naiju non carious

COLLEGE OF DENTAL SCIENCES

DEPARTMENT OF CONSERVATIVE DENTISTRY AND ENDODONTICS

Seminar On

NON-CARIOUS DESTRUCTION AND DISFIGUREMENT OF TEETH

Presented by : -

Dr. Niju Aelias

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.

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.

Other forms of non carious lesions include discolorations which can be

either extrinsic or intrinsic.

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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.

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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

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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 re-

sulting 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.

Treatment Modalities:

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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.

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

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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

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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.

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.

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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

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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 non-

restorative 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 dic-

tated 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.

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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.

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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.

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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 elec-

trolyte drives the fluoride ions deep into the dentin).

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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 tooth-

colored 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 : Erosion can be defined as the loss of tooth structure resulting from

chemico-mechanical 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.

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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

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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.

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.

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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.


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

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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 chemico-

physical 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

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 “Gippo” to distinguish it from

Abrasion and Erosion.

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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.

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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.

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

19

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.

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

20

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 in-

crease 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.

21

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

22

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

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.


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

23

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.

24

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.


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

25

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 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.


Give proper intermediary basing during tooth preparation.

26

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

2. Tobacco

3. Foods and beverages

4. Gingival hemorrhage

5. Restorative materials

6. Medications

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.

27

Clinical Features of Extrinsic Stains:

Bacterial stains are a common cause of surface staining of exposed

enamel, dentin and cementum. Chromogenic bacteria can produce

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.

28

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 per-

meability 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

29

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.

30

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 – 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.

31

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.

Derivatives of tetracyclines are Chlortetracycline (gray-brown),

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.


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

32

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% hy-

drogen peroxide), and place the mixture into the evacuated pulp-root canal

and apply heat inside (110-130° 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.

33


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

Amelogenesis imperfecta may set in during any stage of enamel formation.

34

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.

35

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.

36

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 “Snow-

capped 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.


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

37

during service. If enamel imperfectas are not associated with dentin imperfecta,

the restorative prognosis can be favorable. In any event, conservative non-

restorative 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.

38

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.

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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.

The cementum, periodontal ligament and the alveolar bone

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

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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.


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.

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.

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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.

Dr. Niju Aelias

Reference Articles :

1. Prevalence of Non carious cervical lesions and their relation to

occlusal aspects. A clinical study. Journal of Esthetic Dentistry.

Vol.12 : No.1 2000.

2. Development of Non-Carious cervical Notch lesions : In vitro study.

Journal of Esthetic Dentistry. Vol.11 : No.6 : 1999.

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naiju non carious

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