40 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

2
Dental Caries: Etiology, Clinical
Characteristics, Risk Assessment, and
Management
ANDRÉA G. FERREIRA ZANDONÁ, ANDRÉ V. RITTER, R. SCOTT EIDSON a

T
his chapter presents basic deinitions and information on enamel in a process called remineralization. hus at the tooth
dental caries, clinical characteristics of the caries lesion, surface and subsurface level, dental caries lesions result from a
caries risk assessment, and caries management, in the context dynamic process of damage (demineralization) and restitution
of clinical operative dentistry. (remineralization) of the tooth matter. hese events take place
several times a day over the life of the tooth and are modulated
What I Dental Carie? by many factors including number and type of microbial lora in
the bioilm, diet, oral hygiene, genetics, dental anatomy, dentin
Dental caries is a preventable, chronic, and bioilm-mediated disease and enamel composition, use of luorides and other chemothera-
modulated by diet. his multifactorial, oral disease is caused primar- peutic agents, saliva composition, salivary low, and bufering
ily by an imbalance of the oral lora (bioilm) due to the presence capacity. hese factors are highly individual and tooth speciic,
of fermentable dietary carbohydrates on the tooth surface over and will difer from person to person, tooth to tooth in the same
time. Traditionally, this tooth-bioilm-carbohydrate interaction has individual, and site to site on a same tooth. he balance between
been illustrated by the classical Keyes-Jordan diagram (Fig. 2.1).1 demineralization and remineralization has been illustrated in terms
However, dental caries onset and activity are in fact much more of pathologic factors (i.e., those favoring demineralization) and
complex than this three-way interaction, as not all persons with protective factors (i.e., those favoring remineralization) (Fig. 2.5).2
teeth, bioilm, and consuming carbohydrates will have caries lesions Individuals in whom the balance tilts predominantly toward protec-
over time. Several modifying risk and protective factors inluence tive factors (remineralization) are much less likely to develop dental
the dental caries process, as will be discussed later in this chapter. caries lesions than those in which the balance is tilted toward
At the tooth level, dental caries activity is characterized by pathologic factors (demineralization). Understanding the balance
localized demineralization and loss of tooth structure, the caries between demineralization and remineralization is key to caries
lesion (Figs. 2.2 and 2.3). In health, the microbiome is in symbiosis, management.
the oral commensals striving in a neutral pH. Some bacteria in Repeated demineralization events may result from a predomi-
the bioilm metabolize reined carbohydrates for energy and produce nantly pathologic environment causing the localized dissolution
organic acid by-products. hese organic acids, if present in the and destruction of the calciied dental tissues, evidenced as a caries
bioilm ecosystem for extended periods, can lower the pH in the lesion. he ongoing demineralization at the enamel subsurface
bioilm to below a critical level (5.5 for enamel, 6.2 for dentin). level leads to a collapse of the surface and hence the formation of
his low pH has efects both on the bioilm composition and at a cavitation in the enamel surface. Severe demineralization of dentin
the tooth surface level (Fig. 2.4).132 With extended periods of low results in the exposure of the protein matrix, which is denatured
pH there is a shift in the microbiome to bacteria that are acidogenic initially by host matrix metalloproteinases (MMPs) and subsequently
and acidophilic, causing a dysbiosis in the microbiome. his change degraded by MMPs and other bacterial proteases. Demineralization
in turn will lead to further acidiication of the environment. he of the inorganic phase (dentin mineral), and denaturation and
low pH drives calcium and phosphate from the tooth to the bioilm degradation of the organic phase (primarily dentin collagen) result
in an attempt to reach equilibrium, hence resulting in a net loss in dentin cavitation.3
of minerals by the tooth, or demineralization. When the pH in It is essential to understand that caries lesions, or cavitations
the bioilm returns to neutral and the concentration of soluble in teeth, are signs of an underlying condition, an imbalance between
calcium and phosphate is supersaturated relative to that in the protective and pathologic factors favoring the latter. In clinical
tooth, mineral can then be added back to partially demineralized practice it is very easy to lose sight of this fact and focus entirely
on the restorative treatment of caries lesions, failing to treat the
underlying cause of the disease (Table 2.1). Although symptomatic
a
Dr. Eidson was an inactive author in this edition. treatment is important for many reasons, failure to identify and

40
 CHAPTER 2 Dental Caries: Etiology, Clinical Characteristics, Risk Assessment, and Management

Primary modifying factors: Secondary modifying factors:

• Tooth anatomy • Socioeconomic status
• Saliva • Education
• Biofilm pH • Life-style
• Biofilm composition • Environment
• Use of fluoride •Age(?)
• Diet specifics • Ethnic group (?)
• Oral hygiene • Occupation
• Immune system
• Genetic factors

'----+-- CARIES*

*In the absence of protective factors

and if other risk factors are present

• Fig. 2. 1 Modified Keyes-Jordan diagram. As a simplified description, dental caries is a result of the
interaction of cariogenic oral flora (biofilm) with fermentable dietary carbohydrates on the tooth surface
(host) over time. However, dental caries onset and activity are, in fact, much more complex, as not all
persons with teeth, biofilm, and who are consuming carbohydrates will have caries over time. Several
modifying risk factors and protective factors influence the dental caries process. (Modified from Keyes
PH, Jordan HV: Factors influencing initiation, transmission and inhibition of dental caries. In Harris RJ,
editor: Mechanisms of hard tissue destruction, New York, 1963, Academic Press.)

a 22
b a 21 23 24 25

I
12
11 B
10
8 9
• Fig. 2.3 Extensive active caries in a young adult (same patient as in
B Fig. 2.2). A, Mirror view of teeth No. 20 through 22. B, Cavitated lesions
(a) are surrounded by extensive areas of chalky, opaque demineralized
• Fig. 2.2 A, Young adult with multiple active initial and cavitated caries areas (b). The presence of smooth-surface lesions such as these is associ-
lesions involving teeth No. 8 through 10. B, Cavitated areas (a) are sur- ated with rampant caries. Occlusal and interproximal smooth-surface
rounded by areas of extensive demineralization that are chalky and opaque caries usually occur in advance of facial smooth-surface lesions. The
(b). Some areas of initial (noncavitated) caries have superficial stain. presence of these types of lesions should alert the dentist to the possibility
of a high caries risk patient and possibly extensive caries activity elsewhere
in the mouth. The interproximal gingiva is swollen red and would bleed
easily on probing. These gingival changes are the consequence of long-
standing irritation from the biofilm adherent to the teeth.
42 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

Ne esio ce f
Dynamic stability stage Mild/infrequent

( l u r fa
t m n e a tu
Dominance on non-MS and actinomyces acidification

in reg re sh
er re s in
al ss hin y/h
Acid-induced

ga io y/s ard
adaptation/selection

in n/a mo (d
Acidogenic stage
“low-pH” non-MS
and actinomyces

rr oth ent
Moderate/frequent

es ( in
acidification

t) ena )
m
Aciduric stage Acid-induced

el
)

Ne esio ce f
adaptation/selection

(l urfa
Increase in MS

t m n eat
S
and non-mutans

in init ure d
er ia d ull
aciduric bacteria

al tio ul /so
Severe/prolonged

lo n/ l/ro ft (
acidification

ss pr ug de
og h ( nti
re ena n)
ss m
io el)
n)
• Fig. 2.4 This diagram illustrates how the diet affects the bioilm and consequences on the tooth
surface. In health, the bioilm is in symbiosis. A person who has only occasional consumption of ferment-
able carbohydrates will have a resident microbiome dominated by nonmutans streptococci and actino-
myces in a dynamic stability stage that is adapting to the relatively minor changes in pH. As the diet
changes to more frequent exposures to fermentable carbohydrates, the microbiome adapts to the more
acidic environment in an acidogenic stage, where bacteria that favor low pH lourish. In diets with frequent
exposures to fermentable carbohydrates this constant acid-induced adaptation and selection of the
microbiome continues and leads to an aciduric stage where there is an increase in MS and nonmutans
aciduric bacteria, thus leading to a dysbiosis of the microbiome. At one end of the spectrum, in an envi-
ronment with severe and prolonged acidiication and aciduric bacteria, there is a net mineral loss at the
tooth surface, enamel, or dentin, causing lesion initiation or lesion progression, while at the other end of
the spectrum with only mild acidiication there is a net mineral gain at the tooth surface and consequently
lesion regression or arrest. Certainly this is a simpliied explanation of the changes in the bioilm as the
microbiome adapts to the acidic environment due to cariogenic diets, which does not consider the many
other factors that are at play to either halt the process or boost the process. (From Takahashi N1, Nyvad
B. The role of bacteria in the caries process: ecological perspectives, J Dent Res 90(3):294–303, 2011.
doi:10.1177/0022034510379602)

The “Caries Balance” TABLE 2.1 Caries Management Based on the

Pathological Factors Protective Factors Medical Model
• Acid-producing bacteria • Saliva flow and components
• Sub-normal saliva flow • Remineralization (fluoride, Cariogenic Bioilm Resultant From a
and/or function calcium, phosphate) Primary Etiology Cariogenic Diet
• Frequent eating/drinking of • Good oral hygiene
Symptoms Demineralization lesions in teeth
fermentable carbohydrates • Strategies that maintain a
• Poor oral hygiene healthy microbiome Treatment, therapeutic Improvement of host resistance by (1)
(probiotics, prebiotics bioilm modiication, (2) elevating
(arginine), pH modifiers, bioilm pH, and (3) enhancing
erythritol and xylitol) remineralization
• Strategies that modulate a
dysbiotic microbiome (silver, Treatment, symptomatic Remineralization/arrest of lesions,
peptides, tin, antimicrobials) restoration of cavitated lesions
Posttreatment assessment, Reevaluation of etiologic conditions
therapeutic and primary and secondary risk
Demineralization Remineralization
factors; and continuous
(Caries) (No caries) management based on indings
Posttreatment assessment, Examination of teeth for new lesions,
• Fig. 2.5 The caries balance. The balance between demineralization symptomatic assessment of lesion activity,
and remineralization is illustrated in terms of pathologic factors (i.e., those
assessment of lesion progression
favoring demineralization) and protective factors (i.e., those favoring rem-
ineralization). (Modiied from Featherstone JDB: Prevention and reversal
of dental caries: role of low level luoride, Community Dent Oral Epidemiol
27:31–40, 1999.)
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 43

manage the underlying causative factors of dental caries allows the in-depth information on the dental caries process can be found
disease to continue and increases the chance of treatment failure. elsewhere.133
Caries management eforts must be directed not only at the tooth
level (traditional or surgical treatment) but also at the total-patient
level (caries management by risk assessment). Restorative treatment Ecologic Bai of Dental Carie: The Role of the
does not cure the caries process. Instead, identifying and managing
the risk factors for caries must be the primary focus, in addition Bioilm
to the restorative repair of damage caused by caries. Dental plaque is a term historically used to describe the soft, tena-
his chapter emphasizes the components of a caries management cious ilm accumulating on the surface of teeth. Dental plaque has
program that is based irst on risk assessment and then on modifying been more recently referred to as the dental bioilm or simply the
the bioilm ecology to enhance protective factors and minimize bioilm, which is a more complete and accurate description of its
pathologic factors.4 his chapter also presents information on clinical composition (bio) and structure (ilm).5 he bioilm is composed
characteristics of the caries lesion as they relate to clinical operative mostly of bacteria, their by-products, extracellular matrix, and water
dentistry. Use of correct and consistent terms when referring to (Figs. 2.6, 2.7, 2.8, 2.9, and 2.10). Bioilm is not adherent food
caries and caries lesions is important. Box 2.1 summarizes the debris, as was widely and erroneously thought, nor does it result
most common terms used in this textbook to deine caries lesions from the haphazard collection of opportunistic microorganisms.
based on their location, cavitation status, and activity status. More he accumulation of the bioilm on teeth is a highly organized

• BOX 2.1 Caries Lesion Deinitions

• Caries lesion. Tooth demineralization as a result of the caries process. • Active caries lesion. A caries lesion that is considered to be biologically
Other texts may use the term carious lesion. Laypeople may use the term active—that is, a lesion in which tooth demineralization is in frank activity
cavity. at the time of examination.
• Smooth-surface caries. A caries lesion on a smooth tooth surface. • Inactive caries lesion. A caries lesion that is considered to be biologically
• Pit-and-issure caries. A caries lesion on a pit-and-issure area. inactive at the time of examination—that is, in which tooth
• Occlusal caries. A caries lesion on an occlusal surface. demineralization caused by caries may have happened in the past but has
• Proximal caries. A caries lesion on a proximal surface. stopped and is currently stalled. Also referred to as arrested caries,
• Enamel caries. A caries lesion in enamel, typically indicating that the meaning that the caries process has been arrested but that the clinical
lesion has not penetrated into dentin. (Note that many lesions detected signs of the lesion itself are still present.
clinically as enamel caries may very well have extended into dentin • Rampant caries. Term used to describe the presence of extensive and
histologically.) multiple cavitated and active caries lesions in the same person. Typically
• Dentin caries. A caries lesion into dentin. used in association with “baby bottle caries,” “radiation therapy caries,” or
• Coronal caries. A caries lesion in any surface of the anatomic tooth “meth-mouth caries.” These terms refer to the etiology of the condition.
crown. • Primary dentin. Sound, normal dentin that forms during tooth
• Root caries. A caries lesion in the root surface. development; it is usually completed 3 years after tooth eruption.
• Primary caries. A caries lesion not adjacent to an existing restoration or Histologically, primary dentin has tubules with smooth odontoblastic
crown. processes, with no intratubular crystals. The intertubular dentin has normal
• Secondary caries. A caries lesion adjacent to an existing restoration, cross-banded collagen and normal dense apatite crystals. Clinically,
crown, or sealant. Other term used is caries adjacent to restorations and primary dentin is hard, cannot be easily penetrated with a blunt explorer,
sealants (CARS). Also referred to as recurrent caries, implying that a and can only be cut by a bur or a sharp cutting instrument.
primary caries lesion was restored but that the lesion reoccurred. • Secondary dentin. Sound, normal dentin that forms physiologically on all
• Residual caries. Refers to carious tissue that was not completely internal aspects of the pulp cavity throughout the life of the tooth.
excavated prior to placing a restoration. Sometimes residual caries can be Histologically, secondary dentin resembles primary dentin. Clinically,
dificult to differentiate from secondary caries. secondary dentin is similar to primary dentin.
• Cavitated caries lesion. A caries lesion that results in the breaking of the • Tertiary dentin. Dentin that forms in response to stimuli such as caries,
integrity of the tooth, or a cavitation. attrition, and operative procedures. Also known as reparative or reactive
• Initial caries lesion. A caries lesion that has not been cavitated. In dentin. Usually appears as a localized dentin deposit on the wall of the
enamel caries, initial caries lesions are also referred to as noncavitated or pulp space immediately subjacent to the area of the tooth that has
“white spot” lesions. (Clinically, the distinction between a cavitated and a received the injury. Tertiary dentin is less mineralized than primary and
noncavitated caries lesion is not as simple as it may seem. Although secondary dentin, and contains irregular dentinal tubules. Clinically, tertiary
historically any roughness detectable with a sharp explorer has been dentin is not as hard as primary dentin.
considered a cavitated lesion, more recent caries detection guidelines • Sclerotic dentin. Dentin that forms in response to stimuli such as aging or
establish that only lesions in which a blunt probe penetrates without mild irritation (slow advancing caries). When responding to initial caries
pressure are to be considered cavitated. This distinction has important demineralization events, crystalline material precipitates in intratubular and
implications on lesion management, because most initial caries lesions can intertubular dentin. Sclerotic dentin walls off a lesion by blocking (sealing)
be arrested or remineralized, while most cavitated lesions require the dentinal tubules. This zone can be seen even before the
restorative intervention.) demineralization reaches the dentin and it may not be present in rapidly
• Moderate caries lesion. A caries lesion that may or may not have advancing lesions. Clinically, sclerotic dentin is dark and harder than
cavitated but that has not reached the inner one-third of dentin. This can normal dentin.
be observed clinically by microcavitations in the enamel or a gray shadow. • Leathery dentin. Term used to describe the clinical presentation of the
• Advanced (deep) caries lesion. A deinitely cavitated lesion exposing transition zone between soft and irm dentin (see next section). Technically
dentin. For the purposes of this protocol any lesion that has reached the leathery dentin is part of the irm dentin zone.
inner one-third of the dentin will be considered an advanced lesion.
44 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

er pr
sr

ap p

Longitudinal section Occlusal

of tail of rod
Crystallites
Longitudinal section
of head of rod (4 µm)

Perikymata
Cross-section
of a rod
(head and tail)

Enlarged area
Striae of Retzius in Fig. 2.6C

B Cervical
• Fig. 2.6 A, Composite diagram illustrating the relationship of bioilm (p) to the enamel in a smooth-
surface initial (noncavitated) lesion. A relatively cell-free layer of precipitated salivary protein material, the
acquired pellicle (ap) covers the perikymata ridges (pr). The bioilm bacteria attach to the pellicle. Overlap-
ping perikymata ridges can be seen on the surface of enamel (see Fig. 2.7). (Figs. 2.9 and 2.10 are
photomicrographs of cross sections of bioilm.) The enamel is composed of rodlike structures (er) that
course from the inner dentinoenamel junction (DEJ) to the surface of the crown. Striae of Retzius (sr) can
be seen in cross sections of enamel. B, Higher power view of the cutout portion of enamel in A. Enamel
rods interlock with each other in a head-to-tail orientation. The rod heads are visible on the surface as
slight depressions on the perikymata ridges. The enamel rods comprise tightly packed crystallites. The
orientation of the crystallites changes from being parallel to the rod in the head region to being perpen-
dicular to the rod axis in the tail end. Striae of Retzius form a descending diagonal line, descending
cervically.

and ordered sequence of events. Bacteria seem to occupy the oral bioilm have a precise and well-tuned interaction209 (see
same spatial niche on most individuals. A “hedgehog” formation Fig. 2.6D).
has been recently characterized209 because of the spine of radially Many of the organisms found in the mouth are not found
oriented ilaments. he ilaments are a mass of Corynebacterium elsewhere in nature. Survival of microorganisms in the oral environ-
ilaments with Streptococcus at the periphery. Actinomyces are usually ment depends on their ability to adhere to a surface. Free-loating
found at the base of the bioilm suggesting that Corynebacterium organisms are cleared rapidly from the mouth by salivary low and
attaches to a preexisting bioilm containing Actinomyces. In any frequent swallowing. Although a few specialized organisms, primarily
case it is notable that each taxon is localized in a precise and streptococci, are particularly able to adhere to oral surfaces such
well-deined spatial zone indicating that the microbes in the Text continued on p. 48
 Acquired pellicle
Enamel

30 min-1 hr

1
Head of enamel rod

12-24 hrs
Cocci covering surface

Filamentous bacteria
1-3 days

Palisades of cocci
Filamentous
bacterial
colony

1 week

3 weeks

“Corn cobs”

C Large segment removed

• Fig. 2.6, cont’d C, Drawings 1 through 5 illustrate the various stages in colonization during plaque
formation on the shaded enamel block shown in B. The accumulated mass of bacteria on the tooth
surface may become so thick that it is visible to the unaided eye. Such plaques are gelatinous and tena-
ciously adherent; they readily take up disclosing dyes, aiding in their visualization for oral hygiene instruc-
tion. Thick plaque bioilms (4 and 5) are capable of great metabolic activity when suficient nutrients are
available. The gelatinous nature of the plaque limits outward diffusion of metabolic products and serves
to prolong the retention of organic acid metabolic by-products. Continued
46 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

D
• Fig. 2.6, cont’d D, This illustrates how different taxons inhabit speciic niches on the bioilm creating
microenvironments. There is a ine-tuned synergy among the cells in the oral microbial communities. The
environment and the biochemical gradients drive the selection process. This can be exempliied by the
the role of Streptococcus. Where Streptococcus predominate they create an environment rich in CO2,
lactate, and acetate, containing peroxide and having low oxygen. This environment is advantageous for
the growth of bacteria such as Fusobacterium and Leptotrichia. (From Welch JL, Rossetti BJ, Riekem
CW, et al: Biogeography of a human oral microbiome at the micron scale, Proc Natl Acad Sci USA
9;113(6):E791–E800, 2016. doi:10.1073/pnas.1522149113)

A B

• Fig. 2.7 A, Scanning electron microscope view (600×) of overlapping perikymata (P) in sound enamel
from unerupted molar. B, Higher power view (2300×) of overlapped site rotated 180 degrees. Surface of
noncavitated enamel lesions has “punched-out” appearance. (From Hoffman S: Histopathology of caries
lesions. In Menaker L, editor: The biologic basis of dental caries, New York, 1980, Harper & Row.)
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 47

• Fig. 2.8 Representative 3-D rendering images of mixed-species bioilms in an environment with 1%
(W/V) sucrose. The images show the evolution of the microcolonies over time and the arrangement with
the EPS matrix. (From Xiao J, Klein MI, Falsetta ML, et al: The exopolysaccharide matrix modulates the
interaction between 3D architecture and virulence of a mixed-species oral bioilm, PLoS Pathog
8(4):e1002623, 2012. https://doi.org/10.1371/journal.ppat.1002623)

