Teeth fight back

Publication
Article
Dental Products ReportDental Products Report-2011-04-01
Issue 4

A recent study demonstrating that odontoblast cells are part of the immune system and launch their own response when attacked by bacteria paves the way for possibly reducing the number of unnecessary root canals and shows that these cells are a critical weapon in the fight against dental disease.

A recent study demonstrating that odontoblast cells are part of the immune system and launch their own response when attacked by bacteria paves the way for possibly reducing the number of unnecessary root canals and shows that these cells are a critical weapon in the fight against dental disease.



The 2010 study was done at the University of Washington in Seattle by dentists Dr. Orapin Horst, along with her husband, Dr. Jeremy Horst, and colleagues.
 
Odontoblast cells lay between the pulp and enamel within a tooth and produce a layer of dentin that supports the enamel structurally and forms an extra barrier to protect the pulp from infection.

When bacteria attack, the Horsts’ research showed that odontoblast cells trigger their own immune response, combating the infection by using antimicrobial peptides, which fight the infection directly.  The cells also use protein messengers (chemokines) to recruit white blood cells that bring an inflammatory response to the infection site - but only to the odontoblasts and not the rest of the pulp.

“The study showed how the cells respond to deep cavities and how they fight infection,” Jeremy Horst said. “It (the odontoblast cell layer) doesn’t need the rest of the body to fight infection. It can fight it on its own. Only when inflammation spreads through the pulp is there real trouble.”

It has long been accepted that teeth can protect themselves from bacteria, to some degree, but the inflammation within a tooth can be harmful and, if left untreated, will lead to the demise of the tooth and a spreading abscess.

The study has implications for how tooth infections should be treated.   

“We found that we can trust the odontoblast layer much more than we realized,” Jeremy Horst said. “Maybe we don’t need to do as many root canals. There are cheaper, more efficient ways to treat local infection.”

He said the way dentists today determine if a root canal is needed is imprecise and is based on whether the patient has lingering pain that lasts more than 20 seconds or experiences sudden pain without cause - or simply that a cavity is too deep.

“Right now, there’s a lot of guesswork in our drilling and filling,” he said. “But there is a desire (among dentists) to increase our knowledge base and do the best for our patients. This study gives the first molecular basis for not doing root canals simply because a cavity is too deep.”

Another use intended for this study is the development of a diagnostic test of the inflammatory markers, to be used by dentists to determine if a deep cavity will only need a simple filling, or if the tooth really does need an expensive root canal.

“This study tells us that the tooth has its own antibiotics and maybe we don’t need such invasive treatment,” Jeremy Horst said. "We were surprised that both the microscopy and the molecular markers indicated that these teeth with very deep cavities, more than 2/3 of the way to the pulp, could have been saved with simple fillings."

He said the next step is to repeat the test in patients who have been determined to need a root canal, because of sudden or lingering pain, in order to pinpoint the markers of inflammation that cause the pulp to die.

The Horsts, who currently are working at the University of California at San Francisco, are applying for grants to fund the next steps in the study.

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