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Seminar On


Presented by : -


INTRODUCTION: As we all know, Dental caries is the most common cause of tooth destruction, necessitating operative procedures. However, it has been estimated that 25% of tooth destruction does not originate from caries process. Tooth structure can be lost after its formation by a variety of influences. It is convenient to describe the mechanisms by which tooth tissue is lost other than by caries, trauma or operative procedures as three separate entities namely Attrition, Abrasion and Erosion. These mechanisms often act independently but it is also possible for them to occur in combinations. The three together are termed as wasting diseases and may cause injury to the pulp or affect the esthetics of tooth. The first study on these lesions was conducted by Miller in the year 1907 Tooth tissue loss can be either physiologic or pathologic. A limited degree of tooth wear or alterations in teeth must be accepted as a normal age related change in older patients. On examination of such a patient, if it is found that the patient is left with a dentition that remains functional, symptomless and of reasonable appearance, then the wear may be considered to be physiological or within acceptable limits. If bone wear has already produced an unsatisfactory appearance, sensitivity, or mechanical problems such as reduction in occlusal vertical dimension or very thin teeth, then the process is considered pathologic. Apart from the alterations of the tooth occurring due to wearing of tooth structure, some alterations may be the result of abnormal influence of environmental forces or due to hereditary factors during the development of teeth.


DEFINITION : Tooth tissue loss for reasons other than caries, trauma or operative procedures

Pathological tooth wear : 1. Pulp exposure 2. Loss of vitality 3. Exposure of tertiary dentin 4. Exposure of dentin on buccal / lingual surface 5. Notched cervical surface 6. Cupped incisal / occlusal surface 7. Wear of one arch more 8. Inability to make contact in excursion of mandible 9. Restoration projecting above tooth surface 10. Persistent sensitivity 11. Decrease in length – out of proportion to width Predisposing factors for tooth substance loss : 1. Developmental anomalies 2. Malocclusion / posterior tooth loss 3. Parafunctional habits 4. Restorative materials 5. Diet 6. Systemic disease 7. Natural wear & tear Etiology for tooth substance loss : According to recent concept it is multifactorial , as lesions can occur alone or in combination with each other.

Attrition / Abrasion : Endogenous Parafunction 3

Degluttion Exogenous Mastication Dental hygiene Habits Occupational Dental appliance

Abfraction : Endogenous Parafunction Occlusion Degluttion Exogenous Mastication Habits Occupation Dental appliance

Erosion : Endogenous Plaque GCF Gastric juice Exogenous Diet Occupation Drugs / alcohol


i. ATTRITION : Attrition may be defined as surface tooth structure loss resulting from direct frictional forces between contacting teeth. Attrition is a continuous, age-dependent process, which is usually physiologic. Any contacting tooth surface is subjected to the attrition process, beginning from the time it erupts in the mouth and makes contact with a reciprocating tooth surface. Attrition affects occluding surfaces and results in flattening of their inclined planes and in facet formation. In severe cases, “a reverse cusp� situation might be created in place of the cusp tips and inclined planes. Attrition also affects proximal contact areas; leading to flat, faceted proximal contours, and in some situations, concave proximal surfaces. Attrition is accelerated by parafunctional mandibular movements, noticeably bruxism. Although every person has some signs and symptoms of attrition in their dentition, attrition can predispose to or precipitate any of the following : A. Proximal surface attrition (Proximal surface faceting): This results from surface tooth structure loss and flattening, widening of the proximal contact areas.

Because of this process, the surface area

proximally, which is susceptible to decay, is increased in dimension. At the same time, cleansability will be hindered due to the decrease in dimensions of the surrounding embrasures. Also, the mesio-distal dimensions of the teeth are decreased, leading to drifting, with the possibility that occluding tooth elements will not be physiologically indicated. This mesio-distal reduction of teeth dimensions will lead to overall reduction of the dental arch length, with all its sequelae. Finally, due to the


above-mentioned situations, the interproximal space will be decreased in dimensions, thereby interfering with the physiology of the interdental papillae. This is coupled with the difficulty of plaque control there, that can lead to periodontitis. B. Occluding surface attrition (occlusal wear) This is the loss, flattening, faceting, and/or reverse cusping of occluding elements. This process can lead to loss of the vertical dimension of the tooth. If the wear is severe, generalized, and accomplished in a relatively short time, there would be no chance for the alveolar bone to erupt occlusally to compensate for the occlusal tooth loss. In this case, the vertical loss might be imparted on the face as a loss of vertical dimension. Both situations will result in overclosure during mandibular functional movements. This situation can strain areas in the stomatognathic system, which is not otherwise capable of withstanding these stresses. On the other hand, if the loss occurs over a long period of time (ten years and more), the alveolar bone can grow occlusally, bringing the teeth to their original occlusal termination. In other words, the vertical dimension loss will be confined to the teeth but not imparted to the face. Deficient masticatory capabilities of the teeth can also result from occlusal wear. Blunting (flattening) of the cusps will compel the patient to apply more force on the teeth in an attempt to shear food items into swallowable dimensions. These forces can non-elastically strain the muscles, the teeth (leading to more attrition), the periodontium and the joints. Cheek biting (cotton roll cheeks) is another sequela of occluding surface attrition. With the flattening of cuspal elements through the attrition process, the vertical overlap between the working inclined planes will be lost. This will cause surrounding cheek, lip, or tongue tissues to be fed between the teeth, with a possibility of their being crushed and contused during dynamic tooth contact.


Gingival irritation can also occur, due to food impaction and the closeness of the occlusal table to the gingiva. Decay, as a result of the attrition of the enamel at occluding areas, can occur, because the underlying dentin will be exposed and thereby become more susceptible to decay. This susceptibility is decreased, to some extent, by the high cleansability of the occluding areas (more frictional movements). However, when the attrition creates "reverse" inclined planes or "reverse" cusps, the decay susceptibility will increase. Tooth sensitivity is a symptom that can be due to many factors precipitated by the attrition process, e.g., dentin exposure, pulpal and apical strangulation due to excessive non-physiologic forces, tearing of the periodontal ligaments resulting from the same forces, microcracks (crazings) and stagnation of irritating substrates on the created flat or concave areas of dentin. Usually, the occluding surface will not undergo symmetrical attrition on both sides of the dental arch, or on opposing arches. As a result, unworn occluding areas will act as interfering (deflecting) points for physiologic mandibular movements. TMJ problems can be elicited by one or all of the aforementioned factors, especially the overclosure situation. This condition will overstretch the joint ligaments. Similarly, stomatognathic system musculature problems can be expected as a result of one or more of the aforementioned factors. After severe occluding surface attrition, a predominantly horizontal masticatory movement of the mandible occurs. This type of movement is due to the flat-planed occluding surfaces. To effect some sort of shearing action between opposing teeth, the mandible must be moved farther horizontally, so that the flat-planed teeth can deliver a shearing load on the intervening bolus of food. This horizontal movement can cause extreme strain of the muscles of the stomatognathic system.


Modes to detect attrition : 1. Broca method 2. Photographic & plainimetric method 3. 3 D digital imagery ATTRITION INDEX ( mod. By Richard & Brown ) 0 – No wear 1 – Minimal wear 2 – Noticeable flattening parallel to occlusal plane 3 – Flattening of cusps & grooves 4 – Total loss of contour & / or dentin exposure when identifiable Tooth wear in general with erosion as one of its component Ratings


satisfactory Romeo (R)

No visible wear or change in anatomic form

Sierra ( s)

Limited wear & change in anat. Form

Mike (m)

Considerable wear & change in anat. Form but no treatment

Not acceptable Tango ( t)

Considerable wear & change in anatomic form Further damage to tooth & surrounding tissue.

