Dental plaque-induced gingival disease is compounded by bacterial accumulation that induces pathological changes in the tissues by direct (i.e., bacterial-derived byproducts) and indirect paths (i.e., host-derived inflammatory mediators). Although the microbiology of dental plaque has not been completely characterized, increased subgingival concentrations of Actinomyces spp., Capnocytophaga spp., Leptotrichia spp., and Selenomonas spp. have been found in experimental gingivitis in children when compared with gingivitis in adults.15,16 Histopathological observations have led to the subdivision into three stages that consist of vasodilation, increased gingival crevicular fluid, emigration of neutrophils, and activation of monocytes, lymphocytes, and fibroblasts.11 In addition, normal and abnormal fluctuation in hormone levels can modify the gingival inflammatory response to dental plaque, leading to a diagnosis of puberty or menopausal gingivitis.17,18