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NAD⁺ & NMN
Research brief

NMN-releasing scaffold tested for aged bone repair in rats

In an abstract, researchers describe a proposed two-part bioceramic scaffold that slowly releases NMN and manganese ions; in aged rats with femoral condyle defects it was reported to promote new bone formation and maturation. [1]

Automatic summary · not editorially reviewed

The key findings

  1. The proposed scaffold combines an outer 3D-printed β-tricalcium phosphate hollow tube with an inner freeze-cast manganese-doped tricalcium phosphate rod loaded with NMN. [1]

  2. The authors report the scaffold restored intracellular NAD levels, improved mitochondrial structure and function, and scavenged excess reactive oxygen species. [1]

  3. In aged rats with femoral condyle defects, scaffold implantation reportedly significantly promoted new bone formation and maturation. [1]

The source at a glance

Study type / format
Abstract of a preclinical biomaterial study
Population / context
Aged rats with femoral condyle defects, plus cells in laboratory experiments as described in the abstract.
Summary based on
Study abstract
Original publication
June 27, 2026

Proposed scaffold design for senescent bone

The authors propose a strategy they call senescent metabolism reprogramming. The hierarchical scaffold has an outer 3D-printed β-tricalcium phosphate hollow tube and an inner freeze-cast manganese-doped tricalcium phosphate ceramic rod loaded with nicotinamide mononucleotide (NMN). They say current biomaterial approaches mainly give passive mechanical support or deliver therapeutic factors and do not reverse this pathological microenvironment.

Supporting source [1]

Reported cell and rat findings

During aged bone repair the scaffold is described as releasing NMN and manganese ions over time, aimed at NAD metabolic imbalance and oxidative stress. The authors report it restored intracellular NAD levels, improved mitochondrial structure and function, and scavenged excess reactive oxygen species. This was said to alleviate cellular senescence and, together with inhibited inflammatory responses, promote osteogenic differentiation. In aged rats with femoral condyle defects, implantation reportedly significantly promoted new bone formation and maturation.

Supporting source [1]

Abstract-only scope of this work

The text presents the scaffold as a proposed strategy and reports results without giving sample sizes, follow-up periods or effect sizes. The bone-repair findings come from aged rats with femoral condyle defects, not from people. The abstract does not establish that the approach treats senescence-related diseases in humans; the authors describe that as a future direction. The full text was not reviewed.

Supporting source [1]

How to interpret this

Abstract only; the full text was not reviewed. No sample sizes, follow-up periods or effect sizes are reported. Bone-repair results are from aged rats with femoral condyle defects, not humans, and the scaffold is presented as a proposed strategy.

Based on the study abstract; the full paper, tables and supplementary data were not reviewed.

Source & supporting passages

Read the quoted passagesIn the language of the original source
  1. Finding 1 ↑

    an outer 3D-printed β-tricalcium phosphate (β-TCP) hollow
  2. Finding 2 ↑

    restore intracellular NAD levels for reversing senescence-induced
  3. Finding 3 ↑

    significantly promoted new bone formation and maturation

AI-assisted summary with linked source passages. No independent editorial or clinical review.

Our editorial method

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