It is estimated that six million perinatal deaths occur every year worldwide, with premature birth being the main cause. Scientific evidence has shown that there is an association between periodontal health during pregnancy and adverse outcomes of labor, although interventional studies based on the treatment of periodontitis have failed to document an impact on reducing the incidence of preterm birth (PB) or low birth weight (LBW). Two pathogenic mechanisms have been proposed to explain this association. The direct pathway is based on the presence of gram-negative anaerobic bacteremia originating in the gingival biofilm, whereas the indirect pathway involves the production of pro-inflammatory markers which enter the bloodstream from the gingival submucosa. The result is the same: the development of an immune inflammatory response and/or the local suppression of growth factors in the fetal-placental unit, which in turn triggers labor. In the present review, we describe current concepts pertinent to PB and LBW, chronic and aggressive periodontitis, and the most frequent aspects of periodontal pathology during pregnancy. We evaluate the scientific evidence available to date, and offer a detailed description of the two pathways proposed to explain the association of maternal periodontitis with preterm and LBW delivery.
These results, along with previous findings, show that oral bacteria may be normally present in the placenta, however, the levels of certain oral pathogens in the placenta would highly depend on the mother's periodontal state.
PurposeThe purpose of this report was to describe the clinical and microbiological characteristics of two rare cases of necrotizing stomatitis, and the outcomes of a non-invasive treatment protocol applied in both cases.MethodsWe report two cases of necrotizing stomatitis in a rare location in the hard palate of a 40-year-old woman and a 28-year-old man. Neither had a relevant medical history and both presented with highly painful ulceration in the palate and gingival margin that was accompanied by suppuration and necrosis. 3% hydrogen peroxide was applied to the lesions using sterile swabs, and antibiotic and anti-inflammatory treatment was prescribed to both patients in addition to two daily oral rinses of 0.2% chlorhexidine.ResultsIn both cases, radiological examination ruled out bone involvement, and exfoliative cytology revealed a large inflammatory component and the presence of forms compatible with fusobacteria and spirochetes. There was a rapid response to treatment and a major improvement was observed after 48 hours, with almost complete resolution of the ulcerated lesions and detachment of necrotic areas with partial decapitation of gingival papillae.ConclusionsNecrotizing periodontal lesions can hinder periodontal probing and the mechanical removal of plaque in some cases due to the extreme pain suffered by the patients. We present a non-invasive treatment approach that can manage these situations effectively.
COX-2 protein expression is higher in patients with GV and CP than in individuals without periodontal disease and is inversely correlated with the amount of connective tissue in the lamina propria as determined by image analysis. This finding suggests that COX-2 participates in mechanisms and pathway signaling related to the destruction of fibrillar support structures of the periodontium.
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