TB AND TEETH

By Pam Eastlick

Welcome to The Deep science and technology column where we cover topics from the deep sea to deep space and beyond.

Well, the medical bag is full to overflowing this week so we’ll learn some more tales of the things that affect the human animal. Our first stories deal with one of the planet’s deadliest killers: tuberculosis. We thought we’d all but wiped out this deadly scourge in the middle of the last century when we began to develop our arsenals of antibiotics. But it turns out that TB is not only a deadly enemy, it’s a wily one and our first story should chill you to the bone, given TB’s prevalence, not in some far-off never-never land, but right here in the Marianas.

DISEASE VS. DRUGS

We’ve known for a long time that TB is a shape-shifter when it comes to antibiotics. It seems that virtually every few months we read about yet another strain of TB that’s become resistant to yet another drug developed to combat it. But the latest update has a terrible twist.

Scientists have identified a strain of antibiotic-resistant TB that thrives in the presence of rifampin, a front-line drug used to treat it. The latest strain was identified in a patient in China.

The doctors researching this particular strain discovered that it wasn’t one of the fast growing types UNTIL you treated the patient with rifampin. Then, it took off like a rocket. They also observed that the patient’s condition grew worse when they were given rifampin, but they were cured with rifampin-free regimens.

Roughly 5% of all TB cases are resistant to isoniazid and rifampin, two of the main drugs used to treat the disease. And now we have a TB strain that is feeding on and dependant on the drug that was developed to kill it.

The researchers say that rifampin-dependent tuberculosis is difficult to detect and may be a bigger problem than we currently realize, since the resistant bacteria don’t grow well in culture mediums unless rifampin is added. The researchers urge public health workers to closely examine patients who aren’t getting better when given rifampin, to see if they harbor the rifampin-eating strain.

Unfortunately, the researchers note that drug susceptibility testing is time-consuming and not easily performed in resource-poor settings where tuberculosis is frequently more common.

The World Health Organization (WHO) estimates that tuberculosis kills approximately 2 million people worldwide each year. Multidrug-resistant tuberculosis (MDR-TB) is becoming an increasing problem in many parts of the world, largely because many patients take the antibiotics until they feel better and then they stop taking them. DON’T DO THAT!! That’s how you personally can create drug resistant disease!

And now in a bizarre twist, scientists have discovered that another bacterium that causes disease and kills many people may be an effective weapon against . . . wait for it . . . tuberculosis!

DISEASE VS. DISEASE

It’s been implicated as the bacterium that causes ulcers and the majority of stomach cancers, but studies by researchers at Stanford University, UC Davis, and the University of Pittsburgh have found that Helicobacter pylori (H. pylori) also may play a protective role — against (you guessed it!) tuberculosis.

Jay Solnick, UC Davis professor of medicine and microbiology, and his co-authors report that H. pylori infection may enhance immunity against tuberculosis, a disease endemic in many parts of the world, and for which there is no effective vaccine.

"Here is a bacterium that we know is sometimes harmful and that is clearly associated with cancer," Solnick said. "But it’s not that simple."

Solnick explains that up until the 20th century, when public health improved and antibiotic use was widespread, virtually everyone was infected with H. pylori. That remains the case today in most developing countries, implying that H. pylori may have evolved with its human host because it confers some selective benefit.

"These new findings suggest that one such benefit may that H. pylori provides protection against tuberculosis, and perhaps other infectious diseases as well," he said.

Tuberculosis is second only to HIV as a cause of death due to a single infectious agent; an estimated one third of the world population has latent TB infection. But only 30 percent of people exposed to TB ever become infected, and only 10 percent of those infected will develop active tuberculosis disease.

"One explanation may be the presence of chronic infection of the stomach with H. pylori," Solnick said. The findings also may eventually aid in managing TB, since H. pylori infection may help determine whether someone infected with TB gets a latent, asymptomatic infection or active disease.

Early studies funded by the National Institutes of Health showed that a patient infected with H. pylori had elevated immune responses to TB antigens. The researchers then checked patients from immigrant populations in Santa Clara County, then in households in Gambia and Pakistan, where TB is prevalent. During the two-year study, they found that people exposed to TB who then developed the active disease were less likely to be infected with H. pylori than those who were not infected with H. pylori.

The researchers decided to test their theory in non-human primates. They examined 41 monkeys who were exposed to TB. The results were striking. Of the 30 monkeys that tested positive for H. pylori, only 5 developed active TB, but 6 of 11 monkeys that were negative for H. pylori developed active disease.

The authors acknowledge their findings are preliminary and propose several follow-up studies. First, they want to test whether experimental infection of H. pylori will protect monkeys from TB, and whether it enhances the protective effect of immunization. If successful, they will test a recombinant H. pylori strain that expresses TB antigens for possible immunization against TB.

Electron micrograph of H. pylori. (Credit: Yutaka Tsutsumi, M.D. Professor Department of Pathology Fujita Health University School of Medicine / Courtesy of Wikipedia)

Hmmmm. I think what we have here is a classic case of fighting fire with fire!

