The ‘vacuum’ phenomenon represents a void in the nucleus pulposus filled with air and traces of other gases from surrounding tissues. A void can be created during disc degeneration by the loss of proteoglycans and water from the nucleus pulposus[27] or following endplate damage which allows the endplate to bulge into the vertebral body. In either case, the nucleus becomes ‘stress-shielded’ by the annulus, so that the pressure within it can fall almost to zero[20, 22]. Clefts from the nucleus can extend into fissures in the annulus, which can also become voids during movements such as hyperextension, and appear as a radiolucent area in the discal space in radiographs and CT scans. Alternatively, spinal flexion can cause the VP to decrease in size or even disappear. Hence, the presence of a VP identified by radiographs has long been equated with the presence of “degenerative” disc disease[23, 26]. In each instance, the location and appearance of the gas would appear to indicate the position and extent of cleft formation within the disc, thus providing information as to the nature of the underlying process. Other possible causes of VP include infection (which is also closely associated with Modic changes[28]), osteonecrosis, skeletal metastasis, Schmorls nodes, alkaptonuria, chymopapain chemonucleolysis, and surgical discectomy. Similar phenomena occur in synovial articulations: when vigorous movements distract the apposing articular surfaces, if there is little synovial fluid within the articular cavity, the increasing joint space creates a negative pressure, attracting gas from surrounding extracellular spaces and causing the familiar ‘popping’ sound.
On MRI scans, the classic appearance of a VP is a region of signal void on T1- or T2-weighted images. However, MRI is less sensitive in detecting VP compared with CT[29], as shown here in Table 1. Plain radiographs (DR) detect far fewer VP than CT because CT can remove the illusion caused by overlapping gas in intestines, alveola, or subcutaneous fat fold.
Although a VP is considered to mark end stage disc degeneration, the nutrition still may enter the disc space via the transudate from the diffusion pathway. It has been suggested that fluid flow into and within the disc may enhance the transport of larger molecules[30, 31], and it is now understood that endplates do not generally become less permeable as age and degeneration progress[32].
Studies showed that VP could be related to low back pain, when standing up or rolling over, which may cause pressure changes in the intervertebral discs[33, 34]. Similarly, studies demonstrated that low back pain might be aggravated by atmosphere depression in patients with lumbar disease associated with VP[35]. And our research found that the prevalence of back pain was higher in the VP group than in the no-VP group, which confirmed that VP should be related to low back pain
Many studies have investigated Modic changes, and it is evident that biomechanical and biochemical factors are both important. As the spine is a nonlinear viscoelastic structure and its vertebral body and endplates are ‘weak links’, Adams et al. [22]concluded that the loss of the nucleus pulposus, resulting from bulging into the adjacent vertebra, or desiccation and dehydration for severe degeneration, could cause stress concentrations on the endplates and subchondral bone trabeculae, resulting in the occurrence of microfractures. Increased communication between the vertebral bone and the disc nucleus could lead to inflammation, Modic changes, and infections[28]. Disc prolapse may also create Modic changes, because many herniations of disc material include hyaline cartilage which is presumably pulled off the underlying endplate, exposing cortical bone with many large perforations in it. Such events may explain the endplate ‘erosions’ which are common in the lower lumbar spine[4] where they are closely associated with Modic changes[36], and pain[5]Mechanical events readily explain why Modic changes are most common at the lowest two levels[36].
The prevalence of Modic changes varies from 18 to 62% in the patients with LBP, with different ratios for each type[7, 9, 37–40]. According to the results of previous studies, type I and type II are the most common patterns in the lumbar spine, although it is uncertain whether type II is more frequent than type I. Chung et al.[41] found 11 type I and 38 type II Modic changes in 590 lumbar vertebral endplates of 59 asymptomatic subjects. Weishaupt et al.[42], reported a distribution of 2% type I, 7% type II, and 2% type III. These studies showed type II is more frequent than type I, as in the present study.
In our study, we found that the presence of a VP was significantly correlated with the presence of Modic changes at the L5-S1 level and also at the L4-5 level, and we think that the endplate degeneration might be the origination of the VP. Due to the endplate calcification and activated cytokines, the transport pathway of the nutrition for the intervertebral disc was blocked, resulting in the metabolic unbalance and decrease of the synthesis of matrix structural proteins. It could promote the matrix decomposition, causing the quantity of matrix to decrease and the stress in intervertebral disc to change. As a result, the structure of intervertebral discs became unstable. While compression happened, the intravertebral cleft could occur and be gradually filled with gas, which may cause low back pain and aggravate the intervertebral discs.
Our study has some limitations. The relatively small sample size prevented us from seeking to correlate the severity of VP (reflected as the percentage of the volume of VP in disc) and the severity of Modic changes, as suggested by Wang et al.[43], and it probably explained why VP and Modic changes did not increase with age, as might be expected[36].
Nevertheless, we suggest that the results of the present study have clinical significance. They show that the presence of Modic changes can be anticipated by finding a VP on CT or plain radiographs. Recent research is showing how endplate lesions (as indicated by Modic changes) are strongly implicated in endplate injury, inflammation, infection and pain, so that the radiographic demonstration of a VP may be considered grounds for further imaging studies in patients with low back pain.