Initiation and accumulation of loading induced changes to native collagen content and microstructural damage in the...

Injury to the cartilaginous endplate (CEP) is linked to clinically relevant low back disorders, including intervertebral disc degeneration and pain reporting. Despite this link to clinical disorders, the CEP injury pathways and the modulating effect of mechanical loading parameters on the pace of damage accumulation remains poorly understood.

This study examined the effect of cyclic loading on the initiation and accumulation of changes to native collagen content (type I, type II) and microstructural damage in the central region of cadaveric porcine CEPs.

In vitro longitudinal study.

One hundred fourteen porcine cervical spinal units were included (N=6 per group). The study contained a control group (no cyclic loading) and 18 experimental groups that differed by loading duration (1,000, 3,000, 5,000 cycles), joint posture (flexed, neutral), and cyclic peak compression variation (10%, 20%, 40%). Multicolor immunofluorescence staining was used to quantify loading induced changes to type I (ie, subchondral bone) and type II (ie, endplate) native collagen content (fluorescence area, fluorescence intensity) and microstructural damage (pore area [transverse plane], void area along the CEP-bone border [sagittal plane]).

Significant main effects of loading duration and posture were observed for fluorescence area and fluorescence intensity of type I and II collagen. In the transverse plane, type II fluorescence area significantly decreased following 1,000 cycles (-12%), but a significant change in fluorescence intensity was not observed until 3,000 cycles (-17%). Type II fluorescence area (-14%) and intensity (-10%) were both significantly less in flexed postures compared to neutral. Similar trends were observed for type I collagen in the sagittal plane sections. Generally, significant changes to fluorescence area were accompanied by the development of microstructural voids along the endplate-subchondral bone border.

These findings demonstrate that microstructural damage beneath the endplate surface occurs before significant changes to the density of native type I and II collagen fibers. Although flexed postures were associated with greater and accelerated changes to native collagen content, the injury initiation mechanism appears similar to neutral.

Neutral joint postures can delay the initiation and pace of microdamage accumulation in the CEP during low-to-moderate demand lifting tasks. Furthermore, the management of peak compression exposures appeared relevant only when a neutral posture was maintained. Therefore, clinical low back injury prevention and load management efforts should consider low back posture in parallel with applied joint forces.