Vertebral Endplate

A great review of vertebral endplate
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16816945#CR15

Introduction and conclusion From Bone. 2009 Feb;44(2):372-9. Epub 2008 Nov 11

The cranial endplate of thoracolumbar vertebrae is injured more often than the caudal [1], [2], [3], [4], [5] and [6], and anterior wedge fractures in elderly patients usually involve the cranial rather than caudal endplate [7] and [8]. Schmorl's nodes, which represent a bony reaction to endplate defects, are also more common in the cranial endplate [4]. Mechanical experiments on cadaveric spines suggest that the cranial endplate is more vulnerable to compressive damage than either the caudal endplate or the intervertebral disc [9], and indentation experiments on isolated endplates suggest that cranial are weaker than caudal [10] even though there is little difference in their bone density [11]. These curious facts have been reported, but not explained. Cranial and caudal endplates of adjacent vertebrae are subjected to the same compressive loading by the intervertebral disc that lies between them, and cranial endplates tend to fail in-vitro even if specimens are tested upside down [9]. Therefore this asymmetry in fracture pattern suggests an underlying structural asymmetry in the vertebrae.

In the human thoracolumbar spine, pedicles join the vertebral body at above mid-height. Bone mineral density (BMD) is higher in the pedicles than in the vertebral body [1], and trabecular arcades from the pedicles appear to reinforce the lower endplates more than the upper, at least at some spinal levels [12]. However, the neural arch largely resists axial rotation [13] and [14] and shear [15] B.M. Cyron and W.C. Hutton, Articular tropism and stability of the lumbar spine, Spine 5 (2) (1980), pp. 168–172. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (35)[15] acting on the spine, and there is no obvious reason why trabeculae from the neural arch should be deployed to enhance the compressive strength of the vertebral body.

Structural asymmetry may lie in the endplate itself rather than in its trabecular support. A vertebral endplate consists of perforated cortical bone with a layer of hyaline cartilage bonded to its disc surface. The cortical bone layer contains a radiating anastomosing network of small marrow cavities [16] which allow bone marrow to lie adjacent to calcified hyaline cartilage for approximately 10% of the central endplate area [17], and this is widely regarded as an important route for metabolite transport into the avascular intervertebral discs [18]. Certainly, calcification and blocking of the endplate route is associated with disc degeneration [6] and [19]. It seems reasonable to suppose that the nutritional demands of the discs, which are the largest avascular structures in the body, ensure that vertebral endplates are as thin and porous as possible. This may explain why endplate fracture is so common, but it does not explain why cranial endplates should be more vulnerable than caudal.

This is an important clinical problem because endplate fractures and Schmorl's nodes are associated with back pain [20], [21] and [22], even though both lesions often go unidentified so that the scale of the problem may be underestimated [21], [23], [24], [25] and [26]. Typical recovery periods from acute episodes of back pain are consistent with bony injury, as are the protective and accelerated recovery effects of exercise [27] and [28]. Endplate fracture may cause chronic as well as acute back pain because it can lead to disc degeneration, both in humans [29] and [30] and in experimental animals [31]. In elderly people, damage to vertebral endplates and their supporting trabeculae is so common [23] that it largely explains why old endplates develop a concave deformity facing the disc [32]. Damaged endplates decompress the nucleus pulposus of the disc [33] and [34], lead to abnormally-high load-bearing by the annulus fibrosus and neural arch [33] and [34], and probably contribute to pain and disability in patients with senile kyphosis [35]. A greater understanding of the factors that contribute to the increased fragility of the cranial endplate may help to reduce the risk of injury, and to optimise treatments such as vertebroplasty.
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Vertebral compressive failure usually affects the cranial endplate because it is thinner and supported by less-dense trabecular bone. This relative weakness may reflect the fact that most spinal compression arises from muscle tension [37], which is transmitted to the vertebral body via the pedicles. This causes compressive loading to increase down the spine in stepwise fashion, at the level of each pedicle. Each cranial endplate is compressed by the disc above it, whereas the caudal endplate of the same vertebra is also compressed by muscles attached to its pedicles. Hence the structural asymmetry. Unfortunately, this fine match between loading and strength is lost if the spine is compressed by external forces, such as in a fall on the buttocks with the spine flexed, because then the same force passes through both endplates, damaging the weaker (cranial) one. This could explain the preponderance of cranial endplate fractures in the present experiment, where the same compressive force passed through both endplates. It could also explain their preponderance in life, because falls contribute greatly to vertebral fractures [55].

Reduced thickness and density in the central regions of vertebral endplates (Fig. 6) may reflect the precarious supply of nutrients to the adjacent intervertebral discs. Discs rely on the thinness and porosity of endplates for the transportation of metabolites from blood vessels within the vertebral body [18] J.P. Urban, S. Smith and J.C. Fairbank, Nutrition of the intervertebral disc, Spine 29 (23) (2004), pp. 2700–2709. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (57)[18], and nutritional demands are greatest in the disc nucleus [18]. Impairment of this supply is associated with disc degeneration [19] and [56]. Cranial endplates may not thicken in lumbar vertebrae (as caudal endplates do) as a concession to the nutritional demands of the largest discs. Cranial endplates could possibly be singled out for this “sacrifice” because of asymmetries in blood supply to the vertebral bodies although information on this is lacking. Low optical density in the central endplate probably represents a greater concentration of marrow contact channels in the region which is known to be most porous [39]. In the cervical spine, where discs are thinner and have less acute metabolite transport problems, cranial and caudal endplates are equally thick [57].

The apparent weakness of endplates compared to intervertebral discs may have carried little evolutionary disadvantage when average lifespans were short. Longevity in modern humans exaggerates sarcopaenia and osteopaenia, which appear to reduce vertebral strength more than disc strength [58]. Longevity also increases disc degeneration which intensifies focal loading on vertebral endplates [52] and may facilitate fracture. The need to resist focal loading from degenerated discs may explain why BMD in older spines is greater in trabecular bone adjacent to the endplates compared to central regions of the vertebral body [59] and why BMD is greater in the posterior vertebral body, opposite the high stress concentrations which are commonly found in the posterior annulus of the disc [46].