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OCR for page 19
2
DENTAL FLUOROSIS
THE FLUOIUDE CONTENT OF n ETA
A,! humans ingest fluoride to some extent, and fluoride's affinity for
calcified tissues makes it a normal constituent of dental tissues. Up to 4
times as much fluoride is contained in dentin, the bone-like material that
constitutes the bulk of a tooth, as in enamel, the visible outer layer.
Fluoride is not evenly distributed in enamel and is concentrated primarily
on the outer enamel surface. Most fluoride is incorporated into the
crystalline lattice of enamel before tooth eruption, but more is incor-
porated into the enamel crystals immediately after eruption, while the
enamel is still maturing. The capacity for sound, newly erupted] teeth to
absorb fluoride into the enamel's crystalline lattice, however, rapidly
diminishes as the enamel matures (Weatherell et al., 1977~. As a result,
the amount of fluoride in dental enamel does not increase with age to
nearly the same extent as in bone. Enamel that has undergone clemineral-
ization, the first histological effect of dental caries, and subsequent
remineralization contains higher concentrations of fluoride than does
sound enamel (Silverstone, 1977~.
The concentration of fluoride in sound, mature tooth enamel, at a
depth of approximately 2 micrometers (#m), averages 1,700 ppm in
people residing in areas with low concentrations of fluoride in drinking
19
OCR for page 20
20 Health Effects of Ingested Fluoride
water (i.e., fluoride at 0.l mg/L or less) and 2,200-3,200 ppm in areas
with concentrations of fluoride at approximately I.0 mg/L. Enamel
fluoride concentrations of this order have no adverse impact on oral
health; indeed, the presence of fluoride in the crystalline lattice of dental
enamel can only increase the enamel's resistance to dissolution in decay-
causing acids. When drinking water contains naturally occurring fluoride
at 5-7 mg/1= (much higher than recommended), enamel fluoride concen-
trations have been measured at 4,800 ppm (Aasenden, 1974~. No data
could be found on enamel fluoride concentrations in people residing in
areas where drinking water contains I-5 mg/~. People from areas with
high concentrations of naturally occurring fluoride in drinking water (i.e.,
5-7 mg/~) usually exhibit severe dental fluorosis, and their enamel can
become brittle enough to fracture at incisal edges and cusp tips. Caries
might begin in the broken enamel, and, even if it does not, teeth in this
condition often require treatment to restore function.
~. ~ n^^ ~ ~ A ~1 n7AN
FLUORIDE'S ACTION IN
PnEvENTING DENTAL CARIES
Various forms of fluoride have been used in American dentistry over
the past 40 years to prevent tooth decay. The results have been highly
successful, and the prevalence and severity of dental caries in the 199Os
are substantially reduced from the levels seen in the 19SOs.
Fluoride's action in preventing caries comes from both pre-eruptive
and post-eruptive mechanisms (Dawes, 1989~.
In some studies of water
fluoridation, the greatest reductions In caries were seen in children who
were born as fluoridation began or thereafter, evidence that supports a
pre-eruptive effect (Grainger and Coburn, 1955; Forrest and James,
1965; Horowitz and Heifetz, 1967; Katz and Muhier, 1968; Chandra et
al., 1980~.
However, evidence of caries-preventive effects in teeth
already erupted or in the process of erupting when fluoridation began is
also long-standing (Klein, 1945, 1946; Arnold et am 1953; Ast and
Chase, 1953; Backer Dirks et al., 1961; Russell and Hamilton, 1961;
Backer Dirks, 1967) and has been confirmed more recently (Hardwick
et al., 1982~. The relative importance of pre-eruptive and post-eruptive
effects continues to be researched and debated (Groeneveld et al., 1990;
7 ~
OCR for page 21
Dental Fluorosis 21
Horowitz, 1990; Ttlylstrup, 1990), although the mechanisms of the
effects are well-def~ned.
Pre-eruptively, ingested fluoride is incorporated into the developing
enamel hydroxyapatite crystal, where it has the effect of reducing enamel
solubility (Beltran and Burt, 1988~. Pre-eruptive fluoride might prevent
caries more effectively in pit-and-fissure lesions than in smooth-surface
caries (Groeneveld et al., 1990~.
Post-eruptively, the frequent infusion of low-concentration fluoride into
the oral cavity, such as drinking fluoridated water or regular brushing
with a fluoride toothpaste, enhances remineralization (i.e., rebuilding of
the enamel matrix) when demineralization has occurred! in the early stages
of the curious process (Koulourides, 1990~. Some of the fluoride that
comes into the mouth from water, food, or toothpaste concentrates in
dental plaque (Singer et al., 1970), where most of it is held in bounct
rather than free ionic form. The bound fluoride can be releaser! in
response to lowered plaque pH that demineralizes enamel (Tatevossian,
1990), ant] fluoride is taken up more readily by demineralized enamel
than by sound enamel (White and NancolIas, 19901. The availability of
plaque fluoride to respond to acid challenge leads to gradual establish-
ment of well-crystallized and more acid-resistant apatite in the enamel
surface during the frequent demineralization-remineralization cycles
(Ericsson, 1977; TtlyIstrup et al., 1979; Kidd et al., 1980; Chow, 1990;
ThyIstrup, 1990~.
Plaque fluoride also inhibits glycolysis, the process in which sugar is
metabolized by bacteria to produce acid. Plaque fluoride can retard the
production of extracellular polysaccharide by cariogenic bacteria, a
production that is necessary for plaque to adhere to smooth enamel
surfaces and, hence, for caries to occur (Hamilton, 1990~.
