People recovering from broken bones are often told to stop smoking. Now new research explains why—and the reason may surprise you.

A study published in the American Journal of Translational Research suggests that even low doses of nicotine can interfere with the body’s natural bone-healing process, not by killing bone cells, but by stopping them from reaching the fracture in the first place

Bones don’t heal alone – they call for help

When a bone breaks, healing depends on bone marrow stem cells. These special repair cells travel through the body and home in on the fracture, where they turn into bone-building cells and help knit the bone back together.

Think of it like an emergency repair crew rushing to a collapsed bridge.

But according to the researchers, nicotine disrupts the “GPS signals” that guide these repair cells to the injury site.

What the scientists did

Researchers at Wuhan University studied bone healing in mice exposed to nicotine levels similar to those found in smokers.

They tracked fluorescently labelled stem cells and watched how they behaved after a fracture.

The results were striking:

• Stem cells migrated more slowly

• Fewer stem cells reached the broken bone

• Bone repair was significantly delayed, especially in the early weeks

Importantly, this happened even when nicotine levels were too low to kill cells or stop them growing.

The hidden mechanism: broken signalling

Healthy bones release chemical signals—especially one called SDF-1—that act like a distress flare, calling stem cells to the fracture.

Nicotine reduced these signals and also lowered the sensitivity of stem cells to them.

In simple terms:

• The bone called for help more quietly

• The repair cells stopped listening

As a result, fewer cells arrived to do the job.

The damage may not be permanent – but it costs time

By later stages, bones in nicotine-exposed mice did eventually heal. But the delay matters.

In real people, delayed healing can mean:

• Longer pain and immobility

• Higher risk of complications

• Greater chance of poor or incomplete bone repair

This helps explain why smokers are more likely to suffer delayed unions and non-unions after fractures.

Why this matters beyond cigarettes

The findings raise important questions about:

• Nicotine patches and gums during fracture recovery

• Vaping and “low-nicotine” products

• Second-hand nicotine exposure

The study suggests that nicotine itself—not just smoke toxins—can slow bone repair.

The takeaway

Bones rely on mobile repair cells to heal.
Nicotine doesn’t kill those cells—but it prevents them from getting where they’re needed most.

For anyone with a fracture, this research offers a clear message:

Reducing nicotine exposure during recovery may help bones heal faster and more reliably.

And it finally explains, at a cellular level, why doctors have been urging patients to stub out cigarettes when bones break.

👉 Low-dose nicotine reduces the homing ability of murine bone marrow stem cells and delays fracture healing (published 2018 in Wound and Fracture Healing / available on PubMed Central).

You can access it here:
📄 https://doi.org/10.1186/s12967-018-1668-5

Disclaimer

This article is part of the ORIEMS FIT Research Digest series, created to summarise and explain published scientific research in simple language.

The information shared here is for general education only. It is not medical advice, does not diagnose, treat, cure, or prevent any disease, and should not replace advice from a qualified healthcare professional.

The research discussed was conducted in laboratory and animal models. Results in humans may vary. Always consult a medical professional before making decisions related to injury recovery, smoking cessation, or health treatments.

ORIEMS FIT does not claim to heal fractures or replace medical care.