Mechanical crosstalk between the intervertebral disc, facet joints, and vertebral endplate following acute disc injury in a rabbit model

Abstract

BackgroundVertebral endplate sclerosis and facet osteoarthritis have been documented in animals and humans. However, it is unclear how these adjacent pathologies engage in crosstalk with the intervertebral disc. This study sought to elucidate this crosstalk by assessing each compartment individually in response to acute disc injury.MethodsEleven New Zealand White rabbits underwent annular disc puncture using a 16G or 21G needle. At 4 and 10 weeks, individual compartments of the motion segment were analyzed. Discs underwent T1 relaxation mapping with MRI contrast agent gadodiamide as well T2 mapping. Both discs and facets underwent mechanical testing via vertebra—disc—vertebra tension‐compression creep testing and indentation testing, respectively. Endplate bone density was quantified via μCT. Discs and facets were sectioned and stained for histology scoring.ResultsIntervertebral discs became more degenerative with increasing needle diameter and time post‐puncture. Bone density also increased in endplates adjacent to both 21G and 16G punctured discs leading to reduced gadodiamide transport at 10 weeks. The facet joints, however, did not follow this same trend. Facets adjacent to 16G punctured discs were less degenerative than facets adjacent to 21G punctured discs at 10 weeks. 16G facets were more degenerative at 4 weeks than at 10, suggesting the cartilage had recovered. The formation of severe disc osteophytes in 16G punctured discs between 4 and 10 weeks likely offloaded the facet cartilage, leading to the recovery observed.ConclusionsOverall, this study supports that degeneration spans the whole spinal motion segment following disc injury. Vertebral endplate thickening occurred in response to disc injury, which limited the diffusion of small molecules into the disc. This work also suggests that altered disc mechanics can induce facet degeneration, and that extreme bony remodeling adjacent to the disc may promote facet cartilage recovery through offloading of the articular cartilage.

Advancing basic and preclinical spine research: Highlights from the ORS PSRS 6th International Spine Research Symposium

“…Using a rabbit model, Fainor et al show that perturbations in disc biomechanics not only cause local pathological remodeling in structures such as the vertebral endplates, but also in adjacent structures such as the facet joints. 2 Easson et al identified the ion channel transient receptor potential vanilloid 4 (TRPV4) as performing a critical role in mediating the interplay between inflammation and loading in mouse intervertebral discs. 3…”

“…show that perturbations in disc biomechanics not only cause local pathological remodeling in structures such as the vertebral endplates, but also in adjacent structures such as the facet joints. 2 Easson et al…”

Recombinant Laminin-511 Fragment (iMatrix-511) Coating Supports Maintenance of Human Nucleus Pulposus Progenitor Cells In Vitro

“…The IVD comprises three distinct tissue structures: the fibrocartilage ring, termed the annulus fibrosis, that encloses the central gelatinous nucleus pulposus 2 of 16 (NP) tissue, and two cartilaginous endplates where the disc borders the vertebrae. Agerelated disc degeneration is a progressive condition that may impair the stability of the spinal column, giving rise to a variety of spinal disorders [3,4]. This degenerative process of irreversible change is marked by a decline and deterioration in NP cells, resulting in changes in the extracellular matrix (ECM) composition, thereby compromising the disc's biomechanical features [3,5].…”