• Fig. 2.9 Plaque bioilm formation at 1 week. Filamentous bacteria (f)

appear to be invading cocci microcolonies. Plaque near gingival sulcus
has fewer coccal forms and more ilamentous bacteria (860×). (From • Fig. 2.10 At 3 weeks old, plaque bioilm is almost entirely composed
Listgarten MA, Mayo HE, Tremblay R: Development of dental plaque on of ilamentous bacteria. Heavy plaque formers have spiral bacteria (a)
epoxy resin crowns in man. A light and electron microscopic study, J associated with subgingival plaque (660×). (From Listgarten MA, Mayo
Periodontol 46(1):10–26, 1975.) HE, Tremblay R: Development of dental plaque on epoxy resin crowns in
man. A light and electron microscopic study, J Periodontol 46(1):10–26,
1975.)
48 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

• Fig. 2.11 Approximate proportional distribution of predominant cultivable lora of ive oral habitats.
(From Simón-Soro Á, Tomás I, Cabrera-Rubio R, et al: Microbial geography of the oral cavity, J Dent Res
92:616, 2013. DOI:10.1177/0022034513488119.)

as the mucosa and tooth structure, over 700 diferent species of Recent evidence indicates that there are no speciic pathogens
bacteria have been identiied in the oral bioilm. Oral bioilm from that correlate with dental caries, but rather microbial communities.135
healthy teeth have a higher diversity than from carious teeth.134 Nevertheless, the general activity of bioilm growth and maturation
Signiicant diferences exist in the bioilm communities found is predictable and suiciently well known to be of therapeutic
in various habitats (ecologic environments) within the oral cavity importance in the prevention of dental caries.
(Fig. 2.11A and B). he organisms also have unique contributions Professional tooth cleanings are intended to control the bioilm
to the ecosystem (see Fig. 2.11B). Mature bioilm communities (plaque) and prevent caries (and periodontal) disease. However,
have tremendous metabolic potential and are capable of rapid after professional removal of all organic material and bacteria from
anaerobic metabolism of any available carbohydrate (Fig. 2.12). the tooth surface, a new coating of organic material begins to
However, because of the highly structured bacterial microcolonies accumulate immediately. Within 2 hours, a cell-free, organic ilm,
embedded in an exopolysaccharide (EPS)-rich matrix, there are the acquired enamel pellicle (AEP) (see Fig. 2.6A and C), can
acidic regions in the bioilm that are not neutralized by saliva cover the previously denuded area completely. he pellicle is formed
bufers.210 primarily from the selective precipitation of various components
Many distinct habitats may be identiied on individual teeth, of saliva, particularly selective enzymes. he functions of the pellicle
with each habitat containing a unique bioilm community (Table are believed to be (1) to protect the enamel, (2) to reduce friction
2.2; see Fig. 2.11A). Although the pits and issures on the crown between teeth, and (3) to provide a matrix for remineralization.6
may harbor a relatively simple population of streptococci, the root Although the pellicle exhibits antibacterial activity due to the
surface in the gingival sulcus may harbor a complex community presence of several enzymes, it can also function as a facilitator of
dominated by ilamentous and spiral bacteria. Even within the bacterial cononization.136
same anatomic location there can be a considerable diference in
bacterial diversity.134 For example the mesial surface of a molar
Tooth Habitat for Cariogenic Bioilm
may be carious and have a bioilm dominated by large populations
of mutans streptococci (MS) and lactobacilli, whereas the distal he tooth surface is unique because it is not protected by the
surface may lack these organisms and be caries free. Generalization surface-shedding mechanisms (continual replacement of epithelial
about bioilm communities is diicult. cells) used throughout the remainder of the digestive tract. he
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 49

• Fig. 2.12 A, Mature bioilm communities have tremendous metabolic

Caries free potential and are capable of rapid anaerobic metabolism of any available
8.0
Moderate caries activity
carbohydrates. Classic studies by Stephan show this metabolic potential
Extreme caries activity
by severe pH drops at the plaque-enamel interface after glucose rinse. It
is generally agreed that a pH of 5.5 is the threshold for enamel deminer-
7.0 alization. Exposure to a glucose rinse for an extreme caries activity plaque
results in a sustained period of demineralization (pH 5.5). Recording from
a slight caries activity bioilm shows a much shorter period of demineraliza-
pH tion. B, The frequency of sucrose exposure for cariogenic bioilm greatly
inluences the progress of tooth demineralization. The top line illustrates
6.0 pH depression, patterned after Stephan’s curves in A. Three meals per
day results in three exposures of bioilm acids, each lasting approximately
1 hour. The bioilm pH depression is relatively independent of the quantity
of sucrose ingested. Between-meal snacks or the use of sweetened
5.0 breath mints results in many more acid attacks, as illustrated at the
bottom. The effect of frequent ingestion of small quantities of sucrose
results in a nearly continuous acid attack on the tooth surface. (The clinical
consequences of this behavior can be seen in Fig. 2.37.) C, In active
4.0 caries, a progressive loss of mineral content subjacent to the cariogenic
0 10 20 30 40 50 60 bioilm occurs. Inset illustrates that the loss is not a continuous process.
A Minutes after glucose rinse Instead, alternating periods of mineral loss (demineralization) occur, with
intervening periods of remineralization. The critical event for the tooth is
Effect of Frequency of Ingestion of cavitation of the surface, marked by the vertical dashed line. This event
Sugary Foods on Caries Activity marks an acceleration in caries destruction of the tooth and irreversible
loss of tooth structure. An intervention is usually required to arrest the
lesion, often of the restorative nature. (A, Adapted and redrawn from
Three meals per day Stephan RM: Intra-oral hydrogen-ion concentration associated with dental
pH caries activity, J Dent Res 23:257, 1944.)

5.5
8 am Noon 8 pm

Between-meals sugar
pH

5.5 tooth surface is stable and covered with the pellicle of precipitated
salivary glycoproteins, enzymes, and immunoglobulins. It is the
B ideal surface for the attachment of many oral streptococci. If left
Changes in Mineral Content Over Time
undisturbed, bioilm rapidly builds up to suicient depth to produce
an anaerobic environment adjacent to the tooth surface. Given
the right conditions (that is, a conducive diet and poor oral hygiene)
these tooth habitats will become favorable for harboring pathogenic
bioilm and include (1) pits and issures (Fig. 2.13); (2) the smooth
enamel surfaces immediately gingival to the proximal contacts and
in the gingival third of the facial and lingual surfaces of the clinical
crown (Fig. 2.14); (3) root surfaces, particularly near the cervical
line; and (4) subgingival areas (Fig. 2.15). hese sites correspond
to the locations where caries lesions are most frequently found.
Surface
cavitation
Pits and Fissures
White spot Pits and issures are particularly susceptible surfaces for caries lesion
initiation (Figs. 2.16, 2.17, 2.18, 2.19, 2.20; see also Figs. 2.13
Mineral content

formation
to 2.15). he pits and issures provide excellent mechanical shelter
for organisms and harbor a community dominated by S. sanguis
and other streptococci.7 he relative proportion of MS most probably
determines the cariogenic potential of the pit-and-issure community.
In susceptible patients, sealing the pits and issures just after tooth
eruption may be the most important strategy in their resistance
Increasing to dental caries on those surfaces.
cavitation
Smooth Enamel Surfaces
C Initial caries Clinical caries he proximal enamel surfaces immediately gingival to the contact
area are the second most susceptible areas to dental caries lesions
(Figs. 2.21 and 2.22; see also Figs. 2.14 and 2.19). hese areas are
protected physically and are relatively free from the efects of
mastication, tongue movement, and salivary low. he types and
50 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

TABLE 2.2 Oral Habitatsa

Environmental
Predominant Conditions Within
Habitat Species Bioilm
Mucosa S. mitis Aerobic
S. sanguis pH approximately 7
S. salivarius Oxidation-reduction
potential positive
Tongue S. salivarius Aerobic
S. mutans pH approximately 7
S. sanguis Oxidation-reduction
potential positive A C
Teeth (noncarious) S. sanguis Aerobic
pH 5.5
Oxidation-reduction
negative
Gingival crevice Fusobacterium Anaerobic
Spirochaeta pH variable
Actinomyces Oxidation-reduction very
negative
a b c d
Veillonella
E
Enamel caries S. mutans Anaerobic
pH <5.5
Oxidation-reduction
negative
Dentin caries S. mutans Anaerobic
Lactobacillus pH <5.5
Oxidation-reduction
negative
Root caries Actinomyces Anaerobic
pH <5.5
Oxidation-reduction B D
negative
• Fig. 2.13 Developmental pits, grooves, and issures on the crowns of
a
The microenvironmental conditions in the habitats associated with host health are generally the teeth can have complex and varied anatomy. A and B, The facial
aerobic, near neutrality in pH, and positive in oxidation-reduction potential. Signiicant developmental groove of the lower irst molar often terminates in a pit.
microenvironmental changes are associated with caries and periodontal disease. The changes The depth of the groove and the pit varies. C and D, The central groove
are the result of the bioilm community metabolism.
extends from the mesial pit to the distal pit. Sometimes grooves extend
over the marginal ridges. E, The termination of pits and issures may vary
from a shallow groove (a) to complete penetration of the enamel (b). The
end of the issure may end blindly (c) or open into an irregular chamber
(d). The physical nature of the pit and issures allows for bioilm to remain
numbers of organisms composing the proximal surface bioilm stagnated. Additionally, the decreased thickness of enamel (and some-
community vary. Important ecologic determinants for the bioilm times absence of enamel) at the bottom of the pit and issure make these
community on the proximal surfaces are the topography of the surfaces especially susceptible to dental caries.
tooth surface, the size and shape of the gingival papillae, and the
oral hygiene and diet of the patient. A rough surface (caused by
caries lesions, a poor-quality restoration, or a structural defect)
restricts adequate bioilm removal. his situation favors the occur- (particularly near the CEJ), when exposed to the oral environment
rence and progression of caries lesions and/or periodontal disease (because of gingival recession), are often both neglected in hygiene
at the site. procedures and usually not rubbed by the bolus of food. Conse-
quently, these root surfaces also frequently harbor cariogenic bioilm.
Root Surfaces Root-surface caries lesions are more common in older patients
he proximal root surface, particularly near the cementoenamel because of niche availability and other factors sometimes associated
junction (CEJ), often is unafected by the action of hygiene with senescence, such as decreased salivary low due to multiple
procedures such as lossing because it may have concave anatomic medications and poor oral hygiene as a result of lowered manual
surface contours (luting) and occasional roughness at the termina- dexterity and decreased motivation. Caries lesions originating on
tion of the enamel. hese conditions, when coupled with exposure the root are alarming because they (1) have a comparatively rapid
to the oral environment (as a result of gingival recession), favor progression, (2) are often asymptomatic, (3) are closer to the pulp,
the formation of mature, cariogenic bioilm and proximal root- and (4) are more diicult to restore.
surface caries lesions. Likewise, the facial or lingual root surfaces Text continued on p. 58
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 51

Proximal contact
plaque biofilm
Sub-contact
plaque biofilm

Facial
plaque 20 19
20 biofilm
19 19 Continuous
A 20 B C plaque biofilm
formation

20 19
Horizontal 19 Plaque biofilm
cross-section 20
(just below contact)
D
• Fig. 2.14 Bioilm formation on posterior teeth and associated caries lesions. A, Teeth No. 19 and 20
in contacting relationship. B, The crown of tooth No. 20 has been removed at the cervix. The proximal
contact and subcontact bioilm can be seen on the mesial surface of tooth No. 19. The bioilm on the
facial surfaces is illustrated. C, During periods of unrestricted growth, the bioilms on the mesial and facial
surfaces become part of a continuous ring of bioilm around teeth. D, A horizontal cross section through
teeth No. 19 and 20 with heavy bioilm. Inset shows the interproximal space below the contact area illed
with gelatinous bioilm. This mass of interproximal bioilm concentrates the effects of bioilm metabolism
on the adjacent tooth smooth surfaces. All interproximal surfaces are subject to bioilm accumulation and
acid demineralization. In patients exposed to luoridated water, most interproximal lesions become
arrested at a stage before cavitation.

dt
rd
b p
rd dt
s
c

A B C
• Fig. 2.15 A, Caries lesions may originate at many distinct sites: pits and issures (a), smooth surface
of crown (b), and root surface (c). Proximal surface lesion of crown is not illustrated here because it is a
special case of smooth-surface lesion. Histopathology and progress of facial (or lingual) and proximal
lesions are identical. Dotted line indicates cut used to reveal cross sections illustrated in B and C. Lesions
illustrated here are intended to be representative of each type. No particular association between these
lesions is implied. B, In cross section, the three types of lesions show different rates of progression and
different morphology. Caries lesion progression and morphology follows the inclination of the enamel rods
and/or dentinal tubules. Pit-and-issure lesions have small sites of origin visible on the occlusal surface
but have a wide base. Overall shape of a pit-and-issure lesion is an inverted V. In contrast, a smooth-
surface lesion is V shaped with a wide area of origin and apex of the V directed toward pulp (p). Root
caries begins directly on dentin. Root-surface lesions can progress rapidly because dentin is less resistant
to caries attack. C, Although advanced caries lesions produce considerable histologic change in enamel,
dentin and pulp changes in dentin can be seen even before the lesion reached the dentin. Bacterial inva-
sion of lesion results in extensive demineralization and proteolysis of the dentin. Clinically, this necrotic
dentin appears soft, wet, and mushy. Deeper pulpally, dentin is demineralized and is structurally intact.
This tissue appears to be dry and leathery in texture. Two types of pulp–dentin response are illustrated.
Under pit-and-issure lesions and smooth-surface lesions, odontoblasts have died, leaving empty tubules
called dead tracts (dt). New odontoblasts have been differentiated from pulp mesenchymal cells. These
new odontoblasts have produced reparative dentin (rd), which seals off dead tracts. Another type of
pulp–dentin reaction is sclerosis (s)—occlusion of the tubules by peritubular dentin. This is illustrated under
root-caries lesion.
52 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

A
A C

B D
• Fig. 2.16 Progression of caries in pits and issures. A, Initial lesions
develop on the lateral walls of the issure. Demineralization follows the
direction of the enamel rods, spreading laterally as it approaches the
dentinoenamel junction (DEJ). B, Soon after the initial enamel lesion B
occurs, a reaction can be seen in the dentin and pulp. Forceful probing
of the lesion at this stage can result in damage to the weakened porous
enamel and accelerate the progression of the lesion. Clinical detection at
this stage should be based on observation of discoloration and opaciica-
tion of the enamel adjacent to the issure. These changes can be observed • Fig. 2.17 A, Maxillar irst molar has undermined discolored enamel
by careful cleaning and drying of the issure. C, Initial cavitation of the owing to extensive pit-and-issure caries. Note the dark shadow due to
opposing walls of the issure cannot be seen on the occlusal surface. the dentin demineralization underneath the enamel. The lesion began as
Opaciication can be seen that is similar to the previous stage. Reminer- illustrated in Fig. 2.16 and has progressed to the stage illustrated in Fig.
alization of the enamel because of trace amounts of luoride in the saliva 2.16D. B, Discolored enamel is outlined by the broken line in the central
may make progression of pit-and-issure lesions more dificult to detect. fossa region.
D, Extensive cavitation of the dentin and undermining of the covering
enamel darken the occlusal surface (see Fig. 2.17).
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 53

Radiolucency

A B

Radiolucency
Radiopacity

C D

E F
• Fig. 2.18 Progression of pit-and-issure caries. A, The mandibular right irst molar (tooth No. 30) was
sealed. Note radiolucent areas under the occlusal enamel in A and B. The sealant failed, and caries
progressed slowly during the next 5 years; the only symptom was occasional biting-force pain. This
underscores the need to monitor the sealant for failures. C and D, Note the extensive radiolucency under
the enamel and an area of increased radiopacity below the lesion, suggesting sclerosis. Conversely, a
well-sealed surface can prevent lesion progression. E and F, This maxillar irst molar (tooth No. 14) with
a shadow and a radiolucency indicative of dental caries was sealed as part of a clinical study.
Continued
54 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

G H

I J

K L
• Fig. 2.18, cont’d G–J, The tooth was followed clinically and by bitewing radiographs over the next
8 years. K and L, No progression of the lesion was observed. (E–L, Courtesy Dr. Azam Bakhshandeh,
Department of Odontology, Faculty of Health and Medical Sciences, University of Copenhagen, Depart-
ment of Cariology, Endodontics, and Pediatric Dentistry, Copenhagen, Denmark.)
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 55

A B

C D

E F

• Fig. 2.19 A young patient with extensive caries. A and B, The occlusal pits of the irst molar and
second premolar are carious. An interproximal caries lesion is seen on the second premolar. The second
premolar is rotated almost 90 degrees, bringing the lingual surface into contact with the mesial surface
of the irst molar. Normally, the lingual surfaces of mandibular teeth are rarely affected by caries, but here
tooth rotation makes the lingual surface a proximal contact and consequently produces an interproximal
habitat, which increases the susceptibility of the surface to caries. C and D, The irst and second molars
have extensive caries lesions in the pits and issures. E and F, On the bitewing radiograph, not only can
the extensive nature of the caries lesion in the second premolar be seen but also seen is a lesion on the
distal aspect of the irst molar, which is not visible clinically. (Dark areas in B, D, and F indicate caries.)
56 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

Caries

A B

Extensive
caries

C D

• Fig. 2.20 Example of occlusal caries that has undermined enamel. Note the dark shadow from the
dentin next to the stained issure. A and B, Clinical example. C and D, A bitewing radiograph further
conirms the extensive area of demineralization undermining the distofacial cusp.

A B

• Fig. 2.21 Bitewing radiograph of normal teeth, free from caries. Note the uniform density of the enamel
on the interproximal surfaces. A third molar is impacted on the distal aspect of the lower second molar.
The interproximal bone levels are uniform and located slightly below the cementoenamel junctions, sug-
gesting a healthy periodontium.
 A B C D

E F

G H
• Fig. 2.22 Longitudinal sections (see inset for A) showing initiation and progression of caries on interproximal surfaces. A, Initial demineralization
(indicated by the shading in the enamel) on the proximal surfaces is dificult to detect clinically or radiographically. The lesions develop right below the
contact surface. Flossing of the interproximal area and thorough drying will allow for the best conditions to detect these lesions clinically. B, When proximal
caries lesions irst become detectable radiographically, the enamel surface is likely still to be intact. An intact surface is essential for successful remin-
eralization and arrest of the lesion. Demineralization of the dentin (indicated by the shading in the dentin) occurs before cavitation of the surface of the
enamel. Treatment designed to promote remineralization can be effective up to this stage. C, Cavitation of the enamel surface is a critical event in the
caries process in proximal surfaces. After cavitation, lesion arrest becomes more dificult and virtually impossible in an interproximal surface contact.
Restorative treatment to repair the damaged tooth surface is required. Cavitation can be diagnosed only by clinical observation. The use of a sharp
explorer to detect cavitation is problematic because excessive force in application of the explorer tip during inspection of the proximal surfaces can
damage weakened enamel and accelerate the caries process by iatrogenic cavitation. Separation of the teeth using orthodontic separators can be used
to provide more direct visual inspection of suspect surfaces. Fiberoptic illumination although not speciic for cavitation can facilitate detection; an orange
shadow can be seen when lesions reach the dentin. D, Advanced cavitated lesions require prompt restorative intervention to prevent pulpal disease,
limit tooth structure loss, and remove the nidus of infection of odontopathic organisms. E, Radiographic image showing radiolucency on distal of tooth
No. 13 and mesial of tooth No. 14. F, An orthodontic separator was placed and left in place for 3 days. G, Clinical image of the teeth after separation.
H, There was no evidence of cavitation on either surface.
58 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

Oral Hygiene and It Role in the Dental Carie bacterial clearance, direct antibacterial activity, buffers, and
Proce remineralization.10

Oral hygiene, accomplished primarily by proper tooth brushing Bacterial Clearance

and lossing, is another ecologic determinant of dental caries onset Secretions from various salivary glands pool in the mouth to form
and activity. Careful mechanical cleaning of teeth disrupts the whole or mixed saliva. he amount of saliva secreted varies greatly
bioilm and leaves a clean enamel surface. he cleaning process over time. When secreted, saliva remains in the mouth for a short
does not destroy most of the oral bacteria but merely removes time before being swallowed. While in the mouth, saliva lubricates
them from the surfaces of teeth. Large numbers of these bacteria oral tissues and bathes teeth and the bioilm. he secretion rate
subsequently are removed from the oral cavity during rinsing and/ of saliva may have a bearing on dental caries susceptibility and
or swallowing after lossing and brushing, but suicient numbers calculus formation. Adults produce 1 to 1.5 L of saliva a day, very
remain to recolonize teeth. Some fastidious organisms and obligate little of which occurs during sleep. he lushing efect of this salivary
anaerobes may be killed by exposure to oxygen during tooth low is, by itself, adequate to remove virtually all microorganisms
cleaning; however, no single species is likely to be entirely eliminated. not adherent to an oral surface. he lushing is most efective
Although all the species that compose mature bioilm continue to during mastication or oral stimulation, both of which produce
be present, most of these are unable to initiate colonization on large volumes of saliva. Large volumes of saliva also can dilute and
the clean tooth surface. bufer bioilm acids.

