It starts with a white dot on the gum. You know, those annoying canker sores that itch in the mouth. In some countries, it only needs one week to get worse. A hard fever strikes you and if your immune defenses are too weak, it can destroy the hard and soft tissue of your mouth. When it is not treated in time, it perforates your cheek; and if you’re lucky, you’re not part of the 70% to 80% of the victims it kills. But as a survivor, most of the time, you stay disfigured forever.

The Noma is a non-communicable disease of the mouth that mostly affects one to four-year-old children in developing countries. Today, it mainly develops in sub-Saharan Africa. In an article published in the New England Journal of Medicine, Cyril O. Enwonwu, professor at the School of Dentistry and Medicine, University of Maryland, explains that the name “Noma ” derives from the Greek word nemo, meaning “to graze” or “to devour.” The disease dates back to antiquity, but the name was first used by a Danish physician in 1680 and was meant to underscore its astonishingly rapid development.

At the Forsyth Institute in Boston, a majestic stairway leads to a small and tiny office behind a biology lab. There, a researcher looks for a way to better cure the disease that doesn’t exist anymore in the United States. With calm and delicateness, Bruce Paster explains that he is trying to pinpoint which bacteria are responsible for Noma. “Those bacteria could also be responsible for other disease we have in developed countries,” he says, to justify his research. Paster has always tried to define the oral flora of the mouth. When he started in the late 1980’s, he had never heard about the Noma. “I discovered it at a scientific meeting where another scientist was searching for collaborators,” he says. That’s how he started getting interested in the disease.

The Noma was common in Europe and North America until the early 20th century, when it essentially disappeared from developed countries, except from cases found in the concentration camps of Bergen-Belsen and Auschwitz; and more recently in some patients with human immunodeficiency virus (HIV) infection. “We also found some cases among Native American children with severe combined immunodeficiency syndrome,” Paster explains. According to the World Health Organization (WHO), although African countries are the most affected, Asia and Latin America are not exempted.

More than 700 different species of bacteria may be able to live in the human mouth; but not all of them are present in the same mouth at the same time. Many of these oral bacteria are hard to identify because they are impossible to grow outside the mouth. That’s why Paster’s laboratory has been developing new tools to hunt for oral micro-organisms. “We use cloning and sequencing methods to detect the bacteria present in the mouth of Noma cases,” Paster

He collects a mixture of DNA from bacteria he found in Noma cases. Once he has amplified a specific region of the DNA that exists in all the bacteria, he gets a mixture of one specific region of DNA, each of which represents one bacterium. Paster can also mark each region individually and send them one by one to individual cells. Now that he has each specific bacteria separate in an individual cell, he can sequence, or duplicate, its DNA and grow the bacteria population. Finally, each one of the colonies that grow up, matches to one specific bacterium. The biology community has developed a list of numbers that code for each bacterium. Paster now needs to sort his colonies; he compares them one to another and build charts that mimic genealogical trees, to relate the species to each other. “The shorter the branch, the closer the bacteria are,” he explains. Then he can figure out the bacterial population. “It’s like comparing granny apple and mackintosh apple, rather than comparing apples and oranges.”

At the end of the first step of his research, Paster came up with an astonishing result. “The bacteria involved in Noma isn’t necessary different from what we have in our “seine” mouth.” In other words, we all have the same oral bacteria population, but some people are more likely to develop the disease. Paster concluded that it all depended on the body immune system condition. More than half of the bacterial oral populations are opportunistic; meaning that the action of the bacteria depends on the state of the immune system that defends the body. “Those opportunistic bacteria were unbelievably present in most of the Noma cases,” he explains. “[Today], Noma thrives in communities characterized by extreme poverty, severe malnutrition, unsafe drinking water, poor sanitation and poor oral health practice,” he adds. “They’re like smoking guns!”

Enwonwu also concluded that the Noma resulted from complex interactions between malnutrition and infections from diseases like measles or malaria that weakened the immune system of children in developing countries. He named Noma the ulcer of extreme poverty.

But the problem is also cultural. Enwonwu explains in his article that Haussa communities in Nigeria, named the Noma ciwon iska – an unexplained, sudden illness linked to the spirits. “That’s why the disease is often hidden by families who consider it an evil omen,” Paster says. Most of the time, children are taken to traditional healers who diagnose “worms.” “The problem is that those children are living in villages that believe in superstition,” Paster adds. He insists that if the children were treated earlier, none of them would die; because the Noma can be treated easily at the early stage with local disinfection, antibiotics and nutritional rehabilitation.

To his mind, a solution to cure Noma would be to find a way to better educate people about the disease in developing countries. As soon as the white dot appears, Paster would tell them to “go to the doctor, and you’ll get antibiotics. It is not the anger of Gods.”

On the other hand, the only solution for the survivors who stay disfigured is reconstructive facial surgery. Paster collaborated with the Noma Children’s Hospital in Nigeria were doctors and plastic surgeons from Europe would come and reconstruct children’s faces to give them back their smiles. They also aim to sensitize the population there to the disease so that Noma would not spread and eat children’s faces.

In Boston, Paster will continue his research on Noma as he’s just received new funding and will collaborate with a new team of researchers.