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EDUCATIONAL FORUM
Year : 2015  |  Volume : 5  |  Issue : 1  |  Page : 2-6  

Relationship between periodontal diseases and preterm birth: Recent epidemiological and biological data


1 Department of Gynecology and Obstetrics, Christian Medical College, Ludhiana, Punjab, India
2 Department of General Surgery, Christian Medical College, Ludhiana, Punjab, India

Date of Submission27-May-2014
Date of Acceptance27-Jun-2014
Date of Web Publication13-Jan-2015

Correspondence Address:
Navdeep Saini
Department of General Surgery, Christian Medical College, Ludhiana, Punjab
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2229-516X.149217

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   Abstract 

Preterm infants are born prior to completion of 37 weeks of gestation. These patients are seen on the rise despite the efforts put in to control them. Global incidence of preterm birth is around 9.6% of all birth representing 12.9 million births with regional disparities: From 12% to 13% in USA, from 5% to 9% in Europe, and 18% in Africa. First reported by Offenbacher et al. in 1996 relationship exist between maternal periodontal disease and delivery of a preterm infant. This article reviews the recent epidemiological and biological data. The articles were searched on Google, PubMed recent articles were selected. Mainly, three hypotheses by which periodontal bacteria can affect the outcome of pregnancy. Biological hypothesis: (a) Bacterial spreading, (b) Inflammatory products dissemination, (c) Role of fetomaternal immune response against oral pathogens. The promotion of the early detection and treatments of periodontal disease in young women before and during pregnancy will be beneficial especially for women at risk.

Keywords: Disease, infant, periodontal, preterm


How to cite this article:
Walia M, Saini N. Relationship between periodontal diseases and preterm birth: Recent epidemiological and biological data. Int J App Basic Med Res 2015;5:2-6

How to cite this URL:
Walia M, Saini N. Relationship between periodontal diseases and preterm birth: Recent epidemiological and biological data. Int J App Basic Med Res [serial online] 2015 [cited 2020 Sep 29];5:2-6. Available from: http://www.ijabmr.org/text.asp?2015/5/1/2/149217

between periodontal disease and PB incidence increases frequently with the severity of periodontitis, [19],[25],[31],[34] All these data suggest that women populations with a high prevalence of severe periodontitis are at risk for PB.


   Biological Hypothesis Top


Considering epidemiological evidence, biological theories have been proposed to link PB and periodontal diseases. [20] Mainly, three hypotheses are developed - Bacterial spreading; Inflammatory products dissemination; and Role of fetomaternal immune response against oral pathogens.

Bacterial spreading

The current paradigm indicates that the majority of intrauterine infection originates in the lower genital tract. [36] Despite this statement, number of studies report intrauterine infections caused by those species, which are not found in the urogenital tract. The bacterial spreading theory is based on the possible dissemination of oral bacteria including periodontal pathogens through blood circulation to the amniotic fluid and leading to chorioamniotic infections. [37] The frequent gingival inflammation of women presenting periodontal diseases especially the pregnancy associated gingivitis, [38] facilitates bacteremia process. Furthermore, the more periodontal pockets are deep, the more important is the exchange surface between bacteria biofilm and blood circulation (15-20 cm 2 in the most severe cases). [39] Many analyses of amniotic fluid or placenta have been performed and evidence the presence of different oral pathogens such as Bergeyella, Eikenella, [36] Fusobacterium nucleatum, or Porphyromonas gingivalis. [40],[41],[42]

Inside uterus, these pathogens could provoke an inflammatory response. The increase of inflammatory cytokines or metalloproteases synthesis and the neutrophil activation could induce PB process. [36]

In vivo studies show that the invasiveness of uterine tissues largely depends on the type of bacteria. Potential pathological mechanisms of certain periopathogens, especially for P. gingivalis and F. nucleatum, have been studied. For example, P. gingivalis could infect syncytiotrophoblasts, chorionic trophoblasts, decidual cells, and amniotic epithelial cells, [42] and promotes inflammatory process trough Toll-like receptor 4. [43]

Finally, a case-report study has been published in 2010 concerning a stillbirth caused by F. nucleatum from the mother's mouth. [44] This study highlights the fact that an oral periodontal pathogen can, by hematologic pathway, colonize placenta and provoke fetal complications. It is important to notice that such colonization may be dependent from mother's immunological status.