Direct Antibacterial Activity

Saliva: Nature’ Anticarie Agent Salivary glands produce an impressive array of antimicrobial products
Saliva is an extremely important substance for the proper diges- (see Table 2.3). Lysozyme, lactoperoxidase, lactoferrin, and agglu-
tion of foods, and it also plays a key role as a natural anticaries tinins possess antibacterial activity. hese salivary proteins are not
agent (Table 2.3). he importance of saliva for oral health is part of the immune system but are part of an overall protection
dramatically noted after therapeutic radiation to the head and scheme for mucous membranes that occurs in addition to immu-
neck. After radiation, salivary glands become ibrotic and produce nologic control. hese protective proteins are present continuously
little or no saliva, leaving the patient experiencing an extremely at relatively uniform levels, have a broad spectrum of activity, and
dry mouth (xerostomia) (xero, dry; stoma, mouth), a condition do not possess the “memory” of immunologic mechanisms. However,
termed hyposalivation. Such patients may experience near-total it is important to note that the normal resident oral lora apparently
destruction of the teeth in just a few months after radiation has developed resistance to most of these antibacterial
treatment.8,9 Patients that have autoimmune disease (e.g., Sjögren mechanisms.
syndrome) also sufer from hyposalivation and experience severe Although the antibacterial proteins in saliva play an important
xerostomia, and can experience the same devastating efects of role in the protection of soft tissue in the oral cavity from infection
hyposalivation on their dentition. In addition, many common by pathogens, they have little efect on dental caries because similar
medications are capable of reducing salivary low and increas- levels of antibacterial proteins can be found in caries-active and
ing caries risk (Table 2.4). Salivary protective mechanisms that caries-free individuals.11,12 It is suggested that dental caries suscep-
maintain the normal oral lora and tooth surface integrity include tibility in healthy individuals is not related to saliva composition.

TABLE 2.3 Elements of Saliva That Control Bioilm Communities

Names Action Effects on Bioilm Community
Salivary Enzymes
Amylase Cleaves—1,4 glucoside bonds Increases availability of oligosaccharides
Lactoperoxidase Catalyzes hydrogen peroxide–mediated Lethal to many organisms; suppresses bioilm formation
oxidation; adsorbs to hydroxyapatite in on tooth surfaces
active form
Lysozyme Lyses cells by degradation of cell walls, Lethal to many organisms; peptidoglycans activate
releasing peptidoglycans; binds to complement; suppresses bioilm formation on tooth
hydroxyapatite in active conformation surfaces
Lipases Hydrolysis of triglycerides to free fatty acids Free fatty acids inhibit attachment and growth of some
and partial glycerides organisms
Nonenzyme Proteins
Lactoferrin Ties up free iron Inhibits growth of some iron-dependent microbes
Secretory immunoglobulin Agglutination of bacteria inhibits bacterial Reduces numbers in saliva by precipitation; slows bacterial
A(IgA) (smaller enzymes growth
amounts of IgM, IgG)
Glycoproteins (mucins) Agglutination of bacteria Reduces numbers in saliva by precipitation
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 59

TABLE 2.4 Medications With Potential to Cause Hyposalivation or Dry Mouth (Xerostomia)
Action/Medication Group Medicaments Action/Medication Group Medicaments
Sympathomimetic Anticholinergic, Dehydration
Antidepressants Venlafaxine Diuretics Furosemide
Duloxetine Bumetanide
Reboxetine Torsemide
Bupropion Ethacrynic acid
Anticholinergic Sympathomimetic
Tricyclic antidepressants Amitriptyline Antihypertensive agents Metoprolol
Clomipramine Moxonidine
Amoxapine Rilmenidine
Protriptyline
Doxepin Appetite suppressants Fenluramine
Imipramine Sibutramine
Trimipramine Phentermine
Nortriptyline Decongestants Pseudoephedrine
Desipramine
Bronchodilators Tiotropium
Muscarinic receptor antagonists Oxybutynin
Skeletal muscle relaxants Tizanidine
Alpha-receptor antagonists Tamsulosin
Terazosin Antimigraine agents Rizatriptan

Antipsychotics Promazine Synergistic Mechanism

Trilupromazine Opioids, hypnotics Opium
Mesoridazine Cannabis
Thioridazine Tramadol
Clozapine Diazepam
Olanzapine
Unknown
Antihistamines Aziridine H2 antagonists, proton pump inhibitors Cimetidine
Brompheniramine Ranitidine
Chlorpheniramine Famotidine
Cyproheptadine Nizatidine
Dexchlorpheniramine Omeprazole
Hydroxyzine
Phenindamine Cytotoxic drugs Fluorouracil
Cetirizine Anti-HIV drugs, protease inhibitors Didanosine
Loratadine

Adapted from the Kois Center, Support Materials, Always Pages, http://koiscenter.com/store/supmatlist.aspx, accessed January 13, 2012.

Individuals with decreased salivary production (owing to illness, Because saliva is crucial in controlling the oral lora and the
medication, or irradiation) may have signiicantly higher caries mineral content of teeth, salivary testing should be done on patients
susceptibility (see Table 2.4). with signs and symptoms of hyposalivation. Signs include lack of
saliva pool on the loor of the mouth, gingivitis and mucositis
Bufer Capacity (including burning mouth syndrome), cheilitis (inlammation and
he volume and bufering capacity of saliva available to tooth issuring of the lips and/or the tongue), issure in the soft mucosa,
surfaces have major roles in dental caries protection.13 he bufering fungal infections in the mouth such as thrush, glossodynia (painful
capacity of saliva is determined primarily by the concentration of tongue), sialadenitis (salivary gland infection), saliva that seems
bicarbonate ion. Bufering capacity can be estimated by titration thick and stringy, and several caries lesions especially in uncommon
techniques and may be a useful method for assessment of saliva areas such as the lower central incisors. Symptoms include com-
in caries-active patients. Simple commercial kits are available for plaints of “cotton mouth” (xerostomia); bad breath; diiculty
chairside tests. he beneit of the bufering is to reduce the potential chewing, speaking, and swallowing; a changed sense of taste; and
for acid formation; however, in pathogenic bioilms there are highly problems wearing dentures.
compartmentalized clusters of acidic pH and neutral pH that make
neutralization by saliva diicult.210, 211 Remineralization
In addition to bufers, saliva contains molecules that contribute Saliva and bioilm luid are supersaturated with calcium and phos-
to increasing bioilm pH. hese include urea and sialin, the latter phate ions. Without a means to control precipitation of these ions,
of which is a tetrapeptide that contains lysine and arginine. the teeth literally would become encrusted with mineral deposits.
Hydrolysis of either of these basic compounds results in production Saliva contains statherin, a proline-rich peptide that stabilizes
of ammonia, causing the pH to increase. calcium and phosphate ions and prevents excessive deposition of
60 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

these ions on teeth.14 his supersaturated state of the saliva provides large numbers of MS usually are found in carious pits and
a constant opportunity for remineralizing enamel and can help issures.
protect teeth in times of cariogenic challenges. he shape of the pits and issures contributes to their high
susceptibility to caries lesion. he long, narrow issure prevents
adequate bioilm removal (see Fig. 2.13). Considerable morphologic
Diet and Dental Carie variation exists in these structures. Some pits and issures end
High-frequency exposure to fermentable carbohydrates such as blindly, others open near the dentin, and others penetrate entirely
sucrose may be the most important factor in producing cariogenic through the enamel.
bioilm and ultimately caries lesions. Frequent ingestion of ferment- Pit-and-issure caries lesions typically “expand” as they penetrate
able carbohydrates begins a series of changes in the local tooth into the enamel. he entry site may appear much smaller than the
environment, essentially changing the composition of the bioilm, actual lesion, making clinical detection diicult. Caries lesions of
thus favoring the growth of highly acidogenic bacteria that eventually pits and issures develop from demineralization on their walls,
leads to caries lesion formation (see Fig. 2.4). In contrast, when known as wall lesions (see Fig. 2.16A–C). Progression of the dis-
ingestion of fermentable carbohydrates is severely restricted or solution of the walls of a pit-and-issure lesion is similar in principle
absent, bioilm growth typically does not lead to caries lesions. to that of the smooth-surface lesion because a wide susceptible
Dietary sucrose plays a leading role in the development of pathogenic surface area extends inward, paralleling the enamel rods. A lesion
bioilms and may be the most important factor in disruption of originating in a pit or issure afects a greater area of the denti-
the normal healthy ecology of dental bioilm communities. Sucrose noenamel junction (DEJ) than does a comparable smooth-surface
in particular allows the formation of extracellular polysaccharides, lesion. In cross section, the gross appearance of a pit-and-issure
which render the bioilm viscous and sticky. Because the eventual lesion is an inverted V with a narrow entrance and a progressively
metabolic product of cariogenic diet is acid, in addition to caries wider area of involvement closer to the DEJ (see Fig. 2.16D).
lesions the exposure to acidity from other sources (e.g., dried fruits,
fruit drinks, or other acidic foods and drinks) also may result in Smooth Enamel Surfaces
dental erosion. he dietary emphasis must include all intakes that he smooth enamel surfaces of teeth present a less favorable site
result in acidity, not just sucrose. for cariogenic bioilm attachment. Cariogenic bioilm usually
develops only on the smooth surfaces that are near the gingiva or
Clinical Characteritic of the Carie Leion are under proximal contacts. he proximal surfaces are particularly
susceptible to caries lesion formation because of the extra shelter
As discussed, the caries lesion results from disequilibrium between provided to resident cariogenic bioilm owing to the proximal
the demineralization and remineralization processes. However, contact area immediately occlusal to it (Fig. 2.22 and 2.23). Lesions
caries lesions appear in a variety of diferent clinical presentations starting on smooth enamel surfaces have a broad area of origin
depending on lesion location, severity, and progression rate or and a conical, or pointed, extension toward the DEJ. he path of
activity of the demineralization process, among other factors. ingress of the lesion is roughly parallel to the long axis of the
Clinically, caries lesions can be present on various tooth surfaces, enamel rods in the region. A cross section of the enamel portion
can be cavitated or noncavitated, active or inactive, and vary of a smooth-surface lesion shows a V shape, with a wide area of
depending on their severity (initial, moderate, or severe). For a origin and the apex of the V directed toward the DEJ. After the
complete description of current caries classiication criteria based demineralization reaches the DEJ, when there is enamel cavitation
on lesion severity and activity, see Chapter 3. he following sections and bacterial contamination, the bacterial metabolic activity within
will summarize these characteristics. the lesion causes rapid dentin demineralization both laterally and
pulpally (see Fig. 2.22).142,143
Clinical Site for Carie Initiation
he characteristics of a caries lesion vary with the nature of the
surface on which the lesion develops. here are three distinctly
diferent clinical sites for caries lesion initiation: (1) developmental
pits and issures of enamel, which are the most susceptible sites;
(2) smooth enamel surfaces that shelter cariogenic bioilm; and
(3) root surfaces (see Fig. 2.15). Each of these areas has distinct
surface morphology and environmental conditions. Consequently
each area has a distinct bioilm population. he diagnosis, treatment,
and prevention of these diferent lesion types should take into
account the diferent etiologic factors operating at each site.

Pits and Fissures

Bacteria rapidly colonize the pits and issures of newly erupted
teeth. he type and nature of the organisms prevalent in the oral
cavity determine the type of organisms colonizing pits and issures
and are instrumental in determining the outcome of the coloniza-
tion. Large variations exist in the microlora found in pits and
issures, suggesting that each site can be considered a separate • Fig. 2.23 Extracted tooth showing extensive caries lesion just gingival
ecologic system. Numerous gram-positive cocci, especially S. sanguis, to the proximal contact area. (Note the slightly “lat” contact area adjacent
are found in the pits and issures of newly erupted teeth, whereas to marginal ridge.)
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 61

a b c d

B
• Fig. 2.24 A, Cross section of small caries lesion in enamel examined by transmitted light (100×).
Surface (a) appears to be intact. Body of lesion (b) shows enhancement of striae of Retzius. Dark zone
(c) surrounds body of lesion, whereas translucent zone (d) is evident over entire advancing front of lesion.
B, The porosity of the lesion changes across the different zones. Thus a sharp explorer can easily pen-
etrate the outer enamel and cause a small cavitation on an active lesion. (A, From Silverstone LM, et al.
editors: Dental caries, London and Basingstoke, 1981, Macmillan, Ltd. Reproduced with permission of
Palgrave Macmillan. B, Courtesy Dr. Masatoshi Ando.)

Root Surfaces 2.15, 2.16, and 2.22). he time for progression from a noncavitated
he root surface is rougher than enamel and readily allows cariogenic caries lesion to a cavitated caries lesion on smooth surfaces is
biofilm formation in the absence of good oral hygiene. The estimated to be 18 months (± 6 months).19 Peak rates for the
cementum covering the root surface is extremely thin and provides incidence of new lesions occur 3 years after the eruption of the
little resistance to caries lesion activity. In addition, the critical tooth. Occlusal pit-and-issure lesions develop in less time than
pH for dentin is higher than for enamel, so demineralization is smooth-surface caries lesions. Poor oral hygiene and frequent
likely to start even before the pH reaches the critical level for exposures to sucrose-containing or acidic food can produce
enamel (pH = 5.5). Root caries lesions have less well-deined margins noncavitated initial (“white spot”) lesions (irst clinical evidence
than coronal caries lesions, tend to be U shaped in cross section, of demineralization) in 3 weeks. Radiation-induced hyposalivation
and progress more rapidly than coronal caries lesions because of (dry mouth) can lead to development of caries lesions in 3 months
the lack of protection from an enamel covering. In recent years, from the onset of the radiation. Caries lesion progression in healthy
the prevalence of root caries has increased signiicantly because of individuals is usually slow compared with the progression in
the increasing number of older persons who retain more teeth, compromised persons.
experience gingival recession, and usually have cariogenic bioilm
on the exposed root surfaces.15-18 Enamel Carie Leion
An understanding of the enamel composition and histology is
Carie Leion Progreion helpful to understand enamel caries histopathology (see Chapter
he progression and morphology of the caries lesion vary depending 1; Figs. 2.24, 2.25, and 2.26). On clean, dry teeth the earliest
on the site of origin and the conditions in the mouth (see Figs. evidence of caries lesion on the smooth enamel surface of a crown
62 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

is the initial lesion or a “white spot” (Fig. 2.27; see also Figs. 2.2
and 2.3). hese lesions usually are observed on the facial and
lingual surfaces of teeth. Initial lesions are chalky white, opaque
areas that are revealed only when the tooth surface is desiccated
and are termed noncavitated enamel caries lesions or initial lesions.
hese areas of enamel lose their translucency because of the extensive
subsurface porosity caused by demineralization. Care must be
exercised in distinguishing white spots of initial caries lesions from
developmental white spot hypocalciications or other developmental
defects of enamel. Initial (white spot) caries lesions partially or
totally disappear visually when the enamel is hydrated (wet), whereas
hypocalciied enamel is afected less by drying and wetting (Table
2.5). Hypocalciied enamel does not represent a clinical problem
except for its potential esthetically objectionable appearance. he
surface texture of an initial lesion is unaltered and is undetectable
by tactile examination with an explorer. A more advanced lesion
develops an irregular surface that is rougher than the unafected,
normal enamel. Softened chalky enamel that can be chipped away
with an explorer is a sign of active caries. However, injudicious
use of an explorer tip can cause actual cavitation in a previously
• Fig. 2.25 Microradiograph (150×) of cross section of small caries lesion noncavitated area, requiring, in most cases, restorative intervention.
in enamel. Well-mineralized surface (s) is evident. Alternating radiolucent and Similar initial lesions occur on the proximal smooth surfaces,
radiopaque lines indicate demineralization between enamel rods. (From although their detection by visual examination is more challenging.
Silverstone LM, et al, editors: Dental caries, London and Basingstoke, 1981, Tooth separation with orthodontic separators can facilitate visual
Macmillan, Ltd. Reproduced with permission of Palgrave Macmillan.)

4
4 3
3
2 2
zp
1
tz
1

A B C
• Fig. 2.26 A, Cross section of initial caries lesion in enamel examined in quinoline with polarized light
(100×). Advancing front of lesion appears as a dark band below body of lesion. B, Same section after
exposure to artiicial calcifying solution examined in quinoline and polarized light. Dark zone (DZ) covers
a much greater area after remineralization has occurred (100×). C, Schematic diagram of A and B. Left
side indicates small extent of zones 1 and 2 before remineralization. Small circles indicate relative sizes
of pores in each zone. Right side indicates increase in zone 2, the dark zone, after remineralization. This
micropore system must have been created where previously the pores were much larger. (From Silverstone
LM, et al, editors: Dental caries, London and Basingstoke, 1981, Macmillan, Ltd. Reproduced with permis-
sion of Palgrave Macmillan. C was redrawn.)

s
c c
i i

• Fig. 2.27 Facial and lingual smooth-surface caries. This patient has high caries activity with rapidly
advancing caries lesions. Cariogenic bioilm extends entirely around the cervical areas of the posterior
teeth. Several levels of caries involvement can be seen, including cavitation (c); initial (noncavitated) white
spot lesions (i); and stained, roughened, partially remineralized initial (noncavitated) lesions (s).
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 63

TABLE 2.5 Clinical Characteristics of Normal and Altered Enamel

Hydrated Desiccated Surface Texture Surface Hardness
Normal Enamel Translucent Translucent Smooth Hard
Hypocalciied Enamel Opaque Opaque Smooth Hard
Active Initial Caries Translucent (early lesions) Opaque Rough Softened
Opaque (more established initial lesions) Opaque Rough Softened
Arrested Initial Caries Shiny and/or dark Shiny and/or dark Smooth Hard
Active Moderate Caries Opaque Opaque Rough Softened
Arrested Moderate Caries Shiny and/or dark Shiny and/or dark Smooth Hard
Active Advanced Caries Opaque Opaque Rough Softened
Arrested Advanced Caries Shiny and/or dark Shiny and/or dark Smooth Leathery or hard

Histopathology
1 2 3a 3b 4a 4b 5 6

Bitewing 4 Naked eye

?

