The biology, prevention, diagnosis
and treatment of dental caries
Scientific advances in the United States
Domenick T. Zero, DDS, MS; Margherita Fontana, DDS, PhD;
E. Angeles Martínez-Mier, DDS, MSD, PhD; Andréa Ferreira-Zandoná, DDS, MSD, PhD;
Masatoshi Ando, DDS, PhD; Carlos González-Cabezas, DDS, MSD, PhD; Stephen Bayne, MS, PhD
ental scientists living
and working in the
United States during
the last 50 to 60 years
have contributed to our
understanding that dental caries is
a chronic, dietomicrobial, sitespecific disease caused by shifts
from protective factors favoring
tooth remineralization to destructive factors leading to demineralization. We now know that caries
results from complex interactions
among the tooth structure, the
dental biofilm, and dietary, salivary and genetic influences. The
distribution of caries has changed
in the last century. Relatively
recent data indicate that about 90
percent of carious lesions occur in
the pits and fissures of permanent
posterior teeth and that molar
teeth are most susceptible to
caries.1 The disease is unequally
distributed in the U.S. population;
people who are minorities, homeless, migrants, children with disabilities and of lower socioeconomic
status have the highest prevalence
and severity of caries.1 This article
briefly outlines major scientific
advances in cariology—with, in
honor of the 150th anniversary of
the American Dental Association
(ADA), an emphasis on contributions made by those living and
working in the United States.
D
ABSTRACT
Background. Scientific advances in cariology in the past 150 years
have led to the understanding that dental caries is a chronic, dietomicrobial, site-specific disease caused by a shift from protective factors favoring
tooth remineralization to destructive factors leading to demineralization.
Epidemiologic data indicate that caries has changed in the last century; it
now is distributed unequally in the U.S. population. People who are
minorities, homeless, migrants, children with disabilities and of lower
socioeconomic status suffer from the highest prevalence and severity of
dental caries.
Results. Scientific advances have led to improvements in the prevention, diagnosis and treatment of dental caries, but there is a need for new
diagnostic tools and treatment methods.
Conclusions and Clinical Implications. Future management of
dental caries requires early detection and risk assessment if the profession is to achieve timely and cost-effective prevention and treatment for
those who need it most. Dental professionals look forward to the day
when people of all ages and backgrounds view dental caries as a disease
of the past.
Key Words. Caries; remineralization; saliva.
JADA 2009;140(9 suppl):25S-34S.
Dr. Zero is the associate dean for research, a professor and the chair, Department of Preventive and
Community Dentistry, and the director, Oral Health Research Institute, Indiana University School of
Dentistry, 415 Lansing St., Indianapolis, Ind. 46202-2876, e-mail “dzero@iupui.edu”. Address reprint
requests to Dr. Zero.
Dr. Fontana is an associate professor and the director, predoctoral education, Department of Preventive
and Community Dentistry, School of Dentistry, and the director, Microbial Caries Facility, Oral Health
Research Institute, Indiana University School of Dentistry, Indianapolis.
Dr. Martínez-Mier is an associate professor and the director, the Fluoride Research Program, Department of Preventive and Community Dentistry, Indiana University School of Dentistry, Indianapolis.
Dr. Ferreira-Zandoná is an associate professor and the director, Early Caries Detection Program, Department of Preventive and Community Dentistry, Indiana University School of Dentistry, Indianapolis.
Dr. Ando is an assistant professor, Department of Preventive and Community Dentistry, Indiana University School of Dentistry, Indianapolis.
Dr. González-Cabezas is an associate professor and the director, Secondary Caries Program; director,
Graduate Education, Department of Preventive and Community Dentistry; and director, Laboratory
Research Facility, Oral Health Research Institute, Indiana University School of Dentistry, Indianapolis.
Dr. Bayne is a professor and the chair, Cariology, Restorative Sciences and Endodontics, School of Dentistry, University of Michigan, Ann Arbor.
