Conclusions Development

A carious lesion should be regarded as damage resulting from the infectious disease dental caries. The coronal lesion starts as clinically undetectable demineralization of enamel, visible only at the microscopic level, and proceeds gradually to visible, noncavitated demineralization of first the enamel surface and then the dentin, and finally to cavitation of the dentin. Primary carious lesions are most frequently located supragingivally on the crowns and particularly on the occlusal surfaces of the molars and the approximal surfaces of the posterior teeth. Root caries may occur in elderly people and other adult caries-risk patients with root surfaces exposed by periodontal disease.
Carious lesions may be classified according to type (primary or secondary caries), location (crown, root, and surfaces), size and depth (enamel, dentin, or root cementum), and shape (noncavitated, smooth, rough or soft surface, cavitation, etc). 
From a treatment needs aspect, it is important to evaluate whether the lesions are active or inactive and noncavitated or cavitated.
Enamel lesions develop mainly where cariogenic plaque accumulates and remains undisturbed for lengthy periods. This plaque, together with accessible fermentable carbohydrates, results in prolonged periods of low pH. In toothbrushing populations, these conditions occur most frequently on the approximal surfaces of the posterior teeth (particularly from the mesial surfaces of the second molars to the distal surfaces of the second premolars) and the occlusal surfaces of erupting molars (particularly the distal fossae).
Moderate pH levels result in a noncavitated enamel lesion with a surface zone that is like a micropore filter, and a so-called lesion body where there is greater loss of minerals from every single enamel prism. Such a noncavitated lesion can be arrested without any loss of surface minerals. At very low pH (4.5 to 5.0), an erosive-like enamel lesion will develop with intraprismatic dissolution of the enamel with microcavities. Such a lesion can also be arrested, but with some loss of the enamel surface compared with the surrounding intact enamel. In other words, all noncavitated
as well as more active erosive-like enamel lesions should be diagnosed as early as possible and arrested to prevent extension of the lesion into the dentin, with eventual cavitation, which would generally require operative intervention.
In populations with low or moderate caries prevalence and access to well-organized preventive programs, most enamel lesions will be arrested and therefore never progress into the dentin. On the other hand, in highly caries-active individuals with poor oral hygiene and no daily use of fluoride, enamel lesions can progress to cavitation of the dentin very rapidly (within 6 to 12 months). The demineralization of the dentin at the dentinoenamel junction corresponds to the width of the outer surface of the enamel lesion and progresses in the same direction as the dentinal tubules. Very advanced demineralization of the dentin may occur without enamel cavitation; under such conditions there is no microbial invasion of the dentinal tubules. All noncavitated lesions of dentin can and should, therefore, be arrested and not be treated invasively.
Root caries develops only on root surfaces that are accessible to cariogenic microflora and exposed to the cariogenic plaque (biofilms). The primary lesions develop predominantly at plaque-retentive areas, particularly in the large interproximal areas and along the gingival margin and the cementoenamel junction. These represent stagnant areas where plaque accumulates. The primary root lesion has greater horizontal than vertical dimensions because of the greater thickness of supragingival plaque along the gingivocervical margin. If the exposed root surface is still covered
by a layer of cementum, the early stages in caries development involve a haphazard demineralization of this layer, because of acid formation by the acidogenic bacteria colonizing the root surface. Such initial lesions result in a soft, yellow, but noncavitated root surface that can be arrested.
However, where root cementum has been removed in patches as an iatrogenic effect of aggressive scaling and root planing, the exposed root dentin may be destroyed very rapidly; cavity formation is a combined effect of acidogenic microorganisms and collagenase-producing microorganisms. 
Even cavitated active root lesions can be converted to nonactive brown-black lesions by improved plaque control and use of fluoride. Restoration of such arrested lesions may still be indicated, however, not only to prevent plaque retention, but also to improve esthetics.
