The role of the vertebral end plate in low back pain

J C Lotz, A J Fields, E C Liebenberg, J C Lotz, A J Fields, E C Liebenberg

Abstract

End plates serve as the interface between rigid vertebral bodies and pliant intervertebral disks. Because the lumbar spine carries significant forces and disks don't have a dedicated blood supply, end plates must balance conflicting requirements of being strong to prevent vertebral fracture and porous to facilitate transport between disk cells and vertebral capillaries. Consequently, end plates are particularly susceptible to damage, which can increase communication between proinflammatory disk constituents and vascularized vertebral bone marrow. Damaged end plate regions can be sites of reactive bone marrow lesions that include proliferating nerves, which are susceptible to chemical sensitization and mechanical stimulation. Although several lines of evidence indicate that innervated end plate damage can be a source of chronic low back pain, its role in patients is likely underappreciated because innervated damage is poorly visualized with diagnostic imaging. This literature review summarizes end plate biophysical function and aspects of pathologic degeneration that can lead to vertebrogenic pain. Areas of future research are identified in the context of unmet clinical needs for patients with chronic low back pain.

Keywords: end plate; intervertebral disk; low back pain; spine.

Conflict of interest statement

Disclosures J. C. Lotz, Consultant, Research Support, Stock/Options: Relievant Medsystems, Nocimed LLC A. J. Fields, None E. C. Liebenberg, None

Figures

Fig. 1
Fig. 1
(A) Gross morphology of the lumbar intervertebral joint. (B) Histology section showing regions of interest for panels C, D, and E. (C) End plate detail showing cartilaginous and bony components with hematopoietic marrow elements. (D) Insertion of annular fibers into the end plate cartilage at the inner annulus junction. (E) Vascular sinusoids in the marrow space adjacent to the end plate. Note for panels A and B, left side is anterior.
Fig. 2
Fig. 2
Schematic representation of vertebral end plate development. (A) At embryonic week 6, the sclerotome begins to segment around the notochord to form periodic cartilaginous and fibrocartilaginous precursors to the vertebra and disks, respectively. (B) By embryonic week 15, the notochord atrophies within the vertebra, and ossification begins at the vertebral centers. (C) At embryonic week 25, the ossification centers expand as the vertebrae lengthen. Columnar cartilage develops at the vertebral ends to form the epiphyseal plates. (D) By age 5 years, the ossified portions of the vertebra extend to the lateral margins and the epiphyseal cartilage begins to thin. (E) By age 13 years, peripheral ossification centers outside the epiphyseal plate form the ring apophysis. (F) By age 18 years, the ring apophysis begins to fuse to the osseous mass of the vertebral body.
Fig. 3
Fig. 3
Distribution of protein gene product 9.5 (PGP 9.5)-positive nerve fibers across the end plates (63-year-old woman, L5-S1). Compared with the density of nerves in normal end plate regions, nerve density is higher in end plate regions with damage. Nerve fibers in this disk were observed in the inferoposterior outer annulus. Note: left side is anterior.
Fig. 4
Fig. 4
Midsagittal T1-weighted (A) and T2-weighted (B) magnetic resonance (MR) images of an L1-L2 motion segment with poor end plate signal. (C) Corresponding ultrashort time-to-echo (UTE) MR image showing enhanced end plate signal. Arrows indicate end plate defects shown in Fig. 5A and 5B. (UTE imaging courtesy of Drs. Roland Krug and Misung Han, Department of Radiology, University of California, San Francisco.)
Fig. 5
Fig. 5
Various end plate defects with hypothesized etiologies. (A) End plate cartilage avulsion resulting from bending motion that causes traction at the interface between the end plate and inner annulus. (B) Traumatic node with end plate fragment resulting from excessive compression with a healthy, gel-like nucleus pulposus. (C) Central end plate fracture with exposed trabeculae resulting from excessive compression with a degenerate, fibrous nucleus pulposus.
Fig. 6
Fig. 6
Prevalence of end plate pathologies in different regions may arise from distinct biomechanical conditions. (A) In the lower lumbar spine, the prevalence of end plate cartilage avulsions and erosions increases caudally, mirroring the increase in range of motion (combined flexion/extension data are shown). (B) In the upper lumbar spine, Schmorl nodes increase cranially, mirroring the decrease in trabecular bone mineral density and end plate strength.

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Source: PubMed

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