non-carious/ orthodontic course by indian dental academy

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.
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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.
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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 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.
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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.
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
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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
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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.
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
20

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
21

 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 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
22

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.
23

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
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
24

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.
25

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.
26

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 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.
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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.
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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.
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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
30

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.
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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.
32

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 :
33

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% 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
34

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.
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
35

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 :
36

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.
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.
37

 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 “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.
38

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 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.
39

• 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.
• 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 :
40

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.
 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.
41

 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
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
42

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.
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.
43

2. Development of Non-Carious cervical Notch lesions : In vitro study.
Journal of Esthetic Dentistry. Vol.11 : No.6 : 1999.
44

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