Research has suggested a link between periodontal disease (PD) and preterm birth (PTB). Several studies have indicated that PD may contribute to PTB; however, proof that treating PD will lower the incidence of PTB is still lacking. This article takes a closer look at this issue, but first, it’s important to have an understanding of prematurity.
Preterm birth and risks
Maternal infection is a well-known risk factor for adverse pregnancy outcomes, and infections have been implicated in PTB. Other risk factors include maternal age both high (older than 34 years) and low (younger than 17 years), African American race, low socioeconomic status, inadequate prenatal care, hypertension, diabetes, multiple pregnancies, and drug, alcohol, and tobacco use. Increasing evidence suggests that periodontitis may be a risk factor for delivering preterm, as it results in an immune reaction that triggers PTB or contributes to its onset.
The problem of prematurity
Preterm births, defined as those occurring before 37 weeks’ gestation, complicate 12.2% of births in the United States. There has been an almost 30% increase in PTBs since 1983. In 2003, nearly half a million babies were born prematurely in the United States. PTB is the number one cause of morbidity and mortality, and babies who survive are at risk for lifelong consequences, including cerebral palsy, mental retardation, chronic lung disease, and vision and hearing loss. Nearly 50% of PTBs have no known cause and despite extensive research over the past several decades, the number of PTBs is only slowly declining, with 1 out of every 8 babies born prematurely. The correlation between PD and PTB represents a potentially treatable cause of PTB.
What is periodontal disease, and how might it contribute to PTB?
Periodontal disease (also termed periodontitis) is an oral infection caused by gram-negative bacteria. In 1999, it was approximated that at least 23% of women ages 30 to 54 have periodontitis. PD presents as an infection and creates inflammation of the gingiva and destruction of supporting structures of the teeth. Both infectious organisms and inflammatory mediators have been recovered from the crevicular fluid that bathes the tooth at the gingival margin.
The proposed link to preterm labor involves the descent of microorganisms from the oral cavity and subsequent colonization of the fetal membranes and endometrium. Once bacteria colonize these areas, they release lipopolysaccharides (endotoxins), and trigger systemic inflammation. Inflammatory mediators, such as interleukin-1, interleukin-6, tumor necrosis factor (TNF), and prostaglandin E2 (PGE2), are released and induce uterine contractions, mediate cervical thinning and dilation, and incite premature labor.
Research on the role of PD in PTB
In 1994, Collins and colleagues studied pregnant hamsters injected with a common periodontal pathogen and found that this reduced fetal weight by up to 25%. A subsequent study followed 124 women, either prenatally or within three days of delivering, and conducted full-mouth periodontal exams on each woman. In mothers delivering premature, low-birth-weight (LBW) babies, there was more severe PD than in those delivering at term. The authors concluded that 18.2% of preterm LBW cases may be caused by PD and that periodontitis may be a clinically important risk factor for PTB.
Lopez and colleagues conducted a randomized, controlled study, assigning 400 pregnant women with PD to either receive periodontal treatment before 28 weeks (treatment group) or be treated after delivery (control group). The incidence of PTB in the treatment group was 1.84%, compared to 10.11% in the control group. The study concluded that PD may be an independent risk factor for PTB and that periodontal therapy significantly reduced its occurrence.
In 2005, Boggess and colleagues performed a prospective-observational study following 640 pregnant women, all less than 26 weeks’ gestation. At delivery, umbilical cord blood was collected and analyzed for measures of inflammation and infection, including C-reactive protein (CRP), TNF, PGE2, and immunoglobulin M (IgM). A small number of the women (7.5%) delivered at less than 35 weeks’ gestation. In these preterm deliveries, maternal CRP and TNF levels were increased. More significantly, greater than one-third of early-delivering subjects were IgM-positive for at least one oral pathogen and 26.6% were positive for multiple pathogens. This study demonstrated that fetal exposure to oral pathogens, as evidenced by an IgM response, is associated with PTB.
In 2006, Michalowicz and colleagues conducted a multicenter randomized, controlled trial in which 823 pregnant women with PD were assigned to undergo PD treatment involving scaling and root planing either early in the second trimester or after delivery. Although treatment improved clinical measures of PD and was not associated with adverse medical events, the researchers found that periodontal treatment early in pregnancy did not result in a significant reduction in the rate of PTB, low birth weight, or infants who were small-for-gestational age. PTBs occurred in 12% of the treatment group and 12.8% in the control group. Although this study did not definitely see a reduction in PTB, PD treatment was determined to be a safe care practice in pregnant women. Future studies are needed to determine whether the provision of periodontal treatment even earlier in pregnancy or before conception might improve outcomes.
In a 2009 metaanalysis performed by Polyzos and colleagues, seven randomized trials were reviewed between 2002 and 2007. The authors found that treatment with scaling and root planing reduced the rate of PTB, which was most likely related to the decline in oral cavity pathogens and the reduction of transportation of organisms into the amniotic fluid and chorionic membranes. The authors concluded that treatment significantly lowered PTB, although larger randomized trials are needed.
The state of research and future implications
Currently, three larger ongoing trials funded by the National Institute of Dental Research will attempt to determine whether scaling and root planing in pregnancy to treat PD can reduce the incidence of PTB. If the results of these studies establish that periodontal treatment has any role in reducing the rate of PTB, at-risk patients can be offered the appropriate advice on dental hygiene and PD treatment.
Recommendations for PD evaluation and treatment
The Healthy People 2012 goal is to reduce the number of PTBs from 12.7% to 11.4%, and the March of Dimes 2020 goal is to reduce the rate to 9.6%. This target will be approached by raising public awareness of PTB risk reduction, including ensuring good oral hygiene in women of childbearing age. Proper dental care should begin before conception and continue throughout the pregnancy. Women with PD should be readily identified and treated, and an oral exam should be included in routine prenatal care. According to the American Dental Association, oral health care for pregnant women should include an assessment of periodontal status and, once disease is diagnosed, prompt treatment. Typical treatment of PD involves deep instrumental cleaning, which will decrease the infection and subsequent inflammation.
Although PD can’t be diagnosed by visual examination alone, oral inspection by nurses may pick up on untreated gingivitis, which may eventually lead to PD. Perinatal nurses can be alert to the possibility of periodontitis during pregnancy by examining patients for signs of calculus (tartar) or inflammation, and uncovering evidence of family history of PD. In up to 30% of cases, genetics may play a role in PD. Recommendations for childbearing women should include twice-daily brushing with daily flossing, mouth washing, and routine dental appointments. Preventive oral care is the best method to prevent oral diseases and their potential consequnces on pregnancy.
Jeannie Y. Chan is Staff Nurse III in the Kaiser Permanente Intensive Care Nursery, San Francisco, California. Christine Gallagher Smith is a neonatal nurse practitioner for Intensive Care Nursery and Emergency Transport at UCSF Benioff Children’s Hospital, San Francisco.
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