cons sheet # 7-Wafa'a s3aid

بسم الله الرحمن الرحيم

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Dental Caries Ι & ǁ
1st:Continuation of Dental Caries Ι (Hand-out#6 from page #17 to the end)
-Hidden caries is just a clinical characteristic of some of the pit & fissure caries. It hides on the occlusal tooth surface. You can see very minimal caries involved but when you take a radiograph or you start preparing the cavity, you'll end by having a huge cavity. Basically, some people call it "surprising caries". For the occlusal surface, despite being small at first but in radiographs, it appears huge. Why? Why does that happen? Why we classify it as a separate entity? Because when there's a high remineralization activity on the tooth surface and at the same time there's an active caries process underneath. There's a huge lesion under the surface-mineralized layer.
*In slide#34
- Pic A>> the mesial part of the fissure is slightly carious.
-Pic B>> radiography: arrows point to a radiolucent area. The intensity is not as normal structure of enamel and dentin. There's an area which's more blackish than the rest of the tooth, so we call this area as a radiolucent. Radiolucency on radiographs indicates caries. In this picture, if you compare the extension of the radiolucent area (extension of caries) to the normal tooth, you'll find that almost 1/3 of the tooth is lost.
-Pic C>> when you start doing a cavity preparation, you'll notice the dark-brown color in the cavity. This indicates soft dentin (caries).
-Pic D>> after completing the cavity preparation, notice how much surface is lost. So this is what we call it hidden (surprising) caries.
Q: Is this type of caries chronic or not?
A: yes it's chronic. It's rapidly progressed chronic although the chronic caries progresses slowly, but not all caries progress at the same rate. For example, pits & fissure caries needs 18 ± 6 months. So the one that's -6 months is faster than that of +6 months. Relatively, hidden caries is one of the fastest types of chronic caries.
Q: How much frequent does the hidden caries occur?
A: usually hidden caries occur occasionally. Not more than 3-4% of the cavity preparations we do; because it occurs when the patient has many caries and suddenly, he was motivated to improve his oral hygiene using fluoride in toothpastes and mouth washes, so the surface will be improved by remineralization but still there's an active lesion underneath the surface.
 Smooth enamel caries:
-It's the 2nd type of dental caries.
-Smooth surfaces could be buccal, lingual, mesial or distal.
-In mesial or distal caries, the caries starts in the sub-contact area (underneath the contact area). Not above the contact area because the region above the contact area is:
1- easy to clean 2- there's mastication 3- tongue activity 4-Salivary flow
-However, the sub-contact area is protected from cleaning. It can be cleaned just by floss>> that's why mesial and distal surfaces are highly prone to caries.
-In the incidence of caries, pits & fissure caries takes number one then the proximal surface caries takes number two.
-Buccal and lingual surfaces are prone to caries although there's no contact between teeth in these surfaces. This occurs due to bad oral hygiene, but the most causative factor is that the caries in buccal and lingual surfaces present below the height of contour of the tooth. So these areas are relatively protected from the effect of mastication and salivary flow, although there's salivary flow on the lingual surface but not on the buccal surface. Also there's no tongue activity on the facial surfaces of teeth.
*Factors that cause smooth enamel caries: rough surface on the smooth enamel surface; this surface arises from a faulty restoration that's applied or filling that's not good in terms of margins. So this will accelerate the progression of caries on these surfaces. Sometimes, there're structural defects on smooth surfaces. There should be nothing rough in the oral cavity. Roughness is a very favorable climate for the bacteria.
*How to detect caries under the contact area???
- If it's a small lesion there's difficulty but if it's a large lesion, it'll progress until causing undermining of marginal ridges then the marginal ridges break so it'll be visibly-evident. We detect it in intra-oral examination but if it was small lesion, you won't see it because it's below the contact area and there's decent (adequate) amount of tooth structure buccal and lingual to the lesion. >> So the best way to detect this lesion is to use radiographs.
-In pits & fissure caries, detection is visual. Dentists just look at the pits & fissure of enamel and see if there're signs of caries or signs of undermining enamel. Usually around fissures there's white decalcified margins or greyish discoloration on the fissures>> this tells the dentist that this is caries and not only staining.
-Some people advocate the use of dental explorer or the probe to feel the softness of the fissure. Using a probe, if you feel softness in the fissure some people call this softness as caries and if you don't feel any catch or softness, this is not caries. However, the use of dental explorer is not recommended nowadays. Because the shape of the fissure may be the cause of stickiness to the explorer not by the effect of the softness of dentin but by the shape of the fissure>> so we'll have equivocal diagnosis. It's not obvious if there's really caries, it's just a sticky fissure.
-As we said, the explorer shouldn't be used on the occlusal surface to detect pits & fissure caries; it might be misleading. Because it could be a sticky fissure, the shape of the fissure makes the explorer sticks to the surface. The other reason is: if there's an incipient lesion starting in pits & fissure surface and you examine this surface using an explorer, you'll damage the surface and penetrates it leading to a cavitation. Therefore you accelerate the caries process that could have been reversed because it's less mineralized and softer than normal enamel.
-In class ǁ, it'll be very advanced lesion if you can feel it with the explorer on the proximal surfaces. If you can feel it with the explorer, this is a significant lesion; however, early lesions the only way to diagnose them is to use radiographs.
-In slide#39>> I: Incipient lesion C: cavitated lesion. Any lesion can start as an incipient and then progresses to cavitated one. Usually, we find both incipient and cavitated caries on smooth surface lesions.

