Diagnosis and Treatment of Early Caries Lesions

Treating caries does not mean cleaning and reconstructing a cavity but implementing procedures that create an environment unfavorable to the development and persistence of disease. Dental restoration is simply one stage of treatment. It deals with an outcome of the disease rather than the disease itself. This chapter covers basic concepts of cariology, diagnostic tools designed to identify caries lesions, and procedures for treating early caries lesions, namely remineralization and resin infiltration.

Dental Caries

The primary causes of tooth loss can be attributed to two main tooth and periodontal tissue problems, ie, caries and periodontitis, both caused by bacterial biofilm,1 followed by trauma and a dentist’s actions (iatrogenic causes). Caries is by far the most common disease in the world.

  • More than 40% of the world’s population has at least one untreated caries lesion in their mouth.2
  • More than 90% of human beings will experience caries at least once in their lives.3

Oddly enough, dentists are often unclear what is meant by the term caries. With periodontal disease, there is a clear distinction between outcomes (eg, pockets, recession, bleeding, mobility) and the causal disease. But it is often unclear whether the term caries refers to the disease, ie, a complicated pathologic process that involves initial triggers, a causal chain of events, and final outcomes, or to one outcome, ie, the caries lesion.4

Continuing the parallel with periodontitis, it is very clear that once signs of disease are identified, the affected patient must undergo several meticulous clinical (Fig 3-1) and radiographic (Fig 3-2) investigations designed to identify and evaluate the situation through the calculation of numeric indices and very specific, staged checks. Based on the extent and severity of the situation, it will be possible to draw up a diagnosis, ie, to categorize the underlying disease (eg, periodontitis) using adjectives such as chronic, aggressive, localized, and generalized. These adjectives will be able to guide the subsequent causal therapy and reach an appropriate prognosis. The clear, well-established rules of nomenclature in periodontology should not be underestimated.5

FIG 3-1 Example of a periodontal chart. (Courtesy of University of Bern, Switzerland.)

FIG 3-2 Radiographic status of a patient with periodontal disease. (Courtesy of Dr F. Manfrini, Riva del Garda, Italy.)

In cariology, however, things are generally more vague; typically, only one finding is sought: a cavitated caries lesion. It is very difficult to objectively establish the severity of the condition under examination, given the widespread confusion over terminology4 and lack of importance attached to the topic of caries, which many consider to be basic knowledge that one automatically acquires by osmosis after enrolling in dentistry school.

Causal therapy is generally associated with treatment of periodontal disease but should be applied to nearly any abnormal processes, including caries.6 As the name suggests, causal therapy should address the causes giving rise to a disease; actions aimed at mere treatment of outcomes or symptoms are not worthy of the same medical standing.

Dental caries is a communicable disease of bacterial origin. Physically removing a lesion and replacing it with a restoration will not eliminate the bacteria or stop the caries spreading to the rest of the mouth and the margins of the recently performed restoration7 (Figs 3-3 and 3-4). Causal therapy is generally achieved by adopting an almost identical approach in all medical disciplines:

FIG 3-3 Secondary caries lesion near a composite restoration. The caries lesion did not develop because of the restoration but because nothing was done to reduce the risk of caries before or immediately after the restoration was performed.

FIG 3-4 Recurrent caries lesions that developed apical to two restorations, caused by failure to remove biofilm from the interproximal areas.

  1. Diagnosis
  2. Informing and educating the patient about the causes of disease (eg, making the patient understand the link between diet, cariogenic biofilm, acids, and disease)
  3. Giving the patient instructions for controlling the causes of its prevalence (eg, lifestyle, smoking habits, diet, and hygiene)
  4. Direct treatment of removable causes and outcomes of disease (eg, removing any excess filling material and calculus and/or restoring cavitated caries lesions)
  5. Regular patient assessment

It is easy to understand how this type of approach comes close to the true concept of curing a disease; it is a set of etiopathogenic actions initiated with the aim of completely eradicating disease processes that are ongoing (causal therapy) or potential (primary prevention). These actions also take place at an individual level and can be described as disease management. The action of managing outcomes or symptoms (point 4 in the list above) cannot be called a cure, however useful and necessary it may be; this action can only be described as treatment. It is important to understand the macroscopic difference between a care plan, implicitly including all medical actions, even those of a preventive nature aimed at eliminating or reducing the influence of disease triggers (eg, referring patients for help in giving up smoking or advising them to drink plenty of water), and a treatment plan, which is simply a list of interventions (albeit important) to be performed at a dental clinic.

