Journal of Indian Society of Periodontology
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Year : 2018  |  Volume : 22  |  Issue : 1  |  Page : 50-54  

Maternal periodontal disease and preeclampsia in Jaipur population

1 Private Practitioner, Ex-Senior Lecturer, Rajasthan Dental College, Jaipur, Rajasthan, India
2 Department of Periodontics, Faculty of Dentistry, Ibn Sina National College for Medical Science, Jeddah, Saudi Arabia
3 Department of Periodontics and Oral Implantology, Government Dental College, Jaipur, Rajasthan, India
4 Department of Oral and Maxillofacial Surgery, Government Dental College, Jaipur, Rajasthan, India

Date of Submission28-Sep-2015
Date of Acceptance19-Jan-2018
Date of Web Publication28-Feb-2018

Correspondence Address:
Dr. Girija Jaiman
Rajasthan Dental College, Jaipur, Rajasthan
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jisp.jisp_363_15

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Background: Preeclampsia is identified as an important cause for mother and newborn mortality. Inspite of extensive research, the exact etiological relations have not been established. Hence, an attempt has been made in this study to evaluate the relationship between the preeclampsia and maternal periodontal disease. Materials and Methods: The case–control study comprised of thirty pregnant women distributed equally in the case (preeclampsia) and control (healthy) group. Gingival index, plaque index, bleeding on probing, clinical probing depth, and clinical attachment level were measured in both groups. Microbiologic examination for identification of one red complex organism Porphyromonas gingivalis and one orange complex organism Fusobacterium nucleatum were done in plaque and placental blood of cases and controls. The clinical examinations and collection of placental blood were done 24 h before delivery. Results: Periodontal condition in the preeclamptic women was statistically worse compared with the normotensive women. There was no statistically significant association between microorganisms in plaque and placental blood between normotensive control and preeclamptic pregnant women. The preeclamptic women had significantly higher chances of having newborns weighing <2.5 kg than the normotensive women. Conclusion: The preeclamptic women were associated with significantly higher periodontitis and lower fetal birth weight than normotensive women.

Keywords: Normotensive, periodontitis, preeclampsia

How to cite this article:
Jaiman G, Nayak PA, Sharma S, Nagpal K. Maternal periodontal disease and preeclampsia in Jaipur population. J Indian Soc Periodontol 2018;22:50-4

How to cite this URL:
Jaiman G, Nayak PA, Sharma S, Nagpal K. Maternal periodontal disease and preeclampsia in Jaipur population. J Indian Soc Periodontol [serial online] 2018 [cited 2020 Apr 5];22:50-4. Available from:

   Introduction Top

Periodontitis, being a chronic systemic stressor, has been associated with systemic illnesses. Preeclampsia is a condition observed during pregnancy which is rapidly progressing and characterized by increase in blood pressure and the proteinuria.[1] 3% to 5% of pregnancies are affected resulting in high mortality around the world. In India, its incidence is around 10% and 2%–5% in the United States.[2]

The inflammatory response is activated during normal pregnancy which is marked by the expression of various inflammatory mediators. The exacerbation of this inflammatory response could result in complications during pregnancy.[3] It has also been hypothesized that subgingival bacteria from the oral cavity may enter the mother's bloodstream, thus posing a risk of developing preeclampsia, preterm labor and low birth weight newborns.[4]

Maternal periodontal disease is a treatable and preventable disease in contrast to preeclampsia, which can be treated but is difficult to prevent.[5] Hence, maternal periodontal disease must be taken into account as an independent risk factor for adverse pregnancy outcomes during evaluation of pregnant women.

The aim of this study was to find whether an association exists between maternal periodontal disease and preeclampsia based on periodontal parameters and the microbiological examination of plaque samples and placental blood.

   Materials and Methods Top

The present study was planned among fifteen preeclamptic pregnant females and fifteen normotensive pregnant women. The international society for the study of hypertension in pregnancy defines preeclampsia as the appearance of a diastolic blood pressure ≥90 mmHg mercury measured at two different occasions at least 4 h apart in combination with proteinuria (≥300 mg/24 h or +1 dipstick) developing after a gestational age of 20 weeks in a previously normotensive woman.[6] Anticipating 33.3% of normotensive women to have periodontal disease and at least 40% more among the preeclamptic women with 95% confidence at 80% power, 15 women each need to be recruited in the two groups.

Age, occupation, marital status, education level, income level, and family histories of all the participants were obtained through a personal interview before the periodontal examination. The recording of their periodontal parameters (plaque and gingival indices [PIs and GIs], bleeding on probing [BOP], clinical attachment level [CAL] and probing pocket depth) was done 24 h before delivery by a calibrated examiner with the help of a trained assistant. Gestational age of the mother at the time of delivery and birth weight of the child were noted from hospital records.

