The role of the P2X7 receptor on bone loss in a mouse model of inflammation-mediated osteoporosis
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The role of the P2X7 receptor on bone loss in a mouse model of inflammation-mediated osteoporosis. / Kvist, T. M.; Syberg, S.; Petersen, S.; Ding, M.; Jørgensen, N. R.; Schwarz, P.
In: Bone Reports, Vol. 7, 12.2017, p. 145-151.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - The role of the P2X7 receptor on bone loss in a mouse model of inflammation-mediated osteoporosis
AU - Kvist, T. M.
AU - Syberg, S.
AU - Petersen, S.
AU - Ding, M.
AU - Jørgensen, N. R.
AU - Schwarz, P.
PY - 2017/12
Y1 - 2017/12
N2 - In inflammatory autoimmune diseases, bone loss is frequent. In most cases, secondary osteoporosis is caused by treatment with systemic glucocorticoid. However, the pathogenesis behind the bone loss is presumed multifactorial. We aimed to elucidate the role of the P2X7 receptor on bone mineral density (BMD), microarchitecture, and bone strength in a standardized mouse model of inflammation-mediated osteoporosis (IMO). In total 146 mice completed our protocol, 70 wild type (WT) mice and 76 P2X7 −/− (knockout, KO). BMD at the femur and spine decreased significantly from baseline to day 20 in the WT IMO mice (p < 0.01). In the WT vehicle, KO vehicle and KO IMO, no significant BMD changes were found. Bone strength showed a lower mid-shaft max strength (p = 0.038) and also a non-significant trend towards lower strength at the femoral neck of the WT IMO group. Trabecular bone volume fraction (BV/TV) and connectivity density (CD) after 20 days were significantly decreased in the WT IMO group (p = 0.001). In contrast, the WT vehicle and KO vehicle, BV/TV and CD did no change at 20 days. Cortical bone revealed no significant microarchitectural changes after 20 days in the WT IMO group, whereas the total cortical area increased significantly in WT vehicle and KO IMO after 20 days (5.2% and 8.8%, respectively). In conclusion, the P2X7 receptor KO mice did not respond to inflammation with loss of BMD whereas the WT mice had a significant loss of BMD, bone strength and trabecular microarchitecture, demonstrating a role for the P2X7 receptor in inflammatory bone loss.
AB - In inflammatory autoimmune diseases, bone loss is frequent. In most cases, secondary osteoporosis is caused by treatment with systemic glucocorticoid. However, the pathogenesis behind the bone loss is presumed multifactorial. We aimed to elucidate the role of the P2X7 receptor on bone mineral density (BMD), microarchitecture, and bone strength in a standardized mouse model of inflammation-mediated osteoporosis (IMO). In total 146 mice completed our protocol, 70 wild type (WT) mice and 76 P2X7 −/− (knockout, KO). BMD at the femur and spine decreased significantly from baseline to day 20 in the WT IMO mice (p < 0.01). In the WT vehicle, KO vehicle and KO IMO, no significant BMD changes were found. Bone strength showed a lower mid-shaft max strength (p = 0.038) and also a non-significant trend towards lower strength at the femoral neck of the WT IMO group. Trabecular bone volume fraction (BV/TV) and connectivity density (CD) after 20 days were significantly decreased in the WT IMO group (p = 0.001). In contrast, the WT vehicle and KO vehicle, BV/TV and CD did no change at 20 days. Cortical bone revealed no significant microarchitectural changes after 20 days in the WT IMO group, whereas the total cortical area increased significantly in WT vehicle and KO IMO after 20 days (5.2% and 8.8%, respectively). In conclusion, the P2X7 receptor KO mice did not respond to inflammation with loss of BMD whereas the WT mice had a significant loss of BMD, bone strength and trabecular microarchitecture, demonstrating a role for the P2X7 receptor in inflammatory bone loss.
KW - BMD
KW - IMO
KW - Inflammation
KW - Microarchitecture
KW - Osteoporosis
KW - P2X7
U2 - 10.1016/j.bonr.2015.09.003
DO - 10.1016/j.bonr.2015.09.003
M3 - Journal article
C2 - 29276731
AN - SCOPUS:85032881872
VL - 7
SP - 145
EP - 151
JO - Bone Reports
JF - Bone Reports
SN - 2352-1872
ER -
ID: 191189824