Development of Carious Lesions – Enamel caries – Development

Development of Carious Lesions
Enamel caries
The physicochemical integrity of dental enamel in the oral environment is entirely dependent on the composition and chemical behavior of the surrounding fluids: saliva and plaque fluids. The main factors governing the stability of enamel apatite are pH and the free active concentrations of calcium, phosphate, and fluoride in solution. 
The development of a carious lesion in enamel involves a complicated interplay among a number of factors in the oral environment and the dental hard tissues. The carious process is initiated by bacterial fermentation of carbohydrates, leading to the formation of a variety of organic acids and a fall in pH. The pH can fall below the critical value of 5.5, where the aqueous phase becomes undersaturated with respect to hydroxyapatite. This process is described in more detail in chapter 3. 
While the typical carious lesion in enamel is the result of chemical dissolution of the dental hard tissues caused by bacterial degradation products, ie, acids produced by bacterial metabolism of low-molecular weight sugars in the diet, a lesion resulting from chemical dissolution by any other acid-containing agent is defined as erosion. 
The typical carious lesion is characterized by a subsurface demineralized lesion body, covered by a rather well-mineralized surface layer. Whereas in the erosive lesion, however, the surface has been etched away layer by layer, and there is no subsurface demineralization.
Microradiograms by Haikel et al (1983) have shown that early typical noncavitated carious lesions in enamel consist of a porous surface layer, about 20 to 40 um thick, which acts as a “micropore filter,” and a so-called lesion body, where there is more pronounced loss of mineral (Fig 146). A detail of the boundary between the intact enamel and the lesion body reveals the presence of every single enamel prism, even in the lesion body. However, compared to the inner part of the prisms in the intact enamel, the prisms in the lesion body are somewhat demineralized (Fig 147).
On bitewing radiographs, radiolucencies in approximal enamel represent the sum total of this mineral loss from each single enamel prism, all of which are still present, and not a cavity in the enamel. For the clinician, this is of fundamental importance in treatment planning, because all noncavitated lesions can and should be arrested, rather than treated invasively. Enamel carious lesions on the buccal and lingual surfaces, as well as in the fissures, can easily be detected by direct visual inspection, after mechanical removal of plaque. When the carious attack rate is high (a very active lesion associated with very low plaque pH), the surface of the enamel is rough, resembling unglazed china or chalk. Such lesions may develop on the buccocervical surfaces of the incisors during orthodontic treatment of patients with poor oral hygiene (Fig 148).
Scanning electron microscopic (SEM) studies by Haikel et al (1983) have shown that under such conditions (very low plaque pH), most of the mineral loss on the enamel surface is intraprismatic, as in erosion (Fig 149a). On the other hand, when the carious attack rate is slow because of moderate falls in plaque pH, there is limited localized loss of interprismatic minerals (Fig 149b). The outer and most caries-resistant part of the enamel forms a micropore filter through which minerals may be released, not only from the body of an enamel lesion but also from noncavitated lesions of dentin, as long as hydrogen ions (H+) penetrate the enamel surface. 
In children with poor and irregular oral hygiene, primary enamel lesions develop during and soon after eruption, in so-called stagnant areas of the tooth surface, where bacteria can colonize, developing thick cariogenic plaque that is protected and undisturbed from mechanical chewing forces. Typical stagnation areas are the interproximal embrasures, along the gingival margin and the fissures of erupting teeth, and teeth without normal chewing function. Figure 150 shows the plaque accumulation in such stagnant areas after 3 days without toothbrushing. 
Carvalho et al (1989) showed that most occlusal lesions in molars are initiated during eruption, in the distal and central fossae, because plaque reaccumulates much more rapidly in the fissures of erupting molars without normal chewing function, than it does on fully erupted teeth.
In addition, susceptibility to caries is strongly correlated to the posteruptive age of the enamel. The enamel is most susceptible to dental caries during and just after eruption, until secondary maturation is completed, after some years’ exposure to the oral environment (Kotsanos and Darling, 1991). During this risk period, plaque control and topical application of fluoride should be intensified. 
As early as 1966, Backer-Dirks evaluated the development and arrest of enamel lesions in relation to stage of eruption and the posteruptive age of the enamel. He examined about 90 boys and girls at ages 7 to 15 years, monitoring pits and fissures, approximal surfaces, and free smooth surfaces. Buccal surfaces were examined in more detail than the other surfaces: Each surface was cleaned with a toothbrush and dried with compressed air, and then classified as: sound, white-spot caries (if the surface showed a white opaque lesion, with or without partial loss of surface gloss), and caries with cavitation (if a break in the continuity of the enamel was perceptible with the explorer). 
