Schmorl’s node of primarily developmental cause and Schmorl’s node of primarily acquired cause: two related yet different entities
According to the original definition, Schmorl’s node (SN) corresponds histologically to nucleus pulposus herniation into the vertebral spongy bone with thickened trabeculae around the formed node (1,2). Very conflicting literature on the epidemiology of SN have been reported. Several earlier reports noted that, except for the early childhood period, SN prevalence among age groups remains stable (3-6). Dar et al. (4) studied skeleton vertebrae from a normal adult population and noted that SN was more common in men than in women, but SN was age independent. Hilton et al. (5) found no relationship between age and SN with their study of cadaveric spines and thus proposed a developmental pathogenesis for SN. Chen et al. (7) reported that aging was related to greater odds of endplate lesions; however, the prevalence of focal endplate defects remained stable. Sonne-Holm et al. (6) analysed lateral spine radiographs in an adult Caucasian population cohort and did not note any significant correlation between SN and gender, or age. On the other hand, some authors reported the association of SN with age. Wang et al. (8) reported that greater age was associated with the presence of SN among a male cadaver collection. A male predominance of SN had been frequently reported (5,9-11). Üstündağ (11) studied SN in a post-medieval skeletal sample and noted that males were more affected than females, and there was no relationship found between SN and aging. However, a few studies did not observe an association of SN with gender (6,12,13). The correlation between osteoporosis and SN also remains controversial (14-16). In a study on the cadavers of pre-Hispanic inhabitants González-Reimers et al. (14) did not find a relationship between osteoporosis and SN. On the other hand, other evidence suggests osteoporosis is a cause of SN. Mäkitie et al. (15) reported a high prevalence (61%) of SN in their case-control study of 18 patients diagnosed with WNT mutation-induced osteoporosis. Based on a CT study, Güngör et al. (16) suggested that low bone mineral density may be a predisposing factor for the development of SN in patients younger than 40 years. Recently we (17) described a study of thoracic spine MR imaging among community elderly subjects (mean age: 82 years) and noted a number of features of SN paralleled those of osteoporotic vertebral fracture (OVF). SN prevalence in women (55.5%) almost doubled that in men (25.9%). SN was statistically significantly correlated with lower bone mineral density, and subjects with SN were more likely to have OVF. In vertebrae with osteoporosis, the endplate becomes weakened due to the loss of support from trabecular bone and due to thinning of the endplate itself (18), thus this pathway may exist that: osteoporosis → weakened endplate → SN development → osteoporotic endplate fracture (17).
To make sense of these conflicting literature, we suggest that SNs should be classified into two categories: SN of primarily developmental cause (SNd, Figure 1) and SN of primarily acquired cause (SNa, Figure 2). Note that, SN can be considered as a ‘general phenomenon’ (rather than a specific disease entity) where a portion of disc materials herniated through endplate into the vertebral spongy bone, and the surrounding sclerosis in vertebra reflects reactive healing. An analogy can be made to congenital spondylolisthesis, traumatic spondylolisthesis, and degenerative spondylolisthesis (20).
SNd is characterized by that they more likely involve multiple adjacent vertebrae, more likely to be small or modest in size, they likely to have relatively consistent location and more likely involve a posterior portion of the lower endplate (though other locations are also common). Moreover, compared with SNa, SNd tend to have a more solid border on radiograph due to their longstanding and sometimes static nature. It is also possible some SNd and cupid bow may belong to the same spectrum of developmental changes (Figure 3). Note that Pfirrmann and Resnick described cases showing ‘the transition of Schmorl nodes to a cupid’s bow contour’ (21). SNd are known to be a common but not obligate manifestation of Scheuermann disease. SN associated with Scheuermann disease shall belong to SNd. It is also possible that some very ‘tiny’ SNd may not have clinical relevance (Figure 4), and some SNd may not have a true disc material herniation process. Heritability of SN has also been demonstrated (15,22,23). Though the upper endplate is less resistant to compressive pressure and more likely to fracture (24), in a female twin volunteer study (mean: 53 years), for their study subjects Williams et al. (22) noted that SNs (assumed largely SNd) were more prevalent in lower endplate than in upper endplate.
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 network of small cavities which allow bone marrow to lie adjacent to calcified hyaline cartilage for approximately 10% of the central endplate area, which is an important route for metabolite transport into the discs. The nutritional demands of the discs result in that vertebral central endplates are thin and porous, and which can be subject to fracture under stress force even if bone strength is normal. For the pathogenesis of SNa, whatever the cause of the damage to the cartilaginous endplate, to the subchondral bone of the vertebral body, or to both structures, a weakened area is created that is unable to resist the expansive pressure of the adjacent nucleus pulposus. SNa are more likely to be modest or large in size, and their borders are not always clearly defined on radiograph. Trauma and endplate micro-fractures are triggers for SN (25-29). Dar et al. (25) proposed an axial load model which suggests that the human spine must accommodate increased axial forces in addition to balancing the need for spinal mobility and stability, and it may accumulate micro-traumas that can, over time, lead to the formation of SN. In a cohort of children who had suffered from stable compressive vertebral fractures, Möller et al. (26) reported the occurrence of SN at advanced ages (40 years) at adjacent disc levels. In a study of 70 thoracolumbar spines from cadavers of individuals killed in motor vehicle collisions, Fahey et al. (27) reported a link between trauma and the occurrence of SN. Swärd et al. (28) compared vertebral abnormalities in elite gymnasts versus non-athletes, they found SNs in 17 out of 24 (71%) gymnasts with nodes in 57 endplates and in 7 out of 17 (44%) non-athletes with nodes in 23 endplates. Certain pre-existing conditions can facilitate herniation occurs due to axial forces. The theory of weak spot presence within vertebral endplate has been considered. The possible endplate weakness can be due notochord regression, ossification gaps, or vascular channels (2,30,31). The vertebral level distribution of SNa will be similar to traumatic vertebral fracture (high energy trauma) or OVF (low energy trauma) (19,32). SNa less likely involve posterior portion of an endplate which is not a weak point of biomechanics. Among elderly subjects, SNa more likely involve upper endplate which is the same as osteoporotic endplate fracture (24), and SNa are commonly associated with endplate depression. Osteopenic/osteoporotic SN may be a precursor of OVF, a specific type of endplate fracture, or a co-phenomenon for advanced OVF (Figure 5). Tumorous changes of a vertebra can also increase the fragility of an endplate, and lead to disc materials herniation through endplate into the vertebral spongy bone and form SNa (33,34). In these cases, the surrounding sclerosis may not necessarily develop when the SNa is detected.
Some earlier authors already discussed SN sub-classifications. Hansson and Roos (35) classified the SNs situated just above or below the nucleus pulposus, symmetrically on both sides of the nucleus with well-rounded smooth bone surroundings as type A nodes. The SNs which are situated asymmetrically in relation to the nucleus and/or surrounded by rough often sclerotic bone and were classified into type B. However, according to our reading of the literature, how our classification can correspond to the classification of Hansson and Roos remains unclear. On the other hand, Hansson and Roos did note that some SNs were associated with lower vertebral bone strength while others were not.
We advocate that, for future studies, SNd and SNa should be separately described as much as possible, as SNd and SNa may have different clinical significance. Small SNd may not have clinical relevance, and some SNd may be well covered with the endplate. SNa are usually associated with endplate fracture, and some SNa may be an indicator of compromised vertebral bone strength (17). On the other hand, the physiopathology of SN formation can be multifactorial; and for some SNs, a definite separation of SNd and SNa may not always be possible. More research is required to elucidate the classification of SNs and their relationship to developmental causes or degenerative causes.
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