Non carious destruction and disfigurement of teeth/ dental implant courses by Indian dental academy

PART- I NON CARIOUS DESTRUCTION & DISFIGUREMENT OF TEETH Non carious loss of tooth tissue is a normal physiological process and occurs throughout life. If the Rate of loss is likely to prejudice the survival of the teeth OR is a source of concern to the patient, then it may be considered pathological.

Although decay is the usual cause of tooth destruction necessitating operative procedures. It has been estimated that 25/- of tooth destruction does not originate from a carious process. The following are the possible non-caries destructive processes: •

ATTRUTION

•

ABRASION

•

EROSION

•

ABFRACTION

•

LOCALIZED NON-HEREDITARY ENAMEL HYPOPLASIA

•

LOCALIZED NON-HIREDITARY ENAMEL HYPOCALCIFICATION

•

LOCALIZED NON-HEREDITARY ENAMEL DEMIN HYPOPLASIA

•

LOCALIZED NON-HIREDITARY ENAMEL HYPOCALCIFICATION

•

DISCOLORATIONS

•

MALFORMATION

•

AMELOGENESIS IMPERFECTA

•

DENTINOGENESIS IMPERFECTA

•

TRAUMA

- DENTAL COMPRESSION SYNDROME

The prevalence of tooth wear is on the increase and a significant proportion of a dentists time will need to be devoted to the management of this problem.

ATTRITION DEFINITION; 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 physiological. Any contacting tooth surface is subjected to attrition process beginning from the time it erupts in the mouth and makes contact with a Reciprocating tooth surface.

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: •

PROXIMAL SURFACE ATTRITION (PROXIMAL SURFACE FACETING) The results from surface tooth structure loss and

flattening-widening of proximal contact areas. because of this process surface area proximally

susceptible to

decay is increased in dimension At the same time, cleansibility will be hindered Due to in dimensions of the surroundings embrasures Also M-D dimensions of the teeth are deceased leading to drifting, will lead to overall Reduction of dental ach length Interproximal space will be deceased in dimensions

Interfering with the physiology of interdental papillae •

OCCLUDING SURFACE ATTRITION COCCLUSAL 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.

On the other hand, if the loss occurs over a long period of time (10 years or more) Deficient masticatory capabilities Cheek biting (cotton Roll cheeks) due to flattening Vertical overlap between the working inclined planes will be lost.

Gingival irritation due to food impaction & closeness of occlusal table Decay exposure of underlying dention Horizontal masticatory movement

extreme

strain of muscles of stomato-gnathic systems SIGNS & SYMPTOMS Key presenting signs are •

After mandibular and maxillary teeth simultaneously.

•

Even contact between worn mandibular and maxillary teeth in excursive movements.

•

Tooth sensitivity

ABRASION Definition: The surface loss of tooth structure resulting from direct friction forces between the teeth, and external objects, or from frictional forces between contacting teeth components in the presence of an abrasive mediums.

Although abrasion like attrition

Stimulate the formation of dentin intrapulpally Causing Recession of the pulp and Root canal Sometimes the abrasion Rate is faster than the deposition Rate Result is direct OR indirect pulpal involvement The most predominant abrasion is tooth brush abrasion Occurring cervically usually to the most facially prominent teeth in the arch. i.,e caniness and bicuspids.

Right & left hand Surface Extent, depth, and Rate depends on Direction of brushing Strokes The size of the abrasive % of abrasive Type of abrasive Diameter of bristles, Force used in brushing, Type of tooth tissue abraded.

SIGNS & SYMPTOMS •

Linear in outline, following the path of brush bristles

•

The peripheries of the lesion are very angular demarcated from the adjacent tooth surface.

•

The surface of the lesion is extremely smooth and polished, and it seldom has any plaque accumulation or carious activity in it.

•

The surrounding walls of abrasion lesion tend to make a V-shape, by meeting at an acute angle axially

•

Probing of stimulating (hot, cold, or sweets) the lesion can elicit pain.

OTHER FORMS OF ABRASION •

DEPRESSION ABRASION ____ PIPE SMOKING

•

Generalized occlusal surface abrasion _____chewing tobacco

•

Proximal abrasion __Forcing a toothpick, interdental stimulator.

•

Professional habits_______ cutting sewing thread, pulling nails, abrasives in the working enviornment.

•

Pica syndrome----------habit of chewing clay, occlusal abrasion

pattern.

•

Iatrogenic tooth abrasion

Porcelain teeth apposing natural teeth cast alloys having extremely

Extremely rough occluding surface of a Restoration

high abrasive resistance EROSION Defn The loss of tooth structure resulting from chemico-mechanical acts in the absence of specific microorganisms