 Root caries:
-Root caries could be on any surface of the root; buccal, lingual, mesial or distal. Usually there're different types of bacteria that contribute the most to root caries. Actinomyces species especially Actinomyces viscous bacteria is the predominant bacteria.
-Root caries has less dentinal margins than other types of caries (pits & fissure and smooth enamel caries have defined margins).
-Root caries has less distinct margins and usually "U"-shaped whereas in smooth surface, it's cone-shaped.
*There're some facilitating factors to root caries:
1- Gingival recession.
2- Poor oral hygiene, especially in old patients who have lower digital dexterity and decreased motivation of oral hygiene.
-If we have any anatomic surface that comes towards contour, it facilitates root caries. Examples of anatomic contours in the root: Facets and concavities. Facets and concavities are hard to clean even by floss. So the only way to clean them is by the dentist.
- Also lack of rubbing by food boluses accelerates root caries.
*Root caries is alarming!
- It's alarming because of its rapid progression. There's no enamel but there's cementum and then dentin and as you know, dentin is much softer than enamel.
-It's often asymptomatic. Same as chronic caries; pain is not a common feature.
-It's close to the pulp.
-It's difficult to restore. Restoration is somewhat challenging; because it's close to the pulp. If we make bonded restoration, there's no enamel bind to it. Binding to cementum and dentin is not always predictable.
-Root caries is faster than crown caries; because in the root there's nothing to go through except a thin layer of cementum and then rapidly to dentin.
-Thickness of dentin in crown is much more than that in the root. >> So it's not right to say dentin caries and root caries; because root caries involve dentin caries.
Q: How this lesion could be asymptomatic although it occurs in dentin near the pulp?
A: The patient would feel symptoms from root caries once it reaches dentin almost at or near the pulp. Plus the fact that in elderly, formation of much more secondary dentin so pulp chamber is much narrower.

