SNs are common spinal lesions in the general population, in which the majority are asymptomatic and require no treatment [2–4]. However, patients with endplate fractures around the SNs could result in acute back which is refractory to conservative treatment. Our results showed that PVP was an effective and minimally invasive surgery for this special type of endplate fracture.
Chronic low back pain commonly originates from the intervertebral disc, facet joint, sacroiliac joint and other spinal anatomic structures. Any spinal structures that are innervated by nerves could become source of pain if tissue damage occurs. According to previous studies, SNs could cause severe back pain through the release of inflammatory mediators or cause adjacent endplate fractures [7, 12]. Although the precise relationship between SNs and back pain remain unclear, a specific subgroup of patients with SNs whose spinal MRI showed a high signal intensity on fat-suppression sequences in the vertebral endplate surrounding the SNs, appear to have severe low back pain that originated from the edematous vertebral endplate[18–24]. The same signal changes in MRI images was defined as inclusion criteria in our study.
An array of studies attempted to elaborate the possible etiology of SN development. To-date, no consensus has been reached. Recent studies show that SNs development may be related to subchondral osteonecrosis of the endplate followed by disc materials protruding into the weakened vertebral endplate [7]. Others suggest that SNs correspond to an abnormal development of the vertebra blood vessels. The abnormal presence of vertebral vessels in the adult population may weaken the vertebral endplate, resulting in development of SNs [8]. Observational imaging study have demonstrated a possible relationship between vertebral fractures and SNs. Patients with a history of vertebral fractures during childhood were at increased risk of developing SNs at the index fracture level[15].
Based on previous studies, patients with painful SNs who are refractory to conservative treatment show improvement through several surgical procedures including discoblock, percutaneous vertebroplasty, spinal fusion, and tumor necrosis factor alpha (TNF-a) inhibition [18–26]. The use of these surgical options is based on the causative factors of low back pain, generated from endplate fractures or from degenerative disc materials that result in a special type of discogenic back pain.
SNs could cause chronic back pain through inflammatory mediators and cytokines, which are produced by degenerative disc (annulus rupture) and osteonecrosis of the endplate [26]. Pathophysiological mechanisms of painful SNs are identified with the degenerative disc diseases, resulting in a special type of discogenic back pain, in which provocative discography is typically positive and spinal MRI shows a low signal intensity on T1WI, and a high signal intensity on T2WI (Mordic-I change), indicating degenerative changes of the disc material[25]. Surgical procedures including spinal fusion and discoblock can be used to manage this type of painful SN[25, 26].
Another mechanism of painful SNs are associated with occult trabecular bone fractures in the endplate around the SNs. In the general population, the vertebral body and endplate are composed of trabecular bones. However, for some patients with SNs, the normal trabecular bony structure is impaired due to subchondral osteonecrosis or traumatic history [7, 8, 15]. It is important to note the characteristic changes in spine MRI. Impaired endplates around the SNs usually result in high signal intensity on fat-suppression sequences of spine MRI, indicating an acute stage of bone marrow edema, similar to the pathophysiological changes observed for vertebral compression fractures. Instability, inflammatory mediators, and mechanical pressure over the oedematous endplate can induce acute and severe back pain [12]. A long term improvement of vertebroplasty in patients with osteoporotic fractures has been shown [27–29]. To-date, a paucity of studies have reported the outcome of this specific subgroup of painful SNs with endplate fractures treated by vertebroplasty[18–24].
Painful SNs treated by PVP were first described in 2006 by Masala and colleagues in 18 patients with SNs who showed an improvement in their back pain after PVP [22]. Subsequently, Markus Wenger and coworkers reported a case of painful SNs treated by PVP under computer navigation to access the node without entering the cavity of the SNs [20]. Recently, Sun Zhi-Yong and colleagues reported 32 patients who were successfully treated with Percutaneous Balloon Kyphoplasty (PKP). The height of the vertebral body restoration and functional improvements were maintained during a mean follow-up period of 5 years [19]. Some studies suggested to insert the working cannulas directed towards the apex of the SNs to fill the polymethylmethacrylate (PMMA) around the profile of the SNs in an eggshell shape [18, 21]. However, studies highlighting these procedures are limited to retrospective studies study [18–24]. Hence, In our study, we treated 65 patients with severe back pain by PVP that were suspected to be secondary to fresh endplate fractures (with high signal intensity on fat-suppression sequences in spinal MRI) around SNs. Clinical data from these patients was prospectively collected. The VAS and ODI scores significantly improved after PVP, and were well maintained in the mean post-operative follow-up of 14.82 months. Cement leak into the disc space occurred in 5 patients (7.7%) without symptomatic leakage. Adjacent segment refractures occurred in 2 patients (3.1%), and all were managed successfully after secondary PVP procedures. No other surgical complications were found.
Endplate fractures around the SNs differ from those of common osteoporotic vertebral compression fractures. In our experience, surgical technique tips and specific radiographic change should be paid more attention to. Firstly, fresh endplate fractures must be confirmed by preoperative magnetic resonance imaging (MRI) with high signal intensity on fat-suppression sequences around SNs. For the surgical technique, cement should be injected towards the high signal intensity on fat-suppression sequences area in the endplate around the SN to stabilize and fill the occult trabecular bone fracture. This tough eggshell shaped cement around the SNs can prevent progression of SNs and minimize refractures of the endplate. In the period of PMMA injection, surgeon should perform carefully and gently with frequent X-ray imaging examinate to evaluate the diffusion of cement and prevent cement leakage.
To our knowledge, this is the first prospective study that has reported the outcome of the use of PVP for the treatment of fresh endplate fractures around the SNs. However, small series cases were included in our study, hence, a prospective study with large sample should be performed to investigate our results.