Periodontitis as a Risk Factor for Preterm Low Birth Weight

Ismail Marakoglu; Ulvi Kahraman Gursoy; Kamile Marakoglu; Hulya Cakmak; Tamer Ataoglu

doi:10.3349/ymj.2008.49.2.200

Abstract

Purpose

There is growing evidence showing that a number of complex human diseases are caused or are at least influenced by periodontal diseases. Such diseases include cardiovascular diseases, respiratory diseases, diabetes mellitus and osteoporosis. The aim of study was to evaluate periodontal diseases as a risk factor for a preterm low birth weight.

Materials and Methods

A total of 48 mothers, 20 of who had a preterm low birth weight delivery, were examined in the Clinics of Periodontology, Faculty of Dentistry, Cumhuriyet University. The periodontal exams consisted of a full mouth pocket depth, a Loe and Sillness Gingival index score measurements, and a panoramic radiograph analysis. Information on any other factors that may cause a preterm low birth weight was obtained from the family physician.

Results

The study results indicated that periodontitis (OR: 3.6 95% CI: 1.06 - 12.18) together with bacterial vaginosis (OR: 11.57 95% CI: 1.26 - 105.7) were independent risk factors of a preterm low birth weight. According to the data obtained from this study, the paternal age, tobacco use and the mothers' height were not significant risk factors for a preterm low birth weight.

Conclusion

Within the limits of this study, it is concluded that a poor periodontal health status of the mother may be a potential risk factor for a preterm low birth weight.

INTRODUCTION

Preterm infants who are born with a low birth weight (PLBW) are a major social and economic public health problem in both developed and developing countries.1 Birth weight is a single outcome of a complex multifactorial system, and has been chosen in many studies as a key indicator of the underlying health of the population under investigation.2

Disorders related to a shorter gestation period and PLBW are among the leading causes of death in infants.3,4 Low birth weight (LBW) infants have a higher mortality rate during the neonatal period normal birth weight infants,5,6 and LBW survivors face neuro-developmental problems,7,8 respiratory problems,9,10 congenital anomalies,11,12 and complications due to neonatal intensive care,13 causing a tremendous impact on the health care system and the survivors own family.

Some risk factors that have been associated with a PLBW include a high (> 34 years) and low (< 17 years) maternal age, African-American heritage, a low socioeconomic status, inadequate prenatal care, drug abuse, alcohol and tobacco use, hypertension, diabetes, and multiple pregnancies. Despite increasing efforts to diminish the effects of these risk factors through preventive interventions during prenatal care, there has been a only small decrease in the number of PLBW infants.14-19

There is a reason to believe that other unrecognised risk factors may contribute to the continuing prevalence of PLBW infants. One possible contributing factor to this phenomenon is the effect of an infection on PLBW. It is possible that subclinical genitourinary and periodontal infections can adversely affect the pregnancy outcomes. 20-22 A periodontal infection may influence the pregnancy outcomes by providing a source of gram-negative anaerobic organisms and bacterial components such as lipopolysaccharides. These can trigger the release of immune modulators such as PGE₂ and TNF-α, which are normally involved in normal parturition, and in turn, may influence the course of pregnancy.23,24

The aim of this study was to evaluate the periodontal health of the mothers to determine if it is a risk factor for preterm low birth weight infants.

MATERIALS AND METHODS

Patient selection

This case-control study requested the participation from women who were in-patients in the Department of Family Physician at the Medical School of Cumhuriyet University. A total of 50 volunteer mothers were enrolled in this study. However, two were excluded due to a genitourinary tract infection with concurrent antibiotic therapy. The total study sample size was 48 mothers (20 cases and 28 controls). Detailed data on the outcome of the current pregnancy was gathered from the patient's prenatal record and history from the current pregnancies.

As stated in an early study reported by Offenbacher et al.,24 PLBW cases are defined as mothers delivering an infant weighing < 2,500g and born before 37 weeks' of gestation. The controls were mothers delivering an infant weighing more than 2.500g born after 38 weeks' gestation.

Administered structured questionnaire

Information was collected on the known risk factors22,24 and included the following: a previous preterm delivery, the socio-economic status (annual income, educational level), maternal age, number of gestations, previous pregnancy history, maternal complications (smoking, illicit drug use, alcohol use, lack of prenatal care), infectious diseases (chorioamniotis, bacterial vaginosis, asymptomatic bacteriuria, cervical/vaginal colonization), uterine causes (myomata, uterine septum, bicornuate uterus, cervical incompetence), eclampsia, preeclampsia and Rh factor iso-immunity.

Measurement of periodontal status

A full-mouth periodontal exam was performed on 48 mothers early after the birth of their children. In order to diagnose the periodontal status, the same examiner (U.K.G.) performed all the measurements. Full-mouth data included measuring the pocket depths (PD) on six sites per tooth using a Florida probe (Version 2.75 Florida Probe Corporation, Gainesville, FL, USA), bleeding on probing and the LoeandSillness Gingival index (GI)25 scores.