2nd :Dental Caries ǁ (Hand-out # 7)
*Pathophysiology of caries:
-We talked about the incipient lesion as it appears intra-orally as a white spot lesion when it dries but if it gets wet, the water will fill the porosities inside the incipient lesion. These porosities result from demineralization; the ions are removed leaving a space. So this space if it's filled with water, the lesion will have the same refractive index as the enamel. However, if it's an advanced incipient lesion, usually there's no much change in color; it remains whitish. But if it's small incipient lesion when it gets wet it doesn't show.
-look at the picture in slide#2>> there's a white band on the facial surface of the molar. This is a smooth surface caries. This incipient lesion may progresses to cavitation. Cavitation is an accelerating factor for the caries process; the cavitation will form a shelter of more advanced species of plaque to develop and florish such as lactobacilli. Streptococcus mutans start first because it can adhere to tooth structure then after cavitation; lactobacilli appear in the cavitation in which they accelerate the loss of tooth structure. Cavitation is irreversible. We should always remember that caries process is a balance between demineralization and remineralization that has been reached. If there's a balance, you won't see anything. But if the imbalance occurs, you see cavitation.
-In slide#4 >> 1st pic>>the brownish band on the occlusal surface represents the caries that will extend rapidly to form a cavitation.
-Cavitation is a retentive surface for the bacteria; it allows filamentous bacteria like lactobacilli to live and florish. And in the absence of change in the host's diet or oral hygiene practices, just a presence of cavitation can lead to acceleration of the caries process.
-Cavitation itself is a significant factor that leads to a synergistic acceleration for the growth of the plaque community.
-In class ǁ, particularly proximal caries lesion, we can see the lesion on radiographs if they're small enough but if we see a distinct lesion in enamel on radiographs this indicates that we've a much more involved lesion in dentin. Radiographs are always under-estimating the carious lesion. Whenever you see carious lesion and it reaches DEJ on radiographs, it histologically reaches the DEJ. Usually the incipient lesions appear as a very faint area on radiographs and you'll be guessing whether it's an incipient lesion or not, but actually it's an incipient lesion.
-In incipient lesions the minerals are lost but still there's a substructure of enamel and because the there're acid attacks on enamel, something like an activation occurs. Etching acids cause +ve substructure in enamel that will take much more ions than the normal enamel>> so the incipient lesions take much more ions than the normal enamel takes. Because it lost too much of the minerals and at the same time, the acid etching that occurred because of bacterial products that activated the substructure to receive more ions from the saliva. >>So this helps the remineralization process to be much more rapid.
-The supersaturation of the saliva by ions (calcium & phosphate) that will be a driving force for the ions to go to incipient lesion and reminerlizes. Once the lesion is remineralized, we'll have arrested caries which is a chronic type of caries. It's not a separate entity, it's still chronic because acute can never be arrested.
Incipient lesion remineralization arrested lesion
-In the picture in slide#8>>notice the brownish arrested caries on the distal surface of a premolar (the brownish color occurs due to extrinsic pigmentation; it takes ions from saliva and takes the pigments that present in the oral cavity like coffee, tea...etc or by other staining materials that we eat or drink). The arrested caries is very hard and even harder than the intact enamel.
*Note: Metallic ions contribute the most to the pigmentation process.
Q: Should I restore the arrested caries?
A: No I shouldn't make a restoration because it's a hard structure that resists acid attacks more than the intact enamel. However, if the esthetics is to be concerned, we do a restoration. For example, if the arrested caries present on the labial surface of central incisor.
Q: How could I differentiate between staining and arrested caries?
A: usually for staining to occur, it'll occur generally on the tooth surface, while the arrested caries occur on small lesions 2 or 3 as a maximum. But if there's caries on the occlusal surface, it won't be arrested because of the presence of pits& fissures on the occlusal surface. It's either staining or caries and the difference between them is the diagnosis visually depending of the margins if they're greyish, whitish in color…etc.
 Zones of incipient enamel lesion: these are histological zones
1st: Translucent zone. 2nd: Dark zone. 3rd: Body of the lesion. 4th: surface zone.
1st: Translucent zone.
-It's the deepest zone.
-As the name indicates, in histological sections it won't be evident.
-Look at the picture in slide#10 >> there's a slight demineralization; there're voids (pores). These voids are relatively small in size so it will take the dye that we used in preparing the histological section which is the Quinoline dye. Quinoline dye, once it's up-taken into these voids, it shows the same refractive index as enamel. In this picture, "d" indicates translucent zone while "c" indicates the dark zone. >> So in the picture the light color below the black line (dark zone) represents the translucent area (transparent).
- The voids are almost 1% in volume, about 10 times the size of voids in the natural intact enamel. These voids take the Quinoline dye that's why it shows the same color as the intact enamel, so it appears as transparent.
-But why these voids appear?? When there're bacteria on the tooth surface that releases by-products, acids (mainly lactic acid) and hydrogen ions that penetrate into the surface and stop at the 1st zone of caries process which is the translucent zone>> so these voids contain hydrogen ions in addition to the Quinoline dye.
Q: Does the lesion starts from the bottom to the top?
A: yes the lesion starts from the bottom to the top. Because the enamel surface is intact, it'll start from the subsurface and then advancing downwards and we'll see all these layers (zones1, 2, 3 & 4).
2nd: Dark zone.
-It's the next deepest zone.
-It doesn't transmit polarized light so it appears dark because it contains pores which are too small to be filled with Quinoline dye.
-Total pore volume is 2-4% but the individual pore is very small. These pores don't take the dye, that's why they reflect light; don't let the light to pass through this zone. So it appears as a dark band.
-Dark zone in incipient lesions is a sign of remineralization >> the layer the more darkness it has, the more remineralization that has been occurred. And also there's demineralization in this zone and in the previous zone (transparent zone). There're episodes of demineralization and remineralization but remineralization especially evident in the dark zone.
3rd zone: body of lesion
-Main demineralization occurs in this zone. The demineralization occurs along the Stria of Retzius of the enamel.
** Remember the enamel rods enamel sheath; sheaths have less mineral content and more organic >> so it'll be demineralized first.
-It has a less resistance to acid attacks than the rod itself. >> So there're spin-patterns of Stria of Retizus that present in the body of the lesion because it spreads along these rods.
-Pores are much larger in the in this zone, it's about 5-25% and there's a huge porosity. A lot of mineral dissolution happens in this zone.
4th: Surface zone.
-It's the intact surface layer of the incipient lesion. If there's no intact layer…this wouldn't be classified as an incipient lesion but it'll be classified as a cavitation; because the incipient lesion must have an intact layer.
-It contains pores but they're much less than the rest of zones.
-It's hypermineralized; this helps it to stay intact. Intact surface of incipient lesion is much more mineralized than the intact surface of enamel.
-The surface layer of the incipient lesion is a kind of immunity towards the progression of this lesion but this surface if it's lost, there'll be a very rapid progression of the caries.
-Some people say that the surface layer is not very important by itself but just it protects the surface from being cavitated, that's why it's important. There's nothing special about the surface layer. It's about the protection to the underlying demineralized body of lesion.

