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Table 1 TNF and RANKL blockade differently alter local bone turnover in hTNF-transgenic mice

From: Imbalance of local bone metabolism in inflammatory arthritis and its reversal upon tumor necrosis factor blockade: direct analysis of bone turnover in murine arthritis

Mice OcPm/BPm (%) ObPm/BPm (%) NOc/BPm (cells/mm) NOb/BPm (cells/mm)
Untreated hTNFtg     
   Subchondral bone erosion 26 ± 2 5 ± 2 13.5 ± 1.1 2.5 ± 0.8
   Cortical bone channels 22 ± 1 25 ± 2 9.5 ± 0.7 11.4 ± 1.0
   Endosteal bone surface 1 ± 1 4 ± 1 1.2 ± 0.2 1.4 ± 0.3
OPG-treated hTNFtg     
   Subchondral bone erosion 1 ± 1 0 0.6 ± 0.4 0
   Cortical bone channels 1 ± 1 1 ± 1 0.4 ± 0.4 0.2 ± 0.2
   Endosteal bone surface 0 0 0 0
Anti-TNF treated hTNFtg     
   Subchondral bone erosion 3 ± 3 36 ± 5 4.1 ± 1.2 48.3 ± 11.4
   Cortical bone channels 9 ± 2 43 ± 10 8.7 ± 3.3 26.1 ± 7,2
   Endosteal bone surface 1 ± 1 4 ± 1 2.5 ± 1.2 10.9 ± 5.4
  1. Results presented as the mean ± standard error of the mean. Paw sections of transgenic for human tumor necrosis factor (hTNFtg) mice treated for six weeks with a neutralizing antibody against TNF (anti-TNF) or osteoprotegerin (OPG) were stained for functional osteoclasts and osteoblasts. The fraction of bone surface covered by osteoclasts and osteoblasts (OcPm/BPm, ObPm/BPm) and the numbers of osteoclasts and osteoblasts per bone perimeter (NOc/BPm, NObPm) were assessed and allocated to three skeletal compartments.