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ETIOLOGY OF DENTAL CARIES
Microbial etiology. Willoughby Miller,2 a dentist
and early dental researcher, proposed that oral
bacteria in the presence of fermentable carbohydrates produced acids that dissolved tooth structure. Together with research on plaque by William3
and Black,4 this concept evolved as the foundation
for our current knowledge of caries etiology. However, early caries investigators did not understand
the specific nature of the bacterial infection contributing to caries and that restorative strategies
alone, such as “extension for prevention,”5 were not
successful in controlling the disease. Thus, dentists
dealt mainly with the continuing sequelae of this
widespread disease during the first half of the
20th century.6
Throughout the 20th century, of all possible etiological organisms associated with dental caries, the
mutans streptococci (MS) group captured the
greatest interest. Researchers initially isolated
Streptococcus mutans from human carious lesions,7
but it was not until much later, when researchers
conducted animal studies, that the bacterial etiology of dental caries was established firmly.8,9
Children acquire some oral microorganisms, such
as S. mutans, from their mothers or primary caregivers early in life.10 Therefore, caries is a microbial
disease in which etiologic bacteria are normal constituents of the oral microbiota that cause disease
only when their proportions and pathogenicity
change in response to environmental conditions.11
The key caries-associated microbial virulence traits
include acidogenesis and acid tolerance,12 intracellular polysaccharide storage13 and extracellular
glucan formation, which promotes MS attachment14
and increases plaque’s pH-lowering ability.15,16
Although S. mutans is one of the most researched
cariogenic microorganisms, it is only one of more
than 500 species found in dental plaque.17 In
studies using molecular identification of bacteria,
investigators have reported that diverse bacterial
communities, including some novel species, are
associated with dental caries and that S. mutans is
not detectable in 10 to 20 percent of people who
have severe caries.18,19 Recent evidence also has
supported the role of yeast (Candida albicans) as a
member of the mixed oral microbiota involved in
caries causation.20 These findings provide support
for the ecological plaque hypothesis, which proposes that S. mutans is only one of many endogenous microorganisms involved in the pathogenesis
of caries.11,21,22 A challenge for researchers is to
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characterize this complex biofilm and subsequently
identify microbial risk factors leading to caries
activity, with a view toward developing novel
antimicrobial interventions.
Dietary factors. Dental caries cannot occur in
the absence of dietary fermentable carbohydrates
and, therefore, it has been characterized as a
“dietobacterial” disease.23 Since the original observations of Miller,2 researchers have recognized fermentable carbohydrates as the “fuel” for the caries
process, and in the 1940s, Stephan24,25 demonstrated the relationship between caries and sugar
exposure, leading to the acidification of dental
plaque. Moreover, Weiss and Trithart26 reported a
direct relationship between caries experience and
the frequency of between-meals consumption of
sweet snacks, which findings supported those of
the earlier Vipeholm study in Sweden.27
The role of specific sugars was a subject of great
research interest in the latter half of the 20th century.28 Sucrose (table sugar) has a unique role as
the sole substrate for glucosyltransferases (bacterial enzymes) involved in the synthesis of extracellular glucan, which is an important microbial virulence factor (discussed above). The relative
cariogenicity of starches as compared with that of
sugars has been the subject of considerable controversy.29 Available studies with humans have not
supported the cariogenicity of starches.29 For
example, Newbrun and colleagues30 reported that
people with hereditary fructose intolerance who are
unable to eat fructose and sucrose but consume
large quantities of starch have a much lower caries
experience than do those without fructose intolerance. Highly processed starch-containing foods,
however, have the potential to be cariogenic, especially when combined with sugars, because they
are able to prolong food retention on tooth
surfaces.31,32
The recognition of sucrose as a major factor in
dental caries, as well as work by Bibby33 regarding
ABBREVIATION KEY. ACP: Amorphous calcium phosphate. bis-GMA: Bisphenol-A glycidyl methacrylate.
CAD-CAM: Computer-aided design/computer-aided manufacturing. CO2: Carbon dioxide. Er,Cr:YSGG: Erbiumchromium–doped yttrium scandium aluminum garnet.
Er:YAG: Erbium-doped yttrium aluminum garnet. FOTI:
Fiber-optic transillumination. ICDAS: International
Caries Detection and Assessment Criteria. LED: Lightemitting diode. MS: Mutans streptococci. Nd:YAG:
Neodymium-doped yttrium aluminum garnet. OCT:
Optical coherence tomography. QLF: Quantitative lightinduced fluorescence.
