The discovery could help babies with genetic diseases, elderly people and even astronauts, they say.
The findings in mice, published in Scientific Reports, showed cells in the fluid strengthened bone and cut fractures by 80%.
Human clinical trials are planned within the next two years.
The amniotic fluid protects the baby and helps it develop inside the mother’s womb.
It also contains stem cells that are the building blocks of other tissues.
The researchers collected the amniotic stem cells from material left over from screening tests during pregnancy or collected immediately before birth.
The team at the Institute of Child Health – a collaboration of Great Ormond Street Hospital and University College London – injected the cells into diseased mice.
The animals had brittle bone disease or osteogenesis imperfecta.
In people, the condition affects around one in every 25,000 births and can be fatal, with babies born with multiple fractures.
Even those who survive face up to 15 bone fractures a year, brittle teeth, impaired hearing and growth problems.
Tests on mice showed injecting the cells increased the strength, plasticity and structure of the animal’s bones.
The number of fractures was cut to a fifth of their original level.
The impaired maturation of bone-forming osteoblasts results in reduced bone formation and subsequent bone weakening, which leads to a number of conditions such as osteogenesis imperfecta (OI). Transplantation of human fetal mesenchymal stem cells has been proposed as skeletal anabolic therapy to enhance bone formation, but the mechanisms underlying the contribution of the donor cells to bone health are poorly understood and require further elucidation. Here, we show that intraperitoneal injection of human amniotic mesenchymal stem cells (AFSCs) into a mouse model of OI (oim mice) reduced fracture susceptibility, increased bone strength, improved bone quality and micro-architecture, normalised bone remodelling and reduced TNFα and TGFβ sigalling. Donor cells engrafted into bones and differentiated into osteoblasts but importantly, also promoted endogenous osteogenesis and the maturation of resident osteoblasts. Together, these findings identify AFSC transplantation as a countermeasure to bone fragility. These data have wider implications for bone health and fracture reduction.