul, Turkey.
Background: The aim of this study is to examine the association between adding-on (AO) and disc degeneration(DD) of distal unfused levels in Lenke 3 C, 5 C, 6 C adolescent idiopathic scoliosis (AIS) patients with a follow-up of at least two years by comparing preoperative and postoperative magnetic resonance imaging (MRI).
Methods: 47 AIS patients (32 females and 15 males) with structural thoracolumbar/lumbar (TL/L) curves treated with long segment thoracolumbar fusion were retrospectively evaluated. Patients were divided into two groups according to the occurrence of the AO (AO and Non-AO groups).
MANF overexpression ameliorates oxidative stress-induced apoptosis of human nucleus pulposus cells by facilitating mitophagy through promoting MFN2 expression.
Sci Rep
January 2025
Department of Spine Surgery, The First Affiliated Hospital of Xinjiang Medical University, No.137, Liyu Mountain South Road, Urumqi City, 830054, Xinjiang Province, China.
Intervertebral disc degeneration (IDD) is a degenerative condition associated with impaired mitophagy. MANF has been shown to promote mitophagy in murine kidneys; however, its role in IDD remains unexplored. This study aimed to elucidate the mechanism by which MANF influences IDD development through the regulation of mitophagy.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!