Hematogenous dissemination of inflammatory products

Acute inflammation is responsible for a substantial fraction of PB. [45] In 1998, Offenbacher et al. [46] suggested that the cytokines produced by local inflammation in periodontal tissues affected by periodontitis have systemic effects after diffusion of such cytokines through blood flow. Locally, studies show that periodontal diseases increase secretion of several cytokines, notably prostaglandin E2 (PGE-2), tumor necrosis factor-α, interleukin 6 (IL-6) or interleukin 1β (IL-1β).[47],[48] Analysis of amniotic fluid obtained at the time of PB shows elevated levels of inflammatory cytokines. [49] It can be hypothesize that cytokines produced in periodontal tissues promote inflammation in maternal-fetal unit. Clinically, high-gingival crevicular fluid levels of PGE-2, IL-1β, or IL-6 have been associated with their elevated levels in amniotic fluid. [46] The inflammatory response appears to be the privileged pathway of the pathogenic periodontal disease influence on pregnancy, as suggested for other major systemic diseases, including cardiovascular diseases or diabetes. [50]

Role of fetomaternal immune response

The immune and genetic characteristics of the fetus and pregnant women are one of the potential mechanisms linking periodontal diseases to PB. Numerous studies have analyzed fetal and maternal antibodies directed against oral pathogens during pregnancy. In the study of Boggess et al., [51] 35.2% of samples are IgM positive for at least one oral pathogen, and 26.6% are positive for more than one. The presence of IgM is associated to an increased risk of PB. This immune response against oral pathogens could be associated with an inflammatory response, and the synergy between the two mechanisms increases significantly the risk. The mechanisms linking periodontal diseases and PB are not well defined. Further investigations should be performed to evaluate the impact of each theory. Nevertheless, it can be hypothesized that the influence of periodontal diseases on PB is the result of inflammation of the fetomaternal unit that is amplified in women presenting particular phenotype.


   Effects of Periodontal Treatment on Preterm Birth Incidence Top


Considering periodontal diseases as a risk factor for PB, interventional studies have been performed to evaluate the impact of periodontal treatment on pregnancy outcomes. Case-control studies including a relative large number of pregnant women (>400) show some apparent contradictory results and different conclusions. [20],[52],[53],[54],[55],[56] Indeed, the periodontal treatment may improve periodontal conditions and or pregnancy outcomes or not. [53],[55] A recent meta-analysis indicates that the treatment of periodontal diseases does not reduce the rate of PB. [57] However, as discussed above for epidemiological studies, the conclusions of this analysis could be balanced by the relative heterogeneity of studied populations, according to risk factors ethnicity, smoking, socio-educative levels, and periodontal status definition. For instance, the percentage of black people varies considerably between studies: 50-65% of Hispanic and Caucasian; [20],[58] 45-87% of Afro-American. [52],[55] Furthermore, the modalities of periodontal care in the different studies display some differences that may influence periodontal outcomes. A first session of etiologic periodontal treatment, including oral hygiene instructions, scaling, and root planning was generally performed at the end of the first trimester of pregnancy (before 20-28 weeks). This first session could be unique, [53],[55] or reinforced by regular control visits and complementary treatments if necessary until delivery. [20],[52] The local effects of periodontal treatments are generally positive. Gingival inflammation and mean probing pocket depth are reduced, especially in the study using reinforced periodontal treatment modalities. However, a relative high rate of patients demonstrating a periodontitis progression is observed in some studies 70%, [49] , 50%, [48] and 68%, [56] suggesting that periodontal treatments do not work so efficiently than in a general population. [53] Indeed, the relative "narrow therapeutic window" to perform periodontal treatment and to obtain a successful periodontal lesion cicatrization, and the aggressive profile of severe periodontitis in young women could be considered as limiting factors. [53],[56] A recent study performed by Jeffcoat et al., [56] confirms that the efficiency of periodontal treatment should be considered before the analysis of results. In this study, 322 pregnant women with periodontal disease have been followed, 160 have received randomly complete periodontal treatment, and 162 have served as control without treatment. No significant difference was found in the term of PB incidence between the two groups. However, after considering the effect of periodontal therapy, the results demonstrate a strong and significant relationship between successful periodontal treatment and full-term birth ratio (OR = 6.02).

Despite apparent conflicting data, the majority of studies report that periodontal treatment is safe for pregnant women and improve periodontal status. [52],[54],[56] A pregnant woman is a particular patient. In order to decrease the impact of periodontal disease on PB incidence, the early diagnosis promotion of periodontal disease for young women especially for those presenting major risk factors should be recommended.


   Conclusion Top


Periodontal diseases appear to be a potential risk factor for PB. As well as other modifiable risk factors, these diseases must be taken in charge. Cooperation between obstetricians or general practitioners and periodontists should be developed. The promotion of the early detection and treatments of periodontal disease in young women before and during pregnancy will be beneficial, especially for women at risk.

 
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