Their periodontal condition was further stratified by severity according to the criteria using scores of GI given by Löe and Silness 1963,[7] probing pocket depth, and CALs.

Inclusion criteria were nonsmoker and nonalcoholic preeclamptic and normotensive pregnant women with normal response to glucose tolerance testing, no evidence of recent infections such as hepatitis B or C, rubella, toxoplasma, no fetal structural anomaly, and absence of uterine contractions.

The pregnant women with a history of periodontal treatment within 6 months and with preexisting hypertension before 20 weeks of gestation ≥140/90 mmHg or using medications for hypertension, women on antibiotic prophylaxis for any dental treatment, taking medication influencing sex steroid metabolism, women with renal or cardiovascular disease, diabetes mellitus or any other systemic illness, and women aged <18 years were all excluded from the study.

The purpose of the study was informed to all the participants and their informed written consent was obtained for the same purpose, at the beginning of the study. After investigation, the periodontal status and the need for treatment after delivery were explained to each participant.

Maternal periodontal examination was carried out under proper light and infection control conditions on the hospital bed using sterile mouth mirrors, periodontal probes (William's), and head light. PIs and GIs, BOP, probing depth (PD), and CAL were recorded. All measurements were rounded to the nearest millimeter. GI and PI were recorded according to criteria of Löe and Silness[7] and Silness and Loe,[8] respectively. Adequate care was taken to assess the periodontal parameters accurately although it was not evaluated on the dental chair.

Sterile Gracey curette were used to collect the plaques samples from the deepest pocket, transferred to vials containing reduced transport fluid and cultured on blood agar (BA) and kanamycin BA (KBA). After inoculation on respective culture media, they were incubated in an anaerobic jar for 48–72 h.

Placental blood of all the participants was collected at the time of delivery using a sterile syringe. About 2 ml of blood was drawn and transferred to a vial containing thioglycolate medium with hemin, Vitamin K, and sodium thioglycolate. Blood samples were collected in transport medium and were cultured on BA.

The periodontal parameters and the microbial data obtained were tabulated in Microsoft Excel. The comparison of periodontal status between the groups was done using Student's t-test. Association of periodontitis and microorganisms in plaque between the groups was done using Chi-square test. The association of microorganisms in plaque and placental blood as well as birth weight between the two groups was done using McNemar–Bowker test. The significance level in all tests was set at 95% confidence interval (P ≤ 0.05).

   Results Top

All the clinical parameters of maternal periodontal disease were more evident in preeclamptic women than in normotensive women, and this difference was statistically very significant [Table 1].
Table 1: Clinical findings of periodontal disease between normotensive control and preeclamptic pregnant women (Student's t-test)

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A statistically significant association between maternal periodontal disease and preeclampsia in pregnant women was observed [Table 2]. The periodontitis (maternal periodontal disease) was more predominant among preeclamptic group (93.3%) as compared to normotensive group (33.3%).
Table 2: Association of periodontitis between normotensive control and preeclamptic pregnant women (Chi-square test)

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[Table 3] reveals no statistically significant association of microorganisms in plaque between normotensive control and preeclamptic cases.
Table 3: Association of microorganisms in plaque between normotensive control and preeclamptic pregnant women (Chi-square test)

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No change was observed in the presence of organisms in plaque and placental blood (P = 0.339). The microorganisms were present in plaque and placental blood of 5 out of 15 preeclamptic pregnant women and not present in all the normotensive women [Table 4].
Table 4: Association of microorganisms in plaque and placental blood between normotensive control and preeclamptic pregnant women (McNemar-Bowker test)

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The association of birth weight between normotensive control and preeclamptic pregnant women was statistically significant. About 80% of preeclamptic women had newborns weighing <2.5 kg whereas only 40% of normotensive women had newborns weighing <2.5 kg [Table 5].
Table 5: Association of birth weight between normotensive control and preeclamptic pregnant women

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   Discussion Top

Periodontal disease during pregnancy has been linked to preterm birth, low child birth weight, early pregnancy loss, and preeclampsia. An increased systemic inflammatory response to pregnancy is proposed to have led to preeclampsia.[9]

The present study showed that birth weight of newborn was significantly less in the preeclamptic group suggesting that maternal preeclampsia could increase the risk for low birth weight in children. This finding is in accordance with the study done in which fetal birth weight was significantly higher in the normotensive group than in the preeclamptic group.[10] There are studies reporting negative correlation of severity of periodontitis with fetal birth weight.[11]

The following significant associations were found in the preeclamptic group in the present study: LBW, PD, CAL, PI, GI and BOP and chronic periodontitis. The GI values were comparable with those of other studies where preeclamptic patients had a higher percentage of areas with BOP compared to the healthy peers.[9] The BOP and GI parameters were higher in the preeclamptic patients which could be due to mere increase in inflammation, and the periodontal inflammation may or may not be the cause for preeclampsia. In contrast, preeclampsia may be suspected for its possible coinduction of periodontal disease during pregnancy.