Victor (v)

Excessive wear , extreme change in anat form Esthetics , function.. Pain on chewing. Damage To the tooth & surrounding tissue

Tooth wear index :


Tooth wear index Score / surface



B / L/ O / I C

No loss of enamel surface characteristics No change of contour



Loss of enamel surface characteristics Min.loss of contour



Loss of enamel exposing dentin ( < 1/3 of surface ) Loss of enamel just exposing dentin Defect less than 1mm deep



Loss of enamel exposing dentin ( > 1/3 of surface ) Loss of enamel & dentin but not exposing pulp Defect 1-2 mm deep

B /L/O I C

Complete loss of enamel or pulp exposure Exposure of pulp / secondary dentin Defect > 2mm deep / pulp or secondary dentin exposure


B – buccal / L – lingual / O – occlusal / I – incisal / C cervical

Treatment Modalities: Attrition can occur in degrees, from involvement of only one inclined plane to involvement of all occluding surfaces, and from fractional tooth loss to loss of the whole crown portion of the tooth. Sometimes, surface attrition is slower than, and compensated by, intrapulpal deposition of secondary and tertiary dentin. At other times, the attrition is faster than the intrapulpal dentin deposition, leading to direct pulp exposures. In many situations, the pulp-root canal tissues undergo irreversible pathologic changes long before they are perforated (due to cracks and strangulation). Therefore, treatment must involve several modalities, which should be chosen and initiated in the following sequence: 1. Pulpally involved teeth should be extracted, or undergo endodontic therapy, according to their restorability and future role in the stomatognathic system. 9

2. Parafunctional activities, notably bruxism, should be controlled with the proper discluding-protecting occlusal splints. 3. Myofunctional, TMJ, or any other symptoms in the stomatognathic system should be diagnosed and resolved. Sometimes, simply modifying the discluding occlusal splint used in (2) can be the treatment modality resolving both situations. 4. Occlusal equilibration should be performed after all notable symptoms are relieved. Occlusal equilibration might be the only treatment needed, if lost tooth structure is minimal and if remaining structure can be reshaped to effect physiologic, mandibular movements. Occlusal equilibration, by selective grinding of tooth surfaces, should include rounding and smoothening the peripheries of the occlusal tables. Also, one should create adequate overlap between the working inclines. Both features are essential to prevent further cheek biting. 5. During the last three procedures, exposed sensitive dentinal areas should be protected and actual carious lesions should be obliterated. Protection can be accomplished using fluoride solution. The obliteration is achieved by a proper temporary restoration. Also, during the same procedures, the periodontium should be examined and any pathology should be treated. Fortunately, with extreme loss of clinical crown and vertical dimension, the crown: root ratio becomes very favourable, enhancing the health of the periodontium (except when the substantial occluding forces are applied horizontally and/or on the completely flattened inclined planes). 6. Restorative modalities can now be initiated. Lost tooth structure due to attrition is at high stress concentration areas. Therefore, only metallic (metallic-based) restorations should be used to replace them. Restorations are only needed in the following situations: a. Noticeable loss of vertical dimension that has not been compensated for, and that should be regained to effect a physiologic status in the stomatognathic system.


b. There is extensive loss of tooth structure in a localized or generalized fashion, necessitating restoring the tooth (teeth) to form and function. c. Reshaping remaining tooth structures would not, in and of itself, be conducive to occluding inclined planes working in harmony in creating a physiologic mandibular movement. d. Decay or any other cavitating lesion is superimposed on the attrition reduction of a tooth surface. e. Worn tooth contour (usually proximally) is not conducive to proper maintenance of the periodontium. f. A tooth is cracked or endodontically treated. The most involved restorative modalities are those used to regain lost vertical dimension. They should be accomplished very cautiously and carefully in the following sequence. Verify and reverify its necessity, i.e., be sure that the alveolar bone did not grow occlusally at the same pace that attrition occurred, because, if the alveolar bone did grow occlusally, bringing the occlusally worn teeth to their customary occlusal location, any building-up restoration could impinge on the freeway space, eliciting and/or aggravating bruxism or other parafunctional habits. Estimate how much vertical dimension was lost. This can be determined by measuring the vertical dimension for the patient in the same way it is determined for a full denture construction (from the nasion to the gnathion), and by measuring the vertical dimension, when the patient brings the teeth together. The difference between these two measurements minus the customary measurements for the free-way space (2-3 mm) can give us an estimate of how much we should increase the height of the worn clinical crowns. Estimate how much additional vertical dimension the stomatognathic system can accommodate without untoward effects. It is a well established fact


that not all the lost dimension can be tolerated by the stomatognathic system, especially if attrition has occurred over a long period (more than 15 years), because there is a certain permanent physiologic accommodation which should not be disturbed. Therefore, if a substantial increase in vertical dimension is planned (more than 2 mm), it is a wise idea to build a temporary restoration or a removable occlusal splint that can be easily adjusted through subsequent addition or removal of material. Modes of increasing the vertical dimension : 1. crowning or composite build up incrementally till patient can accommodate the increase physiologically. 2. orthodontic intrusion / use of Dahl appliance that is attached to the palatal surface of anteriors thus a space is created in the posteriors so the posterior teeth erupt occlusally to fill the space and come to occlusion thus creating a space in the anteriors. 3. exploiting the horizontal difference between retruded contact position and intercuspal position. 4. canine raising : material is added on the canine only to disocclude it thus creating space. Composite (resinous) temporary restorations are most frequently used. They may be retained by etched enamel or extracoronally prepared teeth. With these temporary restorations, establish the minimum increase in vertical at the beginning, periodically adding to it. However, before any addition, the entire stomatognathic system should be examined to verify that it is tolerating the previous vertical dimension and is ready for an increase. This process is continued until symptoms of intolerance are observed. At that point, it is necessary to minimally reduce vertical, until these symptoms disappear. The vertical dimension thereby created is the one to which permanent restorations should be built. The permanent restoration should be done in a cast alloy (cast alloy based) material. A fully adjustable articulator, hinge axis determination, and


use of pantographic (stereographic) tracing and facebow records are essential for such cases. These restorations should be cemented only temporarily for an extended period of time, until it is established that no untoward symptomatology will occur. It should be mentioned here that cases necessitating this treatment modality are rather rare, and all the teeth are usually involved. Patients restored in this way should undergo periodic occlusal equilibration for these restorations after cementation, and they should be warned about possible separation between the teeth as a result of encroaching on the free-way space together with the bruxing nature of these dentitions. In most situations, no vertical dimension increase is needed. Restorations may still be needed for the other indications, mentioned, and in these cases it is preferable to use cast alloy (cast alloy based) restorations to preserve the remaining tooth structure and to assure the integrity of the supporting tissues. Because of the short crowns in these cases, it may be necessary to use intraradicular retention means, with or without devitalizing the teeth. Also, extracoronal retention may be the one of choice here to affect the change in the contour and occluding surfaces, in addition to attaining sufficient retention. Splinting of these worn teeth via a cast restoration may be indicated in these situations to increase the resistance-retention forms and also to minimize displacement of teeth after restorations with increased vertical dimension are built. In cases with a carious lesion or defects superimposed on attrition facets, if the dimension of the lesion is very limited (as usual) and there is sufficient tooth structure around it to accommodate walls, amalgam or direct gold can be used to restore them. If no walls can be created, a cast alloy restoration has to


be used. Again, most cases will only need occlusal equilibration and nonrestorative protective measures for the exposed dentin. II. ABRASION : Abrasion can be defined as the surface loss of tooth structure resulting from direct frictional forces between the teeth and external objects, or from frictional forces between contacting teeth components in the presence of an abrasive medium. Abrasion is a pathologic process, which is usually inseparable from attrition and/or erosion. Although abrasion, like attrition, can stimulate the formation of dentin intrapulpally, causing recession of the pulp and root canal tissues away from the advancing lesion's pulpal limit, sometimes the abrasion rate is faster than the dentin deposition rate. The result is direct or indirect pulpal involvement. Also, many abrasion lesions are close to the gingiva, so plaque control measures can be hindered by abrasion in these areas. The most predominant abrasion is toothbrush abrasion, occurring cervically, usually to the most facially prominent teeth in the arch (canines and bicuspids). It is usually on the left side for right-handed individuals and vice versa for left-handed people. It progresses very quickly, when the gingiva recedes, exposing root cementum and dentin facially. Tooth brush abrasion's surface extent, depth, and rate of formation is dictated by: a. The direction of brushing strokes. Horizontal directions are the most detrimental. b. The size of the abrasive. The larger and more irregular that the abrasive particles are, the more abrasion there will be. c. The percentage of abrasives in the dentifrice. The higher that the percentage is, the more abrasion there will be.


d. The type of abrasive, e.g., silica abrasives are much more abrading than phosphate and carbonate ones. e. The diameter of brush bristles. The greater that this diameter is, the more abrasion there will be. f. The type of bristles. Natural bristles are more abrasive than synthetic (mylar) ones. g. The forces used in brushing. Of course, more the force used, especially in the horizontal direction, the more abrasion there will be. h. The type of tooth tissues being abraded. The most resistant tissues to abrasion are enamel, especially occlusally. The least resistant is cementum. Dentin, especially cervically, can be very easily abraded. The clinical signs and symptoms of toothbrush abrasion are very characteristic: 1. The abrasive lesion may be linear in outline, following the path of the brush bristles. 2. The peripheries of the lesion are very angularly demarcated from the adjacent tooth surface. 3. The surface of the lesion is extremely smooth and polished, and it seldom has any plaque accumulation or carious activity in it. 4. The surrounding walls of the abrasive lesion tend to make a V-shape, by meeting at an acute angle axially. 5. Probing or stimulating (hot, cold, or sweets) the lesion can elicit pain. Other forms of abrasion: Pipe smoking or "depression abrasion", is an abraded depression on the occluding surfaces of teeth at a latero-anterior portion of the arch coinciding with the intraoral location of the pipe stem, results from intrusion and abrasion of the tooth. Chewing tobacco, can create a generalized occluding surface abrasion.