In assessing the relative impact of pre-eruptive ant! post-eruptive
effects of fluoride, it became evident by the mid-1970s that a high con-
centration of enamel fluoride could not by itself explain the extensive
reductions in caries that fluoride produced (Levine, 1976~. As clescribed
earlier, enamel fluoride concentrations at a depth of 2 Am average I,700-
4,XOO ppm, depending on age and fluoride exposure. The theoretical
concentration of fluoride in pure fluorapatite that would reduce its acid!
solubility to the extent necessary to explain all reductions in caries is
approximately 3S,000 ppm (Wefe} et al., 1986~. It has also been shown
OCR for page 22
22 Health Effects of Ingested Fluoride
that high concentrations of enamel fluoride do not necessarily mean that
caries will not occur (Arenas and Christoffersen, 1990~. The evidence
collectively demonstrates that fluoride prevents caries by post-eruptive
actions as well as by pre-eruptive incorporation of hydroxyapatite crystals
into the enamel.
In addition, high-concentration fluoride at approximately 12,000 ppm,
as used in professionally applied gels, might have a specific bactericidal
action on cariogenic bacteria in plaque (Bowden, 1990~. Those gels also
leave a temporary layer of calcium fluoride on the enamel surface, which
is available for release when the pH at the enamel surface is lowered
~eGeros, 1990~. The cariogenic bacterium Streptococcus mutans has
been shown to become less acidogenic through adaptation to an environ-
ment where it is regularly exposed to low concentrations of fluoride in
drinking water or to higher concentrations in toothpastes and mouth
rinses (Rosen et al., 1978; Bowden, 1990; Marquis, 1990~. It is plaus-
ible, though not confirmed, that this ecological adaptation reduces the
cariogenicity of S. mutans in humans (van Loveren, 1990~.
HISTOPATHOLOGY OF DENTAL FLUOROSIS
Dental fluorosis is a condition of the dental hard tissues; it is not a
generalized health effect. It is defined as a hypomineralization of enam-
el, characterized by greater surface and subsurface porosity than is found
in normal enamel, and results from excess fluoride reaching the growing
tooth during its developmental stages (Fejerskov et al., 1990~. The
staining, which is characteristic of more severe forms of fluorosis,
actually develops after took eruption, but is seen only when porous
enamel has formed before eruption (Fejerskov et al., 1990~. Surface
enamel that exhibits dental fluorosis contains higher concentrations of
fluoride than does unaffected enamel, and the fluoride content generally
increases with the severity of the condition (Richards et al., 1989~. The
fluoride content of crystals in the hypomineralized subsurface layer is
low, however, when compared with the content of crystals in the more
fully mineralized enamel surface layers (Richards et al., 1989; Yanagi-
sawa et al., 1989), and these subsurface crystals appear stunted when
examined microscopically.
The process of enamel maturation consists of an increase in mineral-
ization within the developing tooth and a concurrent loss of early-secreted
OCR for page 23
Der'tal Fluorosis 23
matrix proteins. Excess fluoride available to the enamel during matura-
tion disrupts mineralization and results in excessive retention of enamel
proteins. This process has been well-illustrated in animal studies. When
rats were given various concentrations of fluoride in their drinking water
over a 5-week period, no differences were found in the protein content
of fluorotic enamel and control enamel during the secretory phase of
enamel formation (Den Besten, 1986~. However, in fluorotic enamel
during the early-maturation stage, animals receiving high doses of fluo-
ride had more enamel proteins retained. At the late-maturation stage,
differences were again less apparent, and only the dental enamel from
animals with the highest fluoride intake contained more protein (Den
Besten, 1986~. This research indicates that the early-maturation stage is
the developmental period when enamel is most sensitive to the effects of
fluoride.
Other research in various animal models (Richards et al., 1986;
Richards, 1990) and humans (Evans and Stamm, 1991a) generally sup-
ports the idea that the early-maturation stage is the most critical develop-
mental period for dental fluorosis, but fluoride at sufficiently high con-
centrations might affect enamel at all stages of its formation (Den Besten
and Crenshaw, 1987; Suckling et al., 19X8~. In humans, the clinical
signs of severe dental fluorosis (ename! pitting and obvious brown stain)
follow the breakdown of the better-mineralized surface layers of enamel
shortly after eruption, resulting in variable uptake of mineral in the
exposed hypomineralized subsurface lesions ~hylstrup, 1983; Fejerskov
et al., 1991~.
Some physiological conditions that affect amelogenesis in humans can
lead to variations in the clinical appearance of dental fluorosis at similar
levels of fluoride intake (Angmar-Mansson and Whitford, 1990~. Cal-
cium deficiency and generalized malnutrition are examples of such
conditions seen in many developing countries. Any condition that de-
creases urinary pH, such as disorders in acid-base balance, can reduce
the renal clearance of fluoride and increase the likelihood of dental
fluorosis (Whitford and Reynolds, 1979; Ekstrand et al., 1982~. Reten-
tion of fluoride in body tissues is increased by high altitudes (Manji et
al., 1986a), although residing at high altitudes, in the absence of fluoride,
has been found to disrupt amelogenesis and produce a condition that can
be clinically confused with dental fluorosis (Angmar-Mansson and Whit-
ford, 1990~.
