The epidemiological data shows 3.8–76% of the general population was diagnosed with SN [11], which is broadly in line with the data from the present study that is showing almost one quarter of the population (22.2%) had SN.
The wide difference in SN prevalence may have different causes, such as different definitions of SN used and different spinal column regions involvement in studies, and some others suggested genetic influence as manifested by variations in ethnic distribution [5, 12].
In the current study, the number of men with SNs was more than women, which in line with previous studies [2, 3, 24]; the research of Dar G. and his collogues considered this high affection among males was due to their larger body size, and taller vertebral bodies and discs both make more mechanical stress on the endplates [5], whilst another study suggested genetic determinants for the male predilection [12].
The prevalence of SN was significantly increased as age advanced, comparable with previous studies that suggested weakened aged cartilaginous endplates and reduced bone density in older age groups; both factors may play a role in pathogenesis of SNs [25,26,27]. The higher lumber levels were affected more, as L1–L2 was the most affected disc (23.6%) in the current study; this was consistent with most of the papers [8, 24, 27]. This could be due to higher mechanical stresses, and the special anatomical features of this part of spine make it more prone to damage by torsional and axial body loads [2].
Several studies did not show significant relation between SNs and disc degeneration nor with disc bulge/herniation, like the current study. As Sonne-Holm S. and his colleagues’ assessed lumbar spine using radiographs in healthy adults [11], whilst Hilton RC and his colleagues studied post-mortem spines, they did not find a significant relation between the SN and DDD at the lumbar region.
Other studies assessed the MRI images of different sample criteria, including healthy twin females [12] and healthy adults [24], a paper analysed discography in adults with back pain [16], and another assessed CT scans of lumber spine [25]; these manuscripts showed a significant relation between SNs and disc degeneration.
This controversy about SN and DDD association might be related to different factors, such as different sample criteria, different radiological modalities used, and other spine region’s involvement with the lumber spine in the studies.
According to this paper, we prefer the theory of endplate osteonecrosis as a cause of SNs, rather than disc degeneration, as a study examined the surgical specimens of SNs proposed that the SNs are the end result of ischemic death of bone beneath the endplate and the herniation of the disc into the body of the vertebra is a secondary phenomenon. The hypothesis of microtrauma is also preferred as Burke et al. found more SN in American soldiers [26]; these minor traumas cause herniation of nucleus pulposus through developmental weak points in the endplates [28]. Also, the developmental models revealed that SNs are already present during skeletal maturation prior the beginning of degeneration [2]. Moreover, the disc degeneration mostly occurs in the lower lumbar levels in reverse to SNs which occurs in the upper lumbar levels.
Modic change was significantly associated with SNs in this study like another study done by Tobias et al .[8]; this result was probably due to disruption of the endplates and the herniation of disc material initiating inflammatory change and edema resembling MC as seen on MRI images.