Table 16 summarizes the fate of the same buccal surface of maxillary first molars from age 8 to 15 years. Only nine of 72 opaque spots progressed to cavitation. More than half the surfaces with white-spot opaque lesions were classified as sound at age 15 years. Reversion from a white-spot lesion to a clinically sound surface occurred at all ages: from 8 to 9, 10 to 11, 12 to 13, and 14 to 15 years, on 11, 10, 12, and 4 surfaces, respectively (37). Because 48% of white-spot lesions were noted within 6 months after eruption, and 84% within 18 months after eruption, it was concluded that, on buccal surfaces, white-spot lesions develop soon after eruption (Backer-Dirks, 1966). 
The disappearance of the opacities on the buccal surfaces was attributed to either
remineralization or surface abrasion, or both. Figures 151 and 152 illustrate the
marked changes in the gingival level of the buccal surface of maxillary first molars
from the ages of 7 to 15 years. During this period, there is gradual physiologic
detachment of the gingival from the surface of the tooth and continuing exposure of
the clinical crown. During this period, the maxillary second molar erupts, leading to a
further repositioning of the gingival attachment on the distal aspect of the first molar.
Thus, the physiologic, passive exposure of the crown leads to a change in local
conditions for plaque accumulation.
It may therefore be concluded from this study that conditions favoring plaque
accumulation along the gingival margin of erupting maxillary first molars lead to
early development of white-spot lesions. Further eruption leads to changes in the local
environment that favor mechanical removal or suppression of cariogenic plaque,
causing either arrest of lesion progression or complete disappearance of lesions.
Similar conditions are frequently found on the buccal and the lingual surfaces of
erupting and newly erupted mandibular first molars.
Another approach to studying the impact of oral mechanical forces on caries
development is to withdraw toothbrushing for controlled periods. In the experimental
caries study by von der Fehr et al (1970), discussed in chapter 2, the subjects were
volunteer dental students. During a preexperimental period, sound gingival conditions
were established. The tooth surfaces were carefully cleaned and thoroughly dried and
scored according to the following Caries Index: 0 = surface appears intact; 1 = limited
grayish tinge, with and without accentuated perikymata; 2 = well-accentuated
perikymata, in some areas forming confluent grayish white spots; and 3 = pronounced
white decalcification. The recordings were made using a binocular dissection
microscope fitted with two spotlights.
All participants then refrained from oral hygiene procedures for 23 days. One group
of subjects was assigned to a sucrose group, which rinsed with 10 mL of dilute
sucrose solution for 2 minutes, 9 times a day, between meals. At the end of the no
hygiene period, the teeth were carefully cleaned, polished, and reexamined for caries.
Oral hygiene was resumed, and the participants were instructed to use 0.2% sodium
fluoride mouthrinse daily. After 1 month, the teeth were cleaned, polished, and
examined for caries. Following a further month of oral hygiene and fluoride rinsing,
the experiment was terminated with a final caries examination of the cleaned and
polished teeth.
At the end of the no hygiene period, the mean Caries Index had increased in both
groups but was considerably higher for the sucrose group than for the control group.
At the end of the two periods with resumption of oral hygiene and fluoride rinsing, the
mean index returned to preexperimental levels. Figure 153 illustrates the typical
appearance of an experimental subject after refraining from oral hygiene for 3 weeks.
On the left side, the plaque has been disclosed: during the first weeks, most plaque
accumulated on the so-called stagnant areas. On the right side, plaque has been
removed, revealing the development of noncavitated enamel lesions (white spots) on
the buccocervical surfaces, where plaque accumulation was greatest.
The study showed that in the absence of daily mechanical removal or disturbance of
bacterial accumulation on the teeth, formation of cariogenic plaque led to the
development of early signs of buccocervical enamel demineralization, and that this
process was accelerated by daily sucrose rinsing between meals. When daily
mechanical plaque control was resumed, and supplemented by daily fluoride rinsing
and professional mechanical toothcleaning (PMTC) on three occasions, there was not
only arrest of caries progression, but also a reversal of the clinical signs of enamel
In principle, identical results were obtained in the study by Loe et al (1972), using a
similar experimental design. In a preliminary reappraisal of the experimental caries
method proposed by von der Fehr et al (1970), Jenkins et al (1973) were unable to
confirm the need for frequent sucrose rinses in inducing carieslike changes in enamel.
Controls who did not rinse with sucrose showed an equal rise in Caries Index scores,
suggesting that, with increased plaque accumulation, dietary carbohydrates dit not
produce a maximal change.
Geddes et al (1978) therefore repeated the experiment, with minor technical
modifications, and used a 14-day experimental period, which gave an adequate
change in Caries Index (Edgar et al, 1978). The results of the new study confirmed the
original findings of von der Fehr et al (1970); the mean Caries Index scores rose
during the period without dental hygiene, and the rise was highest in the group rinsing
with sucrose nine times a day. One month after resumption of oral hygiene, the mean
Caries Index values reverted to preexperimental levels.