Dental fluorosis is a dose-response condition: the greater the intake
OCR for page 24
24 Health E.ffects of Ingested Fluoride
during developmental periods, the more severe the fluorosis will be
(Dean, 1942; Eklund et al., 1987; Larsen et al., 1987; Gedalia and
Shapira, 19X9; Fejerskov et al., 19901. Evidence from animal studies
shows that several patterns of fluoride exposure can disturb amelogenesis.
Early research indicated that the development of fluorosis in the con-
tinuously growing rat incisor was associated with occasional "spikes" in
plasma fluoride concentrations, produced by daily injections, that raised
the plasma fluoride concentration above a presumed threshold value
(Angmar-Mansson et al., 1976; Myers, 1978~. Later research confirmed
that finding (Angmar-Minsson and WhitforcI, 1982) but also showed that
relatively constant, slightly elevates! concentrations of plasma fluoride
produced by constant infusion in rats (approximately 3 micromoles
~mol)/~) also resulted in enamel fluorosis. A subsequent study, which
also employed constant infusion of fluoride in rats, extended the closing
period from ~ to ~ weeks. With longer exposure, enamel fluorosis was
associated with plasma fluoride concentrations of only i.5 ,umol/L
(Angmar-Mansson and Whitford, 1984~. Those results were later con-
firmed by Nelson et al. (1989), who found that more fluorosis-type
lesions were produced in sheep after long-term administration of low
doses of fluoride than after short-term administration of high doses.
Angmar-Mansson and Whitford (1985) also reported that a single high
dose of fluoride (0.75 milligram (mg) or more of fluoride per kilogram
(kg) of body weight) caused enamel fluorosis in rats, even though the
plasma fluoride concentrations returned to pre-dose levels within 24
hours.
It was hypothesized from those results that the pulse loading (single
high dose) and subsequent gradual release of fluoride from bone in the
vicinity of the developing enamel result in local fluoride concentrations
sufficiently high to disturb amelogenesis. That hypothesis was supported
by nuclear microprobe analyses, which showed that the enamel ant!
dentin fluoride concentrations were elevated, in a dose-response manner,
even 70 days after the single fluoride doses, by which time the rats'
incisor teeth would have renewed themselves nearly 2 times (Angmar-
Mansson et al., 1990~.
Dental fluorosis in humans generally is more severe in teeth that
mineralize later in life than in those that mineralize earlier (Larsen et al.,
1985, 19X7, 1988; Pablum et al., 19871. That finding is usually attrib-
uted to greater ingestion of fluoride by older children comparer] with
OCR for page 25
Dental Fluorosis 25
younger (although, as a function of body weight, there is often little
difference in fluoride consumption between older and younger children).
Fluorosis is primarily a condition of permanent teeth; the degree of
fluorosis reported in primary teeth is generally much less than that found
in permanent teeth (Gedalia and Shapira, 1989~. Although extensive
fluorosis of primary teeth has been reported in areas of the world with
high amounts of fluoride ingestion (Thylstrup, 1978; Olsson, 1979;
McInnes et al., 1982; Nair anti Manji, 1982; Larsen et al., 1985; Mann
et al., 1990), it has not been identified as a problem in the Uniter] States.
The lower degree of fluorosis in primary teeth was once believer! to
be clue to the placenta acting as a barrier to the passage of fluoride from
maternal to fetal bloocI, but more recent evidence shows that the placenta
acts as only a limite(l barrier to its passage (Gedalia and Shapira, 19891.
However, fetal blood concentrations usually are lower than maternal
levels. Most fluoride in a tooth's outer enamel layer is clepositec! cluring
the enamel maturation period before eruption, a developmental phase that
lasts only I-2 years in primary teeth but takes 4-5 years in permanent
teeth. The shorter maturation period for primary teeth, adcled to lower
fetal blood fluoride concentrations cluring their prenatal clevelopment, is
probably the main reason why fluorosis in primary teeth is unusual
outside areas of high-fluoride ingestion.
DIAGNOSTIC ISSUES IN
DENTAL FLUOROSIS
Clinical diagnosis of fluorotic lesions has been plagued from the
earliest studies by the fact that not all mottling of dental enamel is caused
by fluoride. During McKay's initial studies in the early years of this
century he referred to this condition as "Coloraclo brown stain," a com-
ment both on the geographic location of his investigations and on the
severity of the condition he found. In his first national publication on the
condition (Black and McKay, 1916), however, it was calle(l "mottled
enamel." The term mottled enamel has since evolved to cover a range
of dental developmental defects, fluorotic and otherwise;- whereas the
term fluorosis more correctly applies only to dental defects of fluorotic
origin. The use of these terms, however, is unfortunately far from
·^
unlrorm.
OCR for page 26
26 Health Effects of Ingested Fluoride
The diagnostic problems that can arise when measuring the prevalence
of dental fluorosis have been well described in the literature (Fejerskov
et al., 1988; Cutress and Suckling, 1990~. Malnutrition, metabolic
disorders, and the presence of other dietary trace elements can lead to
diffuse, symmetrical markings on the enamel that closely mimic the
appearance of fluorosis. Most cases of dental fluorosis are probably
identified correctly by experienced examiners, but high and low popula-
tion prevalences and individual cases have been reported that are incom-
patible with the fluoride histories. In such instances, the likelihood of
misclassification seems strong. When a fluoride history is taken concur-
rently with clinical diagnosis, some argue that the information from the
history biases the diagnostic process.
Those issues deserve to be addressed seriously. It must be remem-
bered, however, that the risk of misclassification has long been recog-
nized as an inherent problem in epidemiological study of any condition.
