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Abstract
Abstract 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.

Log in to Wiley Online Library

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Log in
Purchase Instant Access
48-Hour online access$15.00
Details
Online-only access$25.00
Details
PDF download and online access$59.00
Details
Check out
Abstract
Abstract 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.