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Clinical Feature
Pucker Up - The Effects of Sour Candy on Your Patient's Oral Health
A Review of the dental erosion literature and pH values for popular candies
Robyn R. Loewen, D.D.S.,* Robert J. Marolt, D.D.S.,** and John D. Ruby, D.M.D., Ph.D.†
Although
the harmful effects of acidic beverages on teeth have been well established and
communicated through a variety of clinical articles and public education
pieces, the Minnesota Dental Association’s Public Relations Committee has
determined that the new and emerging concern of the erosive effects of sour
candy on the dentition should be brought to the attention of dental
professionals and the public alike. Furthermore, since the serious irreversible
damage caused by erosion is difficult and costly to treat, early detection and
the initiation of preventive strategies are paramount to minimizing long-term
consequences. The following article should serve as a review of the general
topic of erosion, and should provide additional information about the
increasing prevalence of erosion and the specific risks of sour candy
consumption.
Walk into
any convenience or grocery store candy aisle today, and take a look at the
extensive and colorful array of candy on the shelves. In addition to the
traditional concoctions of chocolate, caramel, and nuts, there has been a
distinct shift in preference for “extreme” or “intense” sour and fruity flavor
experiences. The specific marketing of these sour fruity candies to children
through packaging style and labeling, such as brightly colored plastic baby
bottles filled with citric-acid-laced powder, has increased their appeal and
has led to a popular new source of dietary acid, and unfortunately, a new
contributing factor in the increasing prevalence of dental erosion.
Etiology
of Tooth Wear
Tooth
wear is caused by a complex interrelationship between erosion (dissolution of
hard tissue by acidic substances), attrition (loss of tooth substance from
tooth-to-tooth contact), and abrasion (wear by contact between tooth and
another material). It is difficult to assess the relative influence of each of
these contributing factors to tooth wear.1,2,3 However, the location of the
defects on teeth can assist in making a differential diagnosis.4 • Abrasion, such as that caused by overly aggressive tooth brushing, results in
buccal indentations near the cervical margin or root surface of teeth, usually
without any evidence of decay or decalcification. • Attrition defects are identifiable by matching facets on occluding teeth, fractured
cusps and restorations, and relatively similar wear rates of enamel and dentin. • Erosion from industrial acid exposure typically manifests on the labial
surfaces of maxillary incisors. • Gastroesophageal reflux disease and frequent vomiting cause the loss of lingual
enamel on the maxillary incisors and the lingual surfaces of the maxillary
premolars and molars. • Acidic liquids cause preferential erosion of the anterior maxillary and
mandibular teeth, and are often accompanied by cervical decalcification and
interproximal decay. • Erosion from acidic solids such as candy manifests mainly on posterior teeth
with smooth, glazed enamel which appears to be highly polished, “cupping” of
cusp tips on posterior teeth, and the impression of “raised” restorations from
a loss of the surrounding enamel (Photos 1-6).

Erosion Dental
erosion was described as early as 1803 by John Hunter in his text The Natural
History of the Human Teeth as “decay of the teeth by denudation”. Hunter
specifically differentiated the characteristics of erosion from that of dental
decay of bacterial origin.5 Since that time erosion has been defined as the
irreversible loss of dental hard tissue due to a chemical process, without any
involvement by microorganisms.6 The causative agents are usually acidic
substances, whether intrinsic (gastric acid from reflux or repeated vomiting)
or extrinsic (consumption of acidic foods or beverages, repeated exposure to
chlorinated water, and industrial chemical exposure). Although identification
of patients with intrinsic sources of acid erosion such as gastroesophageal
reflux and those with environmental exposure are critical, this article will
focus on the effects of dietary acids on the dentition, and will introduce new
information on specific risks with frequent consumption of acidic candy.
