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Hygiene hypothesis has been proposed more than two decades back to explain an increasing prevalence of allergic diseases and atopy. It states that, a lack of early childhood exposure to infectious agents increases susceptibility to allergic diseases and atopy later in life. The evidence in relation to hygiene hypothesis is controversial and inconclusive. Moreover, its underlying mechanisms are elusive and remain to be elucidated. Periodontitis is an inflammatory disease initiated by microorganisms present in the plaque biofilm. Association between periodontitis and various systemic diseases has already been established and is currently an area of interest particularly in periodontal research. Consistent with hygiene hypothesis, some researchers believed that pathogens associated with periodontal diseases might have a protective role in the development of asthma and other allergic diseases. Very few studies attempted to explore the concept of association between periodontitis, asthma and other respiratory allergic diseases which could neither support such a protective role for periodontal diseases nor reject such an association. This suggests a need for additional research to examine the relevance of hygiene hypothesis in periodontics. The purpose of the present article is to review the plausible scientific explanations available for hygiene hypothesis, to review some studies relating periodontitis, asthma and other respiratory allergic diseases and to stress the need for further research., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Disorders relating to short gestation and low birth weight are among the leading causes of death and disability in infants. About 25% of pre-term low birth weight (PLBW) cases occur without even a suspected risk factor. Of all PLBW cases, 18.2% may be attributable to periodontitis (Offenbacher et al. 1996 ). Therefore, this study was conducted to assess the views and knowledge of gynaecologist's on association between periodontal disease and pre-term low birth weight and their willingness to advise their patients to seek dental treatment.

Background: The effects of periodontal disease on the oral gingival epithelium (OGE) have not been documented fully because they may not be as dramatic as those seen on the junctional epithelium. The aim of this study was to estimate the changes occurring in the OGE with respect to its proliferation and E-cadherin and cytokeratin 19 (K19) expression during pocket formation. Methods: Gingival samples were collected from 17 periodontally healthy subjects and 18 subjects with chronic periodontitis. K19 and E-cadherin levels were analyzed immunohistochemically. The net proliferative rate was calculated as the difference between the proliferative rate and the apoptotic rate as determined by immunohistochemical analysis of Ki-67 and p53, respectively. Results: There was a significant increase in the net proliferative rate of the OGE during pocket formation (periodontitis group, 220.90 ± 46.85; healthy group, 107.60 ± 25.86; P<0.001). There was a significant reduction in E-cadberin expression (periodontitis group, 0.837 ± 0.428; healthy group, 1.846 ± 0.555) and a significant increase in K19 expression during pocket formation (periodontitis group, 1.45 + 0.686; healthy group, 0.533 ± 0.410). Conclusion: OGE appears to undergo significant changes in proliferation and differentiation during pocket formation that do not seem to be restricted to proteolytic destruction by the invading microorganisms. [ABSTRACT FROM AUTHOR]