Indirect decompression using anterior lumbar interbody fusion (ALIF) for lumbar degenerative spondylolisthesis has been reported [1]. Symptoms from lumbar degenerative spondylolisthesis are a result of vertebral slipping and the thickening and flexure of the ligamentum flavum. Anterior fusion restores disc height and stretches the flexure of the ligamentum flavum, and consequently, the diameter of the spinal canal increases.

We have previously reported 39 cases of patients who underwent noninstrumented stand-alone ALIF for degenerative spondylolisthesis; 29 of these patients had more than 10 years of follow-up [1]. More than 75% of the patients showed satisfactory long-term clinical results [1].

A minimally invasive lateral transpsoas approach to the lumbar spine, also known as extreme lateral interbody fusion (XLIF), has been introduced. XLIF can be used to gain access to the lumbar spine via the psoas major muscle using a direct lateral approach [2]. Furthermore, mini-open anterior retroperitoneal lumbar interbody fusion methods, such as oblique lumbar interbody fusion (OLIF) have been recently applied [345]. Both procedures achieve indirect decompression and correction of sagittal and coronal alignment for lumbar degenerative spondylolisthesis [2345].

Two investigators reported radiographic changes after indirect decompression using magnetic resonance imaging (MRI) and results of stand-alone XLIF surgery and OLIF plus posterior pedicle screw fixation [67]. The cross-sectional area (CSA) of the dural sac was measured pre- and postoperatively. In 19 of the 21 patients, the MRI showed that the XLIF procedure without posterior fixation provided good surgical results and enlargement of the spinal canal after surgery [6]. Substantial improvement was found in all measured variables, with increases of 33.1% in central canal diameter [6]. In another study, the median CSA of the dural sac extension ratio was 30.2% after OLIF plus posterior pedicle screw fixation surgery in 28 patients, which correlated inversely with preoperative CSA [3]. In addition, the central canal diameter did not reach normal size after surgery based on measurements performed at pre- and postoperative time points [67]. As shown in Fig. 1, indirect decompression by OLIF for lumbar degenerative spondylolisthesis in our case could enlarge the spinal canal after surgery. However, the enlargement was not sufficient to lessen the thickness of the ligamentum flavum (Fig. 1). Nevertheless, there are no reports examining whether a change in ligamentum flavum thickness and the CSA of the dural sac occurs during long-term follow-up after anterior fusion surgery.

The aim of the present study was to determine if there is a change in the thickness of ligamentum flavum and the CSA of the dural sac 10 years after ALIF.

Written informed consent was obtained from each patient.

Table 1 shows the demographic characteristics of patients before and after surgery. Low back pain, leg pain, and leg numbness, as evaluated by VAS score, were significantly improved 10 years after surgery compared with before surgery. Evaluation of bone fusion is shown in Figs. 2, 3, 4. All 10 patients retained bone union at the final follow-up. Spinal fusion with correction loss (average, 4.75 mm anterior slip) was achieved in all patients 10 years after surgery.

The average CSAs of the dural sac and ligamentum flavum at L1–2 to L5–S1 were 150 mm² and 78 mm², respectively. The average CSA of the ligamentum flavum at L4–5 (30 mm² at fusion level) was significantly less than at levels L1–2 to L3–4, and L5–S1 (p<0.05). Although patients had an average of 4.75 mm anterior slip, the average CSA of the dural sac at the L4–5 fusion group was significantly larger than at other levels (p<0.05) (Figs. 2, 3, 4, 5, 6).

In the present study, stability of L4–L5 induced a change in the lumbar ligamentum flavum and a sustained remodeling of the spinal canal during a 10-year follow-up. These findings may explain the complete pain relief after indirect decompression fusion surgery in patients with long-term correction loss.

Posture induces physiological changes in the CSA of the spinal canal and neural foramina in young asymptomatic volunteers as seen using MRI [7]. At the disk level, the CSA of the spinal canal varied significantly depending on the body position, most notably between the upright flexed (mean, 268 mm²) and the upright extended (mean, 224 mm²) positions (p<0.0001) [7]. The maximum thickness of the ligamentum flavum was significantly increased in the extended positions (p<0.0001) [7].

