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Bone loss after ovariectomy: the role of RANKL production by B cells


At the age of 7 months, transgenic mice bred to possess B or T lymphocytes incapable of producing RANKL showed similar bone mass to control mice with RANKL-expressing B or T lymphocytes. This suggests that RANKL expressed by B or T lymphocytes does not impact on osteoclastogenesis during mouse development or growth to maturity.

After ovariectomy both sets of knockout mice showed a decrease in bone mineral density at the spine and femur, but the vertebral bone loss was significantly less in mice with B cells that could not produce RANKL. B cell-RANKL knockout mice showed reduced expansion of osteoclasts, which protected them from cancellous bone loss but bone loss still occurred in cortical bone at the same level as controls.

The authors conclude that RANKL expression by mouse lymphocytes does not play a central role in basal bone remodeling. Specific B lymphocyte RANKL expression does partially protect against bone loss due to sex steroid deficiency, but only in the cancellous bone compartment.

Editor's comment: Osteoblasts and T cells are known to be major sources of the indispensable osteoclast-activating factor RANKL. Yet B cells and osteocytes also produce RANKL; the latter were recently shown to play a major role in post-natal bone remodeling. The current study adds to the growing body of evidence showing that different cells control RANKL-mediated bone remodeling in various compartments and under varying hormonal conditions.

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