There was a significant difference in PD measurements between the groups. Contrasting findings were reported by Khader et al.[12] who found no statistical differences between preeclamptic cases and normotensive controls with regard to PD, CAL scores, gingival recession, PI, and GI. One study conducted by Boggess et al. supporting the findings of the present study demonstrated a significant difference in PD between case and control groups.[13]

CAL values in the present study were significantly different between the studied groups. A study has been reported wherein there is a significantly higher PD and CAL scores in the pre-eclamptic group compared with controls.[9] Other studies have also shown significant differences in CAL between the two groups,[6],[9] while another study did not show any statistical significance in sites with CAL ≥3 mm, which is not consistent with the present study.[14]

The findings of CAL, PD, GI, and PI along with the heterogeneity in periodontal pathogen identification might be due to the susceptibility of patients to diseases as well as genetic issues, which are similar to what happens in the periodontal conditions. This draws a conclusion that periodontal or uteroplacental reaction may be prone to biological diversity among various individuals. CAL and PD may be an endpoint parameter showing the history of periodontal destruction and these marked differences in the periodontal inflammatory parameters as was shown in certain studies do not confirm that inflammation is enough for causing preeclampsia[15] as it has been shown that preeclampsia could even result from subclinical inflammation.[16]

Normal pregnancy is a mild pro-inflammatory state whereas preeclampsia indicates a more severe level of inflammation.[1] The subgingival bacteria and their products and pro-inflammatory cytokines from periodontal tissue may enter the bloodstream, reach the maternal–fetal interface, trigger or worsen maternal inflammatory response, increasing the prostaglandin and cytokines levels in the plasma, thereby leading to development of complications in pregnancy.[16]

In the present case–control study, maternal periodontal disease or periodontitis was found more commonly in preeclamptic pregnant women (93.3%) than normotensive women. Significant differences have been reported between the incidence of maternal periodontal disease or periodontitis among the group of individuals with preeclampsia and control groups. The incidence of periodontitis is reported to be 3.17 times higher in preeclampsia women and these women had a poorer periodontal health than normotensive patients.[1] The periodontal disease severity increased with the degree of severity of preeclampsia.[17]

Active maternal periodontal disease may have transient translocation of oral bacteria, through bacteremia to the maternal and fetal blood circulation. This initiates placental inflammation or oxidative stress causing damage to placenta and preeclampsia manifestation.[1] Possible mechanisms by which microbes spread to the uterus which otherwise is a sterile environment include (1) organisms ascend from the vagina and the cervix to the uterus; (2) spread through blood; (3) organisms translocate retrogradely from the peritoneal cavity through the  Fallopian tube More Details; and (4) during invasive procedures accidental inoculation of organisms into the uterine tissues. This association between maternal periodontal disease and pregnancy complications could be due to the decidual tissues being repeatedly exposed to the periodontal pathogens through episodes of transient bacteremia.[16]

In the present study, Porphyromonas gingivalis and Fusobacterium nucleatum have been studied for their presence both in plaque and placental blood of pregnant women. No significant difference was found in microorganisms of plaque and placental blood between normotensive and preeclamptic women. However, limited literature is available for comparison of microorganisms in plaque and placental blood/tissue; P. gingivalis, Eikenella corrodens, and Tannerella forsythensis were found in plaque samples in one study.[1]

Since only P. gingivalis was found in the placental blood of 5 preeclamptic women and comparisons of microorganism in plaque and placental blood between normotensive and preeclamptic women was not statistically significant in the present study, this could suggest that bacterial products rather than whole bacteria penetrate through the placenta and lead to preeclampsia.