Forcing a toothpick, interdental stimulator, or other solid plaque control modes interproximally can create different forms of proximal abrasion. Certain professional habits, such as cutting sewing thread with incisor teeth, holding and pulling nails with front teeth, or abrasives in the working environment itself, can each create a specific localized or generalized form of abrasion. Pica-syndrome, which is due to the habit of chewing clay (mud), has a specific occlusal abrasion pattern, and other systemic disorders. There are some iatrogenic tooth abrasions, such as dentures with porcelain teeth opposing natural teeth, or using cast alloys having an extremely higher abrasive resistance than tooth enamel in a restoration opposing natural teeth, or extremely rough occluding surfaces of a restoration enhancing its abrading capability. This latter situation can create abrasion, even if the restorative material is less abrasive resistant than the tooth. Abrasions caused by these iatrogenic factors can be even more destructive if the restoration has occlusal interferences built into it. Treatment Modalities : After confirming the diagnosis, treatment of abrasion should be pursued in the following sequence: 1. Diagnose the cause of the presented abrasion. There is no use in treating and restoring the teeth if the cause of the abrasion is still in action; otherwise the restoration will be abraded, opposing natural teeth could be abraded, the teeth could move, or the alveolar bone might be resorbed. 2. Knowing the causative factors first correct or replace the iatrogenic dental work. Second try to prevent the patient from practicing the causative habits. If successful in this persuasion, proceed with the restorative treatment as planned.


3. If the habit (practice) cannot be broken, restorative treatment can by-pass the effect of the habit. In other words, if it is localized and not interfering with the physiologic function of the stomatognathic system, endangering the P-D organ. and or the periodontium, (e.g.. pipe smoking anterolateral concavities or other localized forms of abrasion) it may be included in the restoration. The objective of the restoration should be to prevent further destruction of the tooth. Any attempt to restore the tooth to its ideal shape will concentrate intolerable forces (especially abrading ones) on the restoration, with unpredictable and often unfavorable results. If the abrasion is generalized and substantial, the habit (environment) should be discontinued (controlled) by any possible means, because the restorative treatment will involve restoring the teeth to normal configurations in order to establish a functional environment for the stomatognathic system. 4. Abrasive lesions at non-occluding tooth surfaces should be critically evaluated for the need for restoring them. If the lesions are multiple, shallow (not exceeding 0.5 mm in dentin) and wide, there is no need to restore them. If they involve cementum or enamel only, there is no need to restore them. If a restoration is not indicated for the lesion, the edges of the defect should be eradicated to a smooth, non-demarcating pattern relative to adjacent tooth surface. This is done for esthetic and plaque control reasons. The tooth surface then should be treated with fluoride solution to improve its caries resistance. However, if the lesion is wedge (v)-shaped and exceeds 0.5 mm into dentin, it should be restored. 5. If the involved teeth are extremely sensitive, it is preferable to desensitize exposed dentin before restorative treatment is started. This may take several visits. As in many situations, if the sensitive teeth are restored immediately, they will remain sensitive to thermal changes forever. Desensitization can be accomplished by fluoride solution application (8-30% sodium or stanneous fluorides for 4 to 8 minutes), or ionophoresis using an electrolyte containing fluoride ions (galvanic energy supplied to the tooth in the presence of the electrolyte drives the fluoride ions deep into the dentin).


6. Restorative treatment If the abrasive lesion involves an anterior tooth or facially conspicuous area of a posterior tooth, at a non-occluding tooth surface, the restoration can be done in one of the direct tooth-colored materials. In most cases no cavity preparation is needed, if any of the physico-chemically adhering direct tooth-colored materials is used. Similar lesions which involve a non-conspicuous area in a posterior tooth, should be restored with a metallic restoration. If the cavity preparation to accommodate it will impinge on the pulp and root canal system the situation can make the tooth sensitive forever or compromise the P-D organ vitality. In this case, one should use one of the physico-chemically adhering direct toothcolored materials. Although the latter may .not be very durable in posterior teeth, their frequent replacement will be a safer treatment modality than encountering the dangers stemming from a cavity preparation and a metallic restoration there. The restorative treatment may then proceed in the same fashion as detailed for treatment of attrition lesions. III. Erosion :

loss of tooth structure resulting from chemicomechanical acts in the absence of specific microorganisms Until now there is no convincing etiology for erosion. It seems that, like decay, it is caused by multiple factors. Many authorities theorize causes and pathogenesis for erosion, but none can explain the process fully. Of these theories the following are most popular: A. Ingested acid : Ingested acid, with emphasis on citric acid (lemon and citrus fruits), especially if used in large amounts, can participate in or initiate the erosive lesion. Also, other acids, as found in certain beverages and mouth fresheners (deodorizers) can contribute to the erosive process.


B. Salivary citrates : Some authorities have found a correlation between the number and dimensions of erosive lesions and salivary citrates. Others have disproved this correlation. C. Secreted acids : Acids exist in the gingival crevice, due to the occlusal traumatism (bruxism, interferences, or excessive discluding forces). This acidity of the crevicular fluid has been correlated to both occlusal traumatism and to cervical erosion. Although this acidity cannot be fully responsible for an erosive lesion. it can be a participating factor. D. Mechanical abrasion : Abrasion cannot explain the characteristic nature of erosive lesions, it can be a contributing factor. E. Chelating microbial metabolic products : The most prominent product that has been correlated to the erosion processes is pyrophosphate, and although the correlation is not conclusive, it could be one of the contributing factors. F. Acid fumes : Environmental acid fumes has been statistically correlated to the number of erosive lesions in certain populations. G. Excessive tensile stresses at the tooth clinical cervix : Non-elastically deforming tooth contacts, which could be premature or heavy centric, immense working, or balancing, may precipitate intolerable tensile stresses at the tooth cervix, especially facially. The brittle enamel veneer being thin and terminal at this area, could have it's prisms separated from each other, and from underlying dentin. Subsequently it could, be peeled off, or


acquire cracks through which acids penetrate and attack. Both lead to the characteristic wedge shape of some erosive lesions. H. Refused acids : As a result of chronic, frequent regurgitation (forced or non-forced), the stomach's hydrochloric acid can hit the teeth at specific locations, creating a very characteristic type of erosion (lingual surface of the upper teeth, especially molars and premolars. I. Salivary flow : The pattern of the salivary flow, as related to intraoral frictional contact between the moving soft tissues and tooth components. is a very interesting and unusual approach to explaining the pathogenesis of erosive lesions. There have been many attempts to morphologically and therapeutically classify erosive lesions, but none are able to encompass all reported varieties. Acc . to watson & burke(2000) erosion can be classified as :

Extrinsic 1. Environmental 2. Diet 3. Medication 4. Life style

Intrinsic â&#x20AC;˘ Gastric reflux sphincter incompetence inc gastric pr. inc gastric vol. â&#x20AC;˘

Vomiting psycosomatic GI disorders drug induced





Rumination Nomenclature & classification Etiology Extrinsic environment diet medication lifestyle Intrinsic Idiopathic Clinical severity of tooth surface Superficial Generalized Localized Pathogenecity Manifest / active Latent / inactive localization Palatal / occlusal surface of max . Buccal / occlusal surface of mand.


