Bone Metabolism and Remodeling During Lactation

Bone metabolism during lactation represents a finely tuned balance of cellular and molecular processes that ensure adequate milk calcium supply while maintaining skeletal integrity. In response to the substantial calcium demand imposed by milk production, the maternal skeleton undergoes accelerated remodelling: osteoclast-mediated bone resorption increases markedly, mobilising mineral stores, while osteoblast-driven formation may be temporarily uncoupled from resorption. Circulating levels of parathyroid hormone-related protein (PTHrP) rise in concert with declines in oestrogen and insulin-like growth factor I, driving osteoclast differentiation and activity. The resulting demineralisation primarily affects trabecular compartments but extends to cortical bone, altering microarchitecture and reducing bone density.

Post-weaning, a coordinated reversal restores mineral homeostasis as osteoblast activity predominates, facilitating recovery of bone mass. Recent insights highlight an immuno-endocrine crosstalk in which memory T-cells and cytokines such as TNFα and IL-17A further modulate bone turnover. Nutritional factors—particularly dietary protein—also influence the pace and extent of skeletal regrowth. Disruption of these recovery mechanisms, whether by undernutrition, advanced maternal age or hormonal dysregulation, can predispose to persistent bone fragility. Elucidating the signalling networks governing lactation-induced bone turnover has global implications for maternal health, informing dietary guidelines and targeted strategies to preserve long-term skeletal resilience.

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Bone Metabolism and Remodeling During Lactation publication trend

The graph below shows the total number of articles in bone metabolism and remodeling during lactation across all publications each year (not limited to Nature Index journals).

Technical terms

Bone remodelling: Continuous process of bone resorption by osteoclasts and formation by osteoblasts to maintain skeletal strength.

Osteoclast: Multinucleated cell responsible for bone resorption and mineral release.

Osteoblast: Bone-forming cell that secretes matrix and promotes mineralisation.

Parathyroid hormone-related protein (PTHrP): Hormone produced by the mammary gland that stimulates bone resorption during lactation.

Trabecular bone: Spongy, porous bone found at the ends of long bones and within vertebrae, highly responsive to metabolic changes.

Cortical bone: Dense outer layer of bone providing structural support and protection.

Micro-computed tomography (micro-CT): High-resolution imaging technique for quantitative analysis of bone microarchitecture.

Insulin-like growth factor I (IGF-I): Growth factor that promotes bone formation and influences osteoblast activity.

References

1. Memory T-Cells Contribute to Calcium Release from Bones during Lactation in Mice. Nutrients (2024).
2. Recovery of the maternal skeleton after lactation is impaired by advanced maternal age but not by reduced IGF availability in the mouse. PLOS ONE (2021).
3. Low protein intake during reproduction compromises the recovery of lactation‐induced bone loss in female mouse dams without affecting skeletal muscles. The FASEB Journal (2020).