The relationship between periodontal disease, bacterial vaginosis, and preterm birth.
Spontaneous preterm labor leading to preterm birth is a major cause of perinatal mortality and morbidity worldwide. The etiology of spontaneous preterm labor is multifactoral but there is overwhelming evidence to implicate infection in up to 40% of cases. Historically, this infective link has focused on the associations between abnormal genital tract flora in pregnancy (diagnosed by the presence of bacterial vaginosis) and preterm birth. Recently, another condition related to abnormal flora (periodontal disease) has been linked with preterm birth. There are microbiological similarities between the oral cavity and the female genital tract giving rise to a possible common pathophysiology. This review records the interrelationship between periodontal disease, bacterial vaginosis, and preterm birth. We postulate on the mechanism linking the three conditions, particularly through microbiology and gene-environmental interactions. Periodontal disease and bacterial vaginosis may be risk factors in their own rights or may be interrelated. We speculate on whether periodontitisis a marker for an immune hyperresponse to abnormal flora which in the oral cavity results in periodontitis and in the case of bacterial vaginosis might result in preterm birth. We also postulate on the risk of preterm birth by periodontitis alone, bacterial vaginosis alone, or both.
Pretorius
Christopher
C
Department of Obstetrics and Gynecology, Northwick Park and St. Marks Hospitals, Harrow, Middlesex, London, UK.
Jagatt
Anilla
A
Lamont
Ronald F
RF
D005260:Female; D020022:Genetic Predisposition to Disease; D005836:Genitalia, Female / Q000382:microbiology; D006801:Humans; D010510:Periodontal Diseases / Q000382:microbiology / Q000503:physiopathology* / Q000628:therapy; D011247:Pregnancy; D047928:Premature Birth / Q000382:microbiology / Q000503:physiopathology* / Q000517:prevention & control; D016585:Vaginosis, Bacterial / Q000188:drug therapy / Q000382:microbiology / Q000503:physiopathology*