Australian Scientists Now Know How To Stop 3D Printed Body Part Rejection

Australian Scientists Now Know How To Stop 3D Printed Body Part Rejection

Australian researchers have discovered a way to help prevent 3D printed body parts being rejected “as foreign body” by a patient, using anti-osteoporosis medication.

Professor Dietmar W Hutmacher, from QUT’s Australian Research Centre in Additive Biomanufacturing based in the Institute of Health and Biomedical Innovation, said implants trigger what is known as a foreign body response (FBR), causing scar tissue to develop around the implant, stopping it from working effectively in the body.

The researchers had to look into the mechanisms behind the body’s response before they could find ways to change or guide the process – the ideal end result being the 3D printed biodegradable scaffold slowly dissolving away as it is replaced by new living tissue.

The problem is, when tissue is exposed to biomaterial it becomes inflamed before the wound can heal, leading to fibrous tissue scarring. Professor Hutmacher said the team studied the roles of two white blood cell types – monocyctes (which cause inflammation) and M1 macrophages (which help regeneration). Both are associated with scarring, but exactly how wasn’t previously understood.

“Our research into their role found that M1 macrophages joined and became immobilised along the scaffold surface before forming multi-nucleated giant cells which initiated a network of neovessels within the scaffold pores that acted in a way similar to the neovessels that support the growth of fibrous tissue around a tumour”.

Professor Hutmacher says these macrophages and their giant cells produced a growth which led to a dense collagen formation around the implant two to four weeks later. Understanding this process better, the researchers were able to look at “therapeutic intervention”.

“We found that administration of clodronate, an anti-osteoporosis drug, and VEGF Trap, an anti-vascular endothelial growth factor drug, significantly reduced giant-cell accumulation, and the formation of neovessels and fibrosis,” Professor Hutmacher said.

“This represents a promising strategy to modulate both early inflammation and later stage tissue remodelling (weeks to month) to minimise chronic FBR and implant failure.”