Localized Intervertebral Disc Injury Leads to Organ Level Changes in Structure, Cellularity, and Biosynthesis.
Localized Intervertebral Disc Injury Leads to Organ Level Changes in Structure, Cellularity, and Biosynthesis.
复制标题
局部椎间盘损伤会导致结构,细胞和生物合成的器官水平变化。
DOI:
10.1007/s12195-009-0072-8
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发表时间:
2009-09-01
影响因子:
2.8
通讯作者:
Korecki, C. L.
中科院分区:
文献类型:
--
作者:
Iatridis, James C.;Michalek, A. J.;Purmessur, D.;Korecki, C. L.
关键词:
A literature review and new data are presented to evaluate the influence of intervertebral disc (IVD) injury on biomechanics, cellularity, inflammation, and biosynthesis. Literature and new experimental evidence support the hypothesis that localized injury in the disc can lead to immediate and long-term organ level changes in biomechanics and biology of the IVD. Biomechanical properties defining motion segment bending behaviors sensitive to injuries that affect anulus fibrosus (AF) integrity and nucleus pulposus (NP) pressurization. Axial mechanics and IVD height measurements show sensitivity to puncture and other injuries that reduce NP pressurization. Torsional biomechanics are strongly affected by the extent and location of AF lesions but are less sensitive to reduced NP pressurization. IVD injuries such as puncture and stab incisions may also lead to a cascade of biological changes consistent with degeneration, including loss of cellularity, altered biosynthesis and inflammation. New results on effects of 25G needle injection of saline into a bovine IVD organ culture model demonstrated a loss of cellularity and down-regulation of matrix gene expression, providing a specific example of how a minor injury affects the IVD organ response. We conclude that localized injuries in the IVD can induce an organ level degenerative cascade through biomechanical and biological mechanisms, and their interactions. Attempts at IVD repair should target the dual biomechanical roles of the anulus of maintaining nucleus pressurization and transmitting loads across the vertebrae. Biologically, it remains important to maintain IVD cellularity and biosynthesis rates following injury to prevent downstream degenerative changes.
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影响因子:
3.8
作者:
Gu, WY;Yao, H;Flagler, D
通讯作者:
Flagler, D
影响因子:
2.8
作者:
Benneker, LM;Heini, PF;Ito, K
通讯作者:
Ito, K
影响因子:
2.9
作者:
CASSIDY, JJ;HILTNER, A;BAER, E
通讯作者:
BAER, E
影响因子:
15.9
作者:
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通讯作者:
Alini, M
DOI:
10.1302/0301-620x78b6.1287
发表时间:
1996-11-01
影响因子:
--
作者:
Adams, MA;McNally, DS;Dolan, P
通讯作者:
Dolan, P