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the cariogenicity of snack foods, precipitated a
series of ADA conferences in the late 1970s and
early 1980s that culminated in a consensus conference in 1985.34 The conference participants considered several approaches for testing foods to determine their potential cariogenicity, including models
involving animal caries, human plaque acidity and
demineralization and remineralization. They recommended an integrated approach that involved
using combinations of methods to determine the
cariogenicity of foods. They reached a consensus
that foods had “no cariogenic potential” if their
human plaque pH profiles were statistically equivalent to that of sorbitol. Unfortunately, characterization of foods as having “low cariogenic potential”
has not proven to be practical because of individual
variability in eating frequency, sequence of eating
foods, timing of eating (such as eating before bedtime) and after-eating behaviors (oral hygiene, fluoride use, gum chewing).28 It also has been challenging to apply information about food cariogenicity in dietary counseling.35 In the latter part of
the 20th century, scientific interest in the cariogenicity of foods waned with recognition that the
prevalence and severity of caries were declining,
and the U.S. government placed less emphasis on
the need for labeling food regarding its
cariogenicity.
Host salivary and genetic factors. Hostrelated factors are important contributors to a
person’s dental caries susceptibility, resistance or
both. It is well established that saliva plays an
important role in the health of soft and hard tissues in the oral cavity.36 Chronically low salivary
flow rate is one of the strongest indicators of
increased caries risk.37 A subjective complaint of
xerostomia often does not correlate with objective
findings of reduced salivary flow rate.38 This
finding has led to clinical recommendations and
guidelines for the clinical assessment of hyposalivation.39 The objective measurement of salivary
flow is an important cornerstone of caries risk
assessment and management.
Researchers initially believed that genetic factors—such as tooth morphology, position and occlusion; tooth eruption time and sequence; salivary
composition; and sweetness preference—were less
important in determining caries risk than were
environmental influences, such as microbial and
dietary factors.40,41 However, results of recent
studies in populations of twins have shown that
genetic factors may explain more than 50 percent
of the variance in caries experience among
people.42,43 Much remains unknown about geneticenvironmental relationships in caries etiology and
risk assessment, but the future holds interesting
possibilities for improvements in caries diagnosis
and prognosis.
PREVENTION OF CARIES
Risk assessment. Caries risk assessment is the
cornerstone of patient-centered caries management. It is the determination of the probability of a
person’s developing new carious lesions during a
specific period41 and of the probability of a change
in the size or activity of existing lesions across
time.44 It is useful in determining whether additional diagnostic procedures are required; in identifying patients who require caries-control measures;
in assessing the effectiveness of attempts to control
caries; and as a guide in treatment planning and
scheduling recall appointments.44 Investigators
have shown that previous caries experience is the
best predictor of future caries experience in primary teeth, followed by parental education and
socioeconomic status; young children’s age at the
time of MS colonization also was found to be an
important risk factor.45 While previous caries experience may be the most useful criterion for risk
assessment, the information arises too late to be
useful in preventing caries because many irreversible events already have taken place. To enable
effective prevention, researchers must determine
efficient ways to identify children at high risk of
developing caries earlier, shortly after their first
teeth erupt. To accomplish this goal, researchers
must develop molecular and genetic methods to
improve the identification and characterization of
cariogenic microbes and identify ways to reduce or
eliminate harmful effects of their colonization. It
also will be important to develop improved technology to detect and quantify early lesions and to
assess carious lesion activity directly, because this
may prove to be the best strategy to identify
patients in need of intensive caries prevention
efforts.45
Fluoride. American contributions to fluoride’s
role in caries prevention are seminal. They began
at the turn of the 20th century when Frederick
McKay,46 a practicing dentist, associated “mottled