Probe
White spot Cavity Naked eye

Key to histopathology Spaces Demineralization Organic change

Translucent zone 1% 1 —
Dark zone 2-4% 2 —
Body of lesion 5-25% 3 —
Organic change 25% 4 1
• Fig. 2.28 Schematic representation of developmental stages of enamel caries lesion correlated with
radiographic and clinical examination. Cavitation occurs late in development of the lesion. Before cavitation
remineralization is possible, lesion arrest is possible at any stage given the right conditions. (Redrawn
from Darling AI: The pathology and prevention of caries, Br Dent J 107:287–302, 1959. Reproduced by
kind permission of the editor.)

examination of proximal tooth surfaces. Initial enamel lesions It has been shown experimentally and clinically that initial
sometimes may be seen on radiographs as a faint radiolucency that enamel caries lesions can remineralize20,21 whether the dentin is
is limited to the supericial enamel. When a proximal lesion is involved or not. Table 2.5 and Table 2.6 list the characteristics of
clearly visible radiographically, the lesion may have advanced enamel at various stages of demineralization. Initial, noncavitated
signiicantly, and histologic alteration of the underlying dentin enamel lesions retain most of the original crystalline framework
probably already has occurred, whether the lesion is cavitated or of the enamel rods, and the etched crystallites serve as nucleating
not (Fig. 2.28). agents for remineralization. Calcium and phosphate ions from
64 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

TABLE 2.6 Clinical Signiicance of Enamel Lesions

Nonrestorative, Therapeutic
Treatment (e.g., Remineralization,
Bioilm Enamel Structure Antimicrobial, pH control) Restorative Treatment
Normal Enamel Normal Normal Not indicated Not indicated
Hypocalciied Enamel Normal Abnormal, but not weakened Not indicated Only for esthetics
Noncavitated Caries Cariogenic Porous, weakened Yes Not indicated
Active Caries Cariogenic Cavitated, very weak Yes Yes
Inactive Caries Normal Remineralized, strong Not indicated Only for esthetics

Local mechanism of enamel adaptation to the cariogenic challenge to probing and can be easily enlarged by using sharp explorers
and excessive probing force. More advanced cavitated enamel lesions
Mineralization cariogenic challenge

are more obviously detected as enamel breakdown. Although

Saliva-biofilm substrate activity

Tooth
theoretically any caries lesion given the right conditions can be
resistance
arrested and have their progression to larger lesions forestalled,
once cavitation occurs removal of the bioilm is more diicult and
many will require a sealant or restorative intervention. When the
tooth surface cavitates, a more retentive site becomes available to
0

the bioilm community. he cavitation of the tooth surface produces

a synergistic acceleration of the growth of the cariogenic bioilm
community and the expansion of the demineralization with ensuing
expanded cavitation. his sheltered, highly acidic, and anaerobic
1 2 3 4 5
Mineralization-demineralization cycles environment provides an ideal niche for cariogenic bacteria. his
situation results in a rapid and progressive destruction of the tooth
• Fig. 2.29 Diagrammatic representation of enamel adaptation reaction. structure.
Enamel interacts with its luid environment in periods of undersaturation
and supersaturation, presented here as periodic cycles. Undersaturation
periods dissolve most soluble mineral at the site of cariogenic attack, Dentin Carie Leion
whereas periods of supersaturation deposit most insoluble minerals if their
ionic components are present in immediate luid environment. As a result, An understanding of the dentin composition and histology is helpful
under favorable conditions of remineralization, each cycle could lead to understand the histopathology of dentin caries lesions (see
toward higher enamel resistance to a subsequent challenge. (Redrawn Chapter 1; Fig. 2.31). Progression of dental caries in dentin is
from Koulouirides T: In Menaker L, editor: The biologic basis of dental diferent from progression in enamel because of the structural
caries, New York, 1980, Harper & Row.) diferences of dentin (Figs. 2.32, 2.33, and 2.34; see also Fig.
2.31). Dentin contains much less mineral and possesses microscopic
tubules that provide a pathway for the ingress of bacteria and
saliva can penetrate the enamel surface and precipitate on the egress of minerals.
highly reactive crystalline surfaces in the enamel lesion. The When enamel demineralization advances to the DEJ, rapid
supersaturation of saliva with calcium and phosphate ions serves lateral expansion of the caries lesion along the DEJ may occur if
as the driving force for the remineralization process. Artiicial and there is bacterial contamination. his process is still poorly under-
natural caries lesions of human enamel have been shown to regress stood, but it likely occurs only when there is enamel cavitation.
to earlier histologic stages after exposure to conditions that promote For many years this “lateral spread” has been attributed to the
remineralization. he presence of trace amounts of luoride ions DEJ’s lower mineral content compared to primary dentin.137 More
during this remineralization process greatly enhances the precipita- recently, it has been shown that a high concentration of MMPs
tion of calcium and phosphate, resulting in the remineralized enamel is found at the DEJ. MMPs are implied in dentin caries lesion
becoming more resistant to subsequent caries activity because of progression, although this may be a host defense mechanism and
the incorporation of more acid-resistant luorapatite (Fig. 2.29). not necessarily linked to an increase in caries susceptibility.138 What
Remineralized (arrested) lesions may be observed clinically as either is known is that the increased susceptibility to demineralization
intact, smooth white lesions or discolored, usually brown or black, observed at the DEJ on lesions that have reached dentin is a result
spots (Fig. 2.30). he change in color is presumably caused by of bacterial metabolic activity within the dentinal lesion.139-141
trapped organic debris and metallic ions within the enamel. hese Increasing demineralization of the body of the enamel lesion
discolored, remineralized, arrested caries lesion areas are more results in the weakening and eventual collapse of the surface enamel.
resistant to subsequent caries activity than the adjacent unafected he resulting cavitation provides an even more protective and
enamel. hey should not be restored unless they are esthetically retentive habitat for the cariogenic bioilm, accelerating the progres-
objectionable. sion of the lesion. he DEJ provides less resistance to the carious
Cavitated enamel lesions can be initially detected as subtle process than either enamel or dentin. he dentin contamination
breakdown of the enamel surface. hese lesions are very sensitive by bacterial metabolites leads to the lateral spread of the lesion at
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 65

Stained

A B

Arrested
caries

Radiographic
burnout
C D

E
• Fig. 2.30 A and B, Example of arrested caries lesion on the mesial surface of a mandibular second
molar. The area below the proximal contact (A and B, mirror view of tooth No. 18) is partly opaque and
stained. Clinically the surface is hard and intact, yet the area is more radiolucent than the enamel above
or below the stain. C and D, In a different clinical case, caries diagnosis based only on the radiograph
would lead to a false-positive diagnosis (i.e., caries lesion present when it is not). The radiolucency is
caused by the broad area of subsurface demineralization that extends from the facial to the lingual line
angles. The x-ray beam was directed parallel to the long axis of demineralization and consequently pro-
duced a sharply demarcated zone of radiolucency in the enamel. This example illustrates the shortcomings
of radiographic diagnosis. Were there not visual access to the mesial surface of the second molar, it
would be easy to diagnose active caries incorrectly and consequently restore the tooth. E, Cavitated
inactive (arrested) enamel caries lesion on the cervical one third of a central incisor of a 27-year-old patient
with low caries risk. This lesion, if not esthetically offensive, does not require a restoration and should be
monitored.

the DEJ, producing the characteristic second cone of caries activity remineralization. Often pain is not reported even when caries
in dentin (see Figs. 2.16 and 2.22).143 Figs. 2.31, 2.35, 2.36, 2.37, lesions invade dentin except when deep lesions bring the bacterial
and 2.38 illustrate advanced lesions with soft, infected dentin. infection close to the pulp. Episodes of short-duration pain may
Because of these characteristics, dentin caries is V shaped in cross be felt occasionally during earlier stages of dentin caries lesion
section with a wide base at the DEJ and the apex directed pulpally. progression. he pain is caused by stimulation of pulp tissue by
Caries lesions advance more rapidly in dentin than in enamel the rapid movement of luid through the dentinal tubules that
because dentin provides much less resistance to acid demineralization have been opened to the oral environment by cavitation. When
owing to less mineralized content and the presence and orientation bacterial invasion of the dentin is close to the pulp, toxins and
of the dentinal tubules. possibly a few bacteria enter the pulp, resulting in inlammation
he dental caries process produces a variety of responses in of the pulpal tissues, increased pulpal pressure, and thus pulpal
dentin including pain, sensitivity, demineralization, and pain.
66 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

Odontoblast Tubule
a b

1 2 3

B
12 3 • Fig. 2.32 Cross section of demineralized specimen of advanced caries
in dentin. Reparative dentin (A) can be seen adjacent to the most advanced
• Fig. 2.31 Normal and carious dentin. A, Normal dentin has character- portion of lesion. (From Boyle P: Kornfeld’s histopathology of the teeth
istic tubules that follow a wavy path from the external surface of dentin,
and their surrounding structures, Philadelphia, 1955, Lea & Febiger.)
below enamel or cementum, to the inner surface of dentin in the pulp
tissue of the pulp chamber or pulp canal. Dentin is formed from the exter-
nal surface and grows inward. As dentin grows, odontoblasts become
increasingly compressed in the shrinking pulp chamber, and the number
of associated tubules becomes more concentrated per unit area. The
more recently formed dentin near the pulp (a) has large tubules with little
or no peritubular dentin and calciied intertubular dentin illed with collagen
Bacterial biofilm
ibers. Older dentin, closer to the external surface (b), is characterized by
smaller, more widely separated tubules and a greater mineral content in Zone 3: Soft Dentin
intertubular dentin. The older dentin tubules are lined by a uniform layer (Infected dentin/
of mineral termed peritubular dentin. These changes occur gradually from outer carious dentin)
the inner surface to the external surface of the dentin. Horizontal lines
indicate predentin; diagonal lines indicate increasing density of minerals; Zone 2: Firm Dentin
darker horizontal lines indicate densely mineralized dentin and increased (Affected dentin/
thickness of peritubular dentin. The transition in mineral content is gradual, inner carious dentin)
as indicated in Fig. 2.25. B, Carious dentin undergoes several changes. Zone 1: Hard Dentin
The most supericial infected zone of carious dentin (3) is characterized (Reparative dentin)
by bacteria illing the tubules and granular material in the intertubular
space. The granular material contains very little mineral and lacks charac-
teristic cross-banding of collagen. As bacteria invade dentinal tubules, if
carbohydrates are available, they can produce enough lactic acid to
remove peritubular dentin. This doubles or triples the outer diameter of • Fig. 2.33 Cross section of occlusal caries. The occlusal enamel
the tubules in infected dentin zone. Pulpal to (below) the infected dentin appears intact, with a small opening in the occlusal issure. Enamel is
is a zone where the dentin appears transparent in mounted whole speci- darkened where it is undermined by demineralization. The surface of
mens. This zone (2) is the advancing demineralization front, affected enamel may not be clinically cavitated, but usually some discoloration is
carious dentin, and is characterized by loss of mineral in the intertubular observed at the entrance of the issure. The lesion is illed with a bacterial
and peritubular dentin. Many crystals can be detected in the lumen of the plug containing high numbers of MS and lactobacilli. When there is a break
tubules in this zone. The crystals in the tubule lumen render the refractive in the enamel, the dentin underneath the enamel will be highly contami-
index of the lumen similar to that of the intertubular dentin, making the nated below the plug. Deeper dentin is not as heavily contaminated but
zone transparent. Normal dentin (1) is found pulpal to (below) transparent is extensively demineralized. Reparative dentin is being formed below the
dentin. lesion.

he pulp–dentin complex reacts to caries activity by attempting apposition of peritubular dentin or by reparative dentin, as described
to initiate remineralization and blocking of the open tubules. hese in the next paragraphs.
reactions result from odontoblastic activity and the physical process In slowly advancing caries lesions, a vital pulp can repair
of demineralization and remineralization. he pulp–dentin complex demineralized dentin by remineralization of the intertubular dentin
reaction occurs even before the lesion has reached the dentin. and by apposition of peritubular dentin. Initial stages of caries
Dentin can react defensively (by repair) to low-intensity and lesions or mild caries activity produce long-term, low-level acid
moderate-intensity caries lesion progression as long as the pulp demineralization of dentin. Direct exposure of the pulp tissue to
remains vital and has adequate blood circulation. Dentin reaction microorganisms is not a prerequisite for an inlammatory response.
can happen through remineralization of intertubular dentin and Toxins and other metabolic by-products, especially hydrogen ion,
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 67

• Fig. 2.34 A cross section of a caries lesion in dentin and the histologic and clinical manifestations
(adapted from Ogawa et al, 1983). The most supericial outer layer of dentin is heavily contaminated,
necrotic, with irreversible demineralization and denatured collagen ibers. Clinically this is very soft, wet
dentin. This soft, contaminated layer gets progressively harder as the dentin approaches the pulp. The
still demineralized dentin (formerly affected dentin) can feel leathery to the touch or irm, but not as hard
as sound dentin or tertiary dentin (closest to the pulp, dentin formed in reaction to the caries process).
During caries excavation, the goal is to remove only the soft, outer carious dentin (infected dentin), while
the inner carious dentin (affected dentin) is remineralizable and can be maintained. (For orientation of
layers on tooth, see Fig 2.35.) (Modiied from Ogawa K, Yamashita Y, Ichijo T, et al: The ultrastructure
and hardness of the transparent layer of human carious dentin. J Dent Res 62(1):7–10, 1983.)

A B

• Fig. 2.35 A, Rampant caries in a preschool child. B, Rampant

caries in a school-age child. C, Rampant caries in an adult. (A, From
Dean JA, Avery DR, McDonald RE: McDonald and Avery’s dentistry
C
for the child and adolescent, ed 9, St Louis, 2011, Mosby.)

can penetrate via the dentinal tubules to the pulp. Even when the than normal dentin is termed sclerotic dentin. he apparent function
lesion is limited to enamel, the pulp can be shown to respond of the sclerotic dentin is to wall of a lesion by blocking (sealing)
with inlammatory cells.22,23 Dentin responds to the stimulus of the tubules. he permeability of sclerotic dentin is greatly reduced
its irst caries demineralization episode by deposition of crystalline compared with that of normal dentin because of the decrease in
material from the intertubular dentin in the lumen of the tubules the tubule lumen diameter.24 Hypermineralized areas may be seen
in the advanced demineralization front (formally called afected on radiographs as zones of increased radiopacity (often S shaped,
dentin) (see Figs. 2.31 and 2.34). he refractive index of the dentin following the course of the tubules) ahead of the advancing, infected
changes and the intertubular dentin with more mineral content portion of the lesion. Sclerotic dentin formation may also be seen
 A B

C D
Dark areas indicate caries
• Fig. 2.36 Rampant caries in a 21-year-old man. Although occlusal and interproximal lesions exist in
the patient, the progress of the occlusal lesions produced the most tooth destruction. The potential for
developing occlusal lesions could have been reduced by earlier application of sealants. This extensive
amount of caries was the result of the patient’s excessive fear of bad breath. In an attempt to keep his
breath smelling fresh, he kept sugar-containing breath mints in his mouth most of the day. (Dark areas in
B and D indicate caries.)

• Fig. 2.38 Advance cavitated active caries lesions on a 35-year-old

patient with high caries risk. (Courtesy Dr. Ayesha Swarn, DDS, Operative
Dentistry Graduate Program at UNC School of Dentistry.)

• Fig. 2.37 Acute, rampant caries in both anterior (A) and posterior (B)
teeth.
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 69

under an old restoration. Sclerotic dentin is usually shiny and external insults to the enamel.133 Since enamel is a microporous
darker in color but feels hard to the explorer tip. By contrast, solid, stimuli in the tooth surface are transmitted to the pulp. he
normal, freshly cut dentin lacks a shiny, relective surface and irst defense of the pulp is tubular sclerosis, which consists of
allows some penetration from a sharp explorer tip. his repair by mineral deposition in the peritubular dentin and in the dentinal
sclerotic dentin occurs only if the tooth pulp is vital. tubule’s lumen. Wear and age can also cause tubular sclerosis. his
When these afected tubules become completely occluded by the process only occurs in vital pulps. Caries progression in dentin
mineral precipitate, they appear clear when a histologic section of proceeds through three changes: (1) Weak organic acids demineralize
the tooth is evaluated. his portion of dentin has been termed dentin and expose its organic matrix; (2) the organic matrix of
translucent dentin (see Zones of Dentinal Caries Lesions) and is the dentin, particularly collagen, is denatured and degraded; and (3)
result of mineral loss in the intertubular dentin and precipitation the loss of matrix structural integrity is followed by invasion of
of this mineral in the tubule lumen. Consequently, translucent dentin bacteria. hree diferent zones of dentin have been described in
is softer than normal dentin (see Fig. 2.34)25 and is called “irm” moderate and advanced caries lesions (see Figs. 2.33 and 2.35):
(afected) dentin, in contrast to sound dentin that is “hard” dentin. • Soft Dentin (formerly infected dentin). Also called outer carious
More intense caries activity results in bacterial invasion of dentin. dentin, soft (infected) dentin is primarily characterized by
he most supericial (closer to the tooth surface) zone of the carious bacterial contamination. his is the carious dentin closer to the
dentin is the necrotic zone. his very soft (infected) dentin contains tooth surface, characterized by the presence of bacteria, low
a wide variety of pathogenic materials or irritants, including high mineral content, and irreversibly denatured collagen. Histologi-
acid levels, hydrolytic enzymes, bacteria, and bacterial cellular cally this zone may be referred to as necrotic and contaminated.
debris. hese materials can cause the degeneration and death of While soft dentin typically does not self-repair, the advance
odontoblasts and their tubular extensions below the lesion and a front of the soft dentin zone (near irm dentin) is characterized
mild inlammation of the pulp. he pulp may be irritated suiciently by supericial bacterial invasion and the caries process can still
from high acid levels or bacterial enzyme production to cause the be stalled when a good restorative seal is obtained. Clinically,
formation (from undiferentiated mesenchymal cells) of replacement soft dentin lacks structure and can be easily excavated with
odontoblasts (secondary odontoblasts). hese cells produce reparative hand and rotary instrumentation.
dentin (reactionary or tertiary dentin) on the afected portion of • Firm Dentin (formerly afected dentin). Also called inner
the pulp chamber wall (see Figs. 2.31B and 2.33). his dentin is carious dentin, irm (afected) dentin is primarily characterized
diferent from the normal dentinal apposition that occurs throughout by demineralization of intertubular dentin and of initial forma-
the life of the tooth by primary (original) odontoblasts. he structure tion of intratubular ine crystals at the advancing front of the
of reparative dentin varies from well-organized tubular dentin (less caries lesion. As the tubule lumen becomes illed with minerals
often) to very irregular atubular dentin (more often), depending it will give a “transparent” appearance in a section observed in
on the severity of the stimulus. Reparative dentin is an efective a light microscope. Histologically this zone may be referred to
barrier allowing limited difusion of material through the tubules as demineralized. Because of the caries demineralization process,
and is an important step in the repair of dentin. Severe stimuli irm dentin is softer than hard, normal dentin. Although organic
also can result in the formation within the pulp chamber of unat- acids attack the mineral and organic contents of dentin, the
tached dentin, termed pulp stones, in addition to reparative dentin. collagen cross-linking remains intact in this zone and can serve
he success of dentinal reparative responses, either by remineraliza- as a template for remineralization of intertubular dentin.
tion of intertubular dentin and apposition of peritubular dentin or herefore, provided that the pulp remains vital, irm (afected)
by reparative dentin, depends on the severity of the caries challenge dentin is remineralizable. Clinically, irm dentin is resistant to
and the ability of the pulp to respond. he pulpal blood supply hand excavation and can only be removed by exerting pressure.
may be the most important limiting factor to the pulpal responses. he transition between soft and irm dentin can have a leathery
Acute, rapidly advancing caries lesions with high levels of acid produc- texture, particularly in slowly advancing lesions, and has been
tion overpower host defenses of the pulp and result in infection, called leathery dentin. Clinically, leathery dentin does not deform
abscess, and death of the pulp. Compared with other oral tissues, upon pressure from an instrument but can be excavated with
the pulp is poorly tolerant of inlammation. Small, localized infections hand instruments such as spoons and curette without much
in the pulp produce an inlammatory response involving capillary pressure.
dilation, local edema, and stagnation of blood low. Because the • Hard Dentin. Hard dentin represents the deepest zone of a
pulp is contained in a sealed chamber, and its blood is supplied caries lesion—assuming the lesion has not yet reached the
through narrow root canals, any stagnation of blood low can result pulp—and may include tertiary dentin, sclerotic dentin, and
in local anoxia and necrosis. he local necrosis leads to more inlam- normal (or sound) dentin. Clinically this dentin is hard, cannot
mation, edema, and stagnation of blood low in the immediately be easily penetrated with a blunt explorer, and can only be
adjacent pulp tissue, which becomes necrotic in a cascading process removed by a bur or a sharp cutting instrument. (See deinitions
that rapidly spreads to involve the entire pulp. in Box 2.1 for histologic characteristics of hard, tertiary, and
Maintenance of pulp vitality depends on the adequacy of pulpal sclerotic dentin.)
blood supply. Recently erupted teeth with large pulp chambers hese dentin caries zones are most clearly distinguished in slowly
and short, wide canals with large apical foramina have a much advancing lesions. In rapidly progressing caries lesions (see Figs.
more favorable prognosis for surviving pulpal inlammation than 2.36, 2.37, and 2.38), the diference between the zones becomes
fully formed teeth with small pulp chambers and small apical less distinct.
foramina.