Outcomes and Definition of Caries

Cariologists agree that the concept of caries is not interchangeable with the concept of a caries lesion. In essence, caries cannot be removed but rather cured, while a caries lesion can be removed or treated by means of noninvasive, minimally invasive, or invasive procedures.4 A caries lesion is not the only outcome attributable to caries; in addition to broader oral outcomes (eg, chewing difficulties), systemic outcomes (eg, digestive difficulties), and psychologic outcomes (eg, social self-consciousness due to poor esthetics), the following tooth-related effects due to the direct or indirect action of caries can be identified (not necessarily in the order listed):

  • Surface demineralization, noncavitated caries lesion, white spot (WS) (Fig 3-5)

    FIG 3-5 White area of demineralization surrounding a noncavitated pigmented groove.

  • Brown spot, resulting from incorporation of chromogens into a WS (Fig 3-6)

    FIG 3-6 Brown spot affecting the mesial wall of a premolar. The initial WS has incorporated bacterial and food pigments and turned brown over time. This occurrence is often but not always due to a tendency to remineralize.

  • Pulp hyperemia
  • Cavitated caries lesion (Fig 3-7)

    FIG 3-7 Where cariogenic biofilm is present, demineralization continues until the enamel structure collapses and dentinal infection results. Note that brown spots are present on the enamel of the mandibular right first premolar despite the greater tendency of this surface to demineralize.

  • Narrowing of the pulp chamber (Fig 3-8)

    FIG 3-8 (left) Narrowing of the distal pulp horn of the mandibular right first molar resulting from the progression of a preexisting caries lesion.

  • Pulpitis
  • Loss of pulp vitality
  • Partial or total crown fracture
  • Tooth loss (usually by extraction; Fig 3-9)

    FIG 3-9 (right) Edentulous space at the site of the maxillary right first molar, which was extracted because of sequelae of caries-related disease.

Caries or caries-related disease can therefore be defined as an “infectious and communicable process, where a cariogenic biofilm causes demineralization of the tooth’s hard tissues in the presence of oral conditions that are more pathologic than protective.”8 Protective oral conditions are those that promote a remineralizing oral environment, ie, one that is favorable to molecules attaching to the tooth rather than detaching from it (demineralization). These factors can be schematically represented9 as shown in Fig 3-10. A preponderance of pathologic conditions will make certain tooth surfaces (where the cariogenic biofilm can proliferate undisturbed) more inclined to demineralization than to remineralization.

FIG 3-10 Balanced model of caries, indicating protective and pathologic factors and disease indicators. Upstream determinants such as low socioeconomic status or presence of systemic disease also play an important role in disease predisposition. (Modified from Featherstone.9)

Caries is also currently interpreted as a behavioral condition with a bacterial component, where the host behavior is identified as the primary factor responsible for creating an ideal environment for the cariogenic biofilm to become established. Transmission of cariogenic bacterial strains (typically by parents or other children) is most significant during the first months or years of the patient’s life; therefore, the main aim of caries prevention should be to prevent, render unlikely, or postpone this event as long as possible through behavioral and dietary guidance given to children by their parents.

As with many diseases, the mere presence of risk factors (pathologic in this case) does not necessarily indicate that the disease is present and active. Caries-related disease can only be considered present if cavitated or noncavitated active lesions are found. A patient can be considered cured of disease 3 years after the latest treatment of an outcome of caries (eg, one or more restorations or attempts to remineralize an active white spot). Lastly, some outcomes of caries can still be detectable long after recovery even when disease is absent (examples include pulp chamber narrowing or pulpitis that is revealed or occurs long after restoration has been performed). Though not directly related to the oral environment, factors referred to as upstream determinants have also been shown to be related to an increased probability of incurring caries-related disease. These conditions include low socioeconomic status, low level of education, presence of conditions or diseases that are debilitating or have an oral impact, the need to use certain drugs, and inaccessibility of treatment centers.10

Lesion Dynamics and Activity

The dynamics of a caries lesion in a tooth can be summarized as follows11,12:

  1. Acidogenic bacterial plaque ferments carbohydrates introduced with the diet, thus producing acids (lactic, formic, acetic, and propionic) (Fig 3-11).

