Citation

Dudli S, John Ferguson S, Haschtmann D. Spine J. 2014; 14(7): 1256-1264.

Affiliation

Schulthess Klinik, Wirbelsäulenzentrum, Lengghalde 2, CH-8008 Zürich, Switzerland. Electronic address: daniel.haschtmann@kws.ch.

Copyright

(Copyright © 2014, Elsevier Publishing)

DOI

10.1016/j.spinee.2013.07.488

PMID

24583791

Abstract

BACKGROUND CONTEXT: The burst fracture of a vertebra is the result of a complex loading procedure and is often associated with intervertebral disc (IVD) degeneration (DD). Likewise, the presumed etiologies are numerous: (i) the structural perturbation of the IVD/endplate, (ii) the impact loading energy alone, and (iii) the depressurization of the nucleus pulposus. PURPOSE: To describe the pathogenesis of posttraumatic DD by comparing the severity and patterns of degeneration from different injury models. STUDY DESIGN: New data from an in-vitro organ culture study are compared to previous work on the same model system. METHODS: In order to investigate in detail the contribution of each factor (i to iii) to DD, we extended our previous work to compare three different segmental trauma processes in a rabbit full-organ in-vitro model: burst fracture (group A; etiologies (i)-(iii)), equienergetic loading without a fracture (group B; (ii)), and endplate puncturing (group C; (iii)). DD markers (apoptosis, necrosis, matrix remodelling, inflammation) were monitored up to 28 days post-trauma. Gene transcription data were subjected to principle component analysis (PCA) and agglomerative hierarchical clustering (AHC) to identify and compare pathological patterns. This study was funded by the Swiss National Science foundation; project grant number #310010-122105. All authors have no potential conflict of interest. RESULTS: Only group A showed the full profile of DD: reduced glycosaminoglycan content, increased caspase-3/7 and lactate dehydrogenase (LDH) activity, elevated mRNA of catabolic (MMP-1/-3/-13) and pro-inflammatory (TNFIL- 6, IL-8, MCP-1) proteins. In group B, only catabolic and proinflammatory genes were slightly up-regulated. In group C, LDH but not caspase-3/7 activity was increased. Catabolic and pro-inflammatory genes were up-regulated, although less compared to group A. Principle component analysis revealed different transcription patterns for group C. CONCLUSIONS: The structural perturbation of the endplate/IVD, but not the loading energy or nuclear depressurization, promotes DD. In addition, endplate puncturing triggers a different pathogenesis, consistent with a more continuous matrix remodelling process.

Language: en