gms | German Medical Science

Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2018)

23.10. - 26.10.2018, Berlin

Inflammatory stimulation and mechanical loading lead to a weakening of the trans-lamellar bridging network of the anulus fibrosis

Meeting Abstract

  • presenting/speaker Taryn Saggese - Institute of Orthopaedic Research and Biomechanics, Ulm, Germany
  • Lydia Moll - Institute of Orthopaedic Research and Biomechanics, Ulm, Germany
  • Kelly Wade - Institute of Orthopaedic Research and Biomechanics, Ulm, Germany
  • Anna Weigl - Institute of Orthopaedic Research and Biomechanics, Ulm, Germany
  • Graciosa Teixeira - Institute of Orthopaedic Research and Biomechanics, Ulm, Germany
  • Anita Ignatius - Institute of Orthopaedic Research and Biomechanics, Ulm, Germany
  • Hans-Joachim Wilke - Institute of Orthopaedic Research and Biomechanics, Ulm, Germany
  • Cornelia Neidlinger-Wilke - Institute of Orthopaedic Research and Biomechanics, Ulm, Germany

Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2018). Berlin, 23.-26.10.2018. Düsseldorf: German Medical Science GMS Publishing House; 2018. DocST27-543

doi: 10.3205/18dkou144, urn:nbn:de:0183-18dkou1443

Veröffentlicht: 6. November 2018

© 2018 Saggese et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.


Gliederung

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Objectives: Investigate the effects of inflammatory stimulation and mechanical overloading of the trans-lamellar bridging network (TLBN). Anulus fibrosus (AF) disruption can lead to prolapse or herniation of intervertebral discs (IVDs) (Adams et al. Spine 2006). The TLBN is a proteoglycan and elastic fiber-rich structure which separates the lamellae, as well as forming transverse bridges which connect the layers of the AF (Schollum et al. J Anat 2009). Little is known about how mechanobiological factors influence the TLBN and anular wall integrity (Schollum et al. J Anat 2009; Han et al. J Orthop Res 2015; Yu et al. Spine 2015). The current study established a bovine AF organ culture model (AF-OC) which allows defined cyclic strains to be applied to the tissue in vitro. Additionally, IL-1 β media supplementation was used as a concurrent pro-inflammatory stimulus.

Methods: Methods Standardized AF rings were cut and punched from bovine caudal discs. A custom-made electro-mechanical device (Figure 1A [Fig. 1]) was used to exposed the AF-organ cultures (AF-OCs) to high physiological cyclic tensile strain (CTS) for 5 days (9% 1Hz, 3 hours/day). A sub-group was cultured in the presence of IL-1 β (10 ng/ μ L) to simulate a pro-inflammatory environment. PGE2 release and the expression pattern of COX-2, IL-6, and MMP3 in the tissue were assessed by ELISA and immunohistochemistry (IHC) respectively. The mechanical strength of TLBN was evaluated using a peel-test. AF segments were dissected into a 'Y' configuration, and a uniaxial material testing machine was used to measure the force required to separate the AF segment along a lamellar boundary (Gregory et al 2012).

Results: The combination of cyclic strain and IL-1 β (CTS+IL-1 β) resulted in a significant 25-fold increase in PGE2 release compared to controls (p=0,001) (Figure 1B [Fig. 1]). IHC analyses showed that the CTS+IL-1 β group was associated with a higher expression of IL-6 and MMP3 within the TLBN regions compared to adjacent lamellar matrix. Mechanical testing found a significant decrease in the adhesive strength for the CTS+IL1 β group compared to control (p=0,02) (Figure 1C [Fig. 1]).

Conclusion: Our unique organ-culture and mechanical loading approach enables investigation of the AF and TLBN structure-function relationship. Our findings suggest that the combination of cyclic-strain and IL-1 β act synergistically to increase pro-inflammatory and catabolic molecules within the AF, particularly the TLBN matrix, which consequently leads to a weakening of the tissue structure. This new AF-OC model will contribute to a better understanding of the pathomechanism of disc herniation.

Acknowledgements: Supported by the German Spine Foundation.