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Ki Young Lee, Jung-Hee Lee, Kyung-Chung Kang, Sung Joon Shin, Won Ju Shin, Sang-Kyu Im and Joon Hong Park


Maintaining lumbosacral (LS) arthrodesis and global sagittal balance after long fusion to the sacrum remains an important issue in the surgical treatment for adult spinal deformity (ASD). The importance and usefulness of LS fixation have been documented, but the optimal surgical long fusion to the sacrum remains a matter for debate. Therefore, the authors performed a retrospective study to evaluate fusion on CT scans and the risk factors for LS pseudarthrosis (nonunion) after long fusion to the sacrum in ASD.


The authors performed a retrospective study of 59 patients with lumbar degenerative kyphosis (mean age 69.6 years) who underwent surgical correction, including an interbody fusion of the L5–S1, with a minimum 2-year follow-up. Achievement of LS fusion was evaluated by analyzing 3D-CT scans at 3 months, 6 months, 9 months, 1 year, and 2 years after surgery. Patients were classified into a union group (n = 36) and nonunion group (n = 23). Risk factors for nonunion were analyzed, including patient and surgical factors.


The overall fusion rate was 61% (36/59). Regarding radiological factors, optimal sagittal balance at the final follow-up significantly differed between two groups. There were no significant differences in terms of patient factors, and no significant differences with respect to the use of pedicle subtraction osteotomy, the number of fused segments, the proportion of anterior versus posterior interbody fusion, S2 alar iliac fixation versus conventional iliac fixation, or loosening of sacral or iliac screws. However, the proportion of metal cages to polyetheretherketone cages and the proportion of sacropelvic fixation were significantly higher in the union group (p = 0.022 and p < 0.05, respectively).


LS junction fusion is crucial for global sagittal balance, and the use of iliac screws in addition to LS interbody fusion using a metal cage improves the outcomes of long fusion surgery for ASD patients.

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Bum-Joon Kim, Junseok W. Hur, Jong Soo Park, Joo Han Kim, Taek-Hyun Kwon, Youn-Kwan Park and Hong Joo Moon


An in vitro study was performed to understand the potential roles of matrix metalloproteinase (MMP)-2 and MMP-9 in the elastin degradation of human ligamentum flavum (LF) cells via treatment with tumor necrosis factor-α (TNFα) and interleukin-1β (IL-1β). Previous studies have identified a decreased elastin to collagen ratio in hypertrophic LF. Among the extracellular matrix remodeling endopeptidases, MMP-2 and MMP-9 are known to have elastolytic activity. The hypothesis that activated LF cells exposed to inflammation would secrete MMP-2 and MMP-9, thereby resulting in elastin degradation, was examined.


To examine MMP-2 and MMP-9 expression in human LF, cells were isolated and cultured from LF tissues that were obtained during lumbar disc surgery. Isolated LF cells were equally divided into 3 flasks and subcultured. Upon cellular confluency, the LF cells were treated with TNFα, IL-1β, or none (as a control) and incubated for 48 hours. The conditioned media were collected and assayed for MMP-2 and MMP-9 using gelatin zymography and Western blot analysis. The electrophoresis bands were compared on densitometric scans using ImageJ software.


The conditioned media from the isolated human LF cells naturally expressed 72-kD and 92-kD gelatinolytic activities on gelatin zymography. The IL-1β-treated LF cells presented sustained increases in the proenzyme/zymogen forms of MMP−2 and −9 (proMMP-2 and proMMP-9), and activeMMP-9 expression (p = 0.001, 0.022, and 0.036, respectively); the TNFα-treated LF cells showed the most elevated proMMP9 secretion (p = 0.006), as determined by Western blot analyses. ActiveMMP-2 expression was not observed on zymography or the Western blot analysis.


TNFα and IL-1β promote proMMP-2 and proMMP-9 secretion. IL-1β appears to activate proMMP-9 in human LF cells. Based on these findings, selective MMP-9 blockers or antiinflammatory drugs could be potential treatment options for LF hypertrophy.