These experimental caries studies showed that withdrawal of oral hygiene caused
development of caries, with intraindividual and interindividual variations in lesion
progression. Frequent rinsing with sucrose during the experimental period of
undisturbed plaque accumulation seemed to increase the caries progression rate, but
with large individual variations. The deposition of plaque along the gingival margin is
clinically visible less than 24 hours after cessation of toothbrushing (Axelsson, 1989,
1991; Lang et al, 1973). After this initial establishment, plaque rapidly accumulates in
the coronal direction until, after approximately 1 week, the thickness and clinical
extension of the plaque on different teeth and tooth surfaces have reached their
maximum (Listgarten, 1976; Loe et al, 1965).
Whereas there are no major differences in the thickness of the gingivally located
plaque, the occlusal and incisal extension of plaque may vary in different groups of
teeth as well as on the various surfaces, presumably reflecting individual masticatory
patterns. While friction through mastication has an effect on incisal and occlusal
growth of plaque (Carvalho et al, 1989, 1991; Ekstrand et al, 1993), examination of
plaque development (Loe et al, 1965) as well as experimental studies (Lindhe and
Wicen, 1969; Wilcox and Everett, 1963) indicate that the gingival margins and the
cervical areas of the teeth are not subjected to physical stress from food particles in
the modern diet. In the aforementioned studies, developing caries was also observed
along the gingival margin, demonstrating that visible signs of caries develop where
bacterial plaque has been protected from oral mechanical disturbance for the longest
period of time (Thylstrup et al, 1994).
However, compared to individuals with poor and irregular oral hygiene habits, people
who brush meticulously every day exhibit quite a different and limited pattern of
undisturbed plaque. In a toothbrushing population, undisturbed dental plaque is most
likely to persist on the posterior approximal surfaces, where toothbrush accessibility is
limited, and these are the surfaces most frequently decayed. In the above experimental
studies, meticulous PMTC before caries reexamination, in conjunction with
resumption of oral hygiene procedures, resulted not only in arrest of further lesion
progression but also in regression of the superficial enamel lesions to a stage at which
they were no longer readily discernible clinically.
The most extreme model for human experimental caries ensures total elimination of
mechanical forces on tooth surfaces, thereby allowing undisturbed plaque
accumulation. The first such model, by Nygaard Ostby et al (1957), used a gold plate,
retained on the tooth by two pinledges. Opaque spots developed on the enamel over
periods of 4 to 6 weeks.
Von der Fehr (1965) used the same method to examine histologic features of enamel
caries, induced over periods varying from a few weeks to several months.
Corresponding to the area protected by the gold plate, there was macroscopic loss of
enamel translucency, the changes ranging from slight accentuation of the perikymata
to distinct white spots. Microradiographic examination revealed a radiographically
dense surface zone overlying zones with low x-ray absorption (“inner spots”) running
parallel to the outer surface.
Hals and Simonsen (1972) modified the technique, and, in studies of caries around
amalgam restorations in vivo, used a preformed orthodontic band with two metal
posts, 0.3 or 0.5 mm thick, welded to the inner surface to create a space between the
band and the buccal surface of the tooth. This model was applied by Holmen et al
(1988) in 15 children undergoing orthodontic treatment, to investigate the effect of
regular disturbance or removal of dental plaque. Two homologous premolars were
banded for 5 weeks. One tooth in each pair served as a control, to which the band
remained cemented for the entire test period. The other band was removed weekly,
and the buccal surface was cleaned, either by careful pumicing with a nonfluoride
toothpaste or simply by wiping with a cotton pellet. No fluoride of any kind was
added during the entire test period.
The teeth were examined macroscopically, in polarized light, and by SEM. The
enamel changes in the control teeth ranged from slightly accentuated overlapping of
the perikymata to pronounced white opaque lesions. By contrast, all the experimental
teeth appeared clinically sound. In polarized light, the control teeth showed classic
subsurface lesions of varying severity; no subsurface dissolution could be discerned in
any of the experimental teeth, regardless of cleaning procedure (Fig 154).
In SEM, the control teeth showed signs of active carious dissolution. The pumiced
surfaces of the test teeth were characterized by a general smoothing out of surface
irregularities and the presence of microscratches. The appearance of the surfaces
cleaned with cotton pellets was very similar but with less microwear. This study
convincingly demonstrated the importance of intraoral mechanical forces for caries
initiation and progression: complete elimination of mechanical forces (undisturbed
plaque) caused development of caries in all individuals, even without excluding the
complex interplay of other individual factors, as indicated by variations noted in the
rate at which the lesion advanced (Fig 155). The determining factor is mechanical
suppression of bacterial activity, even in the absence of fluoride. The fact that none of
the experimental teeth showed any visible evidence of caries offers further support for
the principle that “clean teeth do not decay.”