enamel”47 with reduced susceptibility to caries; in
collaboration with H.V. Churchill,48 the chief
chemist at the Aluminum Company of America, he
later traced this condition to fluoride. H. Trendley
Dean, the first director of what then was called the
National Institute of Dental Research (now the
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National Institute of Dental and Craniofacial
Research), conducted several studies in the 1930s
and 1940s with colleagues that provided the conclusive epidemiologic evidence linking what they
referred to as “dental fluorosis” or “enamel fluorosis” to excessive fluoride in drinking water.49-51 In
these studies, Dean and colleagues52 also found
that dental fluorosis was associated with lower
caries experience, and their findings served as the
basis for determining the optimal level of water fluoridation for preventing caries and minimizing
dental fluorosis. This research led to the establishment of the first community water fluoridation program targeted at caries prevention, a program that
began in January 1945 in Grand Rapids, Mich. The
results of clinical trials of dietary fluoride supplements resulted in recommendations by the ADA for
fluoride supplementation for people who did not
have access to fluoridated water.53 During the
1940s and 1950s, American researchers, building
on the work of scientists throughout the world,
investigated the synthesis of fluoride compounds
and their potential use in toothpaste for preventing
caries. Scientists from Indiana University, Indianapolis; The Forsyth Institute, Boston; and the
University of Rochester, Rochester, N.Y., conducted
research regarding the inclusion of fluoride in dentifrices.54,55 Interestingly, one of the earliest studies
by Bibby56 involving a dentifrice formulated with
sodium fluoride did not prove successful, because
the presence of calcium in the abrasive interfered
with the action of the fluoride ion.57 The results of
subsequent clinical trials with improved formulations provided conclusive evidence of fluoride’s
caries-preventive benefits when applied topically,
particularly in children.58-61
American scientists contributed to the paradigm
shift in which fluoride’s predominant effect became
viewed as mostly posteruptive and topical. Epidemiologic evidence demonstrated that water fluoridation decreased caries prevalence in both children and adults. The results of animal experiments
and clinical trials supported topical fluoride application and the safe and effective use of fluoride.62
American cariologists contributed to knowledge of
the physicochemical aspects of fluoride-enamel
interactions, the influence of fluoride on the demineralization and remineralization process,63-65 and
the pharmacokinetics of fluoride in the oral
environment.66-68
Diet. Use of fluoride has reduced the need for
strict dietary control of sugar.69 The effectiveness of
dietary measures to control caries is limited
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because modern diets are complex and contain
many natural sugars, refined sugars and sugar
substitutes. However, reducing the amount and
frequency of sugar consumption, including the
“hidden sugars” in many processed foods, is important for people at high risk of experiencing caries.
Parents and caregivers of young children can
reduce children’s caries risk by limiting their consumption of sugar-containing soft drinks70,71 and
increasing their consumption of milk and other
dairy products.72,73 Dairy products have properties
that protect teeth against caries,74 and eating
cheese after exposure to sugar rapidly neutralizes
plaque acidity.75
A wide range of sugar substitutes have low or no
cariogenic potential.76 For example, sucralose is a
high-intensity noncariogenic sweetener,77 and xylitol has been reported to have anticariogenic properties.78 Chewing sugar-containing gum increases
caries risk,79 but chewing sugar-free gum after
meals can reduce caries risk.80 Some food additives
may have protective properties that reduce cariogenicity; for instance, cranberries can reduce bacterial adherence and glucosyltransferase activity of
S. mutans,81 and tea extracts inhibit salivary amylase activity.82
Sealants. Dental scientists in the United States
have been key players in developing ways to
manage and control caries. In 1955, Michael
Buonocore,83 a researcher at the Eastman Dental
Center in Rochester, N.Y., described etching
enamel to improve retention of restorative
materials. Seven years later, R.L. Bowen,84 a scientist at the ADA Research Unit at the National
Bureau of Standards (now the ADA Foundation’s
Paffenbarger Research Center), obtained a patent
for restorations with a tooth-colored plastic,
bisphenol-A glycidyl methacrylate (bis-GMA).