The
mechanism of tooth erosion has been widely described. When salivary pH levels
drop to a critical level, enamel loses calcium by the formation of calcium
citrate complexes, causing an etching of the enamel surface. After this
superficial decalcification of enamel by acid, the remaining three to five
micron layer of demineralized enamel or dentin is more susceptible to the
effects of abrasion or attrition.7 The critical pH for enamel dissolution is
5.5. However, due to the modifying effects of the oral cavity, exposure to
acidic foods and beverages with pH values below 4 can result in dental
erosion.8
There has
been increasing concern over the high prevalence of tooth erosion in children,
with research activity taking place in Europe, Scandinavia,
Australia, and North and
South America within the last decade.9,10,11,12,13 England’s 1993 National Survey of
Child Dental Health included the evaluation of tooth erosion for the first
time.14
Studies
of dental erosion show that the prevalence rates in children seem to be
increasing.15 In epidemiologic studies prior to 2001, the prevalence of erosion
in children had been estimated between 2 and 57%.16,6 In a more recent
Australian study (2007), erosion rates in primary teeth were found to be as
high as 68%.17
Significant
erosion can cause dentin sensitivity and difficulty eating, pulpal inflammation
and/or pulpal exposure, progressive enamel microfracture resulting in a loss of
occlusal vertical dimension, and cosmetic changes due to the exposure of
dentin, making the teeth appear yellow.
Although
acid erosion creates significant enamel damage, caries is not frequently seen
in eroded teeth until the late stages of the condition, when the exposed dentin
is unable to withstand further bacterial acid challenges. Plaque does not
typically build up on the highly polished surfaces. The lack of decay in the
early stages of erosion can deceive patients into a false sense of “dental
health,” which can make any motivation for changes to poor dietary habits
difficult.
Interestingly,
dental erosion is frequently seen in individuals exhibiting high levels of oral
hygiene.18 Toothbrushing immediately following an acid attack can result in
increased abrasion of the soft, demineralized surface.19 Similarly,
toothbrushing immediately prior to the consumption of acidic foods and
beverages results in loss of the protective pellicle, and a greater risk
of decalcification.20,21
Young,
immature enamel is particularly prone to the erosive effects of dietary acid
due to its relative porosity and lack of complete mineralization.22,23,24 The
enamel is also thinner in primary teeth than in permanent teeth, so that the
erosive process may reach dentin more rapidly in primary teeth.17 Also, it has
been shown that children between three and seven years of age have larger
variations and slower salivary sugar clearance rates and also lower salivary
flow rates than older children and adults.25 This suggests that, during the
childhood and early adolescent years, when candy and soft drink consumption may
be the greatest, both primary and permanent teeth are most susceptible to
erosion.
Dietary
Acids Numerous
studies have shown the erosive potential of soft drinks, fruit juices, and sports
drinks.26,27,11,28,29,
30,31,32,8,33,34,35 The degree of enamel dissolution has been shown to be
directly related to the acidity of the substance and varies by type of acid.36
Determinants of acidity include the total amount of acid available (titrable acidity),
the amount of acid present in the solution (H+ ion concentration as measured by
pH), and the strength of the acid (ease of dissociation as expressed by the
acid dissociation constant, pKa). However, the erosive potential of a candy or
beverage is a complex interaction of acidity, pH value, phosphate and fluoride
levels, the type of acid, and its inherent calcium chelating properties. The in
vitro erosive potential is further modified by salivary pH, salivary flow
rates, salivary buffering capacity, calcium, phosphate and fluoride levels in
saliva, duration of exposure, frequency of exposure, and time of day of
exposure. For instance, exposure to acidic foods/beverages just before bedtime
has been shown to be the most harmful.37,38,30,11
The
ability of food acids to chelate calcium is considered to be a major factor in
dental erosion.39 Citric acid is the most erosive component in foods and
beverages, because it chelates calcium even at higher pH levels, such as those
found in buffered saliva.30,40,41,42,43,44,45,8,34 In fact, it is twice as
destructive to dental enamel as hydrochloric or nitric acid.42 Significant
dental erosion has also been shown to result from the use of vitamin C
(ascorbic acid) supplements in tablet form.7 The pH of vitamin C tablets is
1.92, well below the levels considered safe for dental enamel.
