Abstract
Systemic lupus erythematosus (SLE), a chronic inflammatory autoimmune disease, is characterized by loss of B‐cell tolerance to autoantigens. SLE patients are at increased risk for osteoporosis. Mice lacking Fc gamma receptor IIb (Fc©RIIB) exhibit SLE and its restoration rescues the disease. To determine whether deletion of Fc©RIIB induces osteopenia, we analyzed a skeletal phenotype of Fc©RIIB knockouts at 3, 6 and 10 months old. The analysis of anti‐dsDNA antibodies indicated that mice deficient in Fc©RIIB developed spontaneous SLE at 6 months of age. μCT analysis showed that deletion of Fc©RIIB had no effect on cortical and cancellous bone at 3 months of age. In contrast, 6‐ and 10‐month‐old Fc©RIIB −/− males were osteopenic and a severity of bone loss increased with disease duration. Deletion of Fc©RIIB decreased cortical bone area and cancellous bone volume with increased structural model index. Histomorphometry indicated a decrease in cancellous bone volume, trabecular thickness and trabecular number with concomitant increase in trabecular separation in Fc©RIIB−/− males. Ablation of Fc©RIIB increased osteoclast number without any change in osteoblast number. A skeletal phenotype was milder in females. Deletion of Fc©RIIB increased osteoclast differentiation but did not alter alkaline phosphatase activity and mineralization. Breaking strength parameters, including J, Imax, Imin, Imin/Cmin, and Imax/Cmax were decreased in Fc©RIIB deficient mice compared to WT controls. Our data indicate that Fc©RIIB contributes to the regulation of bone turnover and homeostasis subsequent to SLE and that absence of Fc©RIIB induces osteopenia and decreases breaking strength.Support or Funding InformationThe Ratchadapisek Sompoch Endowment Fund (2014, CU‐57‐091‐IC) and the Faculty of Dentistry, Chulalongkorn UniversityThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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