The erosive lesions are pathognomonic in the following aspects: 1. There is no demarcation between the lesion and the adjacent tooth surface, i.e., an explorer can be passed without any interruption from the lesion to the tooth surface. 2. The lesion surface is glazed. 3. Erosion usually does not affect occluding surfaces, except in very advanced situations, and then only indirectly. 4. The erosion rate is the same for enamel, dentin. and cementum, and, sometimes, for restorative material. 5. The P-D organ reacts by both healthy and unhealthy reparative reactions to the stimulation of the erosive lesion. 6. Adjacent gingiva and periodontium are almost always sound and healthy. 7. Tooth sensitivity to physical, chemical, and mechanical stimuli is always evident and the main complaint of the patient. 8. Carious lesions do not usually occur at tooth surfaces attacked by erosion. Erosion usually affects people with good oral hygiene. However, it has been reported in patients with a high plaque index. The rate of erosion in active lesions was estimated to be 1 micron per day. Therefore, perforation to the pulp chamber or root canal is very rare with erosive lesions, as the stimulated secondary and tertiary dentin is usually produced at a faster rate than that (1.5-4 micron/day). Erosion affects upper teeth more than lower teeth, especially attacking the facial surface of cuspids and premolars. The lower anterior teeth facially are a common location for erosion. Topographically, the extent of teeth involvement with erosive lesions can range from a fine unnoticeable line at the cemento-enamel junction to substantial tooth-substance loss making an hour-glass shape out of a tooth. Some times attrition, abrasion, and erosion may work together in creating lesions in teeth, and when all three of these processes are combined, the destruction can be detrimental and rapid.


Treatment Modalities : Although the exact cause for erosion is not known, complete analysis of diet, occlusion, habits, chronic vomiting and environmental factors should be performed for patients exhibiting these lesions. Every attempt should be made to correlate the presence of the lesions to possible causes. After this initial correlation, try to eliminate the causes. The patient should be informed that this may not be the cause, but it is the most probable one. He should be told that the treatment to be pursued is mainly symptomatic, and that corrective therapy will, by no means, stop the disease. He should also be told that the process could recur, not only affecting tooth structures, but the restorative material, as well. Preoperative study models or photographs should be taken and kept for future references. This is to evaluate the progress of the lesion, if no restoration is the treatment modality, and to see the extent of recurrence, if a restoration is the treatment modality. There should not be any rush to attempt restorative modalities, except in extremely symptomatic or disfiguring lesions. It is preferable to observe the rate of the lesion's progress and, according to this observation, choose the most appropriate restorative procedure, or decide if treatment is even indicated at all. The rest of the treatment is exactly as described for abrasion and attrition, except that, if possible, metallic restorations should be the material of choice if restorations are indicated. Metallic restorations have proven to be more resistant to the erosion process than non-metallic ones. Tooth-colored materials capable of chemicophysical bonding to tooth structure can also be used with minimum or no tooth preparation, with the assumption that the restoration may require periodic replacement. The use of these materials is especially indicated when the erosive lesion is extremely deep, badly disfiguring, or when it is expected that the 23

underlying pulp-dentin organ is undergoing advanced degeneration. Again, all this should be done with the understanding that the lesion might progress around these restorations and even involve them. IV. ABFRACTION : Definition : Abfraction is described as wedge shaped defects in the cervical region of the tooth and are hypothesized to be the result of tensile stresses concentrated in this cervical area. The term abfraction was given by â&#x20AC;&#x153;Gippoâ&#x20AC;? to distinguish it from Abrasion and Erosion.

Etiology : The etiology of these lesions is somewhat controversial. Many of these cases cannot be associated with acid exposure or mechanical abrasion and have been termed as Idiopathic Cervical Erosions. In the recent years, investigators have proposed that these defects are created from the occlusal stresses that cause the tooth to bend. This flexure of the tooth from occlusal trauma or stress causes stress concentration at the cervical portion of the tooth disrupting the chemical bonds of the enamel and dentin resulting in loosening and gradual loss of enamel rods. This damaged portion in the cervical area then demonstrates an increased susceptibility to dissolution and abrasion. Mechanism of Formation of Abfraction Lesion : Normally, during mastication, when moving from working side to centric occlusion, lingual slopes of the maxillary cusps contact buccal slopes of


the mandibular cusps. This contact serves as an inclined plane and forces are generated perpendicular to the tangents drawn from the respective cusps. When these eccentrically placed lateral forces are resolved into their two components, the vertical component is directly along the long axis of the tooth and is well tolerated because it is compressive in nature, where as horizontal component is perpendicular to the long axis. In a net result, the transverse force is responsible fro creating deflection / flexure in the tooth structure i.e. the tooth is compressed primarily on the side towards which it is being bent and is subjected to tensile stress on the side away from the direction of bending. For example, in lingually directed forces in a mandibular molar, lingual portion of the tooth is compressed while the buccal portion is stretched, with he fulcrum at the cemento-enamel junction. The region under greatest tensile stress is that closes to the fulcrum, while regions of greatest compressive stress are the occlusal contacts, fulcrum and the apex of the root. Generally, these forces in ideal occlusion create deflection, which is within the tolerable limits of the tooth. However, the magnitude of traverse force (shown for buccal cusps only in the diagram) and the consequent bending movement increases with excessive cuspal slope and/or lingual inclination of the mandibular teeth. Also, masticatory forces in individuals with hyper or malocclusion and parafunctional forces in bruxism may expose one or more teeth to strong lateral forces beyond the capacity of the teeth to withstand, resulting in cervical lesions. Characteristics of Abfraction Lesion : 1) It is always at or near the fulcrum 2) Typical wedge shaped lesion with sharp line angles and is the area of greatest tensile stress concentration. 3) Direction of lateral forces determines the location of lesion. i.e. Number of lesions on same tooth depends upon the number of direction of lateral forces.


4) Size of lesion is determined by the magnitude and frequency of applied tensile force. This Abfraction is not the whole source to produce a cervical lesion. This may be a contributing factor in the formation of the lesion. It must be noted that in all lesions, the concomitant effects of biochemical i.e. salivary ion exchange, which in some instances enhanced by stress corrosion and bioelectric activity are evident and unavoidable.

Classification for treatment Tooth surface loss Localized Generalized Category 1 : Appearance satisfactory Category 2 : Appearance not satisfactory no increase in occlusal ht. req. Category 3 : Appearance not satisfactory increase in occlusal ht. req. i ) sufficient space present ii ) insufficient space present Category 1 • Counseling • Restoration of edentulous space • Control of habits ( bruxism ) • Elimination of occlusal interference • Routine restorative procedures Category 2 26

• Same as above • Counseling • Restoration • monitoring Category 3 • Increase in occlusal vertical dimension • Space obtained by 3 ways Type of restoration • Metal ceramic or gold full coverage posterior rest. • Short crown height • Occlusal build up • Anterior teeth V. DISTURBANCE IN THE STRUCTURE OF TEETH : Enamel is normally formed by the specialized odontogenic epithelial cells called ameloblasts and the entire process of formation of enamel takes place in three distinct stages, which are as follows : Stage I : (Secretary stage) : Enamel matrix formation. Stage II :

: Initial mineralization

Stage III

: Enamel maturation

Enamel matrix formation : In the first stage or Secretary stage the ameloblasts cells cause synthesis and secretion of special proteins namely the amelogenins and enamelins. These two proteins constitute the basic structural elements of the enamel matrix. Initial mineralization :

Initial mineralization starts immediately after the

secretion of enamel matrix proteins and after that enamel microcrystals start to abut the plasma membrane of the ameloblasts cells. 27

Maturation: The stages of maturation is characterized by simultaneous dual activity of withdrawal of protein and water from enamel with concomitant huge increase in its mineral content. All these three stages are completed before the eruption of the tooth in the oral cavity. During the process of enamel formation, the ameloblasts cells are susceptible to various external factors, which can disturb the process and the effect of which is reflected on the surface enamel after the eruption of tooth. Defect in the enamel due to disturbance during its formative process can be either qualitative or it can be quantitative.  Quantitatively defective enamel having normal thickness is known a Enamel Hypoplasia.  Qualitatively defective enamel having normal thickness is called Enamel Hypocalcification. Therefore, depending upon the stages of formation of enamel the defects, which may occur in it under the influence of the external factors, are as follows; Defective Amelogenesis:  Matrix formation – Enamel hypoplasia  Initial mineralization – Enamel hypocalcification  Maturation – Enamel hypomineralization Environmental Enamel Hypoplasia : Enamel hypoplasia may be defined as an incomplete or defective formation of the organic enamel matrix of teeth. Two basic types of enamel hypoplasia exist: (1) a hereditary type, described under Amelogenesis imperfecta, and (2) a type caused by environmental factors.