These two developments initiated a rich era of
adhesive dentistry involving sealants and restorative materials that improved caries prevention and
tooth conservation.85 Sealants prevent food from
collecting in molar pits and fissures and, therefore,
prevent dental caries.86-89 The placement of sealants
over carious lesions arrests the disease process88-92
and is cost-effective compared with routine restorative care.93,94
Remineralization. Joseph Head, a physician
and dentist who practiced dentistry at the Jefferson Hospital in Philadelphia, observed that
demineralized enamel could be “rehardened” to the
point at which “the enamel could no longer be
scratched by a lancet.”95 Decades later, researchers
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conducting clinical studies in Europe demonstrated
that incipient caries could be repaired by saliva
when fluoride application was combined with regular removal of overlying plaque.96-98 These observations were corroborated by Koulourides and colleagues at the University of Alabama,99-101 who
demonstrated in situ that saliva rehardens incipient enamel lesions and small amounts of fluoride
accelerate the process greatly, resulting in a highly
caries-resistant enamel surface. Numerous other
researchers throughout the world also have contributed to our current understanding of remineralization. Partially demineralized enamel and
dentin apatite crystals can be remineralized to
almost their original size under optimal laboratory
conditions. However, once the mineral phase is lost
completely, remineralization is not possible.102,103
The process is diffusion-controlled, and most
remineralization occurs at the surface. This leaves
a sealed surface102 that is more resistant to subsequent demineralization than is sound enamel.101
Nevertheless, attempts to remineralize subsurface
areas of the lesion have continued.104,105
The reversal of incipient carious lesions led to a
paradigm change for caries management, generating great interest in developing new and better
remineralizing therapies. Much of this research is
focused on calcium-containing preparations such as
amorphous calcium phosphate (ACP), which was
developed for dental use by Ming Tung, a
researcher at the ADA Foundation’s Paffenbarger
Research Center,106 and data suggest that some of
these preperations have remineralizing properties.107 Commercial products that contain ACP
and preparations of casein derivatives (casein
phosphopeptide-ACP complex) are commercially
available. Studies have yet to show conclusive evidence of effectiveness in clinical trials108; none has
been shown to be more effective than fluoride.
DIAGNOSIS OF CARIES
Clinical methods. Visual detection of caries was
described as early as 1801, in a book entitled
“Skinner: A Treatise of Human Teeth.”109 One of
the most important early contributions to diagnosis
of dental caries came from G.V. Black, who was a
practicing dentist before becoming dean of the
Northwestern University School of Dentistry in
Chicago.110 Black110 was among the first to
describe, in explicit detail, methods of visual and
tactile detection of dental caries as part of an oral
examination, including the cleaning and drying of
teeth and the use of explorers, that still are in use
100 years later. For detection of proximal caries,
Black described the use of separators to directly
visualize areas of concern and the use of ligatures
(dental floss) passed through the contact point to
detect surface roughness and breakdown.110
Black’s diagnostic methods laid the groundwork
for future criteria for the detection of dental
caries.111-113 Radike111 described detailed criteria for
the visual and tactile detection of dental caries that
until recently were used widely in epidemiologic
and clinical research. They relied heavily on an
explorer “catch” for detection of caries on occlusal
surfaces and recorded cavitated lesions, but not
noncavitated lesions. Because it favored reliability
and comparability, it was the predominant diagnostic system used in the United States.114 Since
the days of Black, our diagnostic understandings
have been far more advanced than simply diagnosing caries at the level of cavitation.115 The latest
contribution to visual diagnostic criteria for caries
are the International Caries Detection and Assessment Criteria (ICDAS), the development of which
involved a joint effort of international cariologists
with significant contributions from the United
States, particularly from the University of
Michigan, Ann Arbor, and Indiana University,
Indianapolis.116 ICDAS was designed to facilitate
the standardized diagnosis of caries on all tooth
surfaces at all stages of severity. An updated version of ICDAS (ICDAS II)117 has been well accepted
in the United States and has been used in clinical
studies with good intraexaminer and interexaminer agreement, as well as satisfactory sensitivity
and specificity.71,116,118-120
Radiographic methods. Less than six months
after W.C. Roentgen’s discovery of the x-ray,
William J. Morton,121 a New York physician, was
one of the first to report (during a meeting of the
New York Odontological Society) that x-rays could
have dental applications. Soon afterward,
C. Edmund Kells,122 a dentist practicing in New
Orleans, reported on the role of radiographs in dentistry. Howard R. Raper, a member of the faculty at
the Indiana University School of Dentistry, further
advanced dental radiography by writing the first
book on the topic,123 and in 1925, he perfected the
intraoral bitewing radiograph, which to this day
remains the conventional method for detecting
proximal caries.124 More recent developments
include higher-speed film and digital radiography.
