Relationship between Periodontitis and Pre-Eclampsia:

A Meta-Analysis
Fabrizio Sgolastra*, Ambra Petrcci, Marco Se!erino, Roberto "atto, Annalisa Monaco
#epartment o$ %i$e, &ealth and En!ironmental Sciences, 'ni!ersity o$ %(A)ila, %(A)ila, *taly
Abstract
Background: Stdies ha!e sggested contro!ersial reslts regarding a possible association between pre-eclampsia
+PE, and periodontal disease +P#, and no meta-analysis has been per$ormed to clari$y this isse-
Methods: A literatre search o$ electronic databases was per$ormed $or articles pblished throgh March ./, .012,
$ollowed by a manal search o$ se!eral dental and medical 3ornals- 4he meta-analysis was condcted according to
the recommendations o$ the 5ochrane 5ollaboration and PR*SMA- 6dds ratios +6Rs, and 789 con$idence inter!als
+5*s, were calclated- &eterogeneity was assessed with the x
.
-based 5ochran : test and *
.
statistic- 4he le!el o$
signi$icance was set at P,0-08-
Results: Fi$teen stdies were inclded, inclding three cohort and 1. case-control stdies- A positi!e association
was $ond between PE and P# +6R .-1;, 789 5* 1-2<=2-/1, P > 0-000<,- &owe!er, a high and signi$icant
heterogeneity was $ond +x
.
> ?.-/., P,0-00001, *
.
> ;89,- *n most cases, sbgrop analysis had low power to
detect signi$icant di$$erences between PE and non-PE grops-
Conclusion: @ased on the $indings o$ the meta-analysis, P# appears to be a possible risA $actor $or PE- &owe!er,
gi!en the important di$$erences in the de$initions and diagnoses o$ P# and PE among the stdies, as well as their
lacA o$ good methodological )ality, $tre trials are needed to con$irm the reslts o$ the present meta-analysis-
5itation: Sgolastra F, Petrcci A, Se!erino M, "atto R, Monaco A +.012, Relationship between Periodontitis and Pre-Eclampsia: A Meta-Analysis- P%oS
6BE <+<,: e;12<;- doi:10-12;1C3ornal-pone-00;12<;
Editor: Masar Datoh, Bational 5ancer 5enter, Eapan
Recei!ed May 1/, .012F Accepted Ely 1, .012F Pblished Agst 17, .012
5opyright: .012 Sgolastra et al- 4his is an open-access article distribted nder the terms o$ the 5reati!e 5ommons Attribtion %icense, which permits
nrestricted se, distribtion, and reprodction in any medim, pro!ided the original athor and sorce are credited-
Fnding: 4he athors ha!e no $nding or spport to report-
5ompeting *nterests: 4he athors ha!e declared that no competing interests eGist-
* E-mail: $abrizio-sgolastraHgmail-com
*ntrodction
Infection and inflammation continue to be at the forefront of
etiologic theories as causative factors of adverse pregnancy outcomes,
such as stillbirth and growth restriction, that affect many women each
year. Previous studies have demonstrated a link between infection or
inflammation and preterm birth, preeclamp-sia (PE, and other
adverse outcomes thought to be secondary to poor placentation !"#$%.
&he prevalence of PE, a multisystem disorder of unclear etiology that
is exclusive to human pregnancy, ranges from '( to )( in developed
countries. PE results in high maternal and neonatal morbidity and
mortality rates, attributable to complications affecting different organs
and systems. In emerging countries, the prevalence of PE is more
than "*( !$%, and the condition is the main cause of maternal death
!+%.
PE occurs usually after '* weeks of gestation. It is characteri,ed by
an abnormal vascular response to placentation, manifesting as
generali,ed vasospasm, activation of the coagulation system, and
reduced organ perfusion affecting the kidney, liver, and brain !$%. &wo
syndromes are included in the definition of PE- maternal,
characteri,ed by endothelial cell activation, perturbations in volume
and blood pressure control, gradual maternal blood pressure
elevation, proteinuria, and generali,ed edema. and fetal, manifested
primarily by intrauterine growth restriction !/#0%. Putative PE risk
factors include advanced maternal age, multifetal
pregnancies, maternal prepregnancy obesity, pregestational hy-
pertension, renal disorders, and diabetes mellitus !1#"'%. In recent
years, infection has been reported to be important in the
pathogenesis of PE, both in terms of its initiation and its
potentiation !),0,"2%.
3everal studies have suggested that periodontal disease (P4, a
chronic inflammatory oral infection, may be associated with an
increased risk for PE development !"$#"1%. P4 affects '*( to
+*( of pregnant women, especially economically disadvantaged
women !'*,'"%. In this inflammatory pathology, the dental pla5ue
# which is a biofilm predominated by 6ram-negative anaerobic
microorganisms # destroys the tooth-supporting tissues. 7ral
microorganisms initiate P4, but the periodontal breakdown is
primarily mediated by the host inflammatory response !'','2%.
P4 may burden pregnant women systemically with endotoxins,
inflammatory cytokines, and oxidative stressors at the maternal-
fetal interface !")%. &hus, P4 may be a vascular stressor that plays
a role in the development of PE in pregnant women.
8ontradictory findings exist regarding the relationship between P4
and PE !"+,'$#'/%, and a previous systematic review did not clarify
this possible association !')%. &herefore, there is a need for a systemic
assessment of the literature on the possible association between P4
and PE. &he aim of the present systematic review and
P%6S 6BE I www-plosone-org 1 Agst .012 I Jolme < I *sse < I e;12<;
Relationship o$ Periodontitis with Pre-Eclampsia