Implant failure may be due to immune system ‘misfire’

Implant failure may be due to immune system 'misfire'

Failure of medical implants such as dental fixtures may be the result of a persistent inflammatory response of the patient’s own immune system, according to new research.

Researchers from the Faculty of Dentistry at the University of Dalhousie, Canada found that the body’s protective immune response was liable to ‘misfire’ against medical implants. Unable to resolve the false threat, the immune system locks into a persistent inflammatory state called glycolysis.

Study leader Neal Callaghan is a research assistant in the Davenport Huyer Lab and an internal medicine resident physician. He said: ‘Implantable devices are everywhere. But in some patients, these devices cause chronic inflammation – not because of the surgery or the device itself, but because of how the immune system reacts.’

How does the immune system cause implants to fail?

The team found that immune cells next to implants switch into a long-term metabolic mode that is at odds with the needs of the body.

Co-leader Christian Rempe, a PhD student in microbiology and immunology, said: ‘Different activities need different kinds of energy. A sprinter and a marathoner don’t fuel the same way. Immune cells are similar, but in chronic inflammation, they get stuck using the wrong energy system.’

The study’s authors applied the metaphor of short and long distance running to further explain this mechanism. When an implant is first fitted, the body ‘sprints’ to respond to the foreign body. While immune cells generally realise that there is no infection and return to an everyday ‘marathon mode’, glycolysis causes them to remain on high alert – fighting a threat that is not there.

Continued activation of the immune system drives long-lasting inflammation and scarring, which could lead to pain, deformity and even implant failure.

How can the research help to prevent implant failure?

Understanding how the body gets ‘stuck’ in glycolysis may allow researchers to design safer implants or develop treatments to return the immune system to its normal state.

Dr Callaghan said: ‘If we can pinpoint the exact immune pathways involved, we can prevent tens of thousands of patients every year from needing painful revision surgeries.’

Further research could include studying unusual immune cells called foreign body giant cells, expanding clinical research using a wider range of patient samples, and testing ‘smart’ implant materials that do not trigger harmful immune responses. 

Dr Callaghan concluded: ‘My biggest goal in medicine is to help more patients. That means understanding disease at its roots, questioning what we assume we already know, and finding the gaps where innovation can happen.’

The study was published in the Science Advances journal.

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