Goodbye root canals? Researchers use lasers to regrow parts of teeth

Goodbye root canals? Researchers use lasers to regrow parts of teeth

Loren Grush

By Loren Grush
·Published May 28, 2014·

For the millions of Americans who suffer cavities each year, the ominous threat of a root canal may soon be a worry of the past.

Now, researchers from Harvard University claim they have discovered a novel way of regrowing parts of people’s teeth using an unlikely tool: Lasers.


In a new study published in the journal Science Translational Medicine, lead researcher Praveen Arany and colleagues detailed how they used focused laser light therapy on rats to stimulate the growth of lost dentin, the calcified tissue that comprises teeth. They noted that if the therapy proves effective in humans, it could potentially eliminate the need for crowns, fillings and other complex dental operations in the future.

The procedure’s success all revolves around a native protein called transforming growth factor beta, or TGF-beta. During preliminary tests of dentin tissues, the researchers discovered that this growth factor changed very drastically when introduced to a focused beam of light. Further analysis revealed that when hit with light, TGF-beta actually stimulated the stem cells already present in dentin.

“Once [TGF-beta] is activated by the laser, it can bind to stem cells resident in the tissue, and then it induces those stem cells to differentiate so they can proliferate and reform dentin,” David Mooney, the Pinkas Family Professor of Bioengineering at Harvard University, told

Numerous studies have focused on ways to manipulate stem cells in order to spur tissue regeneration, but most of these techniques have revolved around reintroducing altered stem cells into the patient or directing stem cell populations externally through added growth factors. With this form of laser therapy, the only external factor that is being introduced is light, which activates TGF-beta that’s already in the body.

According to Mooney, it’s not the laser’s heat that stimulates TGF-beta but the energy of its photons. When light is focused on dentin, the photons get absorbed into the tissue and activate molecules called reactive oxygen species (ROS), which naturally occur in the body. These ROS then stimulate TGF-beta, which spurs the chain reaction ultimately leading to dentin reformation.


However, Mooney noted that the power of the laser must be at a specific level of intensity and cannot produce any heat in order to be effective.

“It’s kind of like Goldilocks, too little won’t do enough and too much will become destructive,” Mooney said. “It has to be just right.”

To test their light therapy’s effectiveness, the researchers created a group of rats with tooth defects, by using a drill to remove pieces of their dentin. They then shined a laser on their exposed tooth structures and soft tissues underneath it. Sure enough, after 12 weeks, the team observed that new dentin had formed in the rats’ teeth.

Given their trial’s success, Arany and his team hope to test this type of dentin regeneration in human clinical trials, which could potentially alter modern dentistry. Currently, if a patient has a chipped or decayed tooth, dentists will use synthetic materials to fix the problem or perform a root canal if the tooth has become too infected. Yet, Arany noted that laser therapy could erase the need for these uncomfortable dental procedures, simply by regrowing the part of the tooth that is missing.

He also noted that focused laser therapy could be used to grow more protective dentin in teeth that have grown sensitive due to gum recession.

“As we grow older our gums recede, exposing our teeth root,” Arany, assistant clinical investigator for the National Institutes of Health, told “The root is covered by cementum, which is not as protective as enamel, so you get dentin sensitivity….What we hope is in tooth sensitivity, [laser therapy] is able to generate an intrinsic protective barrier on the inside of the tooth.”

Expanding beyond the world of dentistry, the researchers note that TGF-beta is found in other bodily tissues, such as skin and bone, and that laser therapy could potentially help regrow tissues in those systems, as well. Also, since TGF-beta is known to control tissue inflammation, the growth factor could perhaps be stimulated to control certain inflammatory diseases.

But for now, the team is focused on TGF-beta in relation to teeth, and they are hopeful that their laser therapy could be used in a clinical setting relatively soon.

“This laser is already a big part of the clinic, since so many of the clinicians use it for other purposes,” Arany said. “So the barrier to clinical trial translation is relatively low.”