    FIG 3-11 (left) Large buildup of bacterial plaque, potentially responsible for caries and/or periodontal disease.

  2. The acids spread into exposed tooth tissues, partially dissolving their constituent mineral crystals (hydroxyapatite carbonate).
  3. Detachment of mineral salts from tooth surfaces leads firstly to roughening, subsurface demineralization, and ultimately cavitation (Fig 3-12).

    FIG 3-12 (above) Polarized photo of a WS in the cervical region of the tooth, showing early signs of cavitation.

  4. The demineralization process can be reversed by calcium, phosphate, and fluoride, which spread inside the tooth tissues and deposit a new mineralized layer on the remaining crystals in noncavitated lesions (remineralization) (Fig 3-13).

    FIG 3-13 WS with areas of partial surface remineralization. The remineralized surface feels the same as unaffected tissue when an instrument is passed over the surface.

  5. When fluoride is present, the new surface is much more resistant to acid attack.
  6. The demineralization-remineralization process takes place several times a day and can give rise to cavitation, repair, or maintenance of the status quo.
  7. The prevalence of demineralization processes leads to the spread of infection with progressive loss of tooth tissue, pulp disease, and tooth loss (Figs 3-14 and 3-15).

    FIG 3-14 Structural failure of the enamel and exposure of dentin.

    FIG 3-15 Extreme outcomes of caries-related disease. The first molar will have to be extracted.

In the case of initial, ie, noncavitated, lesions the International Caries Detection and Assessment System (ICDAS II), which guides the visual diagnosis process for cleaned tooth surfaces, identifies two levels:

  • ICDAS 1: First visual change on enamel surface due to demineralization seen after 5 seconds of air drying
  • ICDAS 2: Distinct visual change in enamel seen whether the surface is wet or dry (see Fig 3-5)

The reader is referred to the ICDAS II Criteria Manual13 for details regarding the remaining categories, ranging from a sound surface (ICDAS 0) to cavitated lesions (ICDAS 3 to 6).

Noncavitated lesions (ICDAS 1 and 2) can also be classified based on their activity. According to the Nyvad et al criteria,14 a noncavitated lesion can be defined as:

  • Active: When the likelihood of lesion progression is greater than the likelihood of nonprogression. The lesion has a rough surface and a chalky, opaque appearance (active WS). Often found at the site of plaque deposits, and the nearby periodontium is often inflamed and bleeds on light probing; the enamel surface is porous and allows acids to pass through to subsurface layers. Feels rough to the touch (see Fig 3-12).
  • Inactive: When the likelihood of lesion nonprogression is greater than that of progression. The surface of the lesion is smooth and shiny; it is generally not located near plaque deposits, and the surrounding gingiva is free of inflammation. The enamel surface has been remineralized through a change in local and general circumstances; white areas often persist in subsurface layers (inactive WS), given that the remineralized surface acts as a strong barrier that prevents minerals from penetrating to greater depth. The surface feels like the sound surrounding surface (see Fig 3-13).

Inactive lesions may still feature persistent whitish areas in subsurface layers or brown pigmented areas during the remineralization process, but this should not detract from positive aspects of the event: an inactive lesion is an active lesion that has been halted through the intervention of optimal protective conditions.

Cavitated lesions may sometimes be present. These are usually brown but meet the typical description of inactive lesions (hard consistency revealed by light probing and located in properly cleaned areas of the dentition). These lesions are generally improperly referred to as dry, ie, early enamel cavitations that have stopped progressing due to an intervening favorable change in the environment (Fig 3-16). Even if such lesions are susceptible to plaque buildup, if located in easily inspected areas, they may simply require regular observation by a dentist if the risk of medium-term reactivation is considered low (3 to 6 months). This is particularly true for low-risk adult and elderly patients.

