ABSTRACT
BACKGROUND: Meniscal injuries are a risk factor for osteoarthritis (OA). While a mechanical pathway between meniscal injury and OA has been described, the biological effects of inflammation on this pathway have yet to be clarified. The aim of our study was to compare levels of specific inflammatory mediators, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and nerve growth factor (NGF), in injured and uninjured meniscal tissue and related knee joint synovium. METHODS: Tissue samples were obtained from 19 patients, 31.1 ± 13.6 years old, who underwent arthroscopic partial meniscectomy. For analysis, tissue samples were categorized into the following groups: injured meniscal site (IM), non-injured meniscal site (NIM), synovium 'nearest' the lesion (NS), and synovium from the opposite knee compartment, 'farthest' synovium (FS). Levels of inflammatory mediators were determined using enzyme-linked immunosorbent assay and between-group differences (IM and NIM; NS and FS) were evaluated using the Wilcoxon signed-rank test. The association between pre-operative pain score and the level of each inflammatory mediator was evaluated using Spearman's correlation. RESULTS: Higher levels of TNF-α and IL-6 were identified in the IM tissue, compared to NIM (p <0.05). IL-6 levels were also higher in the NS compared to the FS (p <0.05). There was no correlation between pre-operative pain score and level of each inflammatory mediator. CONCLUSIONS: Our outcomes confirm a local increase in inflammatory mediator levels, in both meniscal and synovial tissue, which could contribute to development of OA. Management of these biological effects of meniscal injury might be warranted.
ABSTRACT
STUDY DESIGN: A histologic and histochemical study was performed both in the autopsy of a human patient with cervical spinal cord compression caused by ossification of the posterior longitudinal ligament and in a tiptoe-walking Yoshimura mouse model of progressive cervical cord compression. OBJECTIVES: To clarify the mechanism of destructive pathologic changes in the spinal cord under chronic mechanical compression. SUMMARY OF BACKGROUND DATA: Under chronic compression, the spinal cord exhibits destructive changes considered to be causes of profound and irreversible motor paresis. Recently, some investigators have found that apoptosis in acute spinal cord injury induces both secondary degeneration at the site of injury and chronic demyelination of tracts away from the site of injury. However, the mechanism responsible for these destructive spinal cord changes under chronic compression remains unclear. METHODS: The spinal cord was examined histologically, and an attempt was made to detect apoptotic cells using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling in both the autopsy of a human patient and tiptoe-walking mice exhibiting spinal cord compression. RESULTS: Apoptotic cells were observed in the chronically compressed spinal cord in both the autopsy of a human patient and model mice. In tiptoe-walking mice exhibiting spinal cord compression, descending degeneration in the anterior and lateral columns and ascending degeneration in the posterior column were observed. The distribution of oligodendrocytes with positive results from terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling was similar to that for degeneration of the long tracts. CONCLUSIONS: Spinal cord cell apoptosis may produce destructive changes in the spinal cord under chronic compression, with a resulting irreversible neurologic deficit.