Standard procedures have been developed to minimize the chances of
misclassification in data collection ~ilienfeld and Lilienfeld, 1980) and
to reduce its biasing effect in statistical analysis (Kleinbaum et al., 1982~.
During data collection, misclassification can be minimized by cross-
checking with patient records to certify that diagnoses have been cIas-
sified correctly ~ilienfeld and Lilienfeld, PESO). For dental fluorosis
classification, taking a fluoride history seems to be an appropriate part of
a difficult diagnosis. Of course, some diagnostic errors will still be
made, but probably no more than are made in clinical examinations for
caries, loss of periodontal attachment, soft-tissue lesions, or a host of
meclical conditions.
The alternative approach is to avoid fluorosis misclassification in the
data collection by recording less well-def~ned entities, such as "enamel
opacities" or "developmental defects." Whether or not that approach
reduces misclassification, it can yield data that are of limited use in
answering research questions. For example, it is not easy to interpret the
finding that "some type of defective enamel" was found in 50.~% of a
group of schoolchildren, and "white diffuse or patchy" opacities were
found in 10.2% of them (summer et al., 1990~. The latter description
best fits that of dental fluorosis, but the authors of that report do not use
the word fluorosis at all. In another study, "at least one tooth with
defective enamel" was found in 63% of children seen, and 4.4% of them
showed "diffuse patchy opacities" (Suckling and Pearce, 19841. The
latter description is closest to that of dental fluorosis of all the descrip
OCR for page 27
Dental Fluorosis 27
tions given in that report, but again the reader is left to make that inter-
pretation. Others compare the proportion of "blemishes" found in people
in fluoridated and nonfluoridated areas (Dooland and Wylie, 1989) and
the trends in prevalence of "mottling" since the introduction of fluoride
toothpastes (weeks, 1990~.
Even though the problem of misclassifying dental fluorosis is recog-
n~zed during clinical assessments, determination of risk factors for
fluorosis seems more likely to be successful when attempts are made to
measure the condition directly. Russell's guidelines for distinguishing
between enamel opacities of fluoride and nonfluoride origin, now more
than 30 years old (Russell, 1961), are still a valid diagnostic guide.
Taking a fluoride history, when practical, is also a standard and appropri-
ate epidemiological procedure that should not bias the data collected.
INDEXES FOR DENTAL FLUOROSIS
This section provides a brief description and critique of the most
common indexes used to grade dental fluorosis. The detailed clinical
criteria and scoring systems for the three most frequently used indexes
(Dean's, Thylstrup and Fejerskov's, and the Tooth Surface Index of
Fluorosis) are given in Appendix I.
The first index to grade dental fluorosis was developed by Dean in
1934; he called it the Fluorosis Index, but it is usually referred to as
Dean's index. Dean had been assigned by the U.S. Public Health Service
to investigate what was then the newly identified condition of dental
fluorosis and to determine if it was a public-health problem requiring
action. His first index (Dean, 1934) was fairly arbitrary and consisted
of a seven-point ordinal scale from normal to severe. After some years
of use, Dean modified the index to form the six-point ordinal scale that
is still used today (Dean, 1942~. The scores from Dean's index are based
on the two worst-affected teeth in the mouth and are derived from the
whole tooth rather than the worst-affected surface. Water research by
Thylstrup and Fejerskov (197X) states that all surfaces of an affected
tooth should be affected equally.) In the examination, teeth are not dried.
Dean's index has stood the test of time, but even though it is adequate for
broad definition of prevalence and trends, it is not sufficiently sensitive
at both ends of the scale for analytical research.
Dean's index inevitably was modified to meet different conditions in
OCR for page 28
28 Health Effects of Ingested Fluoride
different parts of the world. The ThyIstrup-Fejerskov (TF) index is an
extensive modification of Dean's with a strong biological basis (Thylstrup
and Fejerskov, 1978~. The lO-point ordinal TF index is more sensitive
than Dean's at the high end of the severity scale, and it appears to be
more sensitive at He mild end of the scale because its application calls
for teeth to be dried, which makes the mildest fluorosis more likely to be
detected (Granath et al., 1985; Cieaton-Iones and Hargreaves, 19901.
Indeed, the lowest scores in the TF index reflect such mild fluorosis that
some have questioned whether those categories should be inclucled in the
index as fluorosis categories (O'Mullane and CIarkson, 1990~. The TF
index has been shown to be a valid indication of fluoride content of
fluorotic enamel, although teeth scored in the first three categories of the
index hac! fluoride concentrations that were similar to those in normal
enamel (Richards et al., 1989~. The TF index might be too sensitive in
those categories, which slider only slightly in their clinical appearance,
for purposes other than analytical epidemiology (CIarkson, 19891.
The Tooth Surface Index of Fluorosis (TSTF) was developed by re-
searchers at the National Institute of Dental Research in the early 198Os
(Horowitz et al., 19841. It is intended to be more sensitive than Dean's
index by ascribing a score to each unrestored surface of each tooth
(rather than a single tooth score to the two worst-affected teeth in the
mouth), by eliminating Dean's category of "questionable," and by provi(i-
ing greater range at the high end of the severity scale. The tooth is not
ctried ciuring TSIF examination. Whether it achieves greater sensitivity
with these means has not been conf~rmecI, although it probably provides
a more valic] picture of whole-mouth severity than does Dean's inclex.
Its use of staining as a criterion has been criticized (Fejerskov et al.,
1990), because staining is a post-eruptive phenomenon that is a function
of a person's dietary habits as well as degree of enamel porosity.