FIG 3-16 Inactive cavitated lesion on the occlusal surface of a maxillary molar, regularly cleaned by the patient and periodically checked by a dentist.

Diagnosis in Conservative Dentistry

Proper diagnosis of caries-related disease involves a two-level process:

  1. A higher level, ie, causal or cariologic diagnosis. This involves analyzing factors promoting the disease and staging them based on their impact on the individual patient (or site).15,16
  2. A lower level, ie, outcomes or lesion diagnosis. This involves identifying and recording all the outcomes of the caries activity (starting from stage ICDAS 1) and their effects.14

This chapter does not cover the cariologic diagnosis process. Table 3-1 summarizes the main factors involved in the initiation of caries-related disease and the conditions that promote disease or health. An appropriate treatment plan is the consequence of both diagnostic processes. It will involve treatment of caries-related outcomes as well as strategies that will reduce or eliminate the influence of individual risk factors in the patient. These mainly medical actions must also involve the clinician’s awareness of risk assessment methods and techniques for constructively altering risk factors.15,17,18

TABLE 3-1 Etiologic factors in caries-related disease



Disease promoting

Health promoting






High, organized into biofilm


Predisposing factors for buildup (eg, crowded teeth, orthodontic appliances)

Present and numerous

Absent or scarce


Fermentable carbohydrates

Large amount and intake frequency

Small amount and intake frequency


Large amount and intake frequency

Small amount and intake frequency

Diet: Macro- and micronutrient intake


Healthy and balanced



Scant saliva production

High saliva production


Acidic saliva and/or poor buffering capacity

Neutral or basic saliva

and/or high buffering capacity


Availability of fluoride, calcium, and phosphate




Dental history

High caries incidence

No or low caries incidence


Presence of diseases/conditions with systemic or oral effects



Use of drugs with systemic or oral effects

No use



No use

Socioeconomic status and educational level


Medium, high

Antibacterial substances (eg, xylitol, stannous fluoride, chlorhexidine, dietary)

No use

Deliberate, regular use

Lesion diagnosis

The purpose of the dental diagnostic process is to assess hard tissue conditions, including the presence of anomalies, discoloration, and caries lesions and their activity. These and other caries-related assessments enable the clinician to place the patient in a risk class.

In academic terms, methods of dental diagnosis can be subdivided into two categories:

  1. Standard examinations
    • Medical history and interview
    • Clinical examination
    • Radiographic examination
  2. Supporting examinations
    • Laser fluorescence
    • Transillumination
    • Other diagnostic methods

Medical history

The clinician takes the patient’s medical history to gather data that may have a bearing on the treatment plan. It is essential to create a written document detailing the patient’s current health conditions, allergies and intolerances, voluntary habits (smoking), and dental history and ask the patient to sign it. After finishing this documentation, which will have to be regularly updated, the dentist must spend some time interviewing the patient about their medical history. The aim is to obtain as much information as possible regarding:

  • Patient expectations and requirements
  • Dietary habits
  • Drug treatments
  • Hobbies, sports, habits
  • Smoking/alcohol/drugs
  • Type of toothbrush/toothpaste/dental floss used and method/frequency of use
  • Fluoride prophylaxis and use of mineralizing compounds
  • Willingness to accept treatment and guidance

Clinical examination

A clinical examination is a visual and tactile procedure carried out with the aim of identifying, evaluating, and classifying discolorations, lesions, and anatomical changes affecting inspectable tooth structures and the conditions of preexisting restorations. This procedure must be carried out in accordance with ICDAS II criteria with the teeth thoroughly cleaned, rinsed, and completely dried. It benefits greatly from the use of magnifying systems as well as proper lighting.1921 In addition to the air/water syringe and cleaning devices used for preliminary tooth scaling and cleaning, other instruments useful for clinical examination are:

  • Dental explorer: Instrument with a fine, rounded tip, used to remove any plaque residue and probe grooves and suspect areas. This instrument must never be forced into grooves (maximum force, 25 g), because it can cause irreparable damage to surfaces (Fig 3-17).

    FIG 3-17 Dental explorer with fine, rounded tip. The ends are specifically designed to easily reach all accessible surfaces.