 Dentinal Caries:
-Whenever there's breakage for the surface layer, very rapid progression to the DEJ occurs (lateral spread in DEJ). Then the dentin lesion starts and the progression in dentin is much more rapid than that of enamel due to many things; especially the less mineral content of dentin.
-In dentin, there is variety of symptoms that would happen: pain is a symptom but it's not a commonly encountered symptom.
-Demineralization & remineralization also occur in dentin.

*Zones of dentin:
-1st zone: Normal dentine.
-everything in this layer is normal; normal peritubular dentin, normal intertubular dentin…etc.
-No crystals in the lumen>> so dentinal tubules' lumens are open.
-No bacteria in the tubules.

2nd zone: Subtransparent dentin.
-It's located below the transparent dentin.
-It has demineralization especially in the intertubular dentin. Not in the peritubular dentin but why?? Because the peritubular dentin is much more mineralized than the intertubular dentin and the demineralization starts in an area that's less resistant to acid attacks.
-This zone is the advancing front>> so it goes with the least resistant to acid attacks which is the intertubular dentin first, and then in the peritubular dentin in the next zones.
-There'll be an initial crystal formation in the lumen at the advancing front; these crystals represent remineralization. >> so formation of crystals is a sign of remineralization .
>>So there're two signs; demineralization & remineralization at the same time.
-There would be some damage to the odontoblastic processes; because the odontoblastic processes are very sensitive. If any stimulus or any irritant applied on the surface, the processes will retract from the dentinal tubules or there would be some damage to them.
-There are no bacteria in this zone.

