Each individual has an intrinsic spine shape that is partly maintained during postural changes[7]. Interestingly, we noted a distinct deformity, which is WSV. Most vertebral deformities or fractures involve the mid-thoracic and thoracolumbar junction, which was consistent with the results of previous studies[8–10]. Up to now, vertebral anterior wedge deformities is explained as a two-stage process, with initial endplate damage followed by subsequent collapse of the anterior cortex[11].
In this study, WSV presented in 51.7% patients, which is a relatively high incidence. The problems caused by vertebral wedging include pain, disability and poor quality of life such as exercise intolerance.[12] There are some discussions in the literature regarding the possible etiologies of mild radiographic vertebral changes, including fracture, normal variants, degenerative changes, mild osteoporotic fracture and osteoarthritis.[13–15] In some other studies, a preexisting compression fracture, the L5/S1 disc degeneration grade, and the cross-sectional area of the multifidus and psoas muscle are all the risk factors of WSV.[16] In this study, we excluded the patients with history of trauma. Our study demonstrates that TLWSV are seen in all ages, suggesting that they are likely to be congenital deformities, which is similar to Scheuermann's disease.
The results of this study showed marked radiographic similarities between WSV and SD, such as changes in spine sagittal alignment and intervertebral disc degeneration. This deformity is also similar to compression fracture. We could learn from compression fracture to get a better understanding of biomechanism of WSV. In compression fracture, stress peaks were often presented in the annulus, and became more marked posteriorly when specimens were compressed in extension to simulate erect standing[17]. Fracture reduced intradiscal pressure by 39% and 46% in flexion, and by 57 and 65% in extension, whereas posterior stress peaks increased by 65% and 196% in flexion. Vertebral fracture reduced height, stiffness and pressure in the nucleus of adjacent intervertebral discs, and transferred compressive load-bearing to the neural arch[18]. Wedge fractures decompress the disc, increasing load-bearing by the neural arches, and reducing loading of the anterior vertebral bodies. This compensation may reduce fracture risk in a short time. However, in a long time, stress-shielding of the anterior vertebral body will accelerate bone loss in this region and ultimately increase the risk of further fracture [19]. This mechanism could affect the shape of adjacent vertebral, leading to change in spine saggital alignment.
Based on our observations, ULDD was found to occur frequently in patients with thoracolumbar vertebral wedge-shaped deformities. In WSV patients, sagittal imbalance is a common and disabling condition. There is significant difference in CL, TK and TLK between the two groups. In LLL, WSV group is relatively higher (p = 0.058). To maintain a balanced posture and a forward visualized gaze, hyperkyphosis is commonly compensated with a nonstructural hyperlordosis of other sections of spine in younger people with flexible spines[20], consistent with the result of our study. We supposed that kyphosis in thoracic and thoracolumbar region would account for the compensation in LL. Besides, vertebral could adapted in shape to the new intervertebral disc space with retained signal intensities, may still be functional for weight bearing and stability of the spinal unit[21]. In addition, other compensation is also important, such as splaying of intervertebral space, hip retroversion and knee flexion[20, 22, 23].
WSV easily can be missed in young people. The findings in the lateral radiograph can be slight and obscure, and probably not all children with back traumas are examined radiographically[24]. Therefore, these deformties often are overlooked. They also have been considered unimportant because they are assumed to heal completely without backache later. Based on our observations, WSV is related to ULDD. We should pay attention to the thoracolumbar discs in patients where radiological signs of WSV are present on their spine images and in necessity we maybe need to take some more radical measures.
This study had several limitations. In this study, whole-spine plain roentgenograms and MRIs of every patient are essential. It is difficult to obtain whole-spine plain roentgenograms and MRIs from healthy people. We could get whole-spine plain roentgenograms and MRIs from hospitalized patients easily. So the sample of this study is patients with lumbar disc degeneration visiting our institution for operation.
WSV as a consequence of compression fracture has been published[24–26]. Our study provided novel insights to mechanism of WSV. In this study, we excluded the patients with history of trauma, Scheuermann's disease and its atypical type, other spinal deformities and spinal trauma or tumors. So WSV could be a congenital deformity, which is similar to Scheuermann's disease. Just like Scheuermann's disease[27, 28], the incidence of disc degeneration is significantly higher in WSV patients. In initial stage of WSV, there are many compensation mechanisms. The symptom is not serious. So WSV is often overlooked in younger people. The symptoms get worse and worse with age. because of the change of stress state, lumbar vertebral will experience creep deformation. Creep deformation impacts spine neuromuscular control and stability, and ultimately the development of low back disorders[29].