The effects of dynamic loading on the intervertebral disc

Abstract

Loading is important to maintain the balance of matrix turnover in the intervertebral disc (IVD). Daily cyclic diurnal assists in the transport of large soluble factors across the IVD and its surrounding circulation and applies direct and indirect stimulus to disc cells. Acute mechanical injury and accumulated overloading, however, could induce disc degeneration. Recently, there is more information available on how cyclic loading, especially axial compression and hydrostatic pressure, affects IVD cell biology. This review summarises recent studies on the response of the IVD and stem cells to applied cyclic compression and hydrostatic pressure. These studies investigate the possible role of loading in the initiation and progression of disc degeneration as well as quantifying a physiological loading condition for the study of disc degeneration biological therapy. Subsequently, a possible physiological/beneficial loading range is proposed. This physiological/beneficial loading could provide insight into how to design loading regimes in specific system for the testing of various biological therapies such as cell therapy, chemical therapy or tissue engineering constructs to achieve a better final outcome. In addition, the parameter space of 'physiological' loading may also be an important factor for the differentiation of stem cells towards most ideally 'discogenic' cells for tissue engineering purpose.

Protective effects of paeoniflorin against FasL-induced apoptosis of intervertebral disc annulus fibrosus cells via Fas-FasL signalling pathway

“…Excessive apoptosis causes the death of nucleus pulposus cells (3), and apoptosis is associated with the degeneration of cartilage endplates. In addition, the apoptotic rate has been demonstrated to increase under long-term pressure in intervertebral discs (4). Hence, we speculate that apoptosis is vital in intervertebral disc degeneration.…”

CK8 phosphorylation induced by compressive loads underlies the downregulation of CK8 in human disc degeneration by activating protein kinase C

“…[26][27][28][29] Until now, several lines of evidence have demonstrated that prolonged exposure to hyper-physiological loads is harmful to the disc and consequently contributes to IDD. 21,30 The structure of NP is unique within the intervertebral disc, which is under tremendous forces and compressive load environment. 31,32 The exact mechanisms of this effect are complicated, including decreased proteoglycan production, increased apoptosis, the accumulation of inflammatory agents and cell volume changes.…”

“…Briefly, NP cell samples were subjected to compressive stress environment in a compression culture chamber (Taikang Biological Technology, Xi'an, China), which was linked with a high pressure gas cylinder. Controllable compressive stress was applied to the samples for 4, 24 and 48 h at 3 Mpa or at 0.3, 1.0 and 3.0 MPa for 48 h. [19][20][21] The culture chamber works with compressed gas from the cylinder to the culture dishes, leading to compression of fluid media to the NP cells under controlled pressure. Cells cultured at a similar condition without compression loads were used as control.…”

Poroelastic behaviour of the degenerating human intervertebral disc: a ten-day study in a loaded disc culture system

“…The IVD is a "cushion-like structure" (Chan et al, 2011). Its core is the nucleus pulposus, a gel-like matrix rich in proteoglycans, which is contained by the annulus fibrosus, consisting of alternating lamellae of collagen type-I fibres.…”

“…Its core is the nucleus pulposus, a gel-like matrix rich in proteoglycans, which is contained by the annulus fibrosus, consisting of alternating lamellae of collagen type-I fibres. The IVD's function is essentially mechanical, and can be seen as an elastic hinge that provides flexibility and transfers loads in the vertebral column (Brinckmann and Grootenboer, 1991;Chan et al, 2011). The functional status of IVDs can therefore be described by considering their biomechanical properties.…”