Zones of Dentin Caries Lesions

Carie Rik Aement and Management
Although enamel and dentin have distinct characteristics, the Although it is very important to detect caries lesions, caries detection
reaction observed in dentin is a direct response of the pulp to and caries diagnosis are not exclusively a tooth-centered process.
70 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

It is critical to remember that clinicians treat the entire patient lesions being detected for the patient over the last 2 to 3 years
and not just individual teeth and caries lesions. As noted earlier along with past history of caries lesions in the patient’s
in this chapter, dental caries is a multifactorial medical disease lifetime.39
process, and the caries lesions are the expression of a disease process Historically, dentistry has used a surgical model for dental caries
that involves the patient as a whole. Equally important in the management, which mainly contemplated the biomechanical
management of the caries disease is the ability to individualize excision (removal, excavation) of caries lesions and the restoration
caries diagnosis and treatment or interventions for each patient. of the resultant tooth preparation to form and function with a
To do this, the clinician must formulate a caries risk assessment restorative material. Management of caries disease by a surgical
proile that is based on the individual patient’s current risk factors model consisted of detecting cavitations and “treating” them with
and risk indicators. A risk factor is deined as an environmental, excavation and restorations. Eventually it became apparent that
behavioral, or biologic factor that directly increases the probability dealing only with the end result of the disease and not addressing
that a disease will occur and the absence or removal of which its etiology for each individual patient was not successful in control-
reduces the possibility of disease.37,38 Risk factors are part of the ling the caries disease process. Since surgical management alone
causal chain of the disease process, or they expose the host to the was not successful, a system has been developed using caries
causal chain; but once the disease occurs, removal of a risk factor management strategies. his system looks at individualized caries
may not always result in the disease process being halted. Any risk assessments and uses this information to design treatment
deinition of risk factor must clearly establish that the exposure plans according to the risk assessment indings. hese assessments
has occurred before the outcome or before the conditions are look at each patient’s unique set of pathologic and protective factors.
established that make the outcome likely. his means that longi- Caries management by risk assessment (CAMBRA) represents a
tudinal studies are necessary to demonstrate risk factors. Terms management philosophy that manages the caries disease process
such as risk indicators and risk markers are also used in the caries using a medical model. his process provides an individualized
literature to refer to risk factors, putative risk factors, or something evaluation of a patient’s pathologic factors and protective factors
else entirely. Risk indicators may refer to existing signs of the disease and assesses the patient’s risk for developing future disease. he
process, or signs that the disease process has occurred, but are not risk assessment is then used to develop an individualized evidence-
part of the disease causal chain. For example, existing caries lesions based caries management plan that involves aspects of nonsurgical
would be risk indicators, as they indicate a risk status, but are not therapeutics and dental surgical interventions. Both risk assessment
per se part of the causal chain so they are not risk factors. Multiple and patient-centered interventions are based on the concept of
risk factors (and indicators) have been studied, reviewed, and caries balance as discussed earlier in this chapter (see Fig. 2.1).
validated in the assessment of risk for development of future caries he caries balance model is based on minimizing pathologic factors
disease, but caries risk assessment is not an exact science. Because while maximizing protective factors to attain a balance that favors
caries is a complex multifactorial disease, no single risk factor (or no disease occurring, or health. With the use of CAMBRA for
indicator, or marker) is highly predictive of future caries. However, patient management, mounting evidence suggests that early damage
caries risk assessment is necessary to identify what (if any) interven- to teeth may be reversed and that the incidence of disease manifesta-
tions are needed to lower the patient’s caries risk and activity—which tions can be signiicantly reduced or prevented. CAMBRA is a
is the ultimate goal of caries management when using the medical concept that has gained interest in the United States, and is evolving
model.39,40 A discussion of diferent risk factors will be included into the standard of care in caries management.4,41,144,145 Additionally,
in this section of the chapter. the International Caries Classiication and Management System
Caries risk assessments are speciic for adults and adolescents (ICCMS)146-148 has endeavored to merge caries detection and
older than 6 years and for children under 6 years of age. It is very assessment with an individualized management plan. Another caries
important to spend time with the patient to uncover all relevant risk assessment method that has been validated for children is the
risk factors and indicators currently present. Some risk and protective Cariogram.149,150
factors can be adjusted and modiied by either the patient or the
clinician, such as sucrose intake and luoride exposure; other risk Carie Rik Aement
factors are not easily modiiable, such as hyposalivation as the
result of a needed medication or an existing condition such as he clinical examination process for diagnosis and detection of
Sjögren syndrome. Understanding and controlling risk factors and caries lesions is discussed in detail in Chapter 3. he caries risk
protective factors can be very important in the prevention of new assessment is an important part of this overall process of patient
caries lesion formation and to slow or arrest the progression of care. he clinician must gather all appropriate data from both the
existing caries lesions. interview with the patient and the clinical examination for caries
No consensus exists on exactly how to deine the risk categories detection to formulate an individualized caries risk assessment.
for caries risk assessments. Examples of terms used to describe risk Part of the caries risk assessment identiies the risk (causative)
assessment are “at risk,” “low risk,” “medium risk,” “high risk,” factors, but does not predict the caries outcome. Risk factors can
and “extreme risk.” Assignment of these terms is typically based exist for a patient without the disease being expressed at the time
on the subjective judgment of the clinician with general rules of the examination. he predictive model part of the risk assessment
applied, based on the clinician’s previous clinical experiences and looks at the assessment of caries progression in the future. Risk
training. If a clinician inds no detectable or active caries lesions factors are associated with the variables that have value for prediction
and minimum or no identiiable risk factors, that patient would purposes, which means that the risk factor is present before the
be assigned a low caries risk. In this situation, in the current state disease occurs. As discussed, risk indicators are existing signs of
of the patient’s health, the protective factors for not developing the disease process. hey are examples of what is happening with
caries lesions outweigh the risk factors that could lead to new the patient’s current state of oral health, not how disease occurred.
caries lesions. he strongest predictor for caries risk for patients Risk indicators are clinical observations and detection modalities
in the at-risk and high-risk categories are the number of caries used to identify risk-level status. Examples include visible cavitations
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 71

in pits and issures or in proximal surfaces of teeth, brown spots, identiied as contributing to caries risk include age, gender, luoride
active initial lesions, or cavitated lesions on free smooth surfaces, exposure, home care, smoking habits, alcohol intake, medications,
as well as any restorations in the past 3 years. he ideal caries risk dietary habits, economic and educational status, and general health.
assessment method should be inexpensive and easy to use but at Increased smoking, alcohol consumption, use of medications, and
the same time have high predictive value. It should be valuable in sucrose intake result in increased risk for caries development.42
decision making for caries management in the use of nonsurgical Children and older adults have increased risks. Decreased luoride
therapeutics and surgical interventions that serve the patient in a exposure, lower economic status, and lower educational attainment
cost-efective and health-promoting manner. also increase risk. Poor general health also increases the risk. A
One of the roles of caries risk assessment in caries management strong body of evidence suggests that past caries experience is the
is to assist in determining the current caries lesion activity. Caries best predictor of future caries activity.43 Information that is
lesions may be detected signiicantly before frank cavitation occurs. important and obtained in the patient history interview would be
he diagnosis of caries lesions should include whether they are biologic and environmental factors that include, but are not limited
actively progressing. An inactive lesion may be visible clinically or to, medical history including current and past diseases, current
radiographically; however, it may not be active or progressing over medications, and history of hyposalivation from medications or
time. With a positive shift in protective factors, change in oral conditions; dental history including past history of dental caries,
hygiene, or reduction of pathologic factors, it is possible for caries dental phobias, and history of dental conditions; current home
lesions to change in density, size, hardness, and clinical appearance. care practices and how well this is done; current diet and exposure
hese inactive lesions are arrested and may not require operative to sucrose and other fermentable carbohydrates; and current
intervention. Assessment by the clinician of all the pathologic and exposure to topical luoride products in toothpaste, mouth rinses,
protective factors in the patient’s current history will greatly aid and luoridated water supply. Some of these factors are explored
in the decision regarding current activity. A thorough risk assessment in more detail in the following sections.
allows for a more predictive analysis of current and future disease Fig. 2.39A and B present two examples of caries risk assessment
activity and assists in deciding on nonsurgical or surgical interven- forms that can be used as part of the initial caries diagnosis process;
tions. Caries risk assessment helps the clinician to identify the Fig. 2.39C is an example of a caries assessment form that can be
etiologic causes of the disease for a speciic patient at a speciic used to facilitate communication of the indings with patients.
point in time, and to determine the frequency and treatment his latter caries assessment form is a useful tool to measure changes
protocols for patient follow-up visits. Restorative decisions in terms and determine the efectiveness of caries management procedures.
of material used and cavity preparation design are also inluenced All of these forms can be incorporated into an electronic patient
by the information gathered in the risk assessment process. he management system for increased eiciency.
data gathered establish an important baseline for use in future
reassessments to help the clinician and the patient measure the Social, Economic, and Education Status
efectiveness of the caries management treatment protocol used Social status and economic status are not directly involved in the
for the patient. he systematic use of risk assessment proiles is disease process but are important because they afect the expression
essential in uncovering risk factors that are present before disease and management of the caries disease. he socioeconomic status
manifestation. his information may be useful in the prevention and educational status of the patient have implications on the
of caries lesions in patients who have risk factors present but no necessary compliance and behavioral changes that can decrease
disease expression and then experience a lifestyle change that adds risk for caries development. Socioeconomic status and educational
additional risk factors. he new risk factors then become a tipping status are predictive at the population level but are generally inac-
point for the caries balance equation toward disease expression. curate at the individual level.
For instance, a patient who frequently consumes high-sugar soft
drinks during the day (risk factor) suddenly is prescribed a Diet Analysis
hyposalivation-inducing medication (additional risk factor) that Increased frequency of sugar intake in the form of fermentable
increases caries risk. he informed patient would have the option carbohydrates increases risk for caries by modifying the bioilm to
of making the decision to eliminate a modiiable risk factor (soft support a lower pH environment. he frequent use of candies and
drinks) before expression of the disease and before the introduction lozenges during the day or night increases the risk. Sugar-containing
of the hyposalivation-inducing medication considering this risk acidic beverages, including sport drinks, fruit juices, and soft drinks,
assessment. all contribute to increased risk. Frequent ingestion of fermentable
he incorporation of risk assessments in routine patient care carbohydrates can change the microbiome proile of the bioilm
and in each patient’s caries management program is necessary favoring acidogenic and aciduric bacteria and by inluencing the
because of the multifactorial nature of the caries disease. No one pH of the bioilm to support cariogenic bacteria (see Fig. 2.4).
factor is able to predict the probability of a patient developing
caries lesions. When developing a preventive and restorative caries Salivary Analysis
management plan, consideration of the whole patient is essential Salivary low rate, bufering capacity, and pH all can be measured
to successful outcomes. In addition, recorded speciic risk assessment by various methods (tests). he caries risk predictive value for these
proiles provide patients with an educational tool that empowers tests is not fully demonstrated by strong evidence in all circum-
them to be an important part of managing their disease. Finally, stances. Patients with normal salivary low and adequate bufering
risk assessments provide a means for both the clinician and the capacity may still develop and/or have caries. However, when
patient to monitor and measure the proposed caries management patients have dry mouth symptoms and a salivary low analysis
protocols over time and evaluate and adjust the protocols as needed. leads to a diagnosis of hyposalivation, the decreased salivary low
Risk assessments lead to better treatment outcomes for patients. is a predictive risk factor for root caries in older patients with
Knowing certain factors pertaining to the patient’s history is recession and for increased caries in general in other populations.
key in establishing a caries risk assessment. Factors that have been As discussed, saliva has numerous efects in protection against
72 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

A
• Fig. 2.39 A, Example of a caries risk assessment form recommended by the American Dental Asso-
ciation. B, Example of a caries risk assessment form used by the University of North Carolina, Department
of Operative Dentistry. C, Another caries assessment form used by the University of North Carolina,
Department of Operative Dentistry. This form is very useful for patient communication and compliance.
(A, Copyright 2009, 2011 the American Dental Association.)
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 73

Caries Risk Initial Assessment Risk Low Risk At Risk High Risk
Name___________________________________
Risk Rating Score £3 ≥4 and £8 ≥9
Date____________________________________

Patient Interview Assessment

Dental History Risk Rating Supplemental notes for dental history
1. Had non emergency dental care in last year yes no -1
2. Brushes teeth at least twice daily yes no -3
3. Uses fluoridated toothpaste or product daily yes no -3
4. New caries lesions within the last 3 years yes no 8
5. Patient has teeth sensitive to hot, cold, sweets yes no 3
6. Patient avoids brushing any part of mouth yes no 3

Dietary Assessment
1. Water supply currently fluoridated yes no -2
2. Frequent snacking with sugary foods, Supplemental notes for dietary assessment
acidic foods, fermentable carb foods yes no 8
3. Sugary drinks including soft drinks,
juice, sports drinks, medicinal syrups yes no 8
4. Tobacco use of any kind yes no 3
5. Excessive alcohol or recreational drug use yes no 8
6. Eating disorders yes no 5

Xerostomia Assessment
1. Patient is aware of dry mouth or reduced saliva yes no 10
2. Medications taken that reduce salivary flow yes no 8 Xerostomia Assessments with scores of 8-10
3. Medical conditions affecting salivary flow/content yes no 8 indicate baseline salivary testing is required
4. Saliva flow or content visibly abnormal yes no 10

Patient Clinical Assessment

Clinical Oral Findings
1. Readily visible biofilm/plaque yes no 5
2. Visible cavitated lesions yes no 10
3. Interproximal enamel lesions or radiolucencies yes no 10
4. Visible white spots yes no 5 Clinical Assessments with scores of 10 indi-
5. Visible brown spots or non cavitated caries lesions yes no 3 cate that baseline bacterial testing is required
6. Deep pits or grooves yes no 5
7. Radiographic cavitated lesions yes no 10
8. Restorations with overhangs
and/or margin concerns or open contacts yes no 3
9. Prosthesis ortho, fixed, or removable yes no 3

Risk Rating Total =

This is clinician’s impression of patient’s
10. Clinician’s impression of patient’s risk low at risk high risk if different than would be indicated by
risk factors marked. Describe in box below.
Patient Compliance Assessment
Patient’s attitude and general assessment of patient’s ability to comply for each of the following categories:

Oral hygiene compliance patient limitations yes no This is clinician’s assessment of any perceived
Dietary recommendation patient limitations yes no limitations for the patient to comply with oral hy-
Therapeutic homecare products limitations yes no giene, dietary, or using home care products. Could
be lifestyle, physical, or economic reasons.
Special needs health care (physical or mental compliance issues) yes no Describe in box below.
Patient Clinical In Office Tests Indicated From Risk Score

Cariscreen Meter completed at risk low risk reading _______________

GC America Saliva Check completed at risk low risk
GC America Strep Mutans completed at risk low risk
GC America Plaque Indicator completed at risk low risk
UNC Biologic Testing Lab completed at risk low risk

Notes from oral findings, patient’s attitude, office tests, special circumstances that would influence caries risk or management

• Fig. 2.39, cont’d Continued

74 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

PREPARED FOR PREPARED BY

Name________________________ ________________________.
Caries Assessment Testing Results
Date_________________________

_______________________________________________________________________________________________________
Risk predicts your likelihood of developing future disease. Green is low risk and means you are unlikely to develop a
Your Risk Scores:
cavity whereas red means you are very likely to develop a cavity unless your risk factors are managed. We will use
these results to work with you to develop an individualized plan to control your disease.

Existing Dental Conditions

Your dental condition score is based on current areas of decay, number of cavities in
the last three years, exposed root surfaces, crowns and fillings that are defective. Your
score will also be higher if you wear partial dentures or other appliances.

Saliva Assessment Testing

Your saliva is the main protective factor in the caries risk disease state equation. Yellow
Saliva pH Testing and Red results can produce an increased incidence of cavities. If the pH of the saliva
is low, it sets the stage for the bacteria to grow that cause cavities to form in your
mouth. If the quantity of the saliva is below normal, the healing ability of the saliva to
>6.8 6.0-6.6 <5.8 remineralize your teeth after acidic food and beverages is greatly reduced. This can, in
most incidences, result in a dry mouth that is uncomfortable when eating and lead to an
Saliva Flow and Buffering
increase in cavities on the roots and other surfaces of your teeth. Any change in saliva
content, amount, or pH can increase your risk for cavities to form even if you have not
had cavities in the past. New medications and medical conditions can cause your sa-
Normal Abnormal liva to change rapidly.

Plaque Assessment Testing

Plaque pH Testing
Plaque or biofilm is the mass of bacteria that is always changing and clings to the sur-
faces of your teeth. Plaque is one of the main risk factors that result in cavities. For
plaque to produce the acid that dissolves your teeth and form cavities, it has to be in
>6.8 6.0-6.6 <5.8
an acidic state, or in other words, have a low pH. The more acidic, the more damage
Biofilm Activity that can result. The type of bacteria in the plaque also influences how easy it is for the
damage to occur. The biofilm activity measures the amount of the “bad” bacteria
present in the plaque. The higher the number, the more bacteria are present that cause
<1500 1500-2000 >2000 the cavities to form. The amount of plaque on your teeth means more bacteria are
Visible Plaque present in your mouth. More bacteria produce higher amounts of acid to demineralize
your teeth and cause them to decay.

Low High

Dietary Habits
Frequency of Snacking
A key factor in how you control your disease and prevent cavities is how you eat and
what beverages you consume. Snacking with sweet foods or high carbohydrate foods
that can form sugars causes the plaque to become acidic. This results in more bacteria
<1 2-3 >3
forming that produce even more acid. All of this acid dissolves your teeth and forms
Frequency of sweetened bever- the cavities. Sweetened drinks or drinks high in acid content also produce low pH
ages and sport drinks plaque and more bacteria. Soft drinks and sports drinks like Gatorade are very low in
pH. The more you drink, the more acid the plaque and bacteria produce to cause the
cavities in your teeth.
<1 2-3 >3

• Fig. 2.39, cont’d

 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 75

caries, including inhibition of bacteria, eliminating (clearing of ) surrogate measure of caries activity has also not been identiied to
bacteria from the tooth surface, dilution of bacterial products, be a strong predictor of risk. Although these bacterial tests may
bufering of bacterial acids, and ofering a reparative environment be useful for patient communication by providing insight into the
with necessary calcium and phosphate minerals after bacteria- speciics of the bioilm (bacterial types and resultant environment),
induced demineralization. Since all of these beneits are missing the predictive value (for caries risk) of the evidence of the tests
when patients have salivary hypofunction, patients with “dry mouth” requires further validation by controlled research studies.
are at higher risk for caries. hese patients are more susceptible to
dietary changes that are associated with lower pH foods and bever- Rik Aement Conideration for Children
ages or foods and beverages containing fermentable carbohydrates,
since the protective factors of saliva are diminished in patients Under 6 Year Old
with hyposalivation. In addition to all the above mentioned risk factors for adults and
adolescents, there are age-speciic risk factors and indicators that
Dental Clinical Analysis (Dental Exam) should be considered for children under 6 years. hese include
he dental examination identiies risk indicators more than risk presence of active caries in the primary caregiver in the past year,
factors. his is important as many of the indicators are directly feeding on demand past 1 year of age, bedtime bottle or sippy
related to the current caries activity. Risk indicators and current cup with anything other than water, no supervised brushing, and
caries activity drive the decision-making process toward the type severe enamel hypoplasia.
of intervention that the clinician would prescribe. Visible cavitated
caries lesions and active initial lesions on teeth are both indicators Carie Management and Protocol or Strategie
of caries risk. Visible bioilm may also be considered a risk factor
for caries development. Other examination indings that would for Prevention
inluence increased risk for caries are exposed root surfaces; deep Caries risk assessment is only meaningful if used in conjunction
pits or grooves; ixed, removable prosthesis or orthodontic appliances with a corresponding caries management program. he caries
used; and existing restorations with open contacts, open margins, prevention or management program should comprise a menu of
rough surfaces, or overhangs. prevention therapies and interventions that should be recommended
on the basis of the level of caries risk (Table 2.7 and Box 2.2) and
Bacterial Bioilm Analysis address the patient’s risk factors. However, as discussed in the
Use of supplemental tests to analyze the bacterial component of previous section, no caries risk assessment system is perfect.
the bioilm has little value to determine the patient’s risk level. herefore, in addition to the outcome of the caries risk assessment
For example, the presence of MS or lactobacilli in saliva or plaque tool, the clinician needs to use his or her best clinical judgment,
as a sole predictor for caries in primary teeth has been shown to coupled with the best available research evidence, to design a
have low sensitivity but high speciicity. he measurement of preventive or therapeutic program that works for the patient.
adenosine triphosphate (ATP) activity of the bioilm bacteria as a Needless to say, this is a dynamic process, so monitoring and

TABLE 2.7 Suggested Risk-Based Interventions for Adultsa

Caries Risk Category Ofice-Based Interventions Home-Based Interventions
High
3-month recare examination and oral prophylaxis Brush with prescription luoride dentifrice (e.g., 1/1%/5000 ppm NaF)
Fluoride varnish at each recare visit Use sugar substitutes (e.g., xylitol, erythritol)
Individualized oral hygiene instructions and use of Apply calcium-phosphate compounds (e.g., MI Paste)
specialized cleaning aids (e.g., powered On selected cases use agents to modulate a dysbiotic microbiome
toothbrush, Waterpik) (e.g., xylitol gum or lozenge, chlorhexidine rinse). Use agents to
Dietary counseling encourage a healthy microbiome (probiotics, prebiotics, like arginine)
Bitewing radiographs every 6–12 monthsb If xerostomic, increase salivary function (e.g., xylitol gum, rinses, oral
moisturizers)
Moderate
4–6 month recare examination and oral prophylaxis Brush with luoride dentifrice (e.g., 1450 ppm luoride)
Fluoride varnish at each recall OTC luoride rinse (e.g., 0.05% NaF)
Reinforce proper oral hygiene
Dietary counseling
Low
9–12 month recare examination and oral prophylaxis Brush with luoride dentifrice
Reinforce good oral hygiene

NaF, Sodium luoride; OTC, over the counter; ppm, parts per million.
a
These are general guidelines and should be customized based on the speciic patient’s needs and on weight of individual risk factors uncovered with a caries risk assessment instrument.
b
Data from US Department of Health and Human Services, Public Health Service, Food and Drug Administration; and American Dental Association, Council on Dental Beneit Programs, Council on
Scientiic Affairs. The selection of patients for dental radiographic examinations. Rev. ed. 2004.
Available at www.ada.org/prof/resources/topics/radiography.asp. Accessed January 20, 2012.
Modiied from Shugars DA, Bader JD: MetLife quality resource guide: risk-based management of dental caries in adults, ed 3, Bridgewater, NJ, 2009–2012, Metropolitan Life Insurance Co., p. 6.
76 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