Since the
destructive effects of dietary acids have been well documented, one might ask
why they are used in food products at all. Some of the functions of food
acidulants include flavor enhancement and modification, food preservation,
pectin gelation, the inhibition of enzymatic browning, food leavening, and the
complexation of cation impurities.39 A list of common dietary acids can be seen
in Figure 1.

 Sour
Candy Though
the destructive potential of acidic beverages and fruits has been studied
extensively, there should be growing concern over the preponderance of low pH
candies marketed toward children and their potential for a different pattern of
occlusal enamel erosion, especially on posterior teeth. Dr. John Ruby, a
pediatric dentist and associate professor at the University of Alabama
at Birmingham School of Dentistry, is convinced that the combination of
extremely low pH candies, immature tooth enamel, and a high frequency of ingestion
is causing serious harm to children’s teeth.
Dr. Ruby
recently tested the pH levels of many popular candies, with startling results.
One gram of each candy was dissolved in 5 ml water, then tested with Fisher
Scientific pH paper accurate to within 0.1 unit. Results of his testing can be
found in Figure 2. Most of the sour and fruity candies had very low pH levels.
Some of the more surprising findings from his testing included Warheads Sour
Spray liquid — pH 1.6, and Altoids Citrus Sours hard candies — pH 1.9. (As a
familiar frame of reference, battery acid has a pH of 1.0.) More importantly,
most of the sour fruity candies had lower pH levels than any of the soft drinks
previously studied. Citric acid is the common “sour” flavoring agent in these
products, and as mentioned previously, is the most erosive dietary acid. The
low pH of these candies can also cause localized soft tissue irritation from
surface damage to the mucous membranes of the inner cheek and tongue. In fact,
many of these candy package labels contain a written warning about potential
soft tissue irritation with frequent ingestion.
When
different candy flavorings are compared, the citric-acid-related fruit flavors
of lemon, cherry, and grape destroy much more enamel than the near neutral
aromatic flavors of cinnamon and mint.46 Some examples of currently popular
candies with the potential for erosive damage are the intensely flavored sour
chewy candies, powdered candies, sour gels and sprays, and powder-coated gums.
In addition to a low pH level, the consistency of a candy substance contributes
to the erosive potential of a product as well. For instance, insoluble starchy
“gummy” candies, thick sticky gels, and citric acid powders are particularly
harmful due to their prolonged clearance times
and abrasivity.46
Despite the current lack of in vivo research
specifically addressing the erosion risks from sour, fruity candy, the body of
knowledge regarding the erosive damage caused by other low pH foods and
beverages is significant, and the potential for erosive damage to children’s
teeth with frequent ingestion of these candies cannot be ignored.

Diagnosis
and Intervention Management
of dental erosion consists of five essential components: diagnosis and etiology
assessment, monitoring of the progression of enamel loss, dietary and oral
hygiene modifications, remineralization, and restorative treatment.16 A working
understanding of the complex interaction of dental structures, oral chemistry,
and dietary factors is necessary for proper recognition of erosion,
interpretation of any type of assessment, and appropriate strategies for
treatment.
Diagnosis Determination
of erosion as the specific cause of tooth wear and the subsequent investigation
into possible sources of intrinsic or extrinsic acid are the first steps to
diagnosis. A simple questionnaire can elicit adequate information to begin to
differentiate between the various causes of tooth wear, including erosion,
attrition, abrasion, and possibly abfraction (Figure 3). If other causes of tooth
wear have been ruled out and acid erosion is suspected, a source of acid must
be identified.
Intrinsic
acid sources such as gastroesophageal reflux or frequent regurgitation (eating
disorders, stress vomiting) require referral to an appropriate medical
professional for the patient’s overall health maintenance.47 Environmental
exposure to an acid source requires thoughtful education as to the long term
effects of the exposure, efforts to reduce exposure, and appropriate supportive
care.