  • Mechanical separator: Useful for slightly separating interproximal surfaces to visually evaluate the status of these areas and identify any cavitation (Fig 3-18).

    FIG 3-18 (a) Ivory separator. (b) Elliott separator. (c) Cavitated interproximal lesion, surrounded by brown discoloration, rendered visible after separation.

  • Air-water-glycine (or erythritol) spray: Useful for quickly and gently removing plaque residues from grooves and separated interproximal surfaces (Fig 3-19).

    FIG 3-19 Detail of an air-water-glycine jet able to quickly and easily remove biofilm from tooth surfaces.

Radiographic examination

When diagnosing lesions in lateral and posterior sectors, a radiographic examination plays a fundamental role, particularly in interproximal sectors, provided basic protective principles are observed: justification, optimization, and limitation.2123

Despite the relatively low values of sensitivity (50%) and specificity (87%),21 the main radiographic examination for identifying interproximal lesions is the bitewing. This radiographic projection captures the maxillary and mandibular lateral and posterior teeth on one side, from the distal surface of the maxillary canine to the distal surface of the last tooth present in the arch. In some cases, particularly in adult patients with full dentition (up to third molars), two exposures may be required on each side to display all the required surfaces. This kind of projection is aimed at evaluating interproximal areas, and there should be no radiographic superimpositions in these areas. The use of dedicated centering devices and parallelism aids such as fine wedges (Fig 3-20) or periodontal probes are particularly important for this purpose.

FIG 3-20 (a) The wedge direction indicates the correct radiographic axis. (b) Because the ideal axes are often not parallel, a decision must be taken as to whether to carry out multiple exposures or use alternative tests (eg, separation).

A bitewing examination can often be used to determine:

  • Presence of deep interproximal and occlusal radiolucencies (Figs 3-21 and 3-22)

    FIG 3-21 Numerous interproximal lesions and one buccal lesion on the mandibular left first molar.

    FIG 3-22 Deep occlusal lesion affecting the mandibular right second molar.

  • Extent of residual tooth structure (Fig 3-23)

    FIG 3-23 The maxillary right second premolar is decidedly lacking in crown structure.

  • Dimensions of pulp chamber and presence of pulp calcification (Fig 3-24)

    FIG 3-24 Multiple foci of pulp calcification in pulp chambers of the maxillary right second molar and mandibular right first and second molars. The maxillary right first molar shows narrowing of the pulp chamber.

  • Distance of the lesion or restoration from the pulp chamber (Fig 3-25)

    FIG 3-25 The distal restoration of the maxillary right second premolar is very close to the pulp chamber.

  • Fit and consistency of existing restorations (Fig 3-26)

    FIG 3-26 Numerous poorly fitting restorations.

  • Bone levels, periodontal defects, and furcations (Fig 3-27)

    FIG 3-27 Various areas of reduced periodontal attachment can be identified, albeit peripherally.

  • Presence of interproximal calculus (Fig 3-28)

    FIG 3-28 Numerous calculus deposits can be identified interproximally. It is difficult to see the buccal and palatal/lingual calculus on a radiograph.

  • Presence of anatomical anomalies and/or residual roots (Fig 3-29)

    FIG 3-29 Residual root between the roots of the maxillary left second premolar and first molar.

A pediatric dental evaluation can also be carried out if a young patient’s risk level justifies the examination (Fig 3-30). This examination is fundamental but has limitations, namely:

FIG 3-30 Ten-year-old child with cavitated lesion of the primary maxillary left first molar. Bitewing examination is justified because this condition places the child at high risk of caries.

Radiographic classifications

For many years, radiographic involvement of interproximal dental tissues was studied using the Lutz and Marthaler (L&M) classification, which dates back to 1966. This classification involves four dimensional stages, D1 to D4, based on radiographic lesion size, where D1 and D2 concern the involvement of the outer half (D1) and inner half (D2) of the enamel, while D3 and D4 concern the involvement of the outer half (D3) and the inner half (D4) of the dentin (Fig 3-34).

FIG 3-34 (a to d) Schematic and radiographic representation of the L&M classification.

