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

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

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

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.

ISSN: 1478-6362