Discovery
of a dietary source of acid will require careful questioning and dietary
analysis. A five-day food diary has been suggested, and should include three
weekdays and two weekend days. This diary should include all medicines and
vitamin supplements, as well as the frequency and method of ingestion (i.e.,
chewables, effervescent liquid, swish and swallow, capsules to be swallowed).48
Review and interpretation of the diary can be performed by the dentist, with
specific attention paid to the frequency and pattern of dietary acid
consumption.
Monitoring Ongoing
assessment of enamel loss is challenging in a clinical setting. Although
comparative intraoral photographs and study models will assist in evaluating
long term surface changes, actual quantitative measurements of enamel loss
within short term intervals are more difficult to achieve. Detailed clinical
notes of any visible changes in tooth anatomy, patient sensitivity, or
functional problems are essential in an ongoing assessment of the rate and
progression of enamel loss.
Standardization
of monitoring techniques is needed. Several indices have been proposed for
measuring tooth erosion.49,50,51,4 However, these indices are more useful for
broad-based epidemiological studies of tooth wear, since they fail to localize
and quantify actual enamel loss.9 Salivary tests also need to be developed that
can easily be used in clinical practice to assess salivary buffering capacity,
flow rate, and composition.
 Diet and
Hygiene Modifications The
behavior modifications listed in Figure 4 will aid dentists in coaching
patients to minimize the risk of erosion. Every attempt should be made to
reduce the frequency of consumption of acidic candies, and such foods should be
restricted to main meals.48,52 For example, a change in the timing of eating
sour candy between meals or at bedtime to a mealtime can reduce the severity of
the acid attack due to more efficient clearance time and the buffering benefits
of saliva.37 Encourage patients to finish a meal with something neutral or alkaline
— cheese, milk, or sugar-free chewable antacid tablets. Chewing sugar-free gum
will stimulate saliva flow, providing a natural buffering action. Rubbing
bicarbonate-containing toothpaste on the teeth with a fingertip will reduce the
acid challenge on the tooth surface. Also, rinsing with water rather than
brushing teeth immediately following an acid challenge can reduce
demineralization by clearing the acid from the oral cavity, and will prevent
inordinate damage by toothbrush abrasion of the fragile enamel surface.48
Finally, patients should use less abrasive “sensitive” toothpastes or those
with bicarbonate as an active ingredient, rather than highly abrasive whitening
toothpastes.
Remineralization Treatment
for erosive defects should begin with stabilization of the structural integrity
of the tooth surface and the promotion of remineralization. Topical fluoride
found in over-the-counter rinses and toothpastes, prescription-strength
toothpastes, professionally applied fluoride treatments, and fluoride varnishes
will provide reduced enamel solubility and control the symptoms of tooth
sensitivity.53 Oral hygiene products containing amorphous calcium phosphate can
enhance fluoride uptake for more efficient remineralization and an increased
resistance to further demineralization.
Restoration The goal
of restorative treatment should be to maintain adequate function and esthetics
of primary and permanent teeth. Erosion from the chewing or sucking of acidic
candy primarily affects the occlusal surfaces of the posterior teeth. Eroded
primary teeth should be restored to maintain vertical dimension and
mesial-distal width, reduce symptomatic sensitivity, and provide pulpal
protection for the maintenance of vitality until exfoliation. Frequently,
full-coverage stainless steel crowns are the most appropriate restorative
choice for severely eroded posterior primary teeth.
The
restoration of eroded permanent teeth requires choosing the least invasive
procedure while providing maximum protection from the further loss of tooth
structure. Occlusal sealants and resin-bonded restorations in “cupped” cusp tip
lesions will provide mechanical protection for the affected surfaces, reduce
dentin hypersensitivity, and improve the appearance of severely eroded
posterior teeth.16 Many of these teeth will eventually require full-coverage
cast or ceramic restorations to preserve remaining tooth structure and provide
adequate esthetics and function. Since full-coverage restorations are costly
and involve significant additional loss of tooth structure, it is essential
that appropriate early counseling and behavior modification should occur to
prevent the need for such invasive treatment.
