In recent years, tremendous strides have been made in understanding the etiology of gingivitis. This increase in knowledge has come, for the most part, from basic research in oral microbiology, immunology, histology and pathology. Over the past decade, less progress has been made in further refining the epidemiological relationships between gingivitis and various host and environmental factors. The major restraint has been the great difficulty in reliably measuring gingival inflammation. This problem has resulted in great inter- and intra-study variation in diagnosing the prevalence and severity of gingivitis in human populations. Consequently, it is almost impossible to estimate longitudinal trends in gingivitis and it is nearly as difficult to make comparisons among different population groups studied by different examiners. Nevertheless, by focusing on the most apparent and robust epidemiological relationships, an instructive overview of the epidemiology of gingivitis can be gained. A number of host and environmental factors have been studied in relation to gingivitis and some of these will be reviewed. With respect to age, there is general concensus that marginal gingivitis begins in early childhood, increases in prevalence and severity to the early teenage years, thereafter subsiding slightly and leveling off for the remainder of the second decade of life. Gingivitis during the adult period is much more difficult to characterize due to paucity of data. Estimates of the general prevalence of adult gingivitis vary from approximately 50 to 100% for dentate subjects. In terms of gingivitis prevalence, the dentate elderly do not deviate appreciably from the general adult pattern. When adjusted for cohort effects, gingival disease appears to be on the decline. With the exception of the puberty period, females generally exhibit lower gingivitis prevalence and severity than males. An appreciable number of women exhibit more severe gingivitis during periods of pregnancy. Accurate data comparing gingivitis prevalence between blacks and whites indicate that the former generally experience higher mean levels of gingival inflammation. Frequently, this difference has been partially explained by co-factors such as oral hygiene, socio-economic status and access to dental care. Longitudinal data on race and gingivitis prevalence are not particularly reliable. Bacteria in the gingival crevice and on the gingival margin are most directly responsible for gingivitis. Epidemiologically, this factor may be indirectly assessed by an oral hygiene index. Not surprisingly, the oral hygiene score is most closely correlated with gingivitis among all epidemiological factors. Additional factors which have been assessed for their impact on gingivitis are smoking habits, fluoride use and recent antibiotic history.