For several decades, the accepted method for detecting carious lesions in patients, as well as in clinical trials, has been a combination of clinical visual-tactile (light, mirror, and probing) examination and bitewing radiographs. For most patients, these techniques are still appropriate. However, over the last decade there has been a considerable increase in materials and methods available for this purpose: 
1. The visual method, still used by many general practictioners
2. The visual-tactile method with light, mirror, and gentle probing
3. The conventional visual method in use in European epidemiologic surveys
4. The meticulous clinical visual method based on mechanical cleaning and drying of
the tooth surfaces before examination
5. The visual method with temporary elective tooth separation
6. The visual method with temporary elective tooth separation and the use of
elastomeric impression material for evaluation of the size and depth of cavitated
7. The conventional (bitewing) radiographic technique
8. The digital radiographic method, which minimizes radiation exposure compared to
conventional radiographs
9. The computer-aided radiographic method, which utilizes the measurement potential
of computers in assessing and recording lesion size
10. The fiber-optic transillumination method (FOTI)
11. The electric conductance (fixed frequency) method
12. The endoscopic filtered fluorescence method (EFF)
13. The alternating current impedance spectroscopic technique (ACIST)
14. The quantitative laser (light) fluorescence method (QLF)
The accuracy (sensitivity and specificity) and applicability of these methods vary
considerably. Some, eg, the visual-tactile and European methods, are very rapid and
inexpensive, but subjective, and are therefore useful for large-scale epidemiologic
surveys. Others are objective and offer quantitative diagnosis but are very time
consuming and require costly equipment (ACIST, EFF, and QLF), and to date are
being applied only in limited research projects.
The diagnostic method of choice depends on the purpose of the examination. Apart
from the occult fissure lesion penetrating deeply into the dentin, difficulties in clinical
detection and registration arise not with the advanced lesion but primarily with the
early lesion (confined to the outer enamel), the noncavitated lesion of dentin,
recurrent caries (around the margins of restorations), and subgingival root caries.
The general trend in clinical examination is away from reliance on gentle probing
with a sharp explorer, toward meticulous visual inspection (sharp eyes and a blunt
probe) for early detection of noncavitated lesions: Treatment is directed toward
arresting the lesion and preserving the surface zone, to prevent the initiation of
In general practice, the aforementioned method, in combination with radiographs
(conventional bitewings or digital) and FOTI should be adequate for diagnosis of
carious lesions in patients. Temporary elective tooth separation should be used to
determine whether posterior approximal lesions of dentin are noncavitated or
For diagnosis of occlusal caries, probing offers no advantage in accuracy over visual
inspection after mechanical cleaning and drying. Noncavitated active enamel lesions
should be detectable as white spots on either side of the entrance of the fissures or
pits. However, even noncavitated lesions of dentin occur frequently.
Conventional bitewing radiographs improve the potential for detecting both
noncavitated and cavitated occlusal lesions of dentin. However, there is some risk of
false-positive diagnoses.
A new aid, Diagnodent, based on QLF technique, appears to be advantageous for
detection of occlusal enamel as well as dentin caries lesions.
All noncavitated occlusal lesions, in enamel as well as in dentin, can be arrested by
plaque control and fluoride or treated with noninvasive methods such as fissure
sealants. In a radiographically detected lesion of dentin, or by QLF aid, explorative
opening of the entrance to the fissures may be indicated, to allow direct visual
inspection of possible cavitation through the base of the fissure into the dentin. In the
absence of cavitation, the fissure should be sealed with a fluoride-releasing material
(resin-based glass-ionomer materials or compomers).
Of the recent innovations, the QLF technique followed by the electrical conductance
(fixed frequency) method seems to be the most promising for diagnosis of occlusal
lesions of enamel as well as dentin.
In the anterior teeth, approximal lesions of enamel and dentin, noncavitated as well as
cavitated, are readily detectable by a combination of meticulous clinical visual
examination and FOTI. In the posterior teeth, radiographs (bitewings, digital, or
computer aided) are excellent for detection of approximal lesions in enamel and
dentin, as well as for monitoring progression, arrest, or regression. In this area,
meticulous clinical examination is of limited value in the detection of early lesions.
However, neither radiography nor meticulous clinical examination is useful for
differentiating between cavitated and noncavitated approximal lesions of dentin.
Temporary elective tooth separation is therefore recommended; for visual inspection
with or without a pouring of an impression for future reference. Studies have found no
dentin cavitation in the majority of radiographically detected lesions in the outer half
of the dentin. Such lesions should be arrested rather than restored.