• BOX 2.2 Sample Preventive Protocol for a High-Risk Patient With Cavitated Caries Lesions
1. A comprehensive oral and radiographic evaluation is conducted charting g. A prophylaxis is performed and 5% sodium luoride (NaF) varnish is
caries lesions, periodontal pocket probing, existing restorations, and oral applied to all teeth.
cancer exam; the medical and dental histories are reviewed. In this h. If SDF is used, the lesion should be reassessed 1 to 2 weeks after irst
hypothetical patient, multiple caries lesions, poor oral hygiene, and application to determine if it has arrested. If the lesion has not arrested
generalized marginal gingivitis are noted. a new application of SDF is advised. Lesions that will not be restored
2. A caries risk assessment is completed with emphasis on discovering the need to have a new SDF application every 6 months.
risk factors that are contributing to the causative aspect of the caries i. The microbiologic testing, if done, may be repeated 2 to 4 weeks after
problem and discovering the risk factors for the patient that are predictors initiation of treatment. A reduction in counts can be a great
of future caries risk. A discussion of these risk factors with the patient is motivational tool for patients to continue with their modiications in
essential for understanding of the caries disease process and the patient’s behavior (diet or oral hygiene). Diet analysis is followed up and
role and the provider’s role in controlling the disease. reviewed again. Successes in diet modiications are positively
3. Diagnosis and treatment planning procedures are completed and reinforced. Shortcomings in diet modiications are discussed and
discussed with the patient. options explored with the patient to rectify diet issues, where needed.
4. Nonoperative and operative treatments will be completed in three phases: Home care regimens are reviewed again with patients and reined. It is
(i) a control phase, (ii) a deinitive treatment phase, and (iii) a maintenance important to listen to the patient and work to incorporate diet and
reassessment phase. home care into the patient’s lifestyle and abilities to mentally and
5. CONTROL PHASE (2–4 weeks): physically comply with the recommendations.
a. Oral hygiene procedures are explained and reviewed at each patient 6. DEFINITIVE TREATMENT PHASE:
visit. The frequency of the visits in this initial phase is determined by a. The glass ionomer provisional restorations are replaced (usually by
severity of the disease. This could be weekly or more frequent, quadrants) with deinitive restorations.
depending on the provider’s evaluation. When attempting behavior b. Oral hygiene procedures are reinforced at each visit. Flossing and
modiication, repetition is essential. Review of patient’s current home brushing three times per day with prescription toothpaste is
care techniques and frequency of home care are reviewed along with recommended.
lifestyle issues that might impede compliance. Use of a powered c. Patients with root caries may beneit from chewing xylitol chewing
toothbrush and an oral irrigator for possibly improving patient gum with at least 1 gram of xylitol per piece three to six times per day,
compliance and technique are discussed. Evaluation of the patient’s preferably after meals and snacks.
motivation along with the person’s mental and physical capacity to d. Some patients with low salivary low or low salivary buffering capacity
comply with recommendations for home care must be noted and may beneit from applying casein phosphopeptide–amorphous calcium
considered by the provider. Speciic recommendations are listed for the phosphates (CPP-ACP) to teeth after brushing and lossing prior to
patient to use at home, and the patient agrees that this is practical for retiring to bed.
his or her life situation. e. If reduced salivary low rates are considered to be a major etiologic
b. Prescription luoride toothpaste is prescribed (5000 parts per million factor, the patient should be instructed to chew sugar-free mints
[ppm]) and the patient is instructed to brush with it three times per day several times a day or use other recommended products for
and to use according to given instructions (do not rinse after use, only xerostomia treatment. Prescribing pilocarpine or other salivary
expectorate excess). Any products used for home care should be stimulant should be considered.
carefully reviewed for the pH of the product. Products with pH lower f. When all deinitive restorations are completed, the patient then enters
than 6 should be carefully considered whether their use would the maintenance reassessment phase.
contribute to the pH shift of the bioilm to pathologic for caries lesion 7. MAINTENANCE REASSESSMENT PHASE:
formation. a. The patient should be recalled every 3 months. Oral hygiene and home
c. A diet analysis is completed, analyzed, and reviewed with the patient. care procedures are reviewed and evaluated. Recommendations for
Cariogenic foods and beverages are identiied and alternatives improvement and modiications to home care are evaluated and
suggested. Also acidic foods and beverages that are contributing to the discussed.
pH shift to a lower oral pH environment are identiied and discussed. b. Prophylaxis followed by luoride varnish application is accomplished.
Options for foods that have impact to raise the oral pH are suggested, c. Caries risk assessment is completed again; changes are noted in risk
such as foods rich in arginine. Again the patient’s motivation and factors that have been controlled and those risk factors still listed as
abilities to it the necessary diet modiications into his or her lifestyle causative and predictive factors.
must be evaluated and discussed. d. Diet analysis and recommendations from previous visits are reviewed
d. A microbiologic survey may be completed for patient motivation. This and evaluated.
can be accomplished using either the adenosine triphosphate (ATP) e. Patient continues use of prescription 5000-ppm toothpaste, CPP-ACP
chairside device or formal saliva samples to identify speciic mutans paste, and xylitol chewing gum as advised. Any other recommendations
streptococci (MS) and lactobacilli counts. to changes or additions to the product protocols are reviewed,
e. A saliva analysis is conducted to determine stimulated low rate, discussed, and implemented.
salivary pH and buffering capacity, and viscosity. Treatment protocols f. Every 6 months, salivary evaluations are repeated. Microbiologic
for hyposalivation are recommended for patients with an analysis that evaluations may also be repeated to keep patient motivation.
indicates deiciencies in the above areas. Patients with low salivary pH g. Bitewing radiographs are taken on an annual basis or more frequently
would need to use baking soda rinses during the day and use xylitol if new lesions continue to be detected.
gum or other recommended products to raise pH levels, increase low, h. It is critical for the patient to understand that caries is a disease that is
and increase buffering capacity. only controlled and not “cured.” The protocol that is determined to be
f. Caries control (described elsewhere in this chapter) is completed. This currently successful may have to be periodically reviewed, updated,
may involve use of silver diamine luoride (SDF) for cavitated lesions or and changed. More importantly, the patient will be much like a patient
partial caries removal and interim restoration of all cavitated caries with diabetes, requiring lifetime medication and therapy, diet control,
lesions (usually during one appointment and restoring with glass and lifestyle management for disease stability, and will need to be
ionomer) or a combination of both. This is critical to reduce the dedicated to a lifetime of careful management of caries risk factors to
bacterial load and prevent further progression on the lesion. keep the disease controlled.
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 77

TABLE 2.8 Health History Factors Associated With TABLE 2.9 Clinical Examination Findings Associated
Increased Caries Risk With Increased Caries Risk
History Factor Risk-Increasing Observations Clinical Examination Risk-Increasing Findings
Age Childhood, adolescence, senescence General appearance Appearance: sick, obese, or malnourished
Fluoride exposure No luoride in public water supply Mental or physical Inability or unwillingness to comply with
No luoride toothpaste disability dietary and oral hygiene instruction
Smoking Risk increases with amount smoked Mucosal membranes Dry, red, glossy mucosa, suggesting
decreased salivary low
Alcohol Risk increases with amount consumed
Active caries lesions Cavitation and softening of enamel and
General health Chronic illness and debilitation decreases dentin; circumferential chalky opacity at
ability to give self-care gingival margins
Medication Medications that reduce salivary low Plaque bioilm High plaque scores
Gingiva Puffy, swollen, and inlamed gingiva; bleeds
easily

periodic reassessment and reevaluation of the disease activity and Existing restorations Large numbers, indicating past high caries
rate; poor quality, indicating increased
prevention or management program are critical. habitat for cariogenic organisms
Management of dental caries and its consequences remains the
predominant activity of dentists; however, preventive and diagnostic
services are increasing.44,45 Although these activities relate to a
variety of dental problems, diagnosis and prevention of caries are
major parts of these increases. In a modern practice model, the he efectiveness of a patient’s immune system depends on overall
restoration of a caries lesion can no longer be considered a cure health status. Patients undergoing radiation or chemotherapy
for dental caries. Rather, the practitioner must identify patients treatment have signiicantly decreased immunocompetence and
who have active caries lesions and patients at high risk for caries are at risk for increased caries.
and institute appropriate preventive and treatment measures. his Medically compromised patients should be examined for changes
section presents some measures that may reduce the likelihood of in the following: plaque index, salivary analysis, oral mucosa, gingiva,
a patient developing caries lesions. Depending on the risk status and teeth. Early signs of increased risk include increased bioilm;
of the patient and the risk factors at play for the speciic patient, pufy, bleeding gingiva; dry mouth with red, glossy mucosa; and
the dentist must decide which of these to institute. With this initial caries lesions on teeth. Decreased saliva low is common
paradigm shift, dentistry is focusing increasingly on limiting the during acute and chronic systemic illnesses and is responsible for
need for restorative treatment. the dramatic increase in bioilm. Ambulatory patients with chronic
Preventive treatment methods are designed to limit tooth illnesses often take multiple medications, which individually or in
demineralization caused by cariogenic bacteria, preventing initial combination may reduce salivary low signiicantly (see Table 2.4).
lesions and progression of initial lesions into cavitated lesions. Saliva should be tested for low and bufering capacities when
hese methods include (1) limiting pathogen growth and altering signs or symptoms are detected from an oral examination.
metabolism of the bioilm, (2) increasing the resistance of the
tooth surface to demineralization, and (3) increasing bioilm pH. Diet
A caries prevention and management program is a complex process Dietary sucrose has two important detrimental efects on how
involving multiple interrelated factors (Tables 2.8, 2.9, 2.10, and bioilm afects caries. First, frequent ingestion of foods containing
2.11; see also Table 2.7 and Box 2.2). he primary goals of a caries sucrose provides a change in the bioilm proile from a noncariogenic
prevention program are (1) to modulate the bioilm into a non- bioilm to a cariogenic bioilm.151 Second, mature bioilm exposed
pathogenic bioilm and (2) to create an environment conducive frequently to sucrose rapidly metabolizes it into organic acids,
to remineralization. Prevention should start with a consideration resulting in a profound and prolonged decline in pH. Caries activity
to maintain the patient with a noncariogenic bioilm. Although is most strongly stimulated by the frequency, rather than the
the general health of the patient, luoride exposure history, and quantity, of sucrose ingested. he message that excessive and frequent
function of the immune system and salivary glands have a signiicant sucrose intake can cause caries has been widely disseminated and
impact on the patient’s caries risk, the patient may have little is well known by laypeople. Despite this knowledge, dietary
control over these factors. he patient usually is capable of control- modiication for the purpose of caries control has failed as a public
ling other factors such as diet, oral hygiene, use of agents to modulate health measure. For an individual patient, dietary modiication
the bioilm, and dental care (which may include use of sealants may be efective if the patient is properly motivated and supervised.
and restorations). his section presents a variety of factors that Evidence of new caries activity in adolescent and adult patients
may have an impact on caries prevention. indicates the need for dietary counseling. he goals of dietary
counseling should be to identify the sources of sucrose and acidic
General Health foods in the diet and to reduce the frequency of ingestion of both.
he patient’s general health has a signiicant impact on overall Minor dietary changes such as substitution of sugar-free foods for
caries risk. Declining health signals the need for increased preventive snacks are more likely to be accepted than more dramatic changes.
measures, including more frequent recalls. Every patient has an Rampant (or acute) caries (a rapidly developing process usually
efective surveillance and destruction system for “foreign” bacteria. involving several teeth) is a sign of gross dietary inadequacy, a
78 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

TABLE 2.10 Methods of Caries Treatment by the Medical Model

Method and Indications Rationale Techniques or Material
A. Limit Cariogenic Substrate
Indications: Reduce number, duration, and intensity of Diet diary
Frequent sucrose exposure acid attacks Eliminate sucrose from between-meal snacks
Poor-quality diet Reduce selection pressure for mutans Substantially reduce or eliminate sucrose from meals
streptococci (MS)
B. Modify Microlora
Indications: Modify a dysbiotic bioilm and encourage Bactericidal mouthrinse (chlorhexidine)
High MS counts a healthy bioilm Reduce overall bioilm Topical luoride treatments; probiotics and prebiotics
High lactobacilli counts burden to improve gingival health
C. Disorganize Plaque Bioilm
Indications: Prevents plaque bioilm succession Brushing
High plaque bioilm scores Decreases plaque bioilm mass Flossing
Puffy red gingiva Promotes buffering Other oral hygiene aids as necessary (e.g., electric
High bleeding point score toothbrush)
D. Modify Tooth Surface
Indications: Increase resistance to demineralization Systemic luorides
Noncavitated lesions Decrease plaque bioilm retention Topical luorides
Surface roughening Smooth surface
E. Stimulate Saliva Flow
Indications: Increases clearance of substrate and acids Eat noncariogenic foods that require lots of chewing
Dry mouth with little saliva Promotes buffering Sugarless chewing gum
Red mucosa Medications to stimulate salivary low
Medication that reduces salivary low Use dry mouth topical agents, oral lubricants, etc.
F. Seal Susceptible Surfaces
Indications: Prevents colonization (infection) of Use pit-and-issure and smooth-surface resin
Moderate and high caries risk individuals pit-and-issure system with cariogenic sealants
Teeth with susceptible anatomy (deep plaque bioilm
grooves) Inhibits progression of smooth-surface
Initial noncavitated enamel lesions in high- lesion
risk patients (smooth-surface sealants)
G. Restore Active Cavitated Surfaces
Indications: Eliminate nidus of cariogenic bioilm Apply SDF to caries lesions as indicated Restore all
Cavitated lesions Deny habitat for cariogenic bioilm cavitated lesions
Defective restorations reinfection Correct all defects (e.g., marginal crevices, proximal
overhangs)

TABLE 2.11 Treatment Strategies

Examination Findings Nonrestorative, Therapeutic Treatment Restorative Treatment Follow-upa
Normal (no lesions) None None 1-year clinical examination
Hypocalciied enamel None for nonhereditary lesions; hereditary Treatment is elective; 1-year clinical examination
(developmental white spot) lesions (dentinogenesis imperfecta) esthetics (restore
may require special management defects)
Noncavitated enamel lesions only; Techniques A–E in Table 2.9, as indicated Seal defective pits and 3 months; evaluate: oral lora,
bitewing radiographs indicated issures as indicated mutans streptococci (MS)
(demineralized white spot) counts, progression of white
spots, presence of cavitations
Possible cavitated lesions (active Techniques A–E in Table 2.9, as indicated Techniques F and G 3 months; evaluate: oral lora,
caries) and other noncavitated (restorations, sealants) MS counts, progression of
lesions present; bitewing in Table 2.9 as white spots, presence of new
radiographs indicated indicated cavitations, pulpal response
Inactive caries; no active (new None Treatment is elective; 1-year clinical examination
cavitations) or noncavitated esthetics (restore
lesions defects)
a
These are only generalized follow-up times. Particular circumstances may dictate shorter or longer follow-up intervals, depending on presence of primary and secondary modifying risk factors (see
Fig. 2.1).
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 79

A B w

Caries
C D

• Fig. 2.40 Erosion wear and poor home care leading to caries. A young female patient with severe
wear on the facial surfaces of posterior teeth. This patient subsequently was found to have a hiatal hernia
with frequent regurgitation of stomach acids. Too vigorous brushing and acid demineralization of teeth
accelerated the loss of tooth structure (A and B). Areas of severe wear (w) exhibit dentin hypersensitivity.
Dentin pain was the symptom that caused the patient to seek dental care. Advising the patient to reduce
vigorous tooth brushing resulted in cessation of all brushing. Caries activity rapidly occurred (C and D).

complete absence of oral hygiene practice, systemic illness, or a

combination of these pathologic factors. Rampant caries that is Oral Hygiene
present primarily on proximal surfaces may point more to diet as Bioilm-free tooth surfaces do not decay. Daily removal of bioilm
the main driving factor, whereas rampant caries in the cervical by dental lossing and tooth brushing with a luoridated toothpaste
and interproximal areas may point to diet and hygiene as the is the best patient-based measure for preventing caries and peri-
driving factors. he presence of rampant caries indicates the need odontal disease (Figs. 2.40 and 2.41). Löe established supragingival
for comprehensive patient evaluation. Textbooks on dental caries, plaque as the etiologic agent of gingivitis.47 Longstanding gingivitis
nutrition, and medicine should be consulted as needed. may lead to damage of the epithelial attachment and progression
For high-risk patients, a formal diet analysis should routinely to more serious periodontal disease. Although plaque scores are
be undertaken to identify cariogenic foods and beverages that are not reliable indicators of caries risk, the presence of bioilm over
frequently ingested. his analysis may take place by asking the a lesion may help assess lesion activity.152,153 Efective bioilm control
patient to recall everything that was ingested in the past 24 hours by oral hygiene measures using a luoridated toothpaste results in
(the “24-hour diet interview”). Alternatively, a more detailed diet resolution of the gingival inlammation and remineralization of
analysis may be facilitated by requesting the patient to record a any initially demineralized enamel surface.
diet diary, which consists usually of a 5- to 7-consecutive-day Mechanical bioilm disorganization by brushing and lossing
period with 2 days surveyed being weekend days as patients’ diets has the advantage of not eliminating the normal oral lora. Topical
frequently change considerably on weekends. A form should be antibiotics may control oral bioilm, but long-term use predisposes
provided to the patient that divides each day into six segments the host to infection by antibiotic-resistant pathogens such as
(breakfast, morning, lunch, afternoon, dinner, and evening), and Candida albicans. Frequent mechanical bioilm removal does not
the patient should be instructed to write down everything ingested, engender the risk of infection by opportunistic organisms; rather
including medications, the amount, and the time of consumption. it changes the species composition of bioilm in the selection for
he diary is then analyzed by the dentist, and a discussion is held pioneering organisms and the denial of habitat to potential
with the patient to suggest appropriate alternatives.46 he dentist pathogens. he oral lora on the teeth of patients with good bioilm
should focus on type of cariogenic foods and time intervals between control has a high percentage of S. sanguis or S. mitis and is much
their consumption as well as length of exposure of each cariogenic less cariogenic than older, mature bioilm communities, which
episode. For example, if a patient were to record “10:00 AM 1 have a signiicantly higher percentage of MS.
soda,” the dentist should clarify the type of soda consumed, the Krasse showed that a combination of oral hygiene and diet
quantity of soda, and the duration of time to inish the soda. An counseling is efective in children.48 In this classic study, children
8-oz glass of sugar-containing soda consumed over a 5-minute in two schools were monitored for Lactobacillus levels. he children
period will have a diferent impact than a 20-oz glass sipped over in one school were given feedback about their Lactobacillus levels
a 2-hour period. and proper preventive oral hygiene and dietary instruction. After
80 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

c
c

A B

C D

• Fig. 2.41 A and B, Photograph of the occlusal surfaces of the teeth illustrated in Fig. 2.40. C and D,
After cessation of oral hygiene procedures, caries (c) rapidly developed in the exposed dentin and issures
on the occlusal surfaces. Caries was treated conservatively by excavation of softened dentin and restora-
tion of the excavations and issures with composite.