Current digital imaging technologies generate
images whose diagnostic yield may equal, but not
necessarily exceed, that of images obtained by
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TABLE
Key events in the United States involving restorative materials and
technologies for managing single-tooth problems caused by caries.*
DATE
EVENT, ACCORDING TO MATERIAL/TECHNOLOGY
Early Restorative Materials
1842-1908
Introduction of various restorative materials: gutta-percha, cohesive gold foil, zinc phosphate restorative material and
cement, silicate cement
1895-1935
First experiments with copper-containing amalgam and formulation of low-copper amalgam alloys
1962-1995
Development of high-copper and zinc-free, high-copper dental amalgam; fluoride-releasing dental amalgam; mercury-free
silver filling material
Dental Amalgam
Resin-Based Sealing and Restorative Materials
1947-1960
Introduction of polymethyl-methacrylate–based direct restorative materials
1962
Patenting of bisphenol-A glycidyl methacrylate (bis-GMA)–based dental composites
1968-1977
Introduction of commercial dental composites, commercialization of bis-GMA–based sealants; patenting of radiopacifiers
for composites
1984-2005
Development and commercialization of flowable, packable nano and trimodal composites for dental use
1955-1983
Development and commercialization of acid-etching, enamel and dentin bonding systems
1972-1985
Introduction of glass ionomer restorative materials and glass ionomer admixture with amalgam alloy
1985
Introduction of glass ionomer materials for use with atraumatic restorative technique
1992
Introduction of resin-modified glass ionomers
1860-1870
Introduction of use of zinc oxide eugenol as a cement
1920-1929
Development of first strict formulation of zinc phosphate cement, commercial cavity varnish and calcium hydroxide pulpcapping material
~1969
Development of first hard-set calcium hydroxide composition
1903-1907
Introduction of porcelain jacket crown, lost-wax casting process
1937
Placement of the first Vitallium (Austenal Laboratories, now Dentsply Austenal, York, Pa.) screw implant
1955-1962
Development of titanium casting for single-unit and multiple-unit restorations; patenting of commercial porcelainbonded-to-metal system
1968
Introduction of the first blade-vent implants
~1974- ~1985
Development of plastic extracoronal laminate veneers and subsequent intracoronal porcelain veneers
Adhesive Systems
Glass Ionomers
Varnishes, Liners and Bases
Indirect Restorative Materials for Single Units
using conventional film.125
Other technology-based detection methods.
Technology-based dental caries detection methods
first arose in the United States more than 40 years
ago. In 1968, Lees and Barber126 first suggested the
application of ultrasound in dentistry, and in 1970,
they and Lobene127 published early research
regarding its use for caries detection. The early
applications of electrical conductance128,129 and
fiber-optic transillumination (FOTI)130 in caries
detection had their roots in the United States. A
digital version of the latter system (digital imaging
[DIFOTI], Electro-Optical Sciences, Irvington,
N.Y.),131 was tested in the laboratory132,133 and later
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evaluated in clinical studies.134,135 Optical coherence
tomography (OCT)—which is similar in operation
to ultrasound imaging, but uses light waves rather
than sound waves—has been used in dentistry for
nearly a decade.136,137 Polarization-sensitive OCT is
a variation of conventional OCT that uses polarized
incident light to create images and quantify
caries.138 Fluorescence has received considerable
attention because teeth fluoresce under the excitation of ultraviolet rays.139,140 This idea later led to
the development of the quantitative light-induced
fluorescence (QLF, Inspektor Research Systems
BV, Amsterdam) method in Europe, which has
been studied extensively by investigators at
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TABLE (CONTINUED)
Cavity Preparation and Restoration Equipment
1864-1891
Development of rubber dam, foot-treadle dental engine (700 revolutions per minute [rpm]), electric dental engine (1,000
rpm), steel dental burs
1937
Introduction of automated amalgamation equipment
1942
Introduction of diamond cutting instruments, high-speed dental engine (>10,000 rpm) and tungsten carbide burs
1953
Development of ball-bearing high-speed handpiece (25,000 rpm)
1955-1957
Development of water-turbine (50,000 rpm), belt-driven (150,000 rpm) and air-turbine (300,000 rpm) high-speed
handpieces
1973-1977
Commercial development of ultraviolet-light– and visible-light–curing units
1980-1995
Development of carbon dioxide (CO2), neodymium-doped yttrium aluminum garnet (Nd:YAG), erbium-doped yttrium
aluminum garnet (Er:YAG) and erbium-chromium–doped yttrium scandium aluminum garnet (Er,Cr:YSGG) hydrokinetic