For differential diagnosis and for assessment of treatment needs, root caries should be
classified as active or nonactive and noncavitated or cavitated. This can usually be
done by meticulous clinical examination. A rough, soft plaque-covered surface and
yellow color indicate an active lesion, while a smooth, dark brown or black surface
that is hard to moderate probing pressure indicates an inactive (arrested) lesion.
Cavity formation may be associated with both active and nonactive lesions, but in the
latter the margins appear smooth. On the buccal and lingual surfaces, meticulous
clinical examination should be adequate for diagnosis according to the
aforementioned criteria. Probing with a sharp explorer is contraindicated.
The most difficult type of root lesion to diagnose is located subgingivally on
approximal surfaces. Meticulous clinical examination should be supplemented by
vertical (standing) bitewing radiographs.
As with active enamel lesions, the initial treatment of active root lesions should be
preventive and noninvasive (improved plaque control and use of fluoride), aimed at
arresting the lesion and converting it from active to inactive.
The major emphasis is on the early detection of the noncavitated active lesion.
Treatment is preventive and needs related, aimed at arresting the lesion as soon as
possible. Because the arrested lesion does not progress to cavity formation, there is no
indication for operative intervention (for reviews on the development of carious
lesions, see Thylstrup et al, 1994; Thylstrup and Fejerskov, 1994; for reviews on
diagnosis of carious lesions, see Grondahl, 1994; Ismail, 1997; Pitts, 1997).
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Thanks for the comments! And thank you Verity for poiinntg out an online resource that’s new to me. However, the level of scientific understanding on Raw Food Explained suffers from considerable limitation. For instance, the claims regarding the ‘importance’ of carbohydrates ignore the fact that entire cultures have survived where there has been ne available vegetation, edible or otherwise. The importance is not on carbs but on GLUCOSE. The body’s ability to derive glucose from protein is ignored. I know people who live on a meat-only diet, and yet their digestive processes still run and their heart beats. Carbs are not essential. Some of the nutrition that fruit etc provides is essential, sure, but we can get it from other sources as well. I’m not downplaying the deliciousness of fruit, we should definitely eat it since we have access to it, but rather than looking at the source (fruit) as being the essential element, look at the specific nutrition involved.Too much dietary fat = high blood sugar? This is biologically impossible. That claim is utterly bizarre, and now that I have read the claims made against dietary fat from Raw Food Explained I can guess where you have pulled that from. The backwards understanding presented on that site can be explained with just one quotation : “The consumption of … saturated animal fats destroy the health of the body at the cellular level.” Were that true, the human animal would have died out long before the advent of agriculture provided us with enough edible vegetation to fuel our needs. I do know that I should cut out dairy, but that has nothing to do with any ‘addictive properties’ – the opposite is true; the human diestive system did not evolve to process cow’s milk. Non-human milk can have damaging effects on our system, for some more than others. I am still consuming small amounts of dairy for the satiating effects of healthy fats in cream and cheese. It helps me to stay sated while I am trying to restrict calories for weight loss purposes. I use nuts for the same purpose, but my budget means that I can’t rely solely on nuts as a versatile source of fat just yet. One day…The issue with some fruits is indeed that blood glucose can spike as a result, but moreso that when our tongue picks up sweetness in our food, insulin can be produced, and we all know how devastating insulin production can be, especially when we’re looking for weight-loss. If Steve’s blood sugar levels weren’t adversely changed by the fruit he ate then he must be sensitive to insulin or he used the energy quickly. But form what I can see, he ate mainly berries, which I have already pointed out have a lesser effect on blood sugar than other items. Mangoes and bananas are high-sugar, but their effect on blood sugar is slow (low GL), so again avoiding spikes. Another important realisation you may need to reflect upon is that depending on where you live, fruit and veg may not be consistently available. To suppose the human animal is designed to live off of vegetation requires ignorance of ancient humans wo lived in icy/arid areas. As you say, we’re quite amazing in that we can live off pretty much anything, so to make hard and fast rules about a ‘specific’ diet that ignores aspects of our history is short-sighted at best.Verity, I’m thrilled to know that your diet works for you and you have had success in eradicating your lifestyle illnesses. But be careful not to assume that just because you need to eat a particular way, that everyone else should too. That’s one of the battles I’m fighting as well, so as long as the science supports the choice, and that the diet povides adequate nutrition, that choice is worth supporting.