The Fluorosis Risk Index (FRI) was developed to relate age-specific
fluoride exposure to development of dental fluorosis (PencIrys, 19901. It
divides the surfaces of permanent teeth into two developmentally related
groups of surface zones, which begin formation either during the first
year of life or cluring the third to sixth years. It was developed specifi-
cally for use in case-control studies ant} thus has clear rules for categoriz-
ing subjects as cases, controls, or neither, depending on the distribution
of fluorosis found on designated zones of tooth surfaces. The ability of
FR} in a case-control study to relate fluorosis to enamel developmental
OCR for page 29
Dental Fluorosis 29
periods permitted identification of risk factors that other indexes could
not do (Pendrys and Katz, 1989~. Its use is best restricted to analytical
epidemiology.
The Developmental Defects of Enamel Index (DDE) was developed by
a working group of the Federation Dentaire Internationale, and, as its
name implies, it was intended to be more than a dental fluorosis index
(FDI, 1982~. One of the reasons given for developing the DDE was that
"Classifications based on etiological considerations are premature because
only a few defects can be assigned an etiology" (FDT, 1982~. The
diagnostic problems described in the previous section affect the DDE
because it assigns codes for all types of enamel opacities and thus has
made it difficult for researchers to classify fluorosis as distinct from other
enamel defects. Data analysis in the DDE is also complicated (CIarkson,
1989~. A modified version, intended to make identification of fluorosis
simpler, has been used in a national survey of Ireland (CIarkson and
O'MulIane, 1989~. In this survey, diffuse opacities were found to be the
discriminating factor between fluoridated and nonfluoridated areas.
All the indexes have strengths and deficiencies, and choice of index
should be determined by the purposes of the study. They are not the
only systems for classifying dental fluorosis that have been proposed (Al-
Alousi et al., 1975; Butler et al., 1985a), but they are the ones most in
use at present. The major problem that arises from use of multiple
indexes is that direct comparison of prevalence and severity is difficult
when classifications of cases of fluorosis vary according to the index
used. The review carried out by the U.S. Public Health Service (PHS,
1991) even considered reports in the literature according to the index
used, a conservative approach but one that is hard to criticize purely on
scientific grounds. In this review, we attempt to pool results but focus
comparisons on prevalence and broad categories of "mild to very mild"
and "moderate to severe."
DENTAL F.LUOROSIS AND
FLUORIDE INTAXE
Dean's initial research established I.0 mg/L as the approximate con-
centration of fluoride in drinking water that best preventer] caries while
keeping unsightly dental fluorosis to a minimum (Dean, 1942), but in
OCR for page 40
40 Health Effects of Ingested Fluoride
conclusion was based on data collected in 1980. However, significant
increases in prevalence between 1980 and 1985 were reported in cohorts
13-15 years of] in the Illinois communities (Heifetz et al., 198X), al-
though they could not be discerned in cohorts 8-10 years old over the
same period. Relating age to dental fluorosis and tooth calcification, the
authors concluded that fluoride intake (from all sources) had increased
from 1970 to 1977 but had not increased much since then.
To focus on Me extent of dental fluorosis at higher water fluoride
concentrations uncler modern conditions, Figure 2-5 displays data from
three studies in communities where water fluoride concentrations were
twice the optimal concentration or higher. Overall, prevalence is high,
and most variation seems to come from the proportion of dental fluorosis
graded moderate to severe or mild to very mild. It is difficult to specify
how much of the variation is due to differences among examiners, vary-
ing intakes of fluoride in water and in other sources, differences in other
aspects of diet or physiology, individual biological variations, or some
combination of those possibilities.
loo
80
a'
'' 60
a)
40
20
o
~ ~ Moderate/Severe · Mild/\/ery Mild ~
2 2.3
2.5 2.7 2.7 2.7 2.9 3 3.1
Water Fluoride Concentration (x Optimum)
4.3 5
FIGURE 2-5 Prevalence (percent) and severity of dental fluorosis since 1980
for selected communities in the United States with above-recommended fluoride
concentrations in drinking water. Sources: Segreto et al., 1984; Eklund et al.,
1987; Heifetz et al., 1988.
OCR for page 41
Dental Fluorosis 41
A 199 ~ report from PHS compiled the results of independent investiga-
tions conducted during the 19SOs on dental fluorosis in 24 cities and
compared them with a series of PHS surveys conducted during the late
1930s and early 1940s in 21 cities (Table 2-2~. That comparison showed
that the prevalence of dental fluorosis, most of it mild to very mild, had
increased, although the modern~ay effects of fluoride from sources other
than water were not controlled for. The 19SOs data showed that the
mean prevalence of dental fluorosis in four cities with optimally fluori-
dated water supplies was about 22% (17% very mild, 4% mild, 0.~%
moderate, and 0.~% severe). In another city with a water fluoride
concentration in the range of .-2.2 mg/L, dental fluorosis prevalence
was 53% (23% very mild, 17% mild, 8% moderate, and 5% severe).
In two other cities with water fluoride concentrations greater than 3.7
mg/L, prevalence was about 84% (25% very mild, 27% mild, 19%
moderate, and 14% severe). The data in the PHS report also showed that
the greatest relative increase in fluorosis prevalence since the early
studies was in communities with very low water fluoride concentrations,
demonstrating the influence of sources of fluoride other than water.
Those sources make it difficult to estimate fluoride exposure; they repre-
sent a confounding factor in studies of the relation between fluoride
exposure and dental fluorosis.