A more recent classification, termed E-D, differs from the L&M classification in that it divides the dentin into thirds. Another difference lies in the fact that E indicates involvement of enamel and D indicates involvement of dentin, based on radiographic evidence of the caries lesion2527 (Fig 3-35).

FIG 3-35 (a to e) Schematic and radiographic representation of the E-D classification.

It is legitimate to question the usefulness of a new classification. As already mentioned, and as will be seen later, a demineralized tooth tissue area does not necessarily mean cavitation is present. In vivo assessments carried out on patients27 show that the probability of cavitation being present in permanent teeth based on radiographic involvement (E-D classification) is as follows:

  • E1: 0%
  • E2: 10.5%
  • D1: 40.9%
  • D2 to D3: 100%

The importance of this more up-to-date classification is therefore immediately apparent: in the L&M classification, stage D3 also includes part of the central third of the dentin, which corresponds to stage D2 in the E-D classification. In the latter classification, D2 is always associated with cavitation. This is important because in the absence of cavitation, it is possible to consider minimally invasive intervention methods that do not necessarily require a classic restorative approach to the lesion.28

Laser fluorescence

Laser fluorescence is based on the use of a diode laser able to detect signs of cariogenic bacterial activity inside tooth grooves (Fig 3-36).20 This investigation method results in an easily recordable numeric score. It is particularly recommendable for regular checkups on suspect lesions in grooves, fossae, and foramina that are visibly inaccessible in low-risk patients, where a deep groove or early lesion that is no longer active is considered sound and therefore does not require restoration, only regular monitoring (see Fig 3-16). If the numeric score associated with the area in question remains consistently low and unchanged (or barely fluctuating) during these checkups, the area is likely to be free of caries activity. If the numeric score increases significantly compared with previous scores during regular checkups or an increasing trend is observed, the area under examination is more likely to be subject to caries activity.

FIG 3-36 Diode laser instrument.

The scores provided by the equipment range from 0 to 99, and the results can be interpreted as follows based on histologic investigations29:

  • 0 to 5: Healthy tissue
  • 6 to 14: Demineralization of the outer part of the enamel
  • 15 to 20: Demineralization of the outer and inner part of the enamel
  • 21 to 99: Lesion of the dentin

As with other diagnostic tests, laser fluorescence has its limitations21,29,30:

  • The reading is impaired when strong pigmentations, plaque, and/or calculus are present.
  • Where grooves are very deep, the laser beam may not be able to correctly interpret the lesion.
  • The examination can be impaired by excessive moisture or dehydration.
  • It is not very sensitive (risk of false positives).
  • Equipment cost is high.

Limitations due to contaminants in the grooves can be reduced by always applying the same preparation protocol for the area to be analyzed. For example:

  • Cleaning of the surface with air flow of glycine or erythritol at different angles for 7 seconds (Fig 3-37)

    FIG 3-37 Standardized cleaning stage.

  • Use of a prophylactic brush and glycine or erythritol powder (Fig 3-38)

    FIG 3-38 Further cleaning using small rotating brushes coated with glycine powder.

  • Rinsing of the surface for 10 seconds
  • Drying of the surface for 5 seconds
  • Visual inspection and removal of any residue
  • Repetition of cleaning procedure until acceptable conditions are achieved


Fiber-optic transillumination (FOTI) is an effective aid in the identification of caries lesions because demineralized tissue interacts with light in a different way compared with healthy tissues.20 When used to detect interproximal lesions, a highintensity white light source31 is applied to the buccal or palatal surface and observed through the occlusal surface (posterior teeth) (Fig 3-39) or the surface opposite the light (anterior teeth). A dental curing light can be converted to a FOTI light by applying a special additional tip (Fig 3-40). Enamel lesions look like gray shadows, and dentinal lesions look orange or blue. Although data relating to the sensitivity and specificity of this method are conflicting, there is plenty of evidence in the literature to support its use to detect interproximal lesions in both the anterior and posterior sectors,20,21 particularly when combined with the ICDAS II visual detection method, which can only benefit from this support. The FOTI technique, when combined with visual examination, is currently one of the most effective diagnostic systems. It can be used for anterior teeth but is not recommended for posterior sectors. The latter can be diagnosed using a digital system known as DiFOTI (digital imaging FOTI). This displays images on a screen in grayscale and stores them in the memory of the computer to which the system is connected (by means of dedicated software) (Fig 3-41). Unlike the FOTI technique, which can be performed using a simple and inexpensive fiber-optic lamp, DiFOTI requires more complex equipment as well as a computer and software for processing and storing images.