Panoramic radiographs were taken for each patient. Patients with 3 or more sites with a 4 mm or more pocket depth and bleeding upon probing together with radiographic alveolar bone loss were diagnosed as periodontitis. The amount of alveolar bone loss was measured on the panoramic radiographs and was defined as having a 3 mm or more distance between the cemento-enamel junction and interdental septum.

Statistical analysis

The odds ratios (OR) and 95% confidence intervals (CI) were obtained to indicate an association between PLBW and the potential risk factors (maternal age, maternal height, families income, smoking, bacterial vaginosis, placenta previa and periodontitis).

RESULTS

The unadjusted odds ratio and the 95% confidence limits for several potential risk factors including periodontitis for PLBW are given in Table 1. The odds ratio is a means of comparing whether or not the probability of a certain event occurring is the same for the two groups. Only bacterial vaginosis together with periodontitis appeared to influence the observed frequency of PLBW in this dataset. Odds Ratio analysis suggested that periodontitis increased the risk for PLBW almost 4 times. In addition, bacterial vaginosis raised the incidence of PLBW 12 times. However, this study failed to detect any effect of the maternal age, height, annual income, smoking and placenta previa on a PLBW.

DISCUSSION

The major two subcategories of periodontal diseases are gingivitis and periodontitis. Gingivitis is an inflammatory process and affects only the gingival component of the periodontium. However, the term periodontitis refers to an inflammation of the supporting structures of the teeth; the destruction of the gingival and periodontal fibres, resorption of the crestal bone and the apical proliferation of the junctional epithelium.26

The clinical features of importance for making a diagnosis include alterations in the gingival colour, form, density, the gingival crevice depth, the position of the epithelial attachment, the tendency for bleeding, and any crevicular fluid.26 There are number of indices for an epidemiological study of periodontal diseases. The choice of index should relate to the type and objectives of the study. In this study, in order to diagnose periodontitis in both groups, a GI, PD, BOP and radiographic examination were used. The GI by Loe and Sillness25 was used to evaluate the form, colour, density and the tendency to for the gingiva to bleed. PD measurements require a graded periodontal probe, and measures the distance between the gingival margin to the dento-gingival junction, which is generally 1 - 2 mm. When this distance becomes 3 mm or greater, it refers to the loss of a gingival attachment, which might be the beginning of periodontitis. The BOP confirms the occurrence of gingival inflammation by evaluating gingival bleeding after probing the gingival sulcus with a periodontal probe. Radiographic techniques have improved greatly in recent years. However, in order to use this as a diagnostic tool, a clinician must combine the results with the clinical findings.26 In this study, periodontal disease was diagnosed as periodontitis when the patient has 3 or more dental sites with a 4 mm or more pocket depth and bleeding upon probing together with radiographic alveolar bone loss.

This cross-sectional unmatched case-control study pointed out that the presence of periodontitis and bacterial vaginosis increases the risk for giving birth to a preterm low birth weight infant. The design of this study does not explain the cause of the association between periodontitis and PLBW. However, there are some probabilities, which are supported by biochemical, immunological, and histological evidence.2,20,24

It is believed that in the infection process, the levels of biologically active molecules such as PGE₂ and TNF-α, which are normally involved in normal parturition, are raised to artificially high levels by the infection process. The periodontium can serve as a renewing reservoir for some mediators such as TNF-α, IL-1β and IFN-γ, as well as PGE₂ because they can reach high concentrations in the tissues in periodontitis.24

Galloway first suggested in 1931 that periodontal disease has more than just an an association, but actually contributes to a low birth weight.27 Later in 1996, Offenbacher et al.24 suggested that a periodontal infection could serve as a chronic reservoir of lipopolysaccharide (LPS), which could target the placental membranes via the bloodstream, and LPS has been shown to elicit the production of IL-1β and PGE₂ by the chorioamnionic and trophoblastic cells, a process often associated with preterm parturition. Jeffcoat et al.28 reported that with their existing case-control studies and prospective and uncontrolled intervention studies, there was evidence suggesting that pre-existing periodontal disease in the second trimester of pregnancy increases the risk of a preterm birth.

Maternal age, maternal height, annual income and placenta previa were the other known risk factors for PLBW. However, our results could not show any statistical differences between the groups. The small number of patients in this study may explain this.

A periodontal examination conducted on mothers after giving birth might raise some questions. However, as mentioned in previous studies,24 a periodontal examination conducted at a particular point in time is a measure of the periodontal experience of the individual. Therefore, such an examination is a measurement of a previous disease experience, and provides the same information as any single exam conducted during pregnancy.

Together with other reports,24,29,30 the results of this study provide additional evidence showing that periodontitis is a potential risk factor for PLBW.

Notes

Orally presented in: 31st Scientific Congress of Turkish Society of Periodontology 24-26 May 2001 Izmir-Turkey.

References

1. World Health Organization. The incidence of low birth weight: an update. Weekly Epidemiol Rec. 1984. 59:205–212.

2. Williams CE, Davenport ES, Sterne JA, Sivapathasundaram V, Fearne JM, Curtis MA. Mechanisms of risk in preterm low-birth weight infants. Periodontol 2000. 2000. 23:142–150.