RISK FACTORS IN DENTAL FLUOROSIS
Dental fluorosis is a function of total fluoride intake during critical
dental developmental periods, and in modern conditions, fluoride is
ingested from numerous sources in addition to drinking water. Research
efforts to measure the quantities ingested from all such sources are often
frustratingly imprecise, because quantifying fluoride intake from current
and past use of water, food, and toothpaste, together with past intake
from supplements or infant formula, can be extremely difficult. No
tissues of the body can be measured for lifetime intake of fluoride.
Measurements in plasma might be the best but can be affected by changes
in recent intake. As a relatively invasive procedure, it is also not easy
to use in field studies. Bone obviously cannot be biopsied from volunteer
study participants. Nail clippings reflect only fairly recent fluoride intake
and can be readily contaminated.
Despite these measurement problems, risk factors for dental fluorosis
OCR for page 42
42 Health Effects of Ingested Fluoride
TABLE 2-2 Percent Prevalence of Dental Fluorosis by Clinical Classification
and Concentration of Water Fluoride from Dean's 1940 21-City Survey
and 1980's Sunrey Using Dean's Index
Total No. Cities
and Studies
Water
Fluoride, 1940s 1980s
<0.4
Prevalence, Pa
Mean Sample Size per
City and Study Very Mild
1940s 1980s 1940s 1980s
10 5
360
326
0.9
0.7
4.4
3.0
0.4~.6 3 1 427 126 5.0 ~2.4
1.4
0.7-1.2 4 4 270 471 12.3 + 17.7 +
2.3 16
1.3-1.7 1 3 477 175 27.0 ~19.5 +
4.2 4.1
1.8-2.2 2 1 222 143 35.1 ~23.1
7
2.3-2.7 1 5 4~)4 174 42.1 40.5
7
2.8-3.2 0 3 124 26.2
16
3.3-3.7 0 0
>3.7 0 2 163 24.8
11
Total 21 24
aMean it standard deviation.
Note: The 21 cities represented in the 1940s column are those cities sur-
veyed by Dean in the 1940s. The 24 cities represented in the 1980s column are
those cities surveyed by different investigators using Dean's index in the 1980s.
The means and standard deviations are derived from the cities classified by
respective water fluoride concentrations.
Source: PHS, 1991.
have been identified from epidemiological study, but it is still difficult to
rank their importance with any certainty. One such risk factor is ob-
viously a high fluoride concentration in drinking water (Szpunar and
Burt, 19881; even minor adjustments in water fluoride concentrations can
lead to significant changes in the prevalence of clinically detectable
fluorosis (Evans and Stamm, 199Ib). Other risk factors are ingestion of
OCR for page 43
Dental Fluorosis 43
Prevalence, %. (Continued)
Mild Moderate Severe Total
1940s 1980s 1940s 1980s 1940s 1980s 1940s 1980s
0 2.2 + 0 0.1 + 0 0 0.9 ~6.4 +
2.8 0.3 0.7 2.6
0.6 + 0 0 0 0 0 5.6 + 2.4
0 3 1.2
1.4+ 4.4+ 0 0.8+ 0 0.1 + 13.6+ 22.2+
0.4 2.0 0.3 0.3 2.0 14
3.1 + 5.6 ~0 0.7 + 0 0 30.2 + 25.7 +
1.1 4.7 0.6 4.3 9
7.5 + 2 16.8 1.1 + 8.4 0 4.9 44.0 + 53.2
0.1 6
21.3 29.5 + 8.9 8.4 + 5 1.5 0 73.8 78.5 +
5 9
30.0 + 15.0 + 2.8 + 5 74.0 +
11 16 22
27.8 + 19.3 + 13.9 + 83.4 +
4 17 12 16
fluoride (both intentional and inadvertent from sources other than drink-
ing water. Indeed, most dental researchers (Horowitz, 1991; Rozier,
1991; Szpunar and Burt, 1992) believe that the best approach to stabiliz-
ing the prevalence and severity of dental fluorosis is to control fluoride
ingestion from foods, processed beverages, and dental products rather
than reduce the recommended concentrations of fluoride in drinking
water.
A large number of studies have concluded that fluoride supplements
are a risk factor for dental fluorosis (Holm and Andersson, 1982; Suck
ling and Pearce, 1984; Hellwig and Klimek, 1985; Bohaty et al., 1989;
Dooland and Wylie, 1989; Kumar et al., 1989; Larsen et al., 1989;
OCR for page 44
44 Health Effects of Ingested Fluoride
Pendrys and Katz, 1989; Woolfolk et al., 1989; Woltgens et al., 1989;
Holt et al., 1990; Small et al., 1990; Riordan and Banks, 1991;
Lalumandier, 19921; however, the relation shown was weak in some of
the reports. Other studies have failed to show such a relation (Butler et
al., 1985b; Bagramian et al., 1989; Stephen et al., 1991~. Fluoride
supplements are used widely (Brunelle and Carlos, 1990) and often are
prescribed inappropriately (Pendrys and Morse, 1990; Levy and
Muchow, 1992~. Some of the compliance data are imprecise, however,
because use is usually documented retrospectively. It is not clear wheth-
er it is solely the misuse of supplements that results in dental fluorosis or
whether use at recommended dosages produces the condition (Workshop
Report, 1992~. In either case, the appropriateness of the recommended
supplementation schedules should be considered.