Summary Children’s
increasing preference for “extreme” sour candy and the industry’s response in
the variety of sour candies marketed to children has created a new twist on the
dental erosion front. Additional research is needed to test the actual erosive
potential of sour candies in vivo and the modifying effects of factors such as
salivary buffering capacity. Streamlined measurement tools and standardization
of assessments are needed to enable population-based epidemiological studies of
the effects of all types of tooth wear. New remineralizing products are
reaching the market, but long term efficacy studies on their ability to
actually provide protection from erosive demineralization are needed. Lastly, a
practical clinical method to measure salivary flow rate, salivary pH, and
buffering capacity needs to be developed, so that individual susceptibility factors
can be assessed. However, a simple awareness of the potential for increased
erosion from extrinsic food sources and an understanding of the mechanism of
demineralization are essential to early detection, intervention, and the
prevention of invasive restorative procedures.
 Not only
are extremely sour candies prevalent and readily available at grocery and
convenience stores, as well as athletic and movie concession stands, the
marketing strategy of confection companies directed at very young children
should be particularly disturbing to dentists and parents. For example, “Toxic
Waste” is a sour hard candy presented in a colorful plastic garbage can. The
label offers a challenge to hold the candy in the mouth as long as possible,
with a scoring chart measured by the number of seconds tolerated. In addition,
the label also refers young consumers to a “cool” website offering games and
other activities, as well as advertisements for other candies made by their
company. There is also a warning label on the packaging about potential soft
tissue irritation with continued use.
Other
youth-targeted packaging includes pacifier-shaped suckers, baby bottles filled
with citric acid powder, and sour gel squeezed from a tube with a “real baby
nipple”. Interestingly, the label for the sour gel with the baby nipple claims
the candy has “no refined sugar, less than half the calories of the original and
even better tasting. Real fruit juice concentrates make contents equal to 100%
juice. A portion of the proceeds is donated.” (Since the manufacturer donates a
portion of its proceeds to the American Diabetes Association, the logo for the
American Diabetes Association can also be found on the label.) The label also
has a warning: “Choking hazard – small parts, not for children under 3 years of
age. Avoid getting into eyes. If this occurs, flush eyes with water immediately
for 15 minutes. If irritation persists, consult your doctor. Consuming large
quantities within a brief time period may cause temporary irritation to
sensitive tongues.” …and teeth!
Author’s
Note This
author knows from personal experience as a parent how much these products
appeal to children. Dentists and parents need to realize the possible harm to
their children’s teeth with repeated exposure to these “treats”. As advocates
for our patients and their families, Minnesota
dentists need to spread the word about this emerging trend and its potentially
devastating effects.
References 1. Pindborg J. Pathology of dental hard tissues. Copenhagen, Denmark:
Munksgaard. 1970. 2. Bell EJ, Kaidonis J, Townsend G, Richards L. Comparison of exposed dentinal
surfaces resulting from abrasion and erosion. Aust Dent J 43:362-366, 1998. 3. Smith B. Tooth wear: aetiology and diagnosis. Dent Update 16:204-212, 1989. 4. Eccles JD. Dental erosion and diet. J Dent 2:153-159, 1974. 5. Asa R. Special report: erosion. AGD Impact 35(4):54, 2007. 27Jan2008. 6. Lussi A, Jaeggi T. Dental erosion: from diagnosis to therapy. Monogr Oral Sci
20:140-151, 2006. 7. Giunta JL. Dental erosion resulting from chewable vitamin C tablets. JADA
107:253-256, 1983. 8. Rytömaa I, Meurman JH, Koskinen J, Laakso T, Gharazi L, Turunen R. In
vitro erosion of bovine enamel caused by
acidic drinks and other foodstuffs. Scand J Dent Res 96:324-333, 1988. 9. Gandara BK, Truelove EL. Diagnosis and management of dental erosion. J Contemp
Dent Pract 1(1):16-23, 1999. 10. Deery C, Wagner ML, Longbottom C, Simon R, Nugent ZJ. The prevalence of dental
erosion in a United States and United Kingdom sample of adolescents. Ped Dent
22:505-510, 2000. 11. Milosevic A. Dietary acids – a risk to dental health? British Food Journal.
