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Ncf1 affects osteoclast formation but is not critical for postmenopausal bone loss

Artikel i vetenskaplig tidskrift
Författare Alexandra Stubelius
Annica Andersson
R. Holmdahl
Claes Ohlsson
Ulrika Islander
Hans Carlsten
Publicerad i BMC Musculoskeletal Disorders
Volym 17
Nummer/häfte 1
Sidor 1-7
ISSN 1471-2474
Publiceringsår 2016
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Centre for Bone and Arthritis Research
Institutionen för medicin, avdelningen för invärtesmedicin och klinisk nutrition
Sidor 1-7
Språk en
Länkar dx.doi.org/10.1186/s12891-016-1315-...
Ämnesord Bone mineral density, Estrogen Deficiency, Ncf1, Neutrophil cytosolic factor 1, NOX 2, Osteoclasts, Osteoimmunology, Postmenopausal bone loss, Pre-osteoclasts, Reactive Oxygen Species
Ämneskategorier Reumatologi och inflammation, Immunologi inom det medicinska området

Sammanfattning

Background: Increased reactive oxygen species and estrogen deficiency contribute to the pathophysiology of postmenopausal osteoporosis. Reactive oxygen species contribute to bone degradation and is necessary for RANKL-induced osteoclast differentiation. In postmenopausal bone loss, reactive oxygen species can also activate immune cells to further enhance bone resorption. Here, we investigated the role of reactive oxygen species in ovariectomy-induced osteoporosis in mice deficient in Ncf1, a subunit for the NADPH oxidase 2 and a well-known regulator of the immune system. Methods: B10.Q wild-type (WT) mice and mice with a spontaneous point mutation in the Ncf1-gene (Ncf1*/*) were ovariectomized (ovx) or sham-operated. After 4 weeks, osteoclasts were generated ex vivo, and bone mineral density was measured using peripheral quantitative computed tomography. Lymphocyte populations, macrophages, pre-osteoclasts and intracellular reactive oxygen species were analyzed by flow cytometry. Results: After ovx, Ncf1*/*-mice formed fewer osteoclasts ex vivo compared to WT mice. However, trabecular bone mineral density decreased similarly in both genotypes after ovx. Ncf1*/*-mice had a larger population of pre-osteoclasts, whereas lymphocytes were activated to the same extent in both genotypes. Conclusion: Ncf1*/*-mice develop fewer osteoclasts after ovx than WT mice. However, irrespective of genotype, bone mineral density decreases after ovx, indicating that a compensatory mechanism retains bone degradation after ovx. © 2016 The Author(s).

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