3rd zone: Transparent dentin.
-Lies above the subtransparent dentin.
-The intertubular dentine in this layer has lost its minerals.
-Crystals present inside the lumen but dentin is soft whereas in the subtranparent zone, it's not soft. The loss of minerals didn't significantly affect the hardness of dentin but in the transparent zone it did affect.
-There's no bacterial penetration.
-The picture in slide#24>>look at the pointer that indicates the reparative dentin>> it could be reparative or normal dentin. If it's not located very close to the pulp, you may find tertiary dentin or more formation of secondary dentin. (Notice that the secondary or tertiary dentin is normal dentin not carious dentin).


-Collagen cross-linking in this layer is still intact>> it serves as an intact scaffold; something to hold the minerals and ions on. But if there's no scaffold that holds the ions in a neat organized matter, remineralization won't happen. In dentin the organic matter is the collagen; collagen fibers are cross-linked. If this cross-linkage is disturbed or damaged, there'll be no remineralization>> we'll move to the irreversible phase of caries>> so the transparent dentin is so far good.
-4th zone: Turbid dentin.
-As the name indicates; turbid means that there's something inside. >> So bacteria start to penetrate inside this layer. This is the first layer of bacterial penetration.
-There would be some widening and distortion in the dentinal tubules.
-Dentinal tubules don't contain minerals or contain little>> so loss of minerals takes place in this zone.
-Collagen is irreversibly denatured; so there's no remineralization.
-It's not capable of self-repair.
-5th zone: Infected dentin.
-In this stage everything is disturbed.
-Denaturation of collagen, minerals are lost. It's like a granular mass of bacteria and its by-products.
-It's very soft layer.
-This infected layer of dentin should be completely removed during cavity preparation.
 Affected Vs. Infected:
-Infected dentin: there's bacterial penetration (Zone 4 & 5).
-Affected dentin: this dentin is demineralized but there's no bacterial penetration (Zone2 & 3).
* During cavity preparation, usually we remove the infected dentin and leave the affected dentin without doing anything to it because it doesn't contain bacteria and as we remove the infected dentin, we remove the all of the bacteria>> by doing that, we stop the caries process and then we add a restorative material. But if we remove the affected dentin, this results in an unnecessary cutting.

Q: The affected dentin, how could it be demineralized without the presence of bacteria?
A: This lesion on dentine. The bacteria present on the surface but it starts to make demineralization far away from bacterial penetration, why?? Because in dentin there're many opened-dentinal tubules. The acid that's released from bacteria will enter dentinal tubules and make demineralization before it reaches the dentin.
Q: The affected dentin is weak, how could we add restoration on something weak?
A: Not necessarily, in affected dentin there're two layers; the transparent layer has some softness but the subtransparent is hard. Even the softness that present in the transparent layer is not significantly enough to cause fracture of the restoration.

 Defense mechanism:
1-There're mild, moderate& severe irritants and the reaction of the pulp matches the severity of the irritant.
2-There're reactions for long term low level acid demineralization associated with the slowly advancing lesion.
3- The pulp could react to moderate intensity attacks; also it may react to severe advanced caries characterized by very high acid levels.
-In the 1st & 2nd levels, the pulp may form tertiary dentin, sclerotic dentin, deposition of more minerals…etc. So if the peritubular dentine and the intertubular dentin are filled with more minerals, there would be less irritation to the pulp because the lumen of dentinal tubules will be less (decrease the diameter of lumen causes decrease in the flow of fluids). >>So very much less pain and sensitivity to the pulp.
-All these defense mechanisms occur as long as the pulp is vital. If the pulp is non-vital, there's no defense mechanism.

* Wafa'a Isaid
* Lec#7
*Date of the lec. 1.11.2010