In the hereditary type, both the deciduous and

permanent dentitions are usually involved and generally only the enamel is affected. In contrast, when the defect is caused by environmental factors,


either dentition may be involved and sometimes only a single tooth; both enamel and dentin are usually affected, at least to some degree. Localized Non-Hereditary Enamel Hypoplasia : The ameloblasts that are responsible for forming the enamel are very easily injured. During enamel formation, if these cells are irritated, their metabolic product, i.e., the enamel matrix, will not be properly formed, causing certain interruptions and defects. In certain areas, there may be no enamel at all. When the teeth erupt, these defects will be apparent in the crown portion of the tooth (teeth) and this is called localized, non-hereditary enamel hypoplasia. Lesions range from isolated pits to widespread linear defects, depressions, or loss of a segment in the enamel. These defective areas will have different colors from the surrounding enamel, and the discoloration will increase with age, due to their easy stainability from the environment. At some stage of the tooth's life, the tooth crown will probably look objectionable. In mild environmental hypoplasia, there may be only a few small grooves, pits, or fissures on the enamel surface. If the condition is more severe, the enamel may exhibit rows of deep pits arranged horizontally across the surface of the tooth. There may be only a single row of such pits or several rows indicating a series of injuries. In the most severe cases, a considerable portion of enamel may be absent, suggesting a prolonged disturbance in the function of the ameloblasts. Hypoplasia results only if the injury occurs during the time the teeth are developing or more specifically, during the formative stage of enamel development. Once the enamel has calcified, no such defect can be produced. There are many factors that can injure or destroy the ameloblasts during their formative activities. These include: 1. Nutritional Deficiency (vitamins A, C, and D) 2. Exanthematous Diseases (e.g., measles, chicken pox, scarlet fever).


3. Congenital Syphilis • The hypoplasia due to congenital syphilis is most frequently not of the pitting variety but presents a characteristic, almost pathognomonic, appearance.

This hypoplasia involves the maxillary and mandibular

permanent incisors and the first molars. • The anterior teeth affected are sometimes called “Hutchinson’s teeth”, while the molars have been referred to as “mulberry molars” (Moon’s molars, Fournier’s molars). • Characteristically, the upper central incisor is “screw-driver” shaped, • The mesial and distal surfaces of the crown tapering and converging toward the incisal edge of the tooth rather than toward the cervical margin. • In addition, the incisal edge is usually notched. • The crowns of the first molars in congenital syphilis are irregular and the enamel of the occlusal surface and occlusal third of the tooth appears to be arranged in an agglomerate mass of globules rather than in well-formed cusps. The crown is narrower on the occlusal surface than at the cervical margin. 4. Hypocalcemia • Tetany, induced by a decreased level of calcium in the blood, may result from several conditions, the most common being vitamin D deficiency and parathyroid deficiency. 5. Birth Injury, Prematurity, Rh Hemolytic Diseases 6. Local Infection Or Trauma These include periapical infections of the preceding deciduous tooth (Turner's hypoplasia) or traumatic intrusion of the preceding deciduous tooth. 7. Ingestion Of Chemicals (Chiefly Fluoride) • The ingestion of fluoride containing drinking water during the time of tooth formation may result in mottled enamel.

The severity of the mottling

increases with an increasing amount of fluoride in the water. Thus there is little mottling of any clinical significance at a level below 0.9 to 1.0 parts 30

per million (PPM) of fluoride in the water, whereas it becomes progressively evident above this level. Clinical Features: Depending upon the level of fluoride in the water supply, there is a wide range of severity in the appearance of mottled teeth, varying from (1) Questionable changes characterized by occlusal white flecking or spotting of the enamel, (2) Mild changes manifested by white opaque areas involving more of the tooth surface area (3) Moderate and Severe changes showing pitting and brownish staining of the surface and (4) A Corroded appearance of the teeth. Those teeth which are moderately or severely affected may show a tendency for wear and even fracture of the enamel. 8. Idiopathic Causes. Treatment Modalities : Since these defects vary in extent and location, there will also be a range of treatment modalities. If defects are of minimum size (narrow lines or isolated pits or shallow depressions), selective odontotomy can be performed, blending the defects with the remaining tooth surfaces. However, if odontotomy and esthetic reshaping of the tooth enamel cannot produce a pleasing functional effect, it is necessary to resort to direct tooth-colored resinous materials without any mechanical preparations. In other words, only surrounding enamel is conditioned by acids and the resinous material is inserted. Acid etching of fluoride hypoplastic enamel is extremely difficult and non-conducive to efficient retention. Therefore, several applications of conditioning acids should probably be used. If the defect is at the occluding or contacting area, it is necessary to resort to metallic or cast restorations. However fluoride hypoplastic enamel is


very brittle and chips very easily during tooth preparations and restoration margination. Therefore, every effort should be made to reinforce marginal enamel around these restorations. If the lesions are discolored and veneering procedures are not planned, vital bleaching can be attempted, but it should be done after selective odontotomy (which will eradicate some discolored areas and may remove the most stained superficial area), and before the acid conditioned enamel-retained restoration. If the lesion is completely disfiguring, both in color and in contour, and the involved surface is not an occluding one, laminated tooth-colored resinous or ceramic veneers are the treatment of a choice. If veneering is the only way to mask the defect and/or discoloration, but there is no sufficient amount of enamel (form, thickness, distribution, quality, and presence), the laminated veneer will interfere with occlusion (e.g., labial surface of lower anterior in normal occlusion), the veneering will compromise plaque control measures or if the facial disfigurement is accompanied by tooth structure loss at the contact area, proximal surfaces and/or occluding surfaces, then porcelain fused to metal or cast ceramic full veneering restorations is the modality of choice.

Localized Non-Hereditary Enamel Hypocalcification : As the destruction of ameloblasts interfere with the enamel matrix formation, it can also interfere with the mineralization of this matrix, even if it is well formed. This will lead to non-hereditary enamel hypocalcification. The clinical symptoms of enamel hypocalcification will have the same topography as enamel hypoplasia. However, the appearance will be different. Affected areas will not be defective in any way. However, they will appear


chalky and soft to indentation, and will be very stainable. Therefore, teeth shades change very fast from chalky to yellow, to brown, dark brown, and/or greyish. If extensive, these lesions predispose to attrition and abrasion. Also, the enamel can be chipped if the lesion involves the entire surface of a tooth. Treatment Modalities : No attempt should be made for localized odontotomy, etching restorations, or non-veneering types of restorations. If a diagnosis is made early in the tooth's life, while the uncalcified enamel matrix is still intact and the areas are localized, small, and unstained, an attempt at mineralization of the tooth enamel should be made. This procedure can be done using periodic fluoride applications, fluoride ionophoresis, and strict prevention of plaque accumulation in these areas. In many situations mineralization of these decalcified or unmineralized areas could occur to some extent. Usually, vital bleaching, laminated veneering, composite veneering, and porcelain fused to metal and cast ceramic crowns are the treatments to be used. Localized Non-Hereditary Dentin Hypoplasia : The odontoblasts are also very specialized cells. Their functions and products (dentin) can be disturbed by environmental irritation, leading to deficient or complete absence of dentin matrix deposition. At this point, the resemblance between the ameloblasts and odontoblasts stops. The ameloblasts are irreplaceable cells, and their disappearance means no enamel in this particular area. However, the odontoblasts are replaceable cells. If they disappear, there will be no dentin temporarily, but dentin deposition will be resumed as soon as other pulp cells start depositing it. In these cases, the defect will be isolated within the dentin substance. The causes for these disturbances are exactly the same as those for localized enamel hypoplasia, and as long as they are covered with the dentin and enamel, there will be no apparent destruction to be diagnosed or treated.