18 months, the children in the school receiving preventive counseling even only once every 2 weeks, dramatically reduces the development
had an average of 3.3 new restorations, whereas the control of new caries lesions. here is little evidence that professional
schoolchildren, who received no counseling, averaged 8.2 new prophylaxis at the usual 6-month intervals reduces dental caries
restorations. his study is an excellent demonstration that good levels; therefore it is important to customize recall intervals to the
oral hygiene and dietary improvements may be efective when patient risk. Equal or greater reductions may be expected in patients
using microbiologic testing as a motivational tool. who practice proper oral hygiene methods for bioilm removal.
Rigid oral hygiene programs should be prescribed only to Another adjunct to regular brushing and lossing is the regular
high-risk persons with evidence of active disease. Overzealous, use of electric toothbrushes and oral irrigation devices. A recent
universal application of oral hygiene training programs is frustrating study has demonstrated these devices are efective in the removal
to dentists and their patients. High-risk patients should receive of bioilm and, more importantly, change the composition of the
intensive oral hygiene training usually with a prescription-strength bioilm in a favorable direction when used regularly.50 Since most
luoridated toothpaste (5000 parts per million [ppm] F), dietary patients are not very eicacious on judicious removal of bioilm,
instruction, and preventive dental treatment, as necessary, to control brushing may be viewed more as a delivery mechanism for luoride.
the progress of disease. Adults with a low caries experience probably Recommendations of brushing for at least 2 minutes and not
require less frequency of daily lossing and brushing. rinsing may increase compliance and improve outcomes. Addition-
Bioilm control requires a little dexterity and a lot of motivation. ally, simple suggestions, like feeling tooth surfaces with the tongue
Some knowledge of tooth contours, embrasure form, proximal to assess if the bioilm was removed, may improve awareness and
contacts, and tooth alignment is helpful in optimal bioilm control. assist in eicacy.
Instruction should include the selection and use of mechanical
aids based on patient needs. Professional tooth cleanings can have Fluoride Exposure
an important efect on caries reduction. One study divided grade he highest level of evidence for caries prevention and reduction
school students into three treatment groups: control, monthly supports the exposure of teeth to luoride. Fluoride in trace amounts
professional cleaning, and twice-a-month professional cleaning.49 increases the resistance of tooth structure to demineralization and
In students with low MS levels, the once-a-month cleaning group is particularly important for caries prevention (Fig. 2.42). When
showed ~50% fewer new carious surfaces (0.8 surfaces/student) luoride is available during cycles of tooth demineralization, it is
than the control group (1.8 surfaces/student). In the high MS a major factor in reduced caries activity.51 Fluoride seems to be an
group, the control group had the most new caries (2.5 surfaces/ essential nutrient for humans and is required only in very small
student), whereas the once-a-month cleaning group had similar quantities. Laboratory animals fed a completely luoride-free diet
levels (0.96 surfaces/student) to the low MS group, and the twice- develop anemia and reduced reproduction after four generations.
a-month cleaning group had almost one tenth the number of new When available to humans, luoride produces spectacular decreases
lesions (0.34 surfaces/student) as the control group. his study in caries incidence. he availability of luoride for caries risk
showed that professional bioilm removal on grade school students, reduction has primarily been achieved through the luoridation of
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 81

Posteruptive changes in dental enamel:

the fate of Class V lesions

Age 8 Age 15

Sound enamel 93 74
111 sound
37 enamel
15
41 white
White spot 72 26 spots

4 32 cavitated
9 lesions
A Cavitated lesion 19 19

B
• Fig. 2.42 A, Initial (white spot) lesions of enamel (stage 3 in Fig. 2.28) may remineralize, remain
unchanged, or progress to cavitated lesions. In this study, done in a community with a luoridated public
water supply, only 9 of 72 noncavitated lesions became cavitated. More than half of noncavitated lesions
(37 of 72) regressed to become indistinguishable from normal enamel. B, White spot lesions of enamel
(stage 3 in Fig. 2.28) may remineralize, remain unchanged, or progress to cavitated lesions. A comparison
of a study done in a community with a luoridated public water supply published in 1966 (Backer Dirks,
1966) versus a study completed in a nonluoridated community published in 2012 (Ferreira Zandona et al,
2012). The 1966 study followed 184 smooth surfaces (buccal) over a 7-year period. The 2012 followed
62,812 surfaces over a 4-year period, of those 8652 were buccal surfaces. In both studies only a very
small portion of sound surfaces cavitate (4% versus 1%–2%). Most initial lesions in enamel on smooth
surfaces will not progress to cavitation (only 13% progressed to cavitation in 1966 and only 10% in 2012).
When other surfaces are included the number of lesions that progress to cavitation more than double
(24%) but it still represents only one fourth of all initial lesions. On smooth surfaces even when enamel
cavities are considered, only 20% progress to cavitation exposing the dentin; and, when all surfaces are
included, 30% of enamel cavities do not progress to cavitations exposing the dentin. (A, Redrawn from
Backer Dirks O: Posteruptive changes in dental enamel. J Dent Res 45:503–511, 1966.)

community water systems. Fluoride exposure may occur by means in the enamel becoming more acid resistant (see Fig. 2.29). Second,
of diet, toothpastes, mouth rinses, and professional topical applica- initial caries lesions are remineralized by the same process. hird,
tions. he optimal luoride level for public water systems is 0.7 mg luoride has antimicrobial activity. In low concentrations, luoride
per liter of water.52 he percentage of the U.S. population with ion inhibits the enzymatic production of glucosyltransferase.
public luoridated community water systems has increased from Glucosyltransferase promotes glucose to form extracellular polysac-
62% (140 million) in 1999 to 66% (162 million) in 2000, to charides, which increases bacterial adhesion. Intracellular polysac-
69% (184 million) in 2006,23,54 to 74% (284 million) in 2014. charide formation also is inhibited, preventing storage of
Public water luoridation has been one of the most successful carbohydrates by limiting microbial metabolism between the host’s
public health measures instituted in the United States. For com- meals. In high concentrations (12,000 ppm) used in topical luoride
munities that have luoridated water systems, the annual cost treatments, luoride ion is directly toxic to some oral microorgan-
averages about $0.70 per person.53 For every $1 spent on water isms, including MS. Suppression of growth of MS after a single
luoridation, $6 of health savings are realized. he U.S. Public topical luoride treatment may last several weeks.55 It is possible
Health Service recommends 0.7 ppm of luoride in public water to lengthen this suppression greatly by a change in dietary habits
programs to reap the beneits of water luoridation and reduce the (especially eliminating sucrose) and by the patient’s conscientious
risk of luorosis. Excessive luoride exposure (≥10 ppm) results in application of a good oral hygiene program.
luorosis, which initially causes enamel to become white but may All luoride exposure methods (Table 2.12) are efective to some
eventually cause a brownish discoloration, a condition termed degree. he clinician’s goal is to choose the most efective combina-
mottled enamel. tion for each patient. his choice must be based on the patient’s
Fluoride exerts its anticaries efect by three diferent mechanisms. age, caries experience, general health, and oral hygiene. Children
First, the presence of luoride ion greatly enhances the precipitation with developing permanent teeth beneit most from systemic luoride
into tooth structure of luorapatite from calcium and phosphate treatments via the public water supply. In regions without adequate
ions present in saliva. his insoluble precipitate replaces the soluble luoride in the water supply, dietary supplementation of luoride
salts containing manganese and carbonate that were lost because is indicated for children and sometimes for adults. he amount
of bacteria-mediated demineralization. his exchange process results of luoride supplement must be determined individually. his is
82 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

TABLE 2.12 Fluoride Treatment Modalitiesa

Route Method of Delivery Concentration (ppm) Caries Reduction (%)
Systemic Topical Public water supply 0.7 50–60
Self-application
Low-dose/high-frequency rinses (0.05% sodium luoride daily) 225 30–40
High-potency–low-frequency rinses (0.2% sodium luoride weekly) 900 30–40 after 2 years
Fluoridated dentifrices (daily) 1000–1450 20
Prescription-strength luoridated dentifrices (daily) 4950 32
Professional application
Acidulated phosphate luoride gel (1.23%) annually or semiannually 12,300 40–50
Sodium luoride solution (2%) 20,000 40–50
Sodium luoride varnish (5%) 22,500 30
Stannous luoride solution (8%) 80,000 40–50
Silver diamine luoride (SDF) (38%) 44,800 ~96.1 for caries arrest
~70.3 for caries prevention

ppm, Parts per million.

a
Caries reduction estimates for topically administered luorides indicate their effectiveness when used individually. When they are combined with systemic luoride treatment, they can provide some
additional caries protection.

of particular importance in rural areas with individual wells because agent should be expanded because it has advantages over other
the luoride content of well water can vary greatly within short topical luoride vehicles in terms of safety, ease of application, and
distances. luoride concentration at the enamel surface.6 he American Dental
Topical application of luoride should be done periodically for Association (ADA) Council on Scientiic Afairs recently endorsed
children and adults who are at high risk for caries development. the use of luoride-containing varnishes as caries prevention agents.65
he periodicity varies with the case. Teeth can be cleaned free of Current evidence indicates that luoride varnishes with the
bioilm before the application of topical luorides. Flossing followed concentration of 5% sodium luoride are the most eicacious of
by tooth brushing is recommended for this purpose. Pumicing of all topically applied luoride products.58,66 For patients with a high
teeth (professional prophylaxis) is able to remove a considerable risk of caries, luoride varnish should be applied every 3 months.
amount of the luoride-rich surface layer of enamel and may be For moderate-risk patients, application every 6 months is indicated.
counterproductive. Acidulated phosphate luoride gel is efective, Fluoride varnish is not indicated for low-risk patients.
but a potential risk of swallowing excessive amounts of luoride When applying luoride varnish, the clinician dries of saliva
exists, particularly in young children. Acidulated phosphate luoride from teeth and applies a thin layer of luoride varnish directly
is available in thixotropic gels and has a long shelf life. Stannous onto teeth. Because the luoride varnish sets when contacting
luoride (8% F), another option, has a bitter, metallic taste; may moisture, thorough isolation of the area is not required. Only
burn the mucosa; and has a short shelf life. Although the tin ion tooth brushing, rather than prophylaxis, is necessary before applica-
in stannous luoride may be responsible for staining the teeth, it tion. he main disadvantage of luoride varnish is that a temporary
may also be beneicial in arresting root caries. Topical luoride change in tooth color may occur. Patients should avoid eating for
agents should be applied according to the manufacturer’s recom- several hours and avoid brushing until the next morning after the
mendations and always under supervision so as to limit varnish has been applied.
ingestion. Self-administered luoride rinses have an additive efect (about
Various luoride varnishes are available and are successful in 20% reduction) when used in conjunction with topical or systemic
preventing caries. Varnishes provide a high uptake of the luoride luoride treatment. Fluoride rinses are indicated in high-risk patients
ion into enamel and are widely accepted as the vehicle of choice and patients exhibiting a recent increase in caries activity. Two
for luoride delivery to young adults and older adults alike. Fluoride varieties of luoride rinses have similar efectiveness: (1) high
varnishes are professionally applied and may provide the most dose–low frequency and (2) low dose–high frequency. High-dose
cost-efective means of delivery of luoride to teeth. hese varnishes (0.2% F)–low-frequency rinses are best used in supervised weekly
are efective bactericidal and caries-preventive agents. Fluoride rinsing programs based in public schools. Low-dose (0.05% F)–high-
varnishes were developed several decades ago in an attempt to frequency rinses are best used by individual patients at home. A
improve luoride application techniques and beneits. European high-risk or caries-active patient should be advised to use the rinse
countries have used luoride varnishes for many years. Numerous daily. he optimal application time is in the evening. he rinse
randomized clinical trials conducted outside the United States should be forced between teeth many times and then expectorated,
point to the eicacy and safety of luoride varnishes as caries- not swallowed. Eating and drinking should be avoided after the
preventive agents.56-64 Fluoride varnish enables the deposition of rinse.
large amounts of luoride on an enamel surface, especially on a Routine use of over-the-counter luoride containing dentifrice
demineralized enamel surface. Calcium luoride precipitates on three times per day is recommended for all patients. hese tooth-
the surface, and often luorapatite is formed. he high concentration pastes generally contain 0.32% sodium luoride (1450 ppm). For
of surface luoride also may provide a reservoir for luoride, which moderate-risk and high-risk patients 6 years or older, prescription
promotes remineralization. Although additional research on luoride dentifrices containing higher concentrations of luoride are recom-
varnishes is needed, the use of a luoride varnish as a caries-preventive mended. hese products typically contain 1.1% sodium luoride
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 83

(5000 ppm) and can be safely used up to three times per day in Application of SDF usually only requires removal of the bioilm
this age group.67 For most beneit, patients should be instructed and application of the product with a microbrush for 3 minutes,
to not rinse after brushing and avoid eating or drinking for 30 then either rinsing the area with water or covering the lesion with
minutes after use. luoride varnish. Gingival tissues and lips should be covered with
petroleum jelly to avoid staining. his approach may give patients
Silver Diamine Fluoride who would otherwise be unable to receive treatment a low-cost
Silver diamine luoride (SDF) is a topical solution used as a caries- alternative to arrest caries lesions and preserve their dentition (Fig.
arresting and antihypersensitivity agent.154,155 2.43). However, the anticaries efect of SDF may be reduced over
SDF was recently cleared by the US Food and Drug Administra- time. It has been reported that up to 50% of arrested lesions were
tion (FDA) as an antihypersensitivity agent and is used of-label “reactivated” by 24 months after one application of SDF.161 he
to arrest caries lesions. Both silver and luoride play active roles authors reported that this was likely due to the bioilm-retaining
in their mechanisms of arresting caries development and treatment nature of these cavitated lesions. hus there is a rationale for
of tooth hypersensitivity.156-158 Silver has an antibacterial action restoring these arrested lesions from both the caries management
that slows demineralization and enhances remineralization.159 SDF, approach and for function and esthetics.
due to its ease of use, has been recommended to arrest large cavitated
lesions, allowing not only conservation of tooth structure, but Immunization
delivery of treatment to groups of patients that either do not have For many years, investigators have been trying to develop an efective
access to traditional restorative care or to whom delivery of the anticaries vaccine. Several prototypes have been tested in animals,
standard treatment is challenging. he main drawback of SDF is but at this time neither the safety nor the eicacy of such a vaccine
that with the precipitation of silver, the carious dentin becomes has been demonstrated in humans.68,69
stained black. Some researchers have studied the use of SDF on Even if an anticaries vaccine was developed, some concerns
root caries and have found it to be efective at preventing root remain, which may afect its widespread use. First, the potential
caries lesions.160 adverse efects of a vaccine must be identiied. he safety of such

A B

C D E
• Fig. 2.43 A, Young high caries risk patient. Tooth No. 17 with extensive caries lesion. Tooth was
asymptomatic and roots were still developing. B, Unsupported enamel was removed, soft caries was left
on the pulpal loor to avoid exposing the pulp. C, SDF was applied and left for 3 minutes. Darkened
dentin can be observed. Tooth was restored with amalgam and remained asymptomatic. D, Tooth with
PFM crown and secondary root caries on distal surface with dificult access for restoration. E, SDF applied
and darkened dentin can be observed. (A–C, Courtesy Dr. Nguyen Ngoc, resident Graduate Operative
Program at UNC; D and E, Courtesy Dr. Epure, resident Graduate Operative Dentistry Program at UNC.)
84 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

a vaccine has not yet been shown; concerns about a possible cross- When attempting to improve salivary low rates, a consultation
reaction with human heart tissue remain. Second, its cost must with the patient’s physician may be in order. It may be possible
be compared with that of public water luoridation, which is that a less xerogenic drug be prescribed or the dose of a current
inexpensive and already efective at reducing caries. Vaccination drug reduced. Changing the time of taking the medication(s) may
may be no more efective than luoride therapy, which has a proven be useful. Prescribing salivary stimulants such as pilocarpine or
safety record. It may however be practical to use a caries vaccine cevimeline may be very beneicial in patients with functioning
when public water luoridation is impractical in developed countries, salivar y glands but who have medication-induced
and it may be useful in developing countries. hird, limitations hyposalivation.
imposed by governmental regulatory agencies may afect the Other strategies to improve salivary low rates include increased
widespread use of an anticaries vaccine. water intake, use of sugar-free candies/mints several times a day,
and/or use of xylitol chewing gum. Xylitol will be discussed in
Saliva the next section.
Saliva, as noted earlier in this chapter, provides an efective irst
line of defense against dental caries. Saliva works by diluting acid Chemical Agents
produced in bioilm, washing the acid away (swallowing), bufering Chemical agents to help modulate the bioilm have been proposed.
the produced acid (bicarbonate + phosphate), and assisting in hese agents have been shown to reduce MS levels but this alone
remineralization (calcium + phosphate). Saliva also works by forming has not been shown to modify caries outcomes.71 Prior to initiating
a pellicle. When normal salivary low rates are compromised, patients procedures to reduce the numbers of cariogenic bacteria in the
are usually at high risk for developing caries. oral cavity, bacterial testing should be conducted to determine
Normal aging does not result in reduced salivary low rates; baseline microbiologic variables. Saliva samples may be tested for
however, many older patients have compromised salivary low rates speciic MS and lactobacilli levels; commercial devices may help
as a result of medications taken for systemic conditions. Many evaluate the level of ATP in the bioilm. Bacterial counts or ATP
commonly prescribed medications have hyposalivation as a potential levels are not reliable risk indicators but can be useful as motivational
side efect. A recent study has indicated that 63% of the 200 most tools for patients.
commonly prescribed drugs in the United States have the adverse Various antimicrobial agents are available (Table 2.13). As
efect of reduced salivary low rates.70 discussed, luoride has antimicrobial efects. Two difering strategies
One important strategy for the prevention of caries in such have been suggested for reducing bacterial counts. he traditional
patients is to increase the salivary low rate and, by this, the approach is the use of chlorhexidine (CHX) mouthwash, varnish,
concomitant bufering capacity. For these patients, gathering initial or both, along with prescription luoride toothpaste. When using
baseline data on salivary low rates is critical. Commercial kits are this approach, it may be prudent to use toothpaste free from
available for the assessment of salivary low. hese kits provide sodium laurel sulfate (SLS), which causes the foaming action in
data on simulated low rates, the pH of saliva, and the level of dentifrices. Although data are equivocal, evidence demonstrates
bufering capacity. If saliva samples are sent for microbiologic that SLS reduces the ability of CHX to reduce bioilm formation.72
testing, speciic MS and lactobacilli counts may be determined. Although CHX decreases MS, there is no evidence that it decreases
Speciic strategies for improving low rates and reducing bacterial caries incidence in the absence of luoride.
counts may then be initiated. Subsequent retesting is necessary to CHX was irst available in the United States as a rinse and was
identify the relative eicacy of the strategies. irst used for periodontal therapy. It was prescribed as a 0.12%

TABLE 2.13 Antimicrobial Agents

Spectrum of
Antibacterial Persistence
Mechanism of Action Activity in Mouth Adverse Effects
Antibiotics
Vancomycin Blocks cell wall synthesis Narrow Short Increases gram-negative lora
Kanamycin Blocks protein synthesis Broad Short Can increase caries activity
Actinobolin Blocks protein synthesis Streptococci Long Unknown
Bis Biguanides
Alexidine Antiseptic; prevents bacterial adherence Broad Long Bitter taste; stains teeth and tongue brown;
mucosal irritation
Chlorhexidine Antiseptic; prevents bacterial adherence Broad Long Bitter taste; stains teeth and tongue brown;
mucosal irritation
Halogens
Iodine Bactericidal Broad Short Metallic taste
Fluoride 1–10 parts per million (ppm) reduces Broad Long Increases enamel resistance to caries attack;
acid production; 250 ppm luorosis in developing teeth with chronic
bacteriostatic; 1000 ppm bactericidal high doses
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 85

