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The circadian clock controls bone remodelling

Nature Reviews Rheumatology volume 12, pages 132–133 (2016)Cite this article

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Systemic inactivation of Bmal1 in mice (Bmal1−/− mice) led to impaired longitudinal bone growth, which was associated with an early closure of the growth plate. This finding suggests that BMAL1 regulates chondrocyte functioning during ageing and extends on its previously described role in development and pathology. In addition, Bmal1−/− mice have a low bone mass owing to reduced trabecular and cortical thickness. The observed osteopenia in Bmal1−/− mice can be explained by a defect in osteoblast differentiation. Histological examination of bones of aged Bmal1−/− mice revealed fewer active osteoblasts and osteoctyes, in comparison with wild-type mice. “Given the prominent role of osteocytes in mechanosensing and bone remodelling, it is reasonable to hypothesize that the reduction in osteocytes affects the overall skeletal physiology,” explains Kondratov. In vitro differentiation of mesenchymal stem cells into mature osteoblasts was also impaired by Bmal1 deficiency, suggesting that BMAL1 has a cell-autonomous role in bone formation.

The observed osteopenia in Bmal1−/− mice can be explained by a defect in osteoblast differentiation

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References

  1. Samsa, W. E. Deficiency of circadian clock protein BMAL1 in mice results in a low bone mass phenotype. Bone 84, 194–203 (2016)

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  1. Nature Reviews Disease Primers,

    Liesbet Lieben

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  1. Liesbet Lieben
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Lieben, L. The circadian clock controls bone remodelling. Nat Rev Rheumatol 12, 132–133 (2016). https://doi.org/10.1038/nrrheum.2016.10

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