“…enhanced blood circulation in the end terminal capillary loops and associated increased prevalence of gingivitis/bleeding tendency (Muhlemann 1948, Massler et al 1950, Curilovic et al 1958, Sutcliffe 1972, Daniell 1983 higher bacterial counts (especially Prevotella intermedia (Pi) and Capnocytophaga species) (Kornman & Loesche 1982, Mariotti 1994) During pregnancy increased tendency for gingivitis and larger gingival probing depths (Loe & Silness 1963, Silness & Loe 1964, Miyazaki et al 1991, Robinson & Amar 1992, Machuca et al 1999, Soory 2000a) and periodontitis (Robinson & Amar 1992) increased susceptibility to infection (Cohen et al 1969, Brabin 1985 decreased neutrophil chemotaxis and depressed antibody production (Sooriyamoorthy & Gower 1989b, Raber-Durlacher et al 1991, Raber-Durlacher et al 1993 increased numbers of periodontopathogens (especially Porphyromonas gingivalis and Pi) , Tsai & Chen 1995 increased synthesis of PGE 2 (ElAttar 1976b) (Mittermayer et al 1998) noted (Segal et al 1974) in the luteal phase of the menstrual cycle, although the incidence is low (Segal et al 1974, Ferguson et al 1978. However, the specific mechanism of how steroid sex hormones influence vesicle/ulceration formation remains to be determined (Mariotti 1994).…”