GALVESTON — Tiny babies with miniature fingers and toes are a human wonder. But for those who are born too early, the medical risks are anything but tiny.

Infants born before 37 weeks are more likely to have breathing problems, feeding difficulties and developmental delays.

Preterm birth is the leading cause of infant death, and is a complex problem that has stumped scientists for years.

Now, a new study at the University of Texas Medical Branch, published this month in the American Journal of Pathology, has found a new piece of the puzzle.

“We have identified a major factor in the premature aging of the placenta, which may be responsible for some premature births,” said Dr. Ramkumar Menon, principal researcher of the three-year-study, and an assistant professor in the University of Texas Medical Branch’s department of obstetrics and gynecology.

When the placental membranes age too quickly, these tissues can rupture too soon, leading to a premature birth.

Aging of the placenta and fetal membranes is a natural process expected to happen during labor and after a full-term pregnancy. However, this study shows that the placenta can age prematurely, which can lead to an early birth. This is the first time placental aging has been proven to be a factor in premature rupture and preterm birth, Menon said

In the study, researchers exposed normal fetal membranes to oxidative stress in a laboratory and looked to see whether that caused placental tissue to age more quickly. It did.

This experiment mimicked what researchers saw in placental membranes they studied from premature rupture and preterm birth.

Oxidative stress is caused by environmental toxins, pollution, cigarette smoke, alcohol, poor nutrition and infection, among other things — many inevitable in daily life.

For the purposes of the study, placental tissue was exposed to cigarette smoke as a stress inducer, but the trigger substance was not as important as the process it revealed.

“We were able to show that oxidative stress can lead to premature aging of the placental membranes and can cause a premature rupture and preterm birth,” he said.

When placental membranes cannot provide nutrition and other essential elements to the fetus, it causes a unique inflammatory condition that triggers premature labor.

“Now that we understand the mechanism, we can ask the next question which is, ‘How do we slow down the aging of the placenta?’” Menon said. “It may not be possible to stop oxidative stress, but maybe we can intervene. That is our next line of inquiry.”

Placental aging does not happen overnight, and it is an end effect of a process that continues for days or weeks or longer.

“Ultimately, our investigations could lead to early screening targets, diagnostic targets for high-risk pregnancies and potentially, an intervention to slow down the placental aging process,” he said.

More that 500,000 pregnancies in the U.S. and 15 million worldwide end in preterm births. A healthy pregnancy usually lasts 40 weeks.

Previous studies suggested that infection might be the major cause of preterm premature rupture of the membranes for which antibiotics are standard intervention.

However, interventions such as antibiotics and antioxidants have not been successful in preventing preterm deliveries.

The study is part of an ongoing effort to better understand preterm births before 37 weeks of gestation. It was supported by development funds from the department of obstetrics and gynecology.

Menon is with the university’s division of maternal-fetal medicine perinatal research in the department of obstetrics and gynecology.

Other authors from the medical branch include Dr. George R. Saade, Tariq Ali Syed and Jossimara Polettini, all with maternal-fetal medicine perinatal research division; Istvan Boldogh in microbiology and immunology; Hal K. Hawkins from pathology; Michael Woodson from the electron microscopy core laboratory; and John Papaconstantinou in biochemistry and molecular biology.

Other authors include Stephen J. Fortunato with the Perinatal Research Center, Nashville, and Robert N. Taylor at the Wake Forest School of Medicine, Winston-Salem, N.C.

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