BACKGROUND: More and more attention has been focused on the inflammation or degeneration caused by biochemical factors in radiculopathy during lumbar facet joint degeneration. This study was designed to examine the expression and relationship of MMP-1/TIMP-1 and interleukin-1β (IL-1β), and to analyze the possible mechanism in degenerative lumbar facet joint disease. METHODS: Lumbar facet joint cartilage and synovial tissues in 36 cases of posterior lumbar surgery were harvested to investigate IL-1β and MMP-1/TIMP-1 by immunohistochemistry and Western blot analysis. Double labeling immunofluorescence and real-time PCR, respectively, were used to assess the relationship between IL-1β and MMP-1. RESULTS: IL-1β and MMP-1 were low in the lumbar disc herniation (LDH) group, and increased markedly in the lumbar spinal canal stenosis (LSCS) group (P < 0.05). However, there is no significant difference of TIMP-1 between LDH group and LSCS group (P > 0.05). Double staining results indicated that IL-1β overlapped with MMP-1 in the LSCS group. Moreover, real-time PCR results showed that MMP-1 mRNA in chondrocytes in vitro was affected in a dose- and time-dependent manner in response to IL-1β stimulation. CONCLUSIONS: Overexpression of MMP-1, induced by IL-1β, plays an important role in the inflammatory process of lumbar facet joint degeneration.
BACKGROUND: More and more attention has been focused on the inflammation or degeneration caused by biochemical factors in radiculopathy during lumbar facet joint degeneration. This study was designed to examine the expression and relationship of MMP-1/TIMP-1 and interleukin-1β (IL-1β), and to analyze the possible mechanism in degenerative lumbar facet joint disease. METHODS: Lumbar facet joint cartilage and synovial tissues in 36 cases of posterior lumbar surgery were harvested to investigate IL-1β and MMP-1/TIMP-1 by immunohistochemistry and Western blot analysis. Double labeling immunofluorescence and real-time PCR, respectively, were used to assess the relationship between IL-1β and MMP-1. RESULTS: IL-1β and MMP-1 were low in the lumbar disc herniation (LDH) group, and increased markedly in the lumbar spinal canal stenosis (LSCS) group (P < 0.05). However, there is no significant difference of TIMP-1 between LDH group and LSCS group (P > 0.05). Double staining results indicated that IL-1β overlapped with MMP-1 in the LSCS group. Moreover, real-time PCR results showed that MMP-1 mRNA in chondrocytes in vitro was affected in a dose- and time-dependent manner in response to IL-1β stimulation. CONCLUSIONS: Overexpression of MMP-1, induced by IL-1β, plays an important role in the inflammatory process of lumbar facet joint degeneration.