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Histological and molecular structure characterization of annular collagen after intradiskal electrothermal annuloplasty.

ABSTRACT: The mechanism of pain relief of intradiskal electrothermal annuloplasty (IDET) in the treatment of lumbar diskogenic pain is uncertain. Theories include sealing of annular fissures via collagen denaturation and contraction. Prior studies offer conflicting qualitative data on the ability of IDET to denature collagen. The objective of the present study is to evaluate IDET treatment effect on annular collagen using quantitative data supplied by Fourier-transform infrared imaging spectroscopy. The posterior annulus of disks (n = 3) from an intact human cadaveric spine at room temperature were treated with two different radiothermal catheters using standard intradiskal electrothermal annuloplasty (IDET) heating protocols. Disks were dissected free with catheters in place and fixed in formalin. Channels created by the catheters were marked and catheters were removed. Tissue samples of treated areas adjacent to the channels and internal control areas from the same disk were stained for light microscopy and placed on barium sulfate windows for Fourier transform infrared imaging spectroscopy (FT-IRIS) analysis. Treated areas showed evidence of disruption in the fibrillar organization of annular collagen by light microscopy compared to intact stroma from control areas. Quantitative FT-IRIS analysis compared ratios of wavenumber regions known to be sensitive to collagen denaturation. Mean values for the ratios amide II/1,338 cm(-1) (137.21 +/- 25.84 treated, 76.94 +/- 16.77 control) and 1,640/1,660 cm(-1) (0.98 +/- 0.03 treated, 0.89 +/- 0.03 control) were significantly different between treated and control samples (p < 0.001), indicating a breakdown in collagen integrity. Separate analysis by catheter type suggests that catheter design may impact treatment effect.

SUBMITTER: Southern D

PROVIDER: S-EPMC2504111 | biostudies-other | 2006 Feb

REPOSITORIES: biostudies-other

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Project description:Animal in vivo study.To test the capability of high-density collagen gel to repair annular defects.Annular defects are associated with spontaneous disc herniations and disc degeneration, which can lead to significant morbidity. Persistent annular defects after surgical discectomies can increase reherniation rates. Several synthetic and biological materials have been developed for annular repair. This is the first study to test an injectable biomaterial in vivo.We punctured caudal intervertebral discs in 42 athymic rats, using an 18-gauge needle to create an annular defect. High-density collagen (HDC), either alone or cross-linked with riboflavin (RF), was injected into the defect. There were 4 separate study groups: HDC, HDC cross-linked with either 0.25 mM RF or 0.50 mM RF, and a negative control that was punctured and not treated. The animals were followed for 5 weeks; radiographs were used to assess disc heights and magnetic resonance images were used to evaluate degenerative changes. We developed an algorithm on the basis of T2-relaxation time measurements to assess the size of the nucleus pulposus. Tails were collected for histological analysis to evaluate disc degeneration and measure the cross-sectional area of the nucleus pulposus.After 5 weeks, the control and the uncross-linked HDC groups both showed signs of progressive degenerative changes with minimal or no residual nucleus pulposus tissue in the disc space. Cross-linking significantly improved the ability of HDC gels to repair annular defects. The 0.50 mM RF cross-linked group showed only a slight decrease in nuclear tissue when compared with healthy discs, with no signs of intervertebral disc (IVD) degeneration. The annulus fibrosus was partially repaired by a fibrous cap that bridged the defect. Host fibroblasts infiltrated and remodeled the injected collagen.HDC is capable of repairing annular defects induced by needle puncture. The stiffness of HDC can be modified by riboflavin cross-linking and seems to positively affect the repair mechanism. These results need to be replicated in a larger animal model.N/A.

Project description:It is well established that overstretch of arteries alters their mechanics and compromises their function. However, the underlying structural mechanisms behind these changes are poorly understood. Utilizing a recently developed collagen hybridizing peptide (CHP), we demonstrate that a single mechanical overstretch of an artery produces molecular-level unfolding of collagen. In addition, imaging and quantification of CHP binding revealed that overstretch produces damage (unfolding) among fibers aligned with the direction of loading, that damage increases with overstretch severity, and that the onset of this damage is closely associated with tissue yielding. These findings held true for both axial and circumferential loading directions. Our results are the first to identify stretch-induced molecular damage to collagen in blood vessels. Furthermore, our approach is advantageous over existing methods of collagen damage detection as it is non-destructive, readily visualized, and objectively quantified. This work opens the door to revealing additional structure-function relationships in arteries. We anticipate that this approach can be used to better understand arterial damage in clinically relevant settings such as angioplasty and vascular trauma. Furthermore, CHP can be a tool for the development of microstructurally-based constitutive models and experimentally validated computational models of arterial damage and damage propagation across physical scales. STATEMENT OF SIGNIFICANCE:Arteries play a critical role by carrying oxygen and essential nutrients throughout the body. However, trauma to the head and neck, as well as surgical interventions, can overstretch arteries and alter their mechanics. In order to better understand the cause of these changes, we employ a novel collagen hybridizing peptide (CHP) to study collagen damage in overstretched arteries. Our approach is unique in that we go beyond the fiber- and fibril-level and characterize molecular-level disruption. In addition, we image and quantify fluorescently-labeled CHP to reveal a new structure-property relationship in arterial damage. We anticipate that our approach can be used to better understand arterial damage in clinically relevant settings such as angioplasty and vascular trauma.

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Histological and molecular structure characterization of annular collagen after intradiskal electrothermal annuloplasty.

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