rinse to high-risk patients for short-term use. It is also available in enamel remineralization87-90; however, most of these studies
as a varnish, and the most efective mode of varnish use is as a have not looked at its efect independent of luoride. he CPP-ACP
professionally applied material.73 Chlorhexidine gluconate (0.12%) products must not be prescribed to patients with allergies to dairy
solution is efective in its ability to chelate cations and, as a result, (milk) proteins.
disrupts cell adhesion, cell membrane function, and the ability of
MS to uptake glucose and produce glucans and its metabolism Probiotics
resulting in a decrease in MS counts. Emilson concluded that One novel approach for reducing dental caries that has emerged
CHX varnishes provide efective reduction in MS, although recent in recent years is that of probiotics. he fundamental concept is
evidence is not as conclusive in favor of a CHX rinse.74,75 Despite to inoculate the oral cavity with bacteria that will compete with
some favorable evidence, because there is only a weak correlation cariogenic bacteria and eventually replace them. Obviously the
with a reduction in caries, CHX currently has very limited applica- probiotic bacteria must not produce signiicant adverse efects.
tion as a regularly used caries management antimicrobial agent. A number of commercial products have been introduced and
Xylitol is a natural ive-carbon sugar obtained from birch trees. have been demonstrated to be safe in short-term studies. However,
MS cannot ferment (metabolize) xylitol, so no acid is produced. their relative level of eicacy remains unknown. It has been specu-
Over time xylitol reduces the number of MS in the bioilm. It is lated that for the probiotic microorganisms to gain dominance,
usually recommended that patients chew two pieces of xylitol gum existing pathogens must irst be eliminated. he concept of probiot-
containing a total of 1 g xylitol 3 to 6 minutes after eating or ics holds signiicant promise but considerably more research is
snacking. Chewing any sugar-free gum after meals reduces the required.
acidogenicity of the bioilm because chewing stimulates salivary
low, which improves the bufering of the pH drop that occurs Sealants
after eating.80 Reductions in caries rates are greater however when Although luoride treatments are most efective in preventing
xylitol is used as the sugar substitute.81Although there is some smooth-surface caries, they are less efective in preventing pit-and-
suggestion that xylitol may reduce caries rate,82 enhance remineraliza- issure caries. he use of sealants is an efective preventive treatment
tion, and help arrest dentinal caries,78,79,162 studies in adults have for caries in pit-and-issure areas.91 Sealants have three important
not been able to conirm its role on caries control163 except for preventive efects. First, sealants mechanically ill pits and issures
root caries.164 he evidence supporting the use of xylitol products with a resin-based polymer. Second, because the pits and issures
for the purpose of caries reduction in both adults and children is are physically closed of from the oral environment with the sealant
very weak.165 resin, MS and other cariogenic organisms no longer have access
A myriad of other chemical agents have been suggested to to their preferred habitat. hird, sealants render the surface of the
selectively kill gram-positive cariogenic coaggregates of bacteria. tooth, where the pits and issures are located, easier to clean by
Among these are propolis, nutraceutical phenols from licorice root, toothbrushing and mastication (Figs. 2.44 and 2.45).
arginine, and bactericidal products such as sodium hypochlorite Based on the available scientiic literature, pit-and-issure sealants
0.2% in the form of an oral rinse.166-168 However, despite the efect are appropriate for prevention of caries in susceptible teeth and,
of these strategies on decreasing cariogenic bacteria counts, they within limits, for arresting initial caries lesions.92-96 here is mounting
have not been shown to actually decrease caries incidence in the evidence that sealing initial lesions is an efective means to arrest
absence of luoride. Caries is a bioilm disease modulated by diet; dental caries.169
therefore changes to bacterial counts will have a short-term impact Another strategy recently introduced is the use of extremely
on the caries process. In the absence of other changes, for example low-viscosity resin sealants for the iniltration of white-spot caries
a signiicant reduction in fermentable carbohydrate intake, the lesions on smooth surfaces97 (Fig. 2.46). In situ studies demonstrate
bioilm microbiome will continue to adapt to the acidogenic and the ability of resin sealants, also called iniltrants, to prevent further
aciduric environment caused by a highly cariogenic diet; and these demineralization under cariogenic conditions.98 Resin iniltrants
antimicrobial strategies will have little impact on caries have reportedly been used in free (i.e., facial and lingual) as well
outcomes. as in interproximal enamel surfaces. However, similar to the sealant
technique used in pit-and-issure areas, the technique requires
Calcium and Phosphate Compounds careful attention to detail. A practice-based randomized clinical
Amorphous calcium-phosphate (ACP) products have become research trial has indicated that iniltration was more efective at
commercially available and reportedly have the potential to preventing lesion progression than instructions on oral hygiene,
remineralize tooth structure.83 ACP is a reactive and soluble calcium lossing, and luoride use.170
phosphate compound that releases calcium and phosphate ions to
convert to apatite and remineralize the enamel when it comes in Restorations
contact with saliva. Forming on the tooth enamel and within the he status of a patient’s existing restorations may have an important
dentinal tubules, ACP provides a reservoir of calcium and phosphate bearing on the outcome of preventive measures and caries treatment.
ions in the saliva.84 Casein phosphopeptide (CPP) is a milk-derived Old restorations that are rough and plaque retentive should be
protein that binds to the tooth’s bioilm and is used to stabilize smoothed and polished. If the marginal integrity is inadequate,
ACP. Remineralization products that use CPP as a vehicle to deliver then the restoration should be repaired or replaced. Restoration
and maintain a supersaturation state of ACP at or near the tooth defects such as overhangs, open proximal contacts, and defective
surface have recently been introduced. Some of these products contours contribute to plaque formation and retention. hese
contain other caries-preventive agents such as luoride and xylitol defects should be corrected, usually by replacement of the defective
(e.g., MI Paste Plus, GC America, Alsip, IL). Gum, lozenges, and restoration. Detection of caries around restorations and sealants
topically applied solutions containing CPP-ACP have also been (CARS) (“secondary caries”) may be diicult around old restorations.
reported to remineralize white spots.85,86 Mounting evidence Discoloration of the enamel adjacent to a restoration suggests the
indicates that CPP-ACP complexes, when used regularly, are efective potential for CARS, but is not a deinitive diagnosis. his condition
86 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

Penetrating
pit

A B
A
Sealant

Radiopaque
sealant

B C D
• Fig. 2.44 A and B, Sealant applied to the central fossa of a maxillary
second molar. This tooth was treated because of the appearance of chalky • Fig. 2.45 A and B, Radiograph of a maxillary irst molar with a deep
enamel and softening in the central fossa. A highly illed sealant was used central fossa pit that appears to penetrate to the dentin. C and D, The
(see Fig. 2.43). central pit was sealed with a highly illed, radiopaque sealant. The sealant
is readily visible on the radiograph.

A B

C D
• Fig. 2.46 A, Radiographic image of irst mandibular molar with a proximal lesion on distal surface.
B, Tooth was iniltrated according to manufacturer’s instructions (Icon, DMG America). C and D, Clinical
images of smooth-surface lesions on anterior teeth before and after iniltration, with Icon. (A, Courtesy
Dr. Andrea Cortes, Operative Dentistry Specialization Program, El Bosque University. B, Courtesy Dr. Olga
Lucia Zarta (chair) and Dr. Ainimsay Benitez (resident), Operative Dentistry Specialization Program, Dental
School, El Bosque University, Bogotá, Colombia. C and D, Reprinted with permission from Meyer-Lueckel
H, Paris, Zahnmedizin up2date 267–290, 2017.)
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 87

appears as a localized opalescent area next to the restoration margins. Growing evidence suggests that temporization followed by reentry
(Exception: A bluish color of facial or lingual enamel that directly does not contribute to improved clinical outcomes27, 28; therefore
overlies an old, otherwise acceptable amalgam restoration does not current research supports the placement of a deinitive restora-
indicate replacement unless there is a need for improvement of tion.30,177-181 Selective caries removal allows a restoration to be
esthetics. Such a discoloration may be caused by the amalgam placed while avoiding pulpal exposure.26 Avoiding a pulpal exposure
itself.) Because metallic restorations are radiopaque, the radiolucency has a great impact on the lifetime prognosis of the tooth and
of CARS may be masked. he restoration of cavitated active caries long-term treatment costs.182 Although the residual dentin thickness
lesions is preventive only because it removes large numbers of cannot be accurately assessed clinically, its preservation is a signiicant
cariogenic organisms and some of the sites in which they may be factor in avoiding pulpal distress.183,184
protected, and it restores adequate tooth contours and surface In slowly advancing lesions, it is expedient to remove the soft
smoothness that may facilitate oral hygiene. As emphasized earlier, (infected) dentin until the readily identiiable hard (sclerotic) dentin
the placement of a restoration into a cavitated carious tooth does is reached. In rapidly advancing lesions (see Figs. 2.36, 2.37, and
not cure the caries process. 2.43A), little clinical evidence (as determined by texture or color
Although caries diagnostic and preventive measures have been change) exists to indicate the extent of the soft (infected) dentin.
improved and are more widely used, the repair of destruction For deep lesions, this lack of clinical evidence may result in an
caused by the caries process still is necessary for many patients. excavation that risks pulp exposure. In a tooth with a deep advanced
he treatment regimen is dictated by the patient’s caries status. If caries lesion, no history of spontaneous pain, normal responses to
the patient is at high risk for caries development, treatment should thermal stimuli, and a vital pulp, a deliberate, selective caries lesion
consist of restorative procedures concomitant with many of the removal (as noted) may be indicated. his procedure is supported
preventive measures described previously. he damage done by by a large body of evidence.26-34,99-123,185-192
caries may be repaired while at the same time seeking to lower the Removal of the bacterial infection has been seen as an essential
patient’s risk status for further caries development. Sometimes, part of all operative procedures; however, even removal of dentin
patients present with active caries lesions in numerous teeth. Because up to hard dentin in deep, advanced caries lesions does not ensure
these teeth may be in jeopardy and because of the large numbers a “sterile” dentin as bacteria have been found to be present in all
and sites of cariogenic bacteria, arresting medication for caries dentinal layers in deep caries lesions. Nevertheless, even when
control (e.g., SDF) or restorative treatment for caries control may bacteria are present, compounding evidence indicates that when
be indicated, as described later in this section. his procedure a good seal is present the lesion will arrest193-196 (see Fig. 2.18E–L).
rapidly eliminates the caries lesions, providing better assessment herefore it is not necessary to remove all of the dentin that has
of the pulpal responses of some teeth and greater success of the been compromised by the caries process. Although caries detection
preventive measures instituted. Later, teeth may be restored with solutions such as 1% acid red 52 (acid rhodamine B or food red
more deinitive restorations. 106) in propylene glycol35 have been developed to help stain the
Once caries has produced cavitation of the tooth surface, unless infected layer, these dyes bind and stain the demineralized dentin
the cariogenic bioilm can be removed from a cavitated caries matrix and do not stain bacteria exclusively. Complete removal of
lesion or the lesion has been treated with SDF, preventive measures all stained tooth structure in the preparation therefore ultimately
will be inadequate to prevent further progression of the lesion. leads to signiicantly larger preparations than the traditional visual-
Excision of the lesion (tooth preparation) and proper tooth restora- tactile method of evaluating for caries removal, so their use is no
tion will not only stop the progression of active, cavitated lesions longer recommended.197-199
but also restore tooth function and esthetics. he following are additional clinical considerations for caries
lesion removal:
Clinical Considerations for Caries Removal a. Regardless of which protocol is used for caries removal (caries
Under normal operative clinical circumstances, in a vital permanent removal to irm dentin or selective caries removal to soft dentin),
tooth with no symptoms or signs of pulpal pathology, the extent the tooth may be restored with a inal restoration (Figs. 2.47
of the dentin caries removal (excavation) is dictated primarily by and 2.48). However, the patient should be clearly informed
lesion severity and depth: that in the treatment of advanced (deep) dentin caries some
• Moderate lesions (lesions not reaching the inner one third of leathery and soft dentin may remain under the restoration. his
dentin and with no anticipated risk of pulp exposure) should remaining caries-afected dentin has many implications, including
be excavated to a caries-free DEJ and irm dentin. higher risk for endodontic complications205 (not because “caries
• Advanced (deep) lesions (lesions reaching the inner one third was left under the restoration” but because deep caries was
of dentin and with anticipated risk of pulp exposure) should present to begin with) and a radiographic presentation that
be excavated to a caries-free DEJ and soft dentin, following a may suggest secondary or residual caries.
selective caries removal (SCR) protocol.171,172 b. Although there is overwhelming scientiic evidence in support
For a complete description of current caries classiication criteria of the SCR protocol, this is still a controversial clinical procedure
based on lesion severity and activity, please see Chapter 3. he in certain countries32 with potential liability implications as
SCR protocol is a professionally recognized and accepted tooth-level well as implications for clinical board examinations, most of
caries control treatment,173-176 and it can be used on any tooth which still require complete caries removal (excavation) to hard
with an advanced (deep) caries lesion that is deemed restorable, dentin as a criteria for a successful clinical board
and for which the pulpal and periapical areas are deemed healthy. examination.
Selective caries removal consists of complete caries removal peripher- c. he patient should be clearly informed of the risks and beneits
ally to a sound, caries-free DEJ; axially and pulpally, caries is of the selective caries removal to soft dentin protocol, and
removed to within approximately 1 mm of the pulp within soft provide informed consent. If the patient is not willing to accept
dentin; a glass ionomer (e.g., Fuji IX, GC America, Alsip, IL) the risks, then the alternative, either complete caries removal
temporary restoration or a deinitive restoration is then placed. with a higher risk of complications (endodontic therapy,
88 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

postoperative sensitivity) or tooth extraction, should be remineralize. his allows for the most conservative tooth prepara-
presented. tion without jeopardizing the restoration.
d. A sealed tooth-restoration interface is critical for the success of g. he pulpal diagnoses outlined here rely on signs and symptoms
the restorative procedure (see Fig. 2.18E–L). When a proper of pulp pathology using the best diagnostic tools available.
seal is NOT obtained, or when/if the seal is compromised, However, actual pulpal status is difficult to determine
marginal leakage and ingress of bacteria/luids/nutrients will
allow lesion progression. his is particularly critical when soft
dentin remains under the restoration.
e. When excavating advanced (deep) dentin caries, if a caries-free
DEJ cannot be obtained, a protective restoration (sedative illing,
temporary restoration) should be used and tooth restorability
should be reassessed. A permanent restoration should not be
used unless a sound DEJ (or peripheral dentin margin) is reached
(see Figs. 2.47 and 2.48).
f. In slowly advancing lesions, it is practical to remove the soft
(infected) dentin until irm (demineralized, afected) dentin is A
reached. Despite being demineralized, with adequate marginal
seal, the lesion may arrest and the affected dentin may

Enamel Enamel
Extensive
Extensive
caries lesion
caries lesion
Dentin Dentin

Pulp Pulp

A B

Temporary or
Excavated area definitive
restoration
Base/liner

C D
• Fig. 2.47 Schematic representation of caries-control procedure. A and
B, Faciolingual (A) and mesiodistal (B) cross sections of mandibular irst
molar show extensive preoperative occlusal and proximal caries lesions.
C, Tooth after excavation of extensive caries. Note remaining unsupported
enamel. D, Temporary amalgam restoration inserted after appropriate liner
or base.

D
• Fig. 2.48 A, Preoperative clinical radiograph illustrating extensive
caries lesion in the proximal and occlusal regions of the mandibular right
irst molar. Initial caries excavation of tooth. B, Remaining caries requires
further excavation. Also, note the wedge in place, protecting rubber dam
and soft tissue; it has been lightly shaved by a bur. C, Remaining unsup-
ported enamel under mesiolingual cusp. D, Tooth ready for placement of
temporary restoration. Carious involvement required further extension than
that seen in B and C. Liner or base material has been applied to deepest
excavated areas, and matrix, appropriately wedged, has been placed.
E, Temporary restoration completed for caries-control procedure. Caries
has been eliminated, the pulp adequately protected, and interarch and
intraarch positions of tooth maintained by caries-control procedure.
E
 CHAPTER 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management 89

clinically—bacteria and toxins progressing ahead of caries may TABLE 2.14 Caries-Control Restoration
cause areas of undetectable and asymptomatic pulpal necrosis
or irreversible pulpitis. Initial treatment Caries risk assessment
h. Use of calcium hydroxide (or other liner/base materials) after Education and motivation
Thorough evaluation and documentation of
caries removal and before use of a protective or inal restoration lesions
does not appear to improve outcomes.200 Temporization of all large cavitated lesions by
i. Teeth that are restorable only by use of full cuspal coverage caries-control restorations
restoration generally are not appropriate for the SCR technique Speciic nonrestorative, therapeutic treatment
because of the diiculty of evaluating the tooth for possible (see Table 2.10)
failures such as continuing caries activity under the full coverage Plaque control (see Table 2.10, technique C)
restoration. Another concern is the cost of rectifying failures. Dietary control (see Table 2.10, technique A)
j. his protocol recognizes that exposures will occur despite Preliminary Gingival response as a marker of plaque
admonitions to leave soft and leathery (infected) dentin rather assessment bioilm control effectiveness
than expose the pulp. Whenever there is a pulp exposure, the Arrest of cavitated lesions with SDF as
treatment should be consistent with existing endodontic indicated
guidelines for vital pulp exposures. Pulpal response of teeth with selective
k. Advances in vital pulp therapy may allow successful endodontic caries-excavation and restoration
therapy of pulp exposures without the need for root canal Assessment of patient compliance with
treatment. With the advent of tricalcium silicates, the prognosis medications, oral hygiene, and dietary
of pulp capping (partial and full pulpotomy of permanent mature control measures
teeth) has tremendously improved. Recent observational and Follow-up care Careful clinical evaluation of teeth
randomized trials, as well as systematic reviews and meta-analyses, Replacement of caries-control restorations with
have shown that these procedures have success for pulp vitality permanent restorations
that exceeds 90%.201-203 Complete caries removal with the option Monitoring of plaque bioilm and mutans
of vital pulp therapy should be one of the options ofered to streptococci (MS) levels
the patient during the informed consent process. Further antimicrobial treatment and dietary
reassessment as indicated by new
l. he SCR protocol can be applied either on a single tooth being cavitations, noncavitated lesions, or high MS
treated or to several teeth in a caries control phase treatment. levels
High caries risk patients with multiple cavitated caries lesions
can beneit from a treatment plan designed speciically to gain
control over the rapid progression of their disease. he term
caries control refers to a procedure in which multiple teeth with One of the primary etiologic factors for these patients is their
acute threatening caries are treated quickly by (1) applying a use of prescription drugs for a wide variety of systemic medical
medication (e.g., SDF) to arrest the caries lesions or (2) removing problems. It has been estimated that 63% of the 200 most com-
the infected tooth structure, medicating the pulp if necessary, monly prescribed medications have dry mouth as an adverse efect.
and restoring the defect(s) with a temporary or deinite material. It is the subsequent reduction in salivary low rates and concomitant
he intent of caries-control procedures is immediate, corrective diminished bufering capacity resulting from use of these medications
intervention of advanced caries lesions so as to prevent pulpal that is primarily responsible for the increase in root caries in older
disease and avoid possible sequelae such as toothache, root patients.
canal therapy, or more complex ultimate restorations. The critical pH of dentin (pH at which dentin begins to
his allows the caries process in these cavitated lesions to demineralize) is between 6.2 and 6.7, whereas that of enamel is
be essentially arrested and the overall bacterial load to be reduced. about 5.5.129 As a result, root dentin will demineralize in very
Caries-control procedures must be accompanied by other preven- weak acids, and root caries progresses at about twice the rate of
tive measures (Table 2.14). Teeth rapidly treated by caries-control coronal caries. hus it is critical that all older patients receive
procedures subsequently may be treated by using routine thorough clinical and radiographic examinations on a regular basis.
restorative techniques if appropriate pulpal responses are As described previously in this chapter, a caries risk assessment
obtained. should be carried out for all older patients. Factors that increase
the risk for root caries include the following:
1. Gingival recession
Root Carie Management 2. Poor oral hygiene
It is clear that the baby boom generation of North America is 3. Cariogenic diet
aging. In the year 1900, 3% of the US population was over 60 4. Presence of multiple restorations or multiple missing teeth
years of age, whereas in the year 2000, 13% of the population 5. Existing caries
was over 60 years.124 In the year 2030, it is estimated that at least 6. Xerogenic medications
20% of the population will be 60 years or older. Root caries is a 7. Compromised salivary low rates
pervasive problem in a high percentage of older patients.125,126 Once it has been determined that a patient is at high risk for
Many of these patients have had extensive restorative dentistry root caries, an aggressive preventive protocol should be considered.
done in their lifetimes. Approximately 38% of patients between his protocol is based upon four primary strategies for the prevention
the ages of 55 and 64 years have root caries, and 47% of those of root caries. he irst strategy is to improve salivary low rates
between 65 and 74 years have experienced root caries.127 he and increase the bufering capacity. he second strategy is to modulate
incidence of root caries in old-older adults (over 75 years) is even a cariogenic bioilm in the oral cavity. he third strategy is to
higher.128 reduce the quantity and numbers of exposures of ingested reined
90 C HA P T E R 2 Dental Carie: Etiology, Clinical Characteritic, Rik Aement, and Management

carbohydrates, and the fourth is to attempt to remineralize initial for deinitive restorations of active root caries lesions primarily
lesions and prevent new lesions from developing. In addition to because they bond efectively to both enamel and dentin and
following the aforementioned protocol, three additional consid- they act as reservoirs for luoride, which may be re-released
erations are important: into the oral cavity.130,131 hese materials may be efective as
1. Use of powered toothbrushes and irrigation devices. It is critical anticaries materials only if patients reload the material a
that patients susceptible to root caries practice meticulous oral minimum of three times a day by brushing with luoride-
hygiene. However, many of these patients have physical and containing toothpaste or by using other luoride-containing
visual deiciencies, which makes it diicult for them to adequately products.208 Alternatively these same root caries lesions can be
cleanse the mouth. For these patients, a powered toothbrush arrested by application of SDF (see Fig. 2.43D and E).
may be advantageous.207 Additionally, daily use of a water 3. Educating patients of the necessity for three exposures to luoride
irrigation device (Waterpik, Water Pik Inc., Fort Collins, CO) per day and for reloading the luoride-releasing materials can
may be beneicial. Although the device will not remove bioilm, assist in motivating them to improved levels of compliance.208
studies have shown that daily use will change the composition In summary, many older patients are experiencing an epidemic
of the bioilm in a beneicial way. However, since the toothbrush of root caries, primarily as a result of the hyposalivatory efects of
essentially provides the means of luoride delivery, use of a medications prescribed for systemic illnesses. Many root caries
water irrigation device alone is not indicated unless used with lesions occur in locations that make them diicult if not impossible
a luoridated rinse (e.g., ACT). to restore. he dental profession has a strong track record of preven-
2. Restoration of all root caries lesions with a luoride-releasing tion, and it is clear that with root caries, prevention is much better
material. Resin-modiied glass ionomer materials are preferred than restoration.

Summary
Caries management eforts must be directed not at the tooth level are the result of caries activity. Only implementation of appro-
(traditional or surgical treatment) but at the total-patient level priate caries-preventive measures will lower the probability that
(medical model of treatment). Restorative treatment does not cure caries lesions will recur. Tooth restorations are preventive in the
the caries process. Instead, identifying and eliminating the causative sense that they remove numerous cariogenic organisms in the
factors for caries must be the primary focus, in addition to the afected site and eliminate a protected habitat for other cariogenic
restorative repair of damage caused by caries. bacteria; however, they primarily repair the tooth damage caused
Much of the remainder of this textbook presents information by caries and have only a limited impact on the patient’s overall
on when and how to restore tooth defects. Many tooth defects caries risk.

9. Dreizen SBL: Xerostomia and dental caries. Microbiol Abstr Spec

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