106(6):457-464, 2004. 12. Maupomé G, Ray JM. Structured review of enamel erosion literature (1980-1998):
a critical appraisal of experimental, clinical and review publications. Oral
Diseases 6:197-207, 2000. 13. Imfeld T. Dental erosion. Definition, classification and links. Eur J Oral Sci
104:151-155, 1996. 14. O’Brien M. Children’s dental health in the United Kingdom 1993. Office of
Population Censuses and Surveys. Her Majesty’s Stationary Office, London, 1994. 15. Sheiham A. Dietary effects on dental diseases. Pub Health Nut 4:569-591, 2001. 16. Linnett V, Kim Seow W. Dental erosion in children: a literature review. Ped
Dent 23:37-43, 2001. 17. Kazoullis S, Seow WK, Holcombe T, Newman B, Ford D. Common dental conditions
associated with dental erosion in schoolchildren in Australia. Ped Dent
29:33-39, 2007. 18. Shaw L, Smith AJ. Dental erosion – the problem and some practical solutions.
Brit Dent J 186(3):115-118, 1998. 19. Zero D. Etiology of dental erosion – extrinsic factors. Eur J Oral Sci
104:162-177, 1996. 20. Kuroiwa M, Dodaka T, Kuroiwa M, Abe M. Brushing induced effects with and
without a non-fluoride abrasive dentrifice on remineralization of enamel
surfaces etched with phosphoric acid. Caries Res 28:309-314, 1994. 21. Amaechi B, Higham S, Edgar W, Milosevic A. Thickness of acquired salivary
pellicle as a determinant of the sites of dental erosion. J Dent Res
78:1821-1828, 1999. 22. Massler M. Teen-age cariology.Dent Clin No Am 13:405-423, 1969. 23. Wilson PR, Beynon AD. Mineralization differences between human deciduous and
permanent enamel measure by quantitative microradiography. Arch Oral Biol 34:85-88,
1989 24. Johansson AK, Sorvari R, Birkhed D, Meurman JH. Dental erosion in deciduous
teeth — an in vitro and in vivo study. J Dent 29(5):333-340, 2001. 25. Crossner CG, Hase JC, Birkhed D. Oral sugar clearance in children compared with
adults. Caries Res 25:201-206, 1991. 26. Erickson PR, Alevizos DL, Rindelaub DJ. Soft drinks: hard on teeth. Northwest
Dentistry 2:15-19 27. Toumba J, Duggal MS. Fruit drinks, caries and erosion in children. Dental
Health 38(4):5-8, 1999. 28. Lussi A, Jaeggi T, Jaeggi-Schärer S. Prediction of the erosive potential of
some beverages. Caries Res 29(5):349-354, 1995. 29. Edwards M, Creanor SL, Fore RH, Gilmour WH. Buffering capacities of soft
drinks: the potential influence on dental erosion. Journal of Oral Rehab 26(12):923-927, 1999. 30. Jarvinen VK, Rytömaa I, Heinonen OP. Risk factors in dental erosion. J Dent Res
70(6):942-947, 1991. 31. Meurman JH, Rytömaa I, Kari K, Laakso T, Murtomaa h. Salivary pH and glucose
after consuming various beverages including sugar-containing drinks. Caries Res
21:353-359, 1987. 32. Sorvari R, Kiviranta I, Luoma H. Erosive effect of a sport drink mixture with
and without addition of fluoride and magnesium on the molar teeth of rats.
Scand J Dent Res 96:226-231, 1988. 33. Larsen MJ, Nyvad B. Enamel erosion by some soft drinks and orange juices
relative to their pH, buffering effect and content of calcium phosphate.
