The pathophysiology of the relationship between periodontal infection and preterm low birth weight is thought to involve two possible pathways. One view is that periodontal disease may influence preterm birth directly by causing bacteremia which can lead to the seeding of the genital tract with pathogens resulting in an infection (Dixon et al. 1994, Jeffcoat et al. 2001). This view is supported by the fact that the organisms involved in periodontitis such as Fusobactererium Nucleatum and Capnocytophaga species, are similar to, if not identical with, those associated with upper genital tract infections and it is biologically possible for these organisms to reach the placenta (Jeffcoat et al. 2001). Further, there is substantial data linking lower genital tract infections with premature labour, premature rupture of membranes and low birth weight (Kempe et al. 1992, Hay et al. 1994). Another view is that periodontal disease may influence preterm birth indirectly through the increased production of inflammatory mediators (Offenbacher et al. 1998, Jeffcoat et al. 2001, Mills & Moses 2002, Moore et al. 2004). Endotoxins from the periodontal infection trigger the production of inflammatory mediators such as cytokines and prostaglandin. Both these inflammatory mediators are also known to be associated with the onset of labour and preterm birth (Shub et al. 2009).