The reason for link between periodontal disease and preeclampsia is still not clear. Both diseases have common risk factors. The risk factors such as race, diabetes mellitus, and low socioeconomic status could be corrected in the statistical analyses; no one can rule out the possibility of an unknown factor that predisposes to both preeclamptic and periodontal disease. This unknown factor might be a genetic one.[18] Smoking is a risk factor for periodontal disease, poor fetal growth, and preterm birth, but it reduces the risk of developing preeclampsia. The presence of a chronic infection during pregnancy can be a risk factor for preeclampsia; the preexisting periodontal disease might play a role in the initiation and progression of early-onset preeclampsia.[19]

The present study indicated that the periodontal parameters were worse in women of preeclamptic group than in the normotensive group. The periodontitis was more commonly associated with preeclampsia. No significant association of microorganisms was observed either in plaque or in placental blood among both the groups. The preeclamptic pregnant women had more chances of having newborns weighing <2.5 kg than the normotensive women. The results reported furnish added evidence as to whether periodontal infection is linked to preeclampsia; however, further research is needed to support a causal association and its clinical implications. Research on the subject with larger sample size, analysis of the microbial flora, biochemical, and cytokine analysis is warranted.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Contreras A, Herrera JA, Soto JE, Arce RM, Jaramillo A, Botero JE, et al. Periodontitis is associated with preeclampsia in pregnant women. J Periodontol 2006;77:182-8.  Back to cited text no. 1
Conde-Agudelo A, Villar J, Lindheimer M. Maternal infection and risk of preeclampsia: Systematic review and metaanalysis. Am J Obstet Gynecol 2008;198:7-22.  Back to cited text no. 2
López NJ, Smith PC, Gutierrez J. Higher risk of preterm birth and low birth weight in women with periodontal disease. J Dent Res 2002;81:58-63.  Back to cited text no. 3
Mahendra J, Desai K, Mahendra L. Pre-eclampsia – An oral infectious etiology? Indian J Dent Sci 2011;3:37-40.  Back to cited text no. 4
Erkkola R. Can pre-eclampsia be predicted and prevented? Acta Obstet Gynecol Scand Suppl 1997;164:98-100.  Back to cited text no. 5
Kunnen A, Blaauw J, van Doormaal JJ, van Pampus MG, van der Schans CP, Aarnoudse JG, et al. Women with a recent history of early-onset pre-eclampsia have a worse periodontal condition. J Clin Periodontol 2007;34:202-7.  Back to cited text no. 6
Löe H. Silness J. Periodontal disease in pregnancy. Acta Odontol Scand 1963;21:533-51.  Back to cited text no. 7
Silness J, Loe H. Periodontal disease in pregnancy. II. Correlation between oral hygiene and periodontal condtion. Acta Odontol Scand 1964;22:121-35.  Back to cited text no. 8
Canakci V, Canakci CF, Yildirim A, Ingec M, Eltas A, Erturk A, et al. Periodontal disease increases the risk of severe pre-eclampsia among pregnant women. J Clin Periodontol 2007;34:639-45.  Back to cited text no. 9
Sgolastra F, Petrucci A, Severino M, Gatto R, Monaco A. Relationship between periodontitis and pre-eclampsia: A meta-analysis. PLoS One 2013;8:e71387.  Back to cited text no. 10
Yoseffin O, Gusriani, Mose CJ. Correlations of chronic periodontitis with pre-eclampsia and fetal birth weight. Indones J Obstet Gynecol 2011;35:105-9.  Back to cited text no. 11
Khader YS, Jibreal M, Al-Omiri M, Amarin Z. Lack of association between periodontal parameters and preeclampsia. J Periodontol 2006;77:1681-7.  Back to cited text no. 12
Boggess KA, Lieff S, Murtha AP, Moss K, Beck J, Offenbacher S, et al. Maternal periodontal disease is associated with an increased risk for preeclampsia. Obstet Gynecol 2003;101:227-31.  Back to cited text no. 13
Brown MA, Buddle ML. Inadequacy of dipstick proteinuria in hypertensive pregnancy. Aust N Z J Obstet Gynaecol 1995;35:366-9.  Back to cited text no. 14
Canakci V, Yildirim A, Canakci CF, Eltas A, Cicek Y, Canakci H, et al. Total antioxidant capacity and antioxidant enzymes in serum, saliva, and gingival crevicular fluid of preeclamptic women with and without periodontal disease. J Periodontol 2007;78:1602-11.  Back to cited text no. 15
Barak S, Oettinger-Barak O, Machtei EE, Sprecher H, Ohel G. Evidence of periopathogenic microorganisms in placentas of women with preeclampsia. J Periodontol 2007;78:670-6.  Back to cited text no. 16
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;67:1103-13.  Back to cited text no. 17
Söder PO, Söder B, Nowak J, Jogestrand T. Early carotid atherosclerosis in subjects with periodontal diseases. Stroke 2005;36:1195-200.  Back to cited text no. 18
Herrera JA, Chaudhuri G, López-Jaramillo P. Is infection a major risk factor for preeclampsia? Med Hypotheses 2001;57:393-7.  Back to cited text no. 19


  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]


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