The differences encountered from patient to patient on MRI findings may give rise to diagnostic problems in determining the exact cause of pain [15,16,17,18,19], especially in the absence of clear evidence of disc herniation, root compression, or posterior elements involvement. Data from the literature suggest that as many as 80% of patients complaining of low back pain are categorized as having “non-specific low back pain” . The concept of “active discopathy” is closely related to the subset of patients having non-specific low back pain. From an imaging-based as well as histopathological point of view, active discopathy is characterized by the presence of intervertebral disc changes and adjacent vertebral endplate subchondral bone changes associated with degenerative disc disease (Modic changes type I) . The vertebral body endplates are indeed considered the most vulnerable structure functional spinal unit . They have a bony component and a hyaline cartilaginous component. The bony endplate provides mechanical strength preserving a high intradiscal pressure , whereas the cartilage endplate is more of a biological barrier to reduce transport (of water, inflammatory agents, bacteria, and so forth) between the trabecular bone of the vertebral body and the fibrocartilage of the intervertebral disc [23, 24]. However, these components have to be considered as a single biomechanical unit [25,26,27]. Several grading systems have been proposed to describe and classify disc and endplate degeneration. The most popular MRI grading system for degenerative disc disease was defined by Pfirrmann et al. . The grading system for bone marrow changes near the endplate was implemented by Modic et al. who gave MRI definitions of such alterations [8, 20, 29]. The etiopathogenesis of Modic changes type I is still a matter of debate [20, 30, 31].
According to the theory of “biomechanical stress,” shear, compressive, and bending forces acting on the vertebral endplate adjacent to a degenerated disc lead to endplate microtrauma and subsequent bone marrow oedema . The presence of endplate fissuring and fibrovascular marrow changes has also been confirmed by histopathological studies, supporting this etiopathogenetic theory [20, 32,33,34]. According to this model, Modic changes represent a biomechanical alteration of the normal intervertebral environment associated with endplate damage . In particular, cracks and fissures in both cartilaginous endplates of a disc simultaneously lead to internal disc degeneration and disruption [34,35,36]. Imaging-based evidence of this pathophysiological cascade was presented by Muftuler et al.  who carried out a contrast-enhanced MRI study to investigate endplate dynamics in degenerated discs. He described increased contrast agent accumulation in severely degenerated discs, which provided evidence of disruption of the endplate integrity at later stages of disc degeneration. Another recent work by Rade et al. also reported a strong association between endplate defects and disc degeneration . These findings are in line with previous studies investigating the structural changes in subchondral bone associated with disc degeneration and describing the presence of significant fissures in subchondral bones close to degenerated discs; in particular, a recent study revealed the presence of increased porosity in great detail using µCT . Another mechanical, histological, and micro-CT study of cadaver spines from Zehra et al.  confirmed a stronger association between disc degeneration and large or multiple endplate defects.
The development of endplate cracks and fissures, with consequent increase in subchondral bone marrow porosity, may lead to increased inflow, resulting in higher contrast agent accumulation in the cartilaginous endplate during DCE-MRI acquisition. On the other hand, such disruptions may contribute to the formation of a leaky endplate interface, leading to overall loss of hydration and matrix proteins . We support the view that under sustained load, endplate fissuring may provoke redistribution of water from the reduced and dehydrated disc to the adjacent subchondral bone, leading to marrow oedema and pain, the latter depending on the increased pressure on the marrow.
Using a dedicated MRI unit with a table tilt system, we performed an “in vivo” evaluation of the effects of loading on the discovertebral unit.
According to the literature, the primary consequence of disc degeneration under biomechanical stress is the production of pro-inflammatory soluble mediators such as interleukin 6 and prostaglandin E2 in the nucleus pulposus that, diffusing through vertebral endplate and subchondral bone, can generate local inflammation and oedema . It is well known that biomechanically induced local inflammatory changes are a source of pain. Several clinical studies reveal that surgical stabilization may accelerate Modic I changes and contribute to pain relief. Furthermore, treatment with intradiscal steroid injections was found to be effective in pain reduction and regression of Modic I changes. Altogether, these data support the role of biomechanically and/or biochemically induced local inflammation in the pathogenesis of Modic I changes and related symptoms .
Some authors suggest that Modic changes be the consequence of local anaerobic infection since the environment surrounding disc herniation and annulus fibrosus disruption is favourable to anaerobic germ growth. This theory is supported by the evidence of positive anaerobic culture from surgically harvested disc herniation tissue . The cascade of inflammatory mediators and superimposed low-grade infection, however, is not exclusive of Modic I changes .
Among the Modic endplate changes, MC type I are the most frequently associated with low back pain, but, despite the long debate, the exact relationship remains controversial. Several authors define Modic changes as specific indicators of “discogenic” low back pain with a strong association, while others say that Modic changes are also prevalent in the asymptomatic population [1, 35].
Our results are in line with earlier studies, which suggest that MC type I are associated with low back pain . However, there are indeed other explanations for pain, among which is the reduction in intervertebral space under loading. Disc height reduction is known to affect the size of the foraminal spaces and axial load redistribution to the posterior elements, mainly the facet joints, which cause severe pain due to their innervation. In the present study, we did not evaluate facet joints, spondylolisthesis, or instability, because only sagittal slices were obtained for the follow-up MRI. In previous studies; however, we evaluated the role of weight-bearing MRI in demonstrating “dynamic” joint pathologies, often unmasked by loading [42,43,44].
The clinical relevance of MRI of Modic I changes lies in the increasing acceptance of discogenic pain as a cause of low back pain . Moreover, the natural history of Modic signal changes and associated clinical findings suggest that the treatments able to accelerate the switch to Modic 0 or Modic 2 changes may find a role in the therapeutic planning (surgery, intradiscal steroid, bisphosphonates, exercise, and so forth) . To our knowledge, this is the first study that focuses on the effects of loading on endplate changes. Our study has some limitations: first of all, low back pain is a subjective symptom with multifactorial aetiology. In our analysis, we excluded patients with MR evidence of possible low back pain sources different from Modic I changes, such as facet joint pathology. However, the possible presence of low back pain from other causes not evident at MRI (for example, muscular origin) might not be excluded. In the present study, we also excluded patients with disc extrusion, considered as a confounding factor evaluating low back pain source; indeed, there is evidence that endplate disruption and Modic I changes are closely associated with disc herniation . Disc extrusion appears to be also an important factor allowing disc infection . Another limitation of this study is represented by the low number of patients enrolled; nevertheless, our MRI protocol has proved to be sensitive in detecting MR findings of possible pain sources, not readily evident on standard MRI scans. Lastly, our results lack the evaluation of a control group; comparison with asymptomatic individuals would be interesting, given the evidence of the prevalence of Modic changes also in the asymptomatic population .