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.

Initial research indicated that the levels of interleukin-1beta (IL-1beta) are higher in sites of inflammation than in healthy sites. However, subsequent studies suggest heterogenous responses and indicate the quantitative levels of IL-1beta to be the characteristic of an individual rather than simply being the reflection of the inflammatory status of the tissues. This study has been designed to find out the relationship between IL-1beta levels in the gingival crevicular fluid and the inflammatory status of the periodontal tissues in the Indian population. Sixty patients were selected for the study. They were categorized in to three groups based on their periodontal tissue status as group I (clinically healthy gingiva with no loss of attachment), group II (gingivitis with no attachment loss) and group III (gingivitis with attachment loss). Microcapillary pipettes were used to collect gingival crevicular fluid samples from one site in each person and the samples were analysed for IL-1beta using a commercially available ELISA kit. The concentration of IL-1beta in the gingival crevicular fluid of patients in group III is statistically higher (P < 0.0001) than that in group II and the concentration of IL-1beta in groups II and III is statistically at much higher levels (P < 0.0001) than in the group I subjects. However, there is a significant overlap in the values obtained in groups II and III and the values in both the groups range over a wide spectrum. The composite values obtained within the groups and the overlapping values in groups II and III could indicate the role of genetic polymorphism in determining the quantity of IL-1beta produced and also the contributory role of other cytokines that share similar biologic activity.

It remains a possibility that the absence or low levels of TNF-α in GCF might indicate a stable lesion and elevated levels might indicate an active site but only longitudinal studies taking into account, the disease "activity" and "inactivity" could suggest the possibility of using TNF-α in GCF as an "Indicator" of periodontal disease.

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 characterized by localized infections and inflammatory conditions that directly affect teeth supporting structures which are the major cause of tooth loss. Several studies have demonstrated the involvement of autoimmune responses in periodontal disease. Evidences of involvement of immunopathology have been reported in periodontal disease. Bacteria in the dental plaque induce antibody formation. Autoreactive T cells, natural killer cells, ANCA, heat shock proteins, autoantibodies, and genetic factors are reported to have an important role in the autoimmune component of periodontal disease. The present review describes the involvement of autoimmune responses in periodontal diseases and also the mechanisms underlying these responses. This review is an attempt to throw light on the etiopathogenesis of periodontal disease highlighting the autoimmunity aspect of the etiopathogenesis involved in the initiation and progression of the disease. However, further clinical trials are required to strengthen the role of autoimmunity as a cause of periodontal disease.