However, the situation will be different if these defects are encountered during tooth preparation for a restoration or if the defect is exposed by any other process. In this instance, the defect is part of the preparation or the cavitating lesion that exposed them. Usually, this goes unnoticed, except for sizable defects which change the preparation or the lesion's dimensions. Treatment Modalities : Treatment here could consist of intermediary basing, as it is just an additional dimension to that part of the tooth preparation that is going to be restored. Localized Non-Hereditary Dentin Hypocalcification : These defects have same causes as hypoplasia. Even though the dentin will be present in substance (no vacancy), it will be softer, more penetrable, and less resilient. The very obvious example of this process is interglobular dentin. Most of the time, the lesion is unnoticed, even when uncovered by a tooth preparation or any other cavitating lesions. Treatment Modalities : Give proper intermediary basing during tooth preparation.


VI. Discolorations : This refers to any alteration or change in the colour of the teeth either due to surface stains or deposits or factors, which could have created changes in one or more of, tooth tissues during the development. Correspondingly they may be classified as

Extrinsic Stains. Intrinsic Stains

The causes of extrinsic stains: 1.

Bacterial stains




Foods and beverages


Gingival hemorrhage


Restorative materials



The causes of intrinsic stains: 1. Amelogenesis imperfecta 2. Dentinogenesis imperfecta 3. Dental fluorosis 4. Erythropoietic porphyria 5. Hyperbilirubinemia 6. Localised red cell break down 7. Medication A. Extrinsic Discoloration: Discoloration that is due to surface staining, calculus or any other surface deposits. Proper scaling and polishing with the indicated abrasives can remove these.


Clinical Features of Extrinsic Stains: Bacterial stains are a common cause of surface staining of exposed enamel,








discolorations that vary from green or black brown to orange. These discolorations occur most frequently in children and usually are seen initially on the labial surface of the maxillary anterior teeth in the gingival one third. Extensive use of tobacco products, tea or coffee often results in significant brown discoloration of the surface enamel. The tar within the tobacco dissolves in the saliva and easily penetrates the pits and fissures of the enamel. Foods that contain abundant chlorophyll can produce a green discoloration of the enamel surface. Green staining is also seen secondary to gingival hemorrhage. This is frequently seen in patients with poor oral hygiene and erythematous, hemorrhagic enlarged gingiva. The color results from the breakdown of hemoglobin into green biliverdin. Dental restorative materials especially amalgam can result in black grey discolorations of teeth. This most frequently arises in younger patients who have more open dentinal tubules. This phenomenon is termed as Amalgam blues. Anterior teeth should not be restored with amalgam. A large number of medications may result in surface staining of teeth. Products containing high amounts of iron or iodine were associated with significant black pigmentation of the teeth. Exposure to sulfur, silver nitrate or manganese can cause stains that vary from gray to yellow to brown or black. Copper or nickel may produce a green stain. Cadmium may be associated with yellow to golden brown discolouration.


More recently Stannous fluoride and Chlorhexidine was found to stain the tooth. Chlorhexidine is associated with yellowish brown stain that predominantly involves the interproximal surfaces near the gingival margins. Similar chemicals such as listerine and sanguanarine may also produce extrinsic stains. These stains can be reduced by effective brushing, flossing and scaling procedures. B. Intrinsic Discoloration: Discolouration that could be created from changes in one or more of the tooth tissues. Clinical Features of Intrinsic Stains: 1. Discoloring changes in enamel include hypoplasia and hypocalcification. Very rarely, intrinsic enamel discoloration can be due to externally or internally (systemically) applied agents, due to the extremely low permeability of enamel compared to dentin. Defective enamel from the structural and mineralization aspects can be very permeable and accordingly stainable. 2. Discoloring changes in dentin may result from non-vitality resulting in disintegration of the dentinal tubules' contents or from pigmentation and staining. The latter can result from external sources, e.g., corrosion products of metallic restorations, medicaments, microbial metabolites, etc. This stainability is facilitated by the dentin permeability, especially if it is hypoplastic, hypocalcified, or dead. 3. Discoloring changes in the pulp-root canal system can result from pulpal necrosis, in which the disintegration products diffuse through the dentinal tubules from the root canal-pulp chamber system, discoloring the dentin and entire tooth. Such non-vital discoloration will intensify with time due to more disintegration of the products while in the dentinal tubules. This discoloration is usually grayish to dark black. Internal resorption causes a pinkish discoloration at areas where the pulp tissues come close to the tooth surface following resorption of the pulp 37

chamber or root canal walls. Internal hemorrhage, due to excessive instrumentation, irritation during cavity preparation, can also cause discoloration from the pulp-root canal system. Several systemic disorders can result in the discoloration of the dentition. Congenital Erythropoetic Porphyria (Gunther's disease) : Is an autosomal recessive disorder of porphyrin metabolism that results in the increased synthesis and excretion of porphyrins and their related precursors. Diffused discoloration of the dentition is noted as a result of the deposition of the porphyrin in the hard tissues of the teeth. It is manifested as a reddish brown discoloration that exhibits a red fluorescence when exposed ultraviolet light. Bilirubin is a breakdown product of red blood cells and excess levels can be released into the blood in a number of conditions. The increased amount of bilirubin can result in a yellow green discoloration of the soft tissues. During periods of hyperbilirubinemia, developing teeth also may accumulate the pigment and become intrinsically stained. Biliary Atresia : Biliary atresia is an uncommon congenital disease characterized by narrowing of the ductal element of the biliary system of liver, which results in elevated billirubin levels in blood. Patients with biliary atresia often develop severe jaundice and they also exhibit discoloration of teeth, mainly of the teeth of the deciduous series. The affected teeth appear dark or greenish in color, with roots of the teeth more intensely stained than the crowns. Erythroblastosis Fetalis : Erythroblastosis fetalis is a hemolytic anemia, which develops during intrauterine life and results from incompatible factors in the blood of the mother and the fetus.


An Rh-negative mother normally develops antibodies against the erythrocytes of an Rh-positive fetus. These antibodies when cross the placental barrier attack and destroy the fetal erythrocytes resulting in severe hemolysis. Because of this hemolysis, large amounts of billiverdin and billirubin (blood pigments) are produced in the blood, which later on become deposited into the skin and the tooth. Erythroblastosis â&#x20AC;&#x201C; induced discolorations affect only the primary teeth and their color varies from green or bluish green or yellowish gray. The pigments are largely confined to the dentine and in some cases enamel hypoplasia may also be present. Other diseases less frequently involved are: Congenital hypothyroidism. Significant internal hemorrhage. Neonatal hepatitis. Medications: Several different medications can become incorporated into the developing tooth and result in clinically evident discoloration. Tetracycline discoloration is a sort of permanent staining of the dentin and, to some extent, enamel. Tetracycline administered during the formation of the dentin (enamel) can form complex chelate compounds with both the organic and inorganic components of the dentin (enamel). (The dentin incorporates nine times more tetracycline than enamel). Tetracycline staining occurs frequently due to the prophylactic or therapeutic use of the drug to the pregnant mothers (in the second and third trimester) or the infants (upto the age of seven years). The created compound is very stable. Such tetracycline staining can occur from the drug crossing the placental barrier and/or being secreted in the milk of the lactating mother and bind with the calcium during formation of enamel and dentin.


Clinical Findings : •

Both deciduous and the permanent teeth are affected by this staining.

The intensity and distribution of the color vary depending upon the specific form of tetracycline used and their duration of administration.

The affected teeth exhibit a yellowish or brownish-gray discoloration.

The discoloration is intense at the time of eruption of teeth and gradually the teeth become only “brownish” following exposure to light.

The discoloration is always internal

The section of the tooth often produces bright yellow fluorescence under ultraviolet light.

Chlortetracycline produces brownish-gray color white oxytetracycline tends to produce a yellowish discoloration of teeth.