The swallowing reflex is not fully developed in children of preschool
age, and their inadvertent swallowing of fluoride toothpaste has been
identified as a risk factor (Hellwig and Klimek, 1985: Osuii et al., 19X8;
Pendrys and Katz, 1989; Milsom and Mitropoulos, 1990; Lalumandier,
19921. However, the fluorosis reported was often very mild and barely
discernible. In addition to toothpaste, prolonged use of infant formula in
the fluoridated area of Toronto, Ontario, was identified as a risk factor
for dental fluorosis (Osuji et al., 19881. High socioeconomic status also
emerged as a strong risk factor in a well-conducted case-contro' study
(Pendrys and Katz, 1989), but that finding has not been confirmed in
other studies (Bagramian et al., 1989; Hamdan and Rock, 1991~. Fluo-
ride in foods and beverages processed with fluoridated water has long
been suspected as a risk factor but has not been clearly demonstrated.
Unexpectedly high fluoride concentrations in particular foods and bever-
ages (Clovis and Hargreaves, 1988; Burt, 1992; Pang et al., 1992),
however, might stimulate further research in this area.
Although the subject has received little attention, some data suggest
that dental fluorosis is more prevalent among African-Americans than
among other races or ethnic groups in the same community. Russell
(1962), in the Grand Rapids fluoridation study, noted that fluorosis was
twice as prevalent among African-American children than white children.
In He Texas surveys in the 1980s, the odds ratio for African-American
children having dental fluorosis, compared with Hispanic and non-His-
panic white children, was 2.3 (Butler et al., 1985b). Dental fluorosis
also tended to be more severe among African-American children than
white children in the Georgia study (Williams and Zwemer, 1990),
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Dental Fluorosis 45
although the difference was not statistically significant. In Kenya,
prevalence and number of severe cases were unexpectedly high when
related to fluoride concentrations in drinking water (Manji et al., 1986c),
although nutritional factors could have confounded these results. The
reasons for these findings are unknown and do not appear to have been
explored further.
THE RELATION BETWEEN
DENTAL F1UOROSIS AND CARIES
Dean's studies of this relation in the 1930s showed a sharp reduction
in caries prevalence when communities were ranked from the lowest
water fluoride concentrations (virtually zero) to approximately ~ .0 mg/~.
His data also indicated that caries prevalence leveled out when communi-
ties with water fluoride concentrations above ~ .0 mg/L were rank-orderec]
(Dean, 1942~. On the other hand, caries prevalence was observed to
increase when fluoride concentrations were such that severe dental fluoro-
sis was common and the enamel of affected individuals was friable and
liable to fracture (Grobler et al., 19X6~. Other data on the relation are
inconsistent. Some studies have found that data follow the I-shaped path
shown in Figure 2~: with increasing fluoride concentrations, caries
prevalence diminishes to a certain point and then increases again. How-
ever, a different relation is seen in Figure 2-7, in which caries experience
among adults in Lordsburg, New Mexico, which had 5 times the optimal
fluoride concentration in drinking water, was below that found in the
neighboring community of Deming, which had an optimal concentration.
Differences were found in the amount of dental treatment received be-
tween the two communities, however, a factor that could have influencer!
the results. An earlier Texas study also reported that caries prevalence
among children 12-15 years old continued to diminish even when com-
munity fluoride concentrations were 6-8 times the optimal concentration
(Englander and DePaola, 1979~. These contradictory findings are dif-
ficult to explain and merit further research.
CONCLUSIONS
The data show that the prevalence of dental fluorosis, nearly all of it
OCR for page 46
46 Health Effects of Ingested Fluoride
6
5
In
IL
3
a)
~ 2
~1980 - 19851
o
Optimum 2x optimum 3x optimum
Water Fluoride Concentration
4x optimum
FIGURE 2-6 Canes experience of children 13-15 years of age in Illinois in
1980 and 1985 relative to the fluoride concentration in community drinking
water. DMFS = decayed, missing, and filled surfaces. Source: Heifetzet all,
1988.
mild to very mild (Figure 2-IB and 2-IC), rises with increasing fluoride
concentrations in drinking water. The data also show fairly consistently
that a small, though measurable, proportion of a population exhibits
moderate-to-severe dental fluorosis with .-2.0 times the optimal con-
centration of fluoride in drinking water, and this proportion generally
increases with increasing concentrations of fluoride. However, the data
are not consistent enough to permit a firm definition of the relation
between moderate-to-severe dental fluorosis and water fluoride concentra-
tions. In addition, other uses of fluoride, independent of water fluoride
concentrations, clearly affect the prevalence of dental fluorosis. Develop-
ment of a firm public-policy recommendation is also inhibiter! by lack of
knowledge of the public's perception of less-than-severe fluorosis (Figure
2-1B, 2-IC, and 2-lD).