And now we turn our attention to yet another bane of human existence, at least many of us look at it that way. And that’s the trip to the dentist. Some of us (and you know who you are!) deal with awful pain and unsightly smiles because of our fears. I urge you to visit the dentist if you have problems; particularly if it’s been years since you went. New techniques have definitely eliminated most of the ‘torture-chamber’ aspects of the dentist office. And the following articles tell us about the possible elimination of two more.

LOOK MA, NO MERCURY

Most of us acquired our fear of the dentist in childhood when the dentist made holes in our teeth and filled them up with black stuff. The holes the dentist made were to make holes we already had bigger.

Tooth enamel is the hardest material in the human body because it’s made almost entirely of minerals. As tough as it is, however, enamel can be broken down by bacteria. This forms holes that we all know as cavities and if you don’t go see the dentist regularly, the cavities will eventually destroy the tooth. That’s why dentists repair cavities by filling them with a material to replace the lost enamel. The most common such filling material was invented in the 19th-century and it’s called amalgam — the classic silver-black fillings many people have.

Amalgam works well because it is very durable, easy to use, and (most importantly) cheap. The dark fillings can be unsightly (as a child I had a lovely black hole between my two front teeth) but the real problem is that they contain mercury, a real health and environmental no-no.

Because of the mercury, amalgam has raised health and environmental questions — though according to the American Dental Association, the mercury is bonded in amalgam in such a way that it poses no health hazards.

Dentists would love to have a perfectly white material that mimics natural enamel for repairing cavities in teeth and doesn’t use mercury, but for the most part, they still use amalgam. Other filling materials have been developed, but they often have problems with shrinkage or durability.

Kent Coulter and his colleagues at Southwest Research Institute in San Antonio have developed a new dental restorative material under a program funded by the National Institutes of Health. The new fillings are made with a plastic-like material containing zirconia nanoplatelets — tiny crystals made of the same sort of material used to make fake diamonds and gem stones. Unlike their costume jewelry cousins, the zirconia nanoplatelets are super hard because of a difference in the particular arrangements of the atoms in the material.

Coulter and his colleagues designed a way to make a roll of this material under vacuum. They hope this material can be lifted from the roll and packed in a dental cavity and then cured — using an ultraviolet lamp or some other means — so that it hardens in place without shrinking. Zirconia nanoplatelets are still several years away from the dentist’s chair, however, and the next step will be to see if the new material performs as hoped for people with cavities.

Well, we hope that zirconia works in the mouth as well as it does on the finger, but for most of us dental sufferers, the problem isn’t the nasty black fillings, particularly if they’re inside the mouth and not front and center. The problem that keeps most people out of the dentist’s office is the DRILL. Read on, there may be hope there too!

A STAR IN YOUR MOUTH

One of the first misconceptions I tell my Astronomy students about is the ‘fact’ that the Sun is made from gas. Tell a first-grader this and they automatically assume the Sun is made from burning gasoline. As we get older, we figure out what a gas really is when we learn about the three states of matter, solid, liquid and gas.

Well, that one’s wrong too. There are actually FOUR states of matter and the most common one is the one you’ve never heard of. It’s plasma, the stuff stars are really made of. Plasma is ionized gas and it can have the characteristics of a solid and liquid and a gas.

Plasmas are common everywhere in the cosmos, and one of their characteristics is that they they’re highly reactive. For instance, scientists have discovered that high temperature plasmas react with oxygen and that makes them capable of destroying microbes. These hot plasmas are already used to disinfect surgical instruments.

We know how to make low temperature plasmas too, and it turns out that firing low temperature plasma beams at dentin — the fibrous tooth structure underneath the tooth’s enamel coating — was found to reduce the amount of dental bacteria by up to 10,000-fold. This means that plasma technology could be used to remove infected tissue in tooth cavities — a practice that conventionally involves drilling into the tooth.

Scientists in Germany have used these low temperature plasmas against common oral pathogens. These bacteria form films on teeth surfaces and are capable of eroding tooth enamel and the dentin below it to cause cavities. If left untreated it can lead to pain, tooth loss and sometimes severe gum infections. In this study, the researchers infected dentin from extracted human molars with four strains of bacteria and then exposed it to plasma jets for 6, 12 or 18 seconds. The longer the dentin was exposed to the plasma the greater the amount of bacteria that were eliminated.

These low temperature plasmas are right around body temperature which means that the dentist won’t have to fry your mouth to use them. The low temperature means the plasmas can kill the microbes while preserving the tooth.

The researchers say that plasma technology to disinfect tooth cavities would be welcomed by patients as well as dentists. As most of us know, drilling is usually uncomfortable and sometimes painful. Cold plasma, in contrast, is a completely contact-free method that is highly effective. The scientists are diligently working and they say that a clinical treatment for dental cavities can be expected within 3 to 5 years.

From TB to teeth. Science is an incredibly rich feast.