We have consistently nticoed a similar degree of diffusion restriction with retinoblastomas (probably somewhere between 10-15 untreated cases over the last few years). This could theoretically help differentiate Rb from Coats’ disease, as we would expect much higher ADC with the hypocellular, exudative retinopathy seen in Coats’ (anecdotally, we have seen one case of Coats’ that fit this pattern, brought in from an outside hospital).Another ocular problem-solving area where this may be helpful is in differentiating melanoma (particularly amelanotic) from metastases. The melanosomes and relative dense cellular packing of melanoma typically results in greater diffusion restriction than most other neoplasms. However, that can be a little trickier than the Rb/Coats differentiation or the pseudotumor/lymphoma differentiation. The gap in ADC between diffusion restricted neoplasms and other neoplasms is relatively small. Artifacts in the orbit make the ADC measurements a little less precise, and overlap between lesions becomes a bigger concern. Also, there is a significant effect of volume averaging with small lesions also (< 1 cm). This is an area that probably requires a technical advancement of some sort before it’s ready for everyday use.

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Enjoyed reading this post. That was an entrie comment? Wow! :-DMore like a Paleo primer/treatise!BTW, today on I am doing a targeted ketogenic diet. In the sense that I am going zero (near-zero) carb on three days a week when I fast and don’t do weight training. On the other four days, I will weight train, and eat carbs (reasonable amounts). I think my fat loss will zoom! What say?

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Articles for theme “caries”:
Diagnosis of secondary cariesDefinition and prevalenceSecondary caries has been reported to be eight times more common than primary lesions in adults, particularly in those older than 50 years (Goldberg et al, 1981). However, prevalence may vary markedly in different countries, depending on the total caries prevalence in the population and the level of development of the dental care system. In developing countries with low caries prevalence in the adult population and poor dental care resources, secondary caries may be almost negligible.
Diagnosis of root cariesDefinition and classificationRoot caries usually appears as a shallow area, less than 2 mm deep, a mostly noncavitated, ill-defined, softened, and often discolored lesion, characterized by destruction of cementum and penetration of dentin. Several definitions and classifications have been proposed; Hix and O’Leary (1976) defined root caries as “a cavitation or softened area in the root surface which might or might not involve adjacent enamel or existing restorations (primary and recurrent lesions).
Diagnosis of approximal cariesThe issues to be considered by the clinician with respect to caries of the approximal surfaces are similar to those considered at other sites: Is the surface sound, or is there a lesion? If so, how advanced is the lesion¾involvement of enamel only, enamel and dentinal involvement, or pulpal exposure? Finally, is there cavitation?  Diagnostic methodsMeticulous visual examinationIn the thin anterior teeth, both noncavitated and cavitated approximal lesions are readily detectable by meticulous clinical visual examination.
Diagnostic methodsIn typical fissures, and particularly in atypical sticky fissures (see Fig 203), most of the early stages of the lesion are hidden from the naked eye, although in a clean, dry fissure, it might be possible to observe active noncavitated white-spot lesions on the walls. Soon after eruption, most of these lesions are arrested (see Figs 174, 204a-c, 205c) and take up a brown stain from items in the diet. This diagnostic problem was recognized many years ago by GV Black (1908) who wrote: Very many pits and fissures show evidence of some slight softening in early youth, which is stopped by the coming of immunity or some change of local conditions.
Diagnosis of occlusal cariesIt might be expected that occlusal carious lesions would be fairly easy to diagnose,  because unlike approximal and subgingival root surfaces, these surfaces are readily accessible for visual inspection. However, clinically (visual or visual-tactile by probing) or radiographically, diagnosis of occlusal lesions is a delicate problem, because of the complicated three-dimensional shape of the occlusal surfaces, incorporating fossae and grooves with a great range of individual variations.