These in vivo studies convincingly demonstrate that partial or total elimination of
intraoral mechanical forces leads to evolution of cariogenic plaque, resulting in
carious dissolution of enamel. In addition, they show that reexposure to mechanical
forces not only arrests further progression of the lesion, but also results in partial
regression of the lesion. In all studies, the localized loss of normal enamel
translucency, clinically discerned as white opacities or white spots, served as an
indicator of carious dissolution.
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What comes to mind when you think of the color yellow? You prolabby think “bright,” or “sunny,” or maybe even “cheery.” Did you know that yellow just so happens to be the color of normal, healthy teeth, too? Thank goodness it’s not the traditional color yellow, but a much more subtle hue along the lines of ivory. You see, natural tooth color is produced from within the tooth, and if teeth are healthy there is a slight yellow cast to them which is fine and is pretty much unnoticeable. But that is definitely not the case should your teeth become stained.The most common teeth stains are caused by food and beverage (and tobacco, too, but that will be discussed another time), and are a deep yellow-brown color. Not too attractive. The good news is that these stains can be prevented if we know what foods and drinks cause staining, and how to minimize the risk.The following is a list of teeth-staining offenders:Wine: Red wine is known to stain teeth from the tannins and chromogens (compounds that are changed into pigment) it contains.Tea: Black tea, more specifically. Black tea contains tannins which promotes stains. It even causes worse stains than coffee. (Yes, you read that correctly.) That’s because coffee is chromogen-rich but very low on tannins.Cola: Cola is chromogen-rich and acidic. The acid opens the pores of the tooth’s enamel which in turn makes staining easier. Chromogen-rich and acid – not a good combination at all.Berries: You name the berry and it will cause staining – juice, too.Sauces: Deeply colored sauces such as tomato, soy, and curry are believed to have the potential for significant staining.Sweets: Chewing gum, popsicles, hard candies, and other sugary sweets contain colorings that can stain teeth. Think about suckers: If your tongue can become the color of the sucker, so can your teeth.Now that we know what causes staining, what can we do to prevent it? If coffee, tea, and wine are an absolute must, swallow the liquid promptly. Swallowing without delay is believed to protect teeth from staining, but take time to chew food thoroughly to avoid gulping and possibly choking. While drinking colas or other colored beverages consider sipping them through straws. Then when possible, swish with water after consuming a stain-promoting food or beverage. While these suggestions may help prevent staining, nothing takes the place of good oral hygiene. So remember to brush your teeth and floss twice daily to keep your ivories looking…ivory.

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Articles for theme “caries”:
Development and Diagnosis of Carious LesionsIntroductionA carious lesion should be regarded not as a disease entity, but as tissue damage or a wound caused by the disease dental caries. The coronal lesion begins as clinically undetectable subsurface demineralization of enamel, visible only at microscopic level, and gradually progresses, first to visible demineralization of the enamel surface and to cavitation of the dentin, and finally to complete destruction of the tooth crown despite restoration, but without prevention (Fig 145).
ConclusionsCaries riskFrom a cost-effectiveness aspect caries-preventive measures should be applied strictly according to predicted caries risk. In populations with very high caries prevalence and caries incidence (where almost everyone develops new lesions every year) the traditional whole population strategy would be cost effective. The number of such populations is dwindling, however, particularly in the industrialized countries where caries prevalence was high 20 to 30 years ago.
Cariogram ModelA new model, the Cariogram, was presented in 1996 by Bratthall for illustration of the interactions of caries-related factors. The model makes it possible to single out individual risk or resistance factors. A special interactive version for the estimation of caries risk has been developed.The original Cariogram was a circle divided into three sectors, each representing factors strongly influencing carious activity: diet, bacteria, and susceptibility. The development of the model was based on a need to explain why, in certain individuals, carious activity could be low in spite of, for example, high sucrose intake, poor oral hygiene, high mutans streptococci load, or nonuse of fluorides.
Detailed risk profiles for dental cariesIf a patient is at high risk predominantly for either caries or periodontal disease, a more detailed risk profile is available for the specific disease. Box 19 shows a list of abbreviations for the most important variables related to caries risk.  Figure 138 illustrates how a high-risk patient (C3) has been transformed to a low-risk patient (C1) by improved self-care supplemented by professional preventive measures. The greater the difference between the solid line and the dotted line, the greater the improvement.
Risk ProfilesIntroductionBy combining the symptoms of disease (prevalence, incidence, treatment needs, etc); etiologic factors; external modifying risk indicators, risk factors, and prognostic risk factors; internal modifying risk indicators, risk factors, and prognostic risk factors; and preventive factors, it is possible to present risk profiles for tooth loss, dental caries, and periodontal diseases in graphic form. This can be done manually or by computer. The degree of risk, 0, 1, 2, or 3, is visualized using green, blue, yellow, and red, respectively.