Several authors have reported indirect decompression using a large stand-alone XLIF cage without posterior decompression or pedicle screws, and a stand-alone XLIF showed evidence of solid arthrodesis and improvements in clinical symptoms in more than 80% of patients [8]. Other investigators reported radiographic changes and clinical benefit of stand-alone XLIF surgery. In 19 of the 21 patients in their study, radiographs and MRI showed that the XLIF procedure without posterior fixation provided good surgical results and enlargement of the spinal canal after surgery [6]. Substantial improvement was found in all measured variables, with increases of 41.9% in average disk height, 13.5% in foraminal height, 24.7% in foraminal area, and 33.1% in central canal diameter [6]. Other investigators reported a significant increase in dural sac dimensions of 54% in the anterior–posterior plane and 48% in the medial-lateral plane after XLIF surgery plus fixation of percutaneous pedicle screws, either unilaterally or bilaterally, in 15 patients [9]. In addition, significant improvements in disk height and spinal canal area have been reported after OLIF plus posterior percutaneous screws without direct decompression [3]. The median CSA of the thecal sac extension ratio was 30.2% after OLIF plus posterior percutaneous pedicle screw fixation surgery in 28 patients, and this correlated inversely with preoperative CSA [3]. However, in three reports using MRI evaluations, the central canal diameter did not reach the normal size after surgery, with measurements performed pre- and postoperatively. However, to our knowledge, the change in ligamentum flavum thickness and CSA of dural sac occurring during long-term follow-up after anterior fusion surgery has not yet been reported.

In practice, ligamentum flavum hypertrophy is a multifactorial disease, closely associated with age, activity level, and the extent of mechanical stress [10]. Mechanical stress has been proposed to induce an inflammatory response that triggers ligamentum flavum hypertrophy [101112]. Some factors related to inflammatory response and fibrosis, such as tumor necrosis factor α, transforming growth factor β, connective tissue growth factor, platelet-derived growth factors, matrix metalloproteinases, and tissue inhibitors of matrix metalloproteinases, have been reported to be involved in the development of the hypertrophied ligamentum flavum [1314151617]. However, changes in ligamentum flavum hypertrophy by stabilization or as a result of anti-inflammatory drug use in clinical cases have not been reported.

We have reported that endplate abnormalities (Modic type 1 changes) are related to inflammation and axonal growth into abnormal bone marrow induced by cytokines, such as tumor necrosis factor α [18]. We performed posterior fixation without interbody fusion in patients with Modic type 1 signals before surgery. The Modic type 1 signals changed to normal bone marrow within 2 years of the surgery [19]. Considering the mechanism of ligamentum flavum hypertrophy and these reports about Modic changes, stabilization of the spine may induce an anti-inflammatory effect, and ultimately ligamentum flavum hypotrophy.

Bae et al. [20] have reported risk factors for adjacent segment degeneration (ASD) in 128 patients who underwent instrumented lumbar interbody fusion. Postoperative radiological data showed that further segmental lordosis is a significant risk factor for ASD. This suggests that a larger bone graft or cage can restore lumbar lordosis; however, ASD may be induced after ALIF surgery. In the current study, we observed changes of the ligamentum flavum at the fusion site. Thus, to prevent ASD, appropriate cages for indirect decompression and stability that are sufficient to reduce pain may be recommended.

The present study has the following limitations. First, it is a small retrospective study with a restricted number of patients. Second, the timing of the change of the lumbar ligamentum flavum and remodeling of the spinal canal during the 10 years after surgery is not known. It is also not known if similar changes of the lumbar ligamentum flavum and remodeling of the spinal canal have occurred in cases of nonunion. We could not compare MRI before and after surgery, because we do not have a full MRI set before surgery or early after surgery for all patients. Further studies are required to clarify these points.

In conclusion, the average CSA of the ligamentum flavum at the level of fusion 10 years after indirect decompression using ALIF was significantly less than that before surgery, and the CSA of the dural sac at the level of fusion was significantly larger than at other levels. Stability of the spine may have induced the change of the lumbar ligamentum flavum and remodeling of the spinal canal.