FIG 3-39 Caries lesions affecting the distal wall of a premolar identified using the FOTI technique.

FIG 3-40 A dental curing light can be converted to FOTI by applying an additional terminal.

FIG 3-41 Caries lesions identified using DiFOTI technique.

The benefits of FOTI and DiFOTI techniques include:

  • Absence of ionizing radiations
  • Frequent follow-ups are possible
  • Useful for children and pregnant women
  • Easier detection of cracks, caries infiltrations, and surface discoloration (anterior)
  • Images can be easily compared (DiFOTI)
  • Low cost (FOTI)
  • Information is provided regarding the size and buccopalatal location of the lesion
  • Examination of choice for anterior teeth, when combined with visual inspection (FOTI)

Limitations of the FOTI techniques are:

  • Low sensitivity in posterior sectors
  • Difficult to obtain photographic images and therefore compare different examinations
  • Do not provide information on cavitation and lesion activity

Limitations of the DiFOTI technique are as follows:

  • Initial cost
  • Low sensitivity in detecting apical lesions in the contact area
  • Do not provide information on cavitation and lesion activity
  • Presence of a USB connecting cable
  • Handpiece sterilization is complex (the video camera lens can come into contact with oral fluids because the autoclavable terminal provided has an opening in that area)
  • Not applicable to anterior teeth

Other diagnostic methods

Dental companies are continually developing diagnostic methods that are alternative or supplementary to the ones mentioned previously. These cannot all be described here for obvious reasons, and this does not in any way imply that we are opposed to these methods.

However, additional useful methods aiding the diagnostic process include:

  • Plaque-revealing gels (Fig 3-42), particularly if able to highlight acidogenic plaque. The outcome of caries activity is more likely to be identified in areas where this specific biofilm builds up.

    FIG 3-42 Tooth and periodontal surfaces stained with three-tone plaque-revealing gel: the plaque stained teal is acid producing and therefore potentially cariogenic.

  • Dental floss can help identify roughness and/or discontinuity if it frays when passed through interdental spaces.

Treatment of Early Caries Lesions


Remineralization is defined as the process whereby calcium and phosphate irons supplied by an external source are deposited inside spaces in the crystalline structure of the demineralized enamel to increase the crystalline lattice.32 This is mainly achieved by teaching patients how to prevent caries,33,34 consistently removing biofilm from tooth surfaces,3436 and supplying remineralizing molecules (Box 3-1).37 Remineralization should be considered the best approach to noncavitated white spots originating from caries, ie, white spot lesions (WSLs).38 As already explained, the appearance of a WSL is strictly related to whether or not it is active. Consequently, a positive outcome to the remineralization process is clinically revealed by a change from a rough, opaque surface (active white spot) to a shiny, smooth surface (inactive white spot), which may also incorporate brown pigments over time.14,39 Although white spots can disappear in an entirely natural manner40,41 or by mechanical removal of the demineralized surface,39,42 it is extremely rare for them to disappear altogether.39 Given that remineralization initially takes place primarily in the outer enamel layers, it becomes difficult for the minerals to reach the deepest subsurface layers, which is why such areas are likely to experience incomplete remineralization (Fig 3-43).

FIG 3-43 (a) Active WS on buccal surface of a canine. The lesion is rough when a dental explorer is passed over it. (b) The same WS, now inactive, after 6 months of remineralization.

BOX 3-1 Dentist and patient responsibilities during the remineralization process


  • Knowledge of caries-related disease dynamics
  • Classification of the patient’s risk class and major disease determinants
  • Customized instructions designed to control/stop the disease
  • Scheduling of checkups


  • Noncariogenic diet and habits
  • Consistent biofilm removal
  • Sufficient supply of minerals
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May 25, 2021 | Posted by in General Dentistry | Comments Off on Diagnosis and Treatment of Early Caries Lesions
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