Oxytetracycline (yellow), Minocycline (green-black). Long term use of tetracyclines can result in discoloration of the adult dentition also due to incorporation into the continually forming physiologic secondary dentin. Treatment Modalities : 1. Discoloration due to extrinsic causes can be removed by proper scaling and polishing with the indicated abrasives. 2. Intrinsic discoloration in enamel and dentin can be treated in the same way as localized non-hereditary enamel hypoplasia and hypocalcification is treated. 3. Intrinsic discoloration due to discoloring changes in the pulp-root canal system should be treated as follows. If tooth non-vitality is the cause, endodontic therapy should be instituted. After successful treatment, proceed with the following sequence of treatment: a. Non-vital bleaching :


Evacuate the pulp chamber and root canal portion of the clinical crown from any root canal treatment medicaments or fillings; then. irrigate the evacuated area with a mixture of chloroform and ethyl-ether. Prepare mixtures as in vital bleaching (five parts 30% hydrogen peroxide and one part ethyl-ether in a cotton pellet or a paste of sodium perborate in 30% hydrogen peroxide), and place the mixture into the evacuated pulp-root canal and apply heat inside (110-130째 F). Here, it is possible to maintain the heat for a longer time to obtain better results than with vital bleaching (no pulp tissues to be concerned with). The process can be repeated several times to obtain satisfactory results. b. If non-vital bleaching does not end with pleasing results, it may be necessary to resort to laminated veneer or porcelain fused to metal or cast ceramic veneering restorations as described before. 4. If internal resorption is the cause for the discoloration, initiate endodontic therapy, and after successful completion of the endodontic treatment, clean out the concavity (ies) in the pulp chamber walls created by the internal resorption and fill it with a suitable tooth-colored material, and proceed with the regular restorative procedures. 5. If internal hemorrhage has caused the discoloration, the tooth should be covered with ZOE or a ZOE cemented temporary for a while. This will facilitate the resolution of the hemorrhage. If discoloration does not disappear in time, if darkening occurs, or if confronted with degenerative pulpal symptoms, endodontic therapy may be necessitated. VII.Malformation : Malformation can be either in micro- or macroforms, and is usually of hereditary origin. The most common type of malformation is one or two teeth (usually upper lateral) that are noticeably smaller in size than surrounding ones, with pointed incisal edges (peg teeth). Malformation should be differentiated from the illusion that can occur when there is a substantial discrepancy between


tooth size and jaw size. This situation might give the impression of too large or too small teeth. Nevertheless, this should not be corrected by restorative procedures, but rather with orthodontic treatment. Treatment Modalities : 1. If the affected tooth is properly aligned in the arch and has intact enamel and is not subjected to extensive occluding forces (is not a discluding tooth), conditioning of the enamel and building the tooth up with a direct tooth-colored resinous material will be the treatment of choice, at least for a temporary period of time. 2. If the affected tooth is malaligned, repositioning should be performed before any restorative treatment. 3. If the affected tooth does not have sufficient quality enamel to retain a restoration similar to that described in (1) or if the tooth (after a restoration) can be subjected to excessive occluding forces, it is preferable to select porcelain fused to metal or cast ceramic veneering restorations as the treatment modality. VIII. HEREDITARY DISTURBANCE OF ENAMEL FORMATION Amelogenesis Imperfecta : Definition : Amelogenesis imperfecta is a heterogenous group of hereditary disorders of enamel formation affecting both deciduous and the permanent dentition. The disease involves only the ectodermal component of the tooth (i.e. enamel) while the mesodermal structures of tooth, e.g. dentin, cementum and pulp, etc. always remain normal. Types : Normally the process of enamel formation progresses through three stages : • Stage of enamel matrix formation. • Stage of early mineralization. • Stage of enamel maturation 42

Amelogenesis imperfecta may set in during any stage of enamel formation. • They can be Autosomal Dominant Traits (hypocalcification, hereditary generalized and localized hypoplasia), or can be • X-Linked Trait (hypomaturation) or • A Recessive Trait (pigmented hypomaturation). The abnormality could be in the matrix formation leading to hypoplasia or it could be in the mineralization leading to hypomineralization. Three basic types of Amelogenesis imperfecta have been identified, which correlate with defects in these three developmental stages of enamel. • Hypoplastic type of Amelogenesis imperfecta • Hypocalcification type of Amelogenesis imperfecta • Hypomaturation type of Amelogenesis imperfecta Hypoplastic Type : a. In this type the enamel thickness is usually far below normal since the disease affects the stage of matrix formation. b. The teeth exhibit either complete absence of enamel from the crown surface or there may be a very thin layer of enamel on some focal areas. c. Thin enamel d. Open contact e. Small teeth, with short roots, very limited pulp chambers and root canal dimensions f. Delay in eruption g. Sometimes the enamel is glassy (prismless) h. There may be some discoloration, usually yellow i. The enamel could look wrinkled j. All signs of severe occlusal wear Hypocalcification type : Hypocalcification type of Amelogenesis imperfecta represents that stage of the disease, which has occured due to disturbance in the process of early mineralization of the enamel. 43

In this stage, the enamel is of normal thickness but is soft and can be easily removed with a blunt instrument. 1. The enamel is usually stained (yellow or black). It may be chalky at early stages of life. 2. The enamel chips easily. 3. The enamel can be very soft in consistency (cheesy). 4. Although teeth will have normal forms when they erupt, they have dull surfaces readily stainable by age. The stains become darker with time. 5. The enamel is worn away very easily in life with all signs and symptoms of severe attrition (may be to the gum line). Hypomaturation Type : This type occurs due to interruption in the process of maturation of enamel. Here the enamel is of normal thickness but it does not have the normal hardness and translucency. The enamel can be pierced with an explorer tip with firm pressure. Teeth often show chipping of enamel away from the normal dentin surface. Clinical Features: 

Amelogenesis imperfecta affects both deciduous and the permanent teeth.

Sex predilection varies according to the mode of inheritance.

The color of the teeth is mostly chalky white but sometimes it can be yellow or even dark brown.

The contact points in the proximal surfaces are mostly open while the occlusal surfaces and the incisal edges are severely abraded.

Sometimes the tooth is completely devoid of enamel and the patient shows severe abrasion of the dentin.

The enamel may have a cheesy consistency, which is easily removable form the tooth surface.


On rare occasions, the enamel may look almost normal except the presence of few grooves and wrinkles on its surface.

Amelogenesis imperfecta does not increase the susceptibility of teeth to dental caries.

In the mildest form of hypomaturation type of Amelogenesis imperfecta, the enamel is of near normal hardness and has some white opaque flecks at the incisal areas of the teeth. These type of teeth are known as “Snowcapped teeth”.

Radiographic Appearance : In Amelogenesis imperfecta, the thickness and radiodensity of enamel varies greatly. If the enamel is present at all, it can be found mostly on the tip of the cusps and on the interproximal areas.  In hypoplastic type, the radiodensity of the enamel is usually greater than the adjacent dentin.  The radiodensity of enamel in hypomaturation type is almost equal to that of the normal dentin. Treatment Modalities : Early diagnosis is the key to a relatively successful treatment. Only two modalities can be used in most cases. Selective odontotomy and esthetically reshaping the teeth. This is a repeated procedure that is needed throughout the lifetime of the tooth because of the frequent changes in shape (attrition). Full veneering includes procedures with metallic, metallic based, or cast ceramic restorations. At no time should these restorations oppose a natural tooth, i.e., occluding teeth should be restored at the same time with the same materials. In extensive conditions, lengthy, comprehensive periodic evaluation should be practiced before trying any restorative work on these patients, as the teeth are easily chipped. This situation can happen during a tooth preparation or


during service. If enamel imperfectas are not associated with dentin imperfecta, the restorative prognosis can be favorable. In any event, conservative nonrestorative treatment should be tried first, before resorting to restorative procedures. Dentinogenesis Imperfecta : Definition : Dentinogenesis imperfecta is an inherited disorder of dentin formation, which affects the deciduous as well as the permanent dentition and it usually exhibits an autosomal dominant mode of transmission. The disorder has been classified into three types : Type I : Dentinogenesis imperfecta, which occurs in patients afflicted with Osteogenesis Imperfecta (OI). •

This type is usually inherited as an autosomal dominant trait.

It involves the deciduous teeth more often than the permanent teeth.

Teeth will usually have an opalescent color (as seen in type II as well).

Patients will exhibit features of Osteogenesis Imperfecta (since both conditions occur together), which include bluish sclera of the eyes and several bony defects.

It is important to note that not all cases of Osteogenesis Imperfecta will be associated with Dentinogenesis Imperfecta.

