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TNF is required for the induction but not the maintenance of compression-induced BME signals in murine tail vertebrae: limitations of anti-TNF therapy for degenerative disc disease.

Publication ,  Journal Article
Papuga, MO; Kwok, E; You, Z; Rubery, PT; Dougherty, PE; Pryhuber, G; Beck, CA; Hilton, MJ; Awad, HA; Schwarz, EM
Published in: J Orthop Res
September 2011

While bone marrow edema (BME) is diagnostic of spondyloarthropathy, its nature remains poorly understood. In contrast, BME in ankylosing spondylitis is caused by tumor necrosis factor (TNF)-induced vascular and cellular changes. To investigate the relationship between chronic compression and TNF signaling in compression-induced BME we utilized a tail vertebrae compression model with WT, TNF-Tg, and TNFR1&2-/- mice to evaluate: (i) healing following release of chronic compression, (ii) induction of BME in the absence of TNFR, and (iii) efficacy of anti-TNF therapy. Compression-induced normalized marrow contrast enhancement (NMCE) in WT was significantly decreased threefold (p < 0.01) within 2 weeks of release, while the NMCE values in TNF-Tg vertebrae remained elevated, but had a significant decrease (p < 0.05) by 6 weeks after the release of compression. TNFR1&2-/- mice were resistant to compression-induced BME. Anti-TNF therapy did not affect NMCE versus placebo. Histological examination revealed that NMCE values significantly correlated with marrow vascularity and cellularity (p < 0.05), which account for 76% of the variability of NMCE. Collectively, these data demonstrate a critical role for TNF in the induction of chronic compression-induced BME, but not in its maintenance. Amelioration of BME is achieved through biomechanical stability, but is not affected by anti-TNF therapy.

Duke Scholars

Published In

J Orthop Res

DOI

EISSN

1554-527X

Publication Date

September 2011

Volume

29

Issue

9

Start / End Page

1367 / 1374

Location

United States

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • Tail
  • Stress, Mechanical
  • Spine
  • Recovery of Function
  • Orthopedics
  • Mice, Knockout
  • Mice, Inbred C57BL
  • Mice
  • Male
 

Citation

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Papuga, M. O., Kwok, E., You, Z., Rubery, P. T., Dougherty, P. E., Pryhuber, G., … Schwarz, E. M. (2011). TNF is required for the induction but not the maintenance of compression-induced BME signals in murine tail vertebrae: limitations of anti-TNF therapy for degenerative disc disease. J Orthop Res, 29(9), 1367–1374. https://doi.org/10.1002/jor.21370
Papuga, M Owen, Edmund Kwok, Zhigang You, Paul T. Rubery, Paul E. Dougherty, Gloria Pryhuber, Christopher A. Beck, Matthew J. Hilton, Hani A. Awad, and Edward M. Schwarz. “TNF is required for the induction but not the maintenance of compression-induced BME signals in murine tail vertebrae: limitations of anti-TNF therapy for degenerative disc disease.J Orthop Res 29, no. 9 (September 2011): 1367–74. https://doi.org/10.1002/jor.21370.
Papuga MO, Kwok E, You Z, Rubery PT, Dougherty PE, Pryhuber G, Beck CA, Hilton MJ, Awad HA, Schwarz EM. TNF is required for the induction but not the maintenance of compression-induced BME signals in murine tail vertebrae: limitations of anti-TNF therapy for degenerative disc disease. J Orthop Res. 2011 Sep;29(9):1367–1374.
Journal cover image

Published In

J Orthop Res

DOI

EISSN

1554-527X

Publication Date

September 2011

Volume

29

Issue

9

Start / End Page

1367 / 1374

Location

United States

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • Tail
  • Stress, Mechanical
  • Spine
  • Recovery of Function
  • Orthopedics
  • Mice, Knockout
  • Mice, Inbred C57BL
  • Mice
  • Male