3. Kramer MS. Determinants of low birth weight: methodological assessment and meta-analysis. Bull World Health Organ. 1987. 65:663–737.

4. Day JC. Population projections of the United States by age, sex, race, and hispanic origin: 1995 to 2050, US Bureau of the Census, Current Population Reports, P25-1130. 1996. Washington, DC: US Government Printing Office.

5. Shapiro S, McCormick MC, Starfield BH, Krischer JP, Bross D. Relevance of correlates of infant deaths for significant morbidity at one year of age. Am J Obstet Gynecol. 1980. 136:363–373.

6. McCormick MC. The contribution of low birth weight to infant mortality and childhood morbidity. N Engl J Med. 1985. 312:82–90.

7. Byrne J, Ellsworth C, Bowering E, Vincer M. Language development in low birth weight infants: the first two years of life. J Dev Behav Pediatr. 1993. 14:21–27.

8. Fitzharding PM. Follow-up studies of the low birth weight infant. Clin Perinatol. 1976. 3:503–516.

9. McCall MG, Acheson ED. Respiratory disease in infancy. J Chronic Dis. 1968. 21:349–359.

10. Hack M, Caron B, Rivers A, Fanaroff AA. The very low birth weight infant: the broader spectrum of morbidity during infancy and early childhood. J Dev Behav Pediatr. 1983. 4:243–249.

11. Van den berg BJ, Yerushalmy J. The relationship of the rate of intrauterine growth of infants of low birth weight to mortality, morbidity and congenital anomalies. J Pediatr. 1966. 69:531–545.

12. Cristianson RE, van den Berg BJ, Milkovich L, Oechsli FW. Incidence of congenital anomalies among white and black live births with long-term follow-up. Am J Public Health. 1981. 71:1333–1341.

13. Speidel BD. Adverse effects of routine procedures on preterm infants. Lancet. 1978. 1:864–866.

14. National Center for Health Statistics. Health, United States, 1982. DHHS Pub. No. (PHS) 83-1232. Public Health Service. 1982. Dec. Washington, DC: US Government Printing Office.

15. Waitzman NJ, Scheffler RM, Romano PS. The cost of birth defects: estimates of the value of protection. 1996. Lanham, MD: University press of America.

16. Lewitt EM, Baker LS, Corman H, Shiono PH. The direct cost of low birth weight. Future Child. 1995. 5:35–56.

17. Institute of medicine, committee to study the prevention of low birth weight. 1985. Washington, DC: National Academy Press.

18. Evaldson G, Lagrelius A, Winiarski J. Premature rupture of the membranes. Acta Obstet Gynecol Scand. 1980. 59:385–393.

19. Gortmaker SL. The effects of prenatal care upon the health of the newborn. Am J Public Health. 1979. 69:653–660.

20. Møller M, Thomsen AC, Borch K, Dinesen K, Zdravkovic M. Rupture of fetal membranes and premature delivery associated with group B streptococci in urine of pregnant women. Lancet. 1984. 2:69–70.

21. McDonald HM, O'Loughlin JA, Jolley P, Vigneswaren R, McDonald PJ. Vaginal infection and preterm labour. Br J Obstet Gynaecol. 1991. 98:427–435.

22. Gibbs RS, Romero R, Hillier SL, Eschenbach DA, Sweet RL. A review of premature birth and subclinical infection. Am J Obstet Gynecol. 1992. 166:1515–1528.

23. Scannapieco FA. Position paper of The American Academy of Periodontology: periodontal disease as a potential risk factor for systemic diseases. J Periodontol. 1998. 69:841–850.

24. Offenbacher S, Katz V, Fertik G, Collins J, Boyd D, Maynor G, et al. Periodontal infection as a possible risk factor for preterm low birth weight. J Periodontol. 1996. 67:1103–1113.

25. Loe H, Silness J. Periodontal disease in pregnancy. 1. Prevalence and severity. Acta Odontol Scand. 1963. 21:533–551.

26. Ramfjord SP, Ash MM. Periodontology and Periodontics: modern theory and practice. 1989. St. Louis, Tokyo: Ishiyaku EuroAmerica, Inc.;117–164.

27. Galloway CE. Focal infection. Am J Surg. 1931. 14:643–645.

28. Jeffcoat MK, Geurs NC, Reddy MS, Cliver SP, Goldenberg RL, Hauth JC. Periodontal infection and preterm birth results of a prospective study. J Am Dent Assoc. 2001. 132:875–880.

29. Dasanayake AP. Poor periodontal health of the pregnant woman as a risk factor for low birth weight. Ann Periodontol. 1998. 3:206–212.

30. Dasanayake AP, Boyd D, Madianos PN, Offenbacher S, Hills E. The association between Porphyromonas gingivalis-specific maternal serum IgG and low birth weight. J Periodontol. 2001. 72:1491–1497.