CariesRes 33:81-87, 1999. 34. Asher F, Read MJF. Early enamel erosion in children associated with excessive
consumption of citric acid. Br Dent J 167:384-387, 1987. 35. Jain P, Nihill P, Sobkowski J, Agustin MZ. Commercial soft drinks: pH and in
vitro dissolution of enamel. Gen Dent 55(2):150-154, 2007. 36. McDonald JL Jr, Stookey GK. Influence of different carboxylic acids on enamel
dissolution in the presence and absence of sucrose. J Dent Res 54(4):187, 1975. 37. Millward A, Shaw L, Smith AJ, Rippin JW, Harrington E. The distribution and
severity of tooth wear and the relationship between erosion and dietary
constituents in a group of children. Int J Ped Dent 4:151-157, 1994. 38. Lussi A, Jaeggi T, Schärer S. The influence of different factors on in vitro
enamel erosion. Caries Res 27:387-393, 1993. 39. Kleber CJ, Putt MS, Muhler JC. Enamel dissolution by various food acidulants in
a sorbitol candy. J Dent Res 57:447-451, 1978. 40. West NX, Hughes JA, Addy M. Erosion of dentin and enamel in vitro by dietary
acids: the effect of temperature, acid character, concentration and exposure
time. J Oral Rehab 27:875-880, 2000. 41. McClure FT, Ruzicka SJ. The destructive effect of citrate vs lactate ions on
rats’ molar tooth surfaces, in vivo. J Dent Res 25:1-12, 1946. 42. Elsbury WB. Hydrogen-ion concentration and acid erosion of the teeth. Br Dent J
93:177-179, 1952. 43. Miller CD. Enamel erosive properties of fruits and various beverages. J Am Diet
Assoc 28(4):319-324, 1952. 44. Davis WB, Winter PJ. Dietary erosion of adult dentine and enamel. Br Dent J
143:116-119, 1977. 45. Linkosalo E, Markkanen S, Alakuijala A, Seppa L. Effects of some commercial
health beverages, effervescet vitamin C preparations and berries on human
dental enamel. Proc Finn Dent Soc. 84:31-38, 1988. 46. Bibby BG, Mundorff SA. Enamel demineralization by snack foods. J Dent Res
54:461-470, 1975. 47. Shaw L, Smith A. Erosion in children: an increasing clinical problem? Dent
Update 21:103-106, 1994. 48. Imfeld T. Prevention of progression of dental erosion by professional and
individual prophylactic measures. Eur J Oral Sci 104:215-220, 1996. 49. Smith B, Knight J. An index for measuring the wear of teeth. Brit Dent J
156:435-438, 1984. 50. Aine L, Baer M, Maki M. Dental erosions caused by gastroesophageal reflux
disease in children. J Dent Child 60:210-214, 1993. 51. O’Sullivan E, Curzon M, Roberts G, Milla P. Gastroesophageal reflux in children
and its relationship to erosion of primary and permanent teeth. Eur J Oral Sci
106:765-769, 1998. 52. Moynihan PJ. Dietary advice in dental practice. Brit Dent J 193(10):563-568,
2002. 53. Featherstone JDB. The science and practice of caries prevention. JADA
131:887-899, 2000.
*Dr.
Loewen is a pediatric dentist in private practice in Rochester, Minnesota, and
Diplomate, American Board of Pediatric Dentistry and Fellow, American Academy
of Pediatric Dentistry.
E-mail is rloewen@charterinternet.com
**Dr.
Marolt is a general dentist in private practice in White Bear Lake, Minnesota,
and member, Academy of General Dentistry. E-mail is drbobm@maroltdentistry.com
†Dr. Ruby
is associate professor, Department of Pediatric Dentistry, School of Dentistry,
The University of Alabama, Birmingham, Alabama. E-mail is
john–ruby@cs1dental.uab.edu
Copyright 2008. Minnesota Dental Association
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