Microchip lung catches fatal disease

reposted from:

Microchip lung catches fatal disease

By Francie Diep

Published November 08, 2012


  • lung-chip.JPG

    This plastic device, which is about the size of a flash drive, mimics the function and one of the illnesses of a human lung. (Courtesy Wyss Institute, Harvard University)

This fingertip-size device can’t exactly cough, but it can get a lung disease. For the first time, researchers have reproduced some of the effects of a disease in a microchip. The scientists’ “organ-on-a-chip” technology is still under development, but they hope it someday will help test therapeutic drugs more quickly and reliably than current methods allow.

“There’s a huge need to find more predictive alternatives” to the lab mice that pharmaceutical companies rely on now, said Geraldine Hamilton, who worked on the diseased lung-on-a-chip. Hamilton manages the organs-on-a-chip research program at Harvard University’s Wyss Institute. “We think that the organs on chips truly provide that alternative,” she told TechNewsDaily.

Organs-on-a-chip are plastic microchips designed to act as small, simplified versions of lungs, hearts and other bodily organs. Unlike the microchips in computers, they don’t have circuits imprinted on them. Instead, they’re etched with tiny channels that carry water, air, blood or other biological fluids. The channels are lined with living cells taken from either rats or humans, to help them act more like real organs.

The researchers who make them hope they’ll become more-accurate testing grounds for drugs than lab rats, or simple collections of cells grown in a Petri dish, are. The vast majority of newly invented treatments that work well in lab mice don’t ultimately work in people.

“What happens is the drugs fail when they get to these much later stages, either when they reach clinical trials or even after they get to market,” Hamilton said. That costs drug companies time and money, she said. She and other organs-on-a-chip researchers hope better tests for potential drugs will help labs discover early on which drugs work and which don’t.

U.S. research agencies are investing heavily in organs-on-a-chip tech. The National Institutes of Health plans to give U.S. labs as much as $70 million over five years to develop the chips. The NIH has signed an agreement to give as much as $37 million to the Wyss Institute alone.

In the latest step forward in organs-on-a-chip research, Hamilton and her colleagues re-created a lung condition called pulmonary edema, or fluid leakage into the lungs. Hamilton worked with researchers from Harvard, Children’s Hospital Boston and the drug company GlaxoSmithKline.’

The lung-on-a-chip had two channels, designed to represent an air sac in the lung and an adjacent blood vessel. Hamilton’s team even hooked a tiny vacuum up to chip. The vacuum stretched and released the chip’s “lung” channel as if it were an air sac in a working lung, expanding and deflating with every breath.

To give the chip pulmonary edema, the researchers injected a chemotherapy drug, interleukin-2, into the “blood vessel” channel. Pulmonary edema is a potentially fatal side effect of interleukin-2, also known as IL-2, which treats skin melanomas and kidney cancer. In the lung microchip, researchers used the same doses of interleukin-2 that human patients get, on the same time schedule.

The IL-2 injection caused fluid to leak from the lung-on-a-chip’s blood vessel channel into the lung air sac channel. It also caused blood clots to form in the air sac channel. Such fluid leakage and clot formation also happen in pulmonary edema in people.

The lung-on-a-chip researchers discovered something along the way: They found that the vacuum-created “breathing” action of the chip actually increased the fluid spillage in the chip. “We didn’t expect that mechanical breathing motions would be responsible for the large majority of the edema produced by IL-2,” Hamilton said.

It will be a long time yet before plastic chips replace lab rats and Petri dishes in drug labs. “We are beginning the validation process,” Hamilton said. Wyss scientists are now starting to talk with pharmaceutical companies and regulatory agencies about what experiments they want to see before they would feel confident about using chips instead of lab animals, Hamilton said.

When the technology is ready, however, Hamilton and her colleagues imagine it could test much more than therapeutic drugs. It could test the safety of cosmetics, pollutants or food, she said. It could also teach researchers more about diseases, such as pulmonary edema.

Hamilton and her team published their work Nov. 7 in the journal Science Translational Medicine.

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