lasers for dentistry
1993-1995
Introduction of air-abrasion cutting equipment for dental use
~1995-2000
Development and introduction of high-torque electric dental handpiece
1989
Introduction of second generation of computer-aided design/computer-aided manufacturing (CAD/CAM) equipment
~1998
Introduction of commercial light-emitting diode (LED) light-curing units
* Sources: Buonocore,83 American Dental Association,149 Bayne and Thompson,150 Bower and Marjenhoff,151 Gelbier,152 Mahler,153 Rueggeberg,154
Schulein,155 Thompson and colleagues156 and Wilwerding.157
Indiana University.141-144 QLF is a promising and
nondestructive method of detecting and quantifying carious lesions. It allows for longitudinal clinical monitoring of carious lesions and potentially
can determine carious lesion activity.145 In the late
1990s, European researchers introduced an
infrared laser fluorescence device (DIAGNOdent,
KaVo Dental, Biberach, Germany) for caries detection. It is based primarily on fluorescence absorption by bacterial by-products in porous carious
lesions. Researchers have evaluated this device in
research settings146,147 and as an oral health
screening tool in public schools.148
TREATMENT OF CARIES
Restorative materials. The effects of prevention
on caries prevalence and the advantages of
improved dental materials have shifted the focus in
caries management from surgical methods and
restoring tooth structure to development and use of
dental materials to prevent disease, remineralization procedures, minimally invasive treatments for
difficult-to-access regions and materials with which
early lesions can be impregnated to prevent further
progression.
The table summarizes key historical events in
the United States involving restorative dental
materials, equipment and techniques related to the
treatment of dental caries in single teeth.83,149-157
Whereas this table focuses on accomplishments in
this country, we should note that scientists in
Japan (who developed dentin bonding systems and
glass ionomers, for example) and Europe (who
developed dental amalgam, silicate cements, microfill composites, hybrid composites and glass
ionomers, among others) also have made many significant contributions.
Continuing dental caries disease usually results
in tooth loss. Contributions related to restoration
for tooth replacement are not included here.
Throughout the long history of restorative dentistry, U.S. dental companies have developed many
specialized hand instruments, dental burs, diamond cutting instruments and special finishing
instruments. All of these technical developments in
materials and treatment to restore carious lesions
have involved a strong partnership of academic,
corporate, association-based and governmental
dental research entities and scientists. We
acknowledge the progress they have enabled dentistry to achieve in fighting oral disease.
CONCLUSIONS
Dental caries is a dynamic dietomicrobial disease
involving cycles of demineralization and remineralization. The early stages of this process are
reversible by modifying or eliminating etiologic factors (such as plaque biofilm and diet) and increasing protective factors (such as fluoride exposure and salivary flow). This approach manages
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31S
dental caries by means of prevention and cure,
reserving surgical approaches for those whose disease severity and tissue loss leave no other option.
Our understanding of caries has changed
markedly in the last century. A National Institutes
of Health consensus statement112 acknowledged
that tooth restoration does not stop the caries
process and emphasized the need for improved
diagnosis, prevention and management of caries in
its early (that is, noncavitated) stages. Still, dental
practitioners and researchers alike have an incomplete understanding of the natural history of
caries. Cognizant of the limitations of current clinical diagnostic methods and concerns about potential disease progression, dentists tend to err on the
side of more aggressive operative treatment than
often might be warranted.
Dentistry needs new diagnostic tools and treatment methods to support improved patient care.
Future caries management must include risk
assessment to enable clinicians to provide timely
and cost-effective care to those most in need. We
have made much progress in our knowledge of the
biology, prevention, diagnosis and treatment of
dental caries since the founding of the ADA 150
years ago. However, dental caries remains a significant problem for many Americans, and we look
forward to the day when people of all ages and
backgrounds view dental caries as a disease of
the past. ■
Disclosure. None of the authors reported any disclosures.
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