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AGEING

Bone inflamm-ageing

Nature Reviews Rheumatology volume 15, page 252 (2019)Cite this article

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Bone regeneration and fracture repair mechanisms are compromised as people age. One mechanism to account for this decline is that skeletal stem and progenitor cells (SSPCs) are more prone to differentiate into fat-producing adipocytes than into bone-producing osteoblasts. New research indicates that this switch in SSPC differentiation occurs as a result of chronic inflammation that develops as we age.

Leucht and his team took bone samples from patients undergoing fracture fixation surgery (see image) and found an association between low SSPC number and a slow time to fracture union. This finding was replicated in a mouse tibial monocortical defect model, with better bone regeneration and a greater number of SSPCs in young (12 weeks) mice than in middle-aged (52 weeks) mice.

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  1. Nature Reviews Rheumatology http://www.nature.com/nrrheum/

    Nicholas J. Bernard

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  1. Nicholas J. Bernard
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Correspondence to Nicholas J. Bernard.

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Bernard, N.J. Bone inflamm-ageing. Nat Rev Rheumatol 15, 252 (2019). https://doi.org/10.1038/s41584-019-0216-8

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