Public policy on use of fluoride to promote oral health should be
aimed at keeping dental fluorosis prevalence as low as possible relative
to the benefits of caries control, a classic public-health tracle-off. When
OCR for page 47
Dental Fluorosis 47
12
10
Cl) 8
2
a)
-
2 4
2
| HI Lordsburg ~ Deming |
l
Rl 1~1
R ~ I_ RAIR
R SIR My ~
........ ,,,., , ,,,,, , . , , ,.,,.,.,,,.,,.,,,, . , , ,, , ,,,,,~ ~ 1 , ,.,,,., ,, ,,,,,,,, , , ,.' ,
R IlR I , ~
Rtt. l ! ~ ,
R 89 l i t l
R ~ l l
-------- ---------- -------- ---1 1 .,,, ,,., ~
~ _ 1 2 ' ~. 1 1 . : -i 1
~ ~ 1~ at l 1 .......................... 1
6 ~ · 1 ~ l 1
1:. . 2::::2 2 """"'-. ": _ 1:.-.2.~ 2 : · 2 2 2:2 - :s , 1 ~ ::2 ::::::::- ::.::::2'-.- 1
1:. :::::: ~ : F - - .: -.: :s , I :::::::::::::::.::::--- :: -.- I
1: ".2 2::"2 "::-""2::''-: _ 1:::-"2. --: -:::: - 2-:: - :s , 1 ::: ::::::--::::-.2.2.- :::::::: 1
--- 122222'"2'''"'' I'''' --- 1'''''"''''''"' ~1 .. ,, ,, , ,,,,,,,, , '''''''''''''''''''1
1:::-2:::::: :::::: :::: :.::: _ 1:.2-2." :::: :2 2 - 2-: - 2:.: :s , 1 :::::::2- -::- ::2 - -.2 - 2-:::: 1
2c,,'2:,2f',~,2-~->,-5, ·., ,, ,1
1 '22--- ~1"''''""'''! 1 ............. .1
1:::::::2 2 ::::2::::.'.'.:::::::: ~1:'::: :: .::: :.: .- . :e 1 , ::: :,.: :.-:::::::: 1
1''-''"' ~1'''''''''"! 1 . 1
o
27-40 41-50 51-65
Age Groups
,,,,,,,,,,,,,....,....~
FIGURE 2-7 Caries experience of adults 27~5 years of age in Deming (flu-
onde at 0.7 mg/L) and Lordsburg (fluoride at 3.5 mg/L), New Mexico, in 1984.
Source: Eklund et al., 1987.
drinking water is the only source of fluoride, the evidence supports the
conclusion that water fluoridation at currently recommended concentra-
tions results in prevalence of mild-to-very-mild dental fluorosis of about
10% and very little severe fluorosis. At twice the recommended con-
centrations, the prevalence of moclerate-to-severe clental fluorosis is small
but measurable. At higher concentrations in drinking water, the preval-
ence increases, although limited evidence shows that the extent ant!
distribution of dental fluorosis at 4 times the optimal concentration is not
much higher than that at 2 times the optimum. At 5 times or more,
however, the prevalence of moderate-to-severe dental fluorosis is substan-
tially higher.
Interpretation of current data is difficult because of exposure to fluo-
ride from sources other than drinking water. In the modern U.S. envir-
onment, people are exposer] to fluoride from food, beverages, toothpaste,
and a variety of prescribed or over-the-counter dental products. Many
of these are intended for topical use only, but some inadvertent ingestion,
especially by young children, is unavoiciable. The most effective ap
OCR for page 48
48 Health Effects of Ingested Fluoride
preach to stabilizing the prevalence and severity of dental fluorosis,
without jeopardizing the benefits to oral health, is likely to come from
more judicious control of fluoride in foods, processed beverages, and
dental products, rather than a reduction in the recommended concentra-
tions of fluoride in drinking water. But applying such a policy would be
formidable; reduction of fluoride concentrations in drinking water would
be easier to administer, monitor, and evaluate. If it proved to be scientif-
ically justified, such a policy could be considered.
Current regulations of EPA are that the maximum contaminant level
(MC L) for fluoride in drinking water is 4.0 mg/L, regardless of mean
temperature. That standard is considered low enough to prevent crippling
skeletal fluorosis, and dental fluorosis is accepted as a purely cosmetic
defect with no general health ramifications. However, the most severe
forms of dental fluorosis might be more than a cosmetic defect if enough
fluorotic enamel is fractured and lost to cause pain, adversely affect food
choices, compromise chewing efficiency, and require complex dental
treatment. Severe dental fluorosis has been seen in the United States at
3.5 mg/I~ (in a warm climate, 5 times the recommended fluoride con-
centration), but even in that community the ramifications of fluorosis
were insufficient to recommend a reduction in the MCL. This conclusion
points out the need to revise the PHS guidelines related to temperature
and for more information on the impact on general health that results
from damage to teeth as a consequence of the severest forms of fluorosis.
If recommended fluoride concentrations in drinking water should still be
expressed in a range related to mean temperature, the MCL might also
be expressed more logically as a temperature-related range rather than a
single figure.
Overall, the evidence of the current current relation of dental fluorosis
to fluoride in drinking water in the United States is still sparse, and the
evidence that does exist is too inconsistent to be used as a basis for
recommending changes in EPA regulations. When the results of further
research become available, EPA's regulations might need further review
and modification.
RESEARCH RECOMMENDATIONS
Studies should be conducted on the sources of fluoride during the
OCR for page 49
Dental Fluorosis 49
critical stages of tooth development in children and on the contribution
of the various sources to dental fluorosis etiology. Such information
would permit more precise regulation of fluoride products to control
fluorosis while retaining fluoride's substantial cariostatic benefits.
Studies should be conducted on the relation between water fluoride
concentrations and dental fluorosis in various climatic zones. Findings
could serve as a basis for any needed revision of the 1962 PHS guide-
lines.
The lowest concentration of fluoride in toothpaste that produces ac-
ceptable cariostasis should be determined. That information would
permit the marketing of children's toothpastes that would retain anticaries
benefits while minimizing the risk of fluorosis.
Further studies should be conducted on the contribution of ingested
fluoride and fluoride applied topically to teeth to prevent caries. The
results would permit more efficient use of fluoride for caries prevention,
thus reducing the risk of fluorosis.
OCR for page 50
Representative terms from entire chapter:
drinking water
