Non-surgical periodontal therapy can reduce the risk for preterm births in mothers who are affected by periodontitis. Additional multicentered, randomized, controlled clinical trials are required to confirm this link between periodontitis and PLBW.

In the recent decades, periodontal disease has been identified as a risk factor for pre-term deliveries. Hence, it is important to evaluate the awareness of health-care providers of the association between periodontal diseases and pre-term birth. A self-administered questionnaire was distributed to random samples representing general medical practitioners (GMPs), general dental practitioners (GDPs) and Gynecologists for this study. A knowledge score was calculated for correct answers to 11 survey questions related to oral health effects during pregnancy and compared among the three groups. In this study, 133 physicians, 135 dentists and 100 Gynecologists completed the questionnaire. More GDPs (67.4%) than GMPs (56.4%) and Gynecologists (63%) reported there was an association between periodontal disease and pre-term low birth weight. Efforts to increase this awareness may prove valuable in improving preventive care during pregnancy.

Periodontal diseases are inflammatory diseases of supporting structures of the tooth. It results in the destruction of the supporting structures and most of the destructive processes involved are host derived. The processes leading to destruction and regeneration of the destroyed tissues are of great interest to both researchers and clinicians. The selective susceptibility of subjects for periodontitis has remained an enigma and wide varieties of risk factors have been implicated for the manifestation and progression of periodontitis. Genetic factors have been a new addition to the list of risk factors for periodontal diseases. With the availability of human genome sequence and the knowledge of the complement of the genes, it should be possible to identify the metabolic pathways involved in periodontal destruction and regeneration. Most forms of periodontitis represent a life-long account of interactions between the genome, behaviour, and environment. The current practical utility of genetic knowledge in periodontitis is limited. The information contained within the human genome can potentially lead to a better understanding of the control mechanisms modulating the production of inflammatory mediators as well as provides potential therapeutic targets for periodontal disease. Allelic variants at multiple gene loci probably influence periodontitis susceptibility.

Periodontal infections, which serveas a reservoir of inflammatory mediators such as prostaglandin E 2 (PGE 2 ), may pose a threat to the fetal-placental unit and cause preterm delivery. This study was conducted to estimate the levels of PGE 2 in gingival crevicular fluid (GCF) and serum to explore the possible use of the GCF-PGE 2 level as a risk predictor of preterm low birth weight (PLBW). Twenty-two pregnant female patients were selected for the study. Samples of GCF and serum were collected from each patient, and sampling was repeated at one month after parturition. The level of PGE 2 in GCF and serum was estimated using a commercially available ELISA kit (NeogenTM). The mean serum PGE 2 level was 4.4 ng/ml and 1.64 ng/ml before and after parturition, respectively, and the difference was statistically significant (P < 0.001). The mean GCF-PGE 2 level was 5.8 ng/ml and 5.5 ng/ml before and after parturition, respectively, but the difference was not significant. There was positive correlation between the serum-PGE 2 and GCF-PGE 2 levels, and there was a negative correlation between PGE 2 level and gestational age. The present findings suggest that there is a weak correlation between maternal GCF-PGE 2 level and birth outcome. Further clinical trials with a larger sample size are warranted for further investigation of the association between GCF-PGE 2 level and PLBW. (J Oral Sci 53, 293-300, 2011)

Background: Pharmaceutical inhibition of host response pathways may be an adjunctive or alternative strategy for treating periodontal diseases. In addition to inhibition of prostaglandin synthesis, aspirin is known to modify the action of cyclooxygenase, changing its activity to a lipoxygenase and leading to formation of lipoxins which have a proresolving effect. This study evaluated the periodontal attachment level of subjects on long-term low dose aspirin therapy. Methods: Oral hygiene index simplified, clinical attachment loss and bleeding index were recorded for 162 subjects who were on long-term (>6 months) low dose (75 mg and 150 mg) aspirin therapy (study group) and 146 subjects not taking the drug (control group). Results: Mean clinical attachment loss was 2.38 ± 0.49 mm in the control group and 2.01 ± 0.69 mm in the study group. The difference was statistically significant at p < 0.001. Correlation analysis suggested that there was a negative correlation between clinical attachment loss and duration of aspirin intake but the clinical attachment loss was not significantly different in the two dosage groups. Conclusions: The results of this study suggest that low dose aspirin may reduce the risk of periodontal attachment loss. This hypothesis needs to be tested by larger sample sized prospective cohort studies.