Moreover, there is no correlation between Dentinogenesis Imperfecta and the severity of the osseous defects present in Osteogenesis Imperfecta.

Type II : Dentinogenesis Imperfecta, which is not associated with Osteogenesis Imperfecta. •

This type of Dentinogenesis Imperfecta is often known as “hereditary opalescent dentin” and this variant is more commonly encountered than the other two types of Dentinogenesis Imperfecta.

It is the most common type among all the three types of the disease, having incidence rate about 1 in 8000 people. 46

The condition is inherited as an autosomal dominant trait.

Involves deciduous and permanent teeth with equal frequency.

The color may be from grey, brown, yellow-brown to violet.

Most of them exhibit a translucent hue.

The enamel, although intact, is easily chipped because of the defective dentino-enamel junction.

The crowns are overcontoured.

The roots are short and slender.

There are signs and symptoms of extensive attrition.

The dentin is devoid of tubules.

The dentin contains a lot of interglobular dentin.

The decay process, if initiated, will spread laterally.

Root canal and pulp chamber space is obliterated.

Dentin hardness and resilience is almost half that of normal dentin.

Type III : Dentinogenesis Imperfecta Type III or the “Brandywine type” is a rare condition and is inherited as an autosomal dominant trait.  It is commonly seen in a racial isolate area in the state of Maryland.  It affects both dentitions.  Clinically the disease is same as type I and type II variants, however it often exhibits multiple pulp exposures and periapical lesions in deciduous teeth. Clinical Features of Dentinogenesis Imperfecta : In all three types of Dentinogenesis Imperfecta both deciduous and permanent dentitions are affected with variable clinical presentations. 

The condition affects males and females with almost equal frequency.

On eruption, the teeth exhibit a normal contour but they have an opalescent ‘amber like’ appearance.

Few days after eruption, the teeth may achieve an almost normal color, following which they become translucent. 47

Finally the teeth become either gray or brownish in color with a bluish reflection from the enamel.

The overlying enamel is structurally normal in most cases, however it is lost rapidly from the surface soon after the teeth have erupted and as a result the teeth often develop severe attrition.

In some cases of Dentinogenesis Imperfecta, the affected teeth may also exhibit hypomineralized areas on the surface enamel.

Teeth are not particularly sensitive even when most of the surface enamel is lost, it happens since the dentinal tubules are haphazardly arranged and most of them are devoid of the odontoblastic processes.

Although the dentin is soft and easily penetrable in Dentinogenesis Imperfecta, these teeth are not caries prone. The possible reason could be the structural change in the dentin itself, which provides little scope for the entry of the cariogenic microorganisms into the tooth since most of the dentinal tubules are obliterated in this disease.

Type III cases of Dentinogenesis Imperfecta are often associated with multiple pulp exposures (mostly due to attrition) and periapical pathology.

Radiographic Features : Radiographically Dentinogenesis Imperfecta reveals the following features ; 

The Type I and Type II diseases are radiographically similar and they often exhibit “bulb shaped” or “bell shaped” crowns of the teeth with abnormally constricted cervical areas.

The roots of the teeth are thin and spiked.

Depending on the age of the patient, the teeth exhibit varying degrees of obliteration of the coronal as well as the radicular pulp chamber.









radiographically appear normal. 

The type III dentinogenesis imperfecta may reveal radiographic features, which are similar to those of the type I and type II, although in many cases


the affected teeth exhibit extremely large pulp chambers surrounded by a thin shell of dentin and enamel. 

Because of their typical appearance the affected teeth are often called “shell” teeth.

These teeth frequently exhibit multiple pulp exposure and associated periapical pathology.

Treatment Modalities : Any possible success for treatment depends upon early diagnosis and care. Only two possible treatment modalities can be used here, namely, selective odontotomy and permanent full veneering. The treatment in Dentinogenesis Imperfecta is mostly aimed at preventing excessive tooth attrition and improving esthetics of the patients. 

Metal and ceramic crowns are given.

These teeth are not suitable candidates for playing the role of abutments for any bridge work since the roots are small and they also tend to fracture under frictional stress.

In case of severe generalized attrition, complete denture prosthesis may be necessary. There should not be any false security in preparing these teeth, because

of the absence of the pulp chamber and root canals, as these teeth are very susceptible to fracture, especially by instrumentation forces. There should not be any attempt to use intracoronal or intraradicular retention modes. Therefore, the only retention possible is an extracoronal reinforcing-protecting veneering restoration. Splinting between these teeth is one way to avoid root fracture, which, unfortunately, should be expected by both the patient and the dentist. TRAUMA : Ellis Classification Class 1 : simple fracture of the tooth crown involving little or no dentin Class 2 : extensive fracture of the tooth crown involving considerable dentin but no pulp


Class 3 : extensive fracture of the crown involving considerable dentin and exposing the pulp Class 4 : A non vital traumatized tooth with or without loss of crown structure Class 5 : Tooth loss as a result of trauma Class 6 : fracture of the tooth root , with or without loss of crown structure Class 7 : displacement without fracture of crown or root Class 8 : fracture of crown enmasse Class 9 : cracked tooth Class 10 : cyclic incomplete dislocation of the tooth WHO classification from 1978 (code no corresponding to the international classification of diseases; ) 873.60 Enamel fracture 873.61 Crown fracture involving enamel and dentin 873.62 Crown fracture involving pulp 873.63 Root fracture 873.64 Crown root fracture 873.66 Luxation 873.67 Intrusion or extrusion 873.68 Avulsion 873.69 Other injuries TREATMENT MODALITIES : Three therapeutic bases â&#x20AC;&#x201C; 1. Accurate & detailed diagnostic data should be taken . 2. Patient should be aware that the vitality of the tooth may not be maintained as the degenerative process starts after trauma and the tooth may become non vital later. 3. If trauma has occurred during incomplete tooth development or the early stages of passive tooth eruption then tooth first stabilized with provisional restoration or endodontic treatment followed by permanent restoration after stabilization. CLASS 1 : 1. Smoothening the peripheries of the defect. 50

2. Esthetically reshaping of the involved area . 3. In large defects , use direct tooth coloured restorative materials CLASS 2 : Use of adhesive direct tooth colored restorations . CLASS 3 : Root canal treatment followed by post and core . CLASS 4 : Root canal treatment followed by crown . CLASS 5 : Intentional RCT followed by placing the tooth back into socket and splinting the tooth . If this cannot be done then placing a bridge. CLASS 6 : Horizontal fracture – Cervical – poor prognosis . RCT can be done followed by post & core or crown lengthening procedure followed by crown . Middle – root canal followed by intraradicular splinting Apical – RCT leaving the apical segment as it is or removing it surgically. CLASS 7 : Reduction of tooth in its socket followed by splinting . RCT if indicated. CLASS 8 : RCT followed by reattachment procedure for crown or post and core or crown given. CLASS 9 : Immediate therapy : splint stabilize relieve occlusion RCT if indicated


coronal restoration removed periodontal defect corrected Permanent restoration : reinforcing â&#x20AC;&#x201C; protecting cast / cast based restoration foundation treatment depends on the degree of fracture can be treated accordingly as class 1,2 or 3. CLASS 10: Extent of periodontal involvement is assessed followed by occlusal equilibration and then treatment of periodontal defect. SUMMARY: Wear is a natural process that occurs whenever two or more surfaces move in contact with one another. In the complex environment of the oral cavity where the teeth with any restorations move in contact with one another, wear is inevitable. As patients are now retaining their natural dentition for many more years the clinical problems associated with advanced wear is also increasing. The management of wear involves the replacement of missing tooth tissue with dental materials together with an attempt to minimise the causative factors. Therefore it is vital that we should have good knowledge of the etiology and contributory factors of the different forms of wear seen in the tooth tissues and their management.


Reference Articles : 1.

Retention of a resin modified glass ionomer adhesive in non carious

cervical lesions- 6yr.

Follow up.

J dent. 2005 aug 33 (7); 541 -547. (van dijken jw ) 2. 3yr clinical evaluation of a compomer & a resin composite as a cl v filling material Oper dent 05. may 30 (3), 275 – 81.( Gallo jr., Burgess jo ) 3. Attrition , abrasion, erosion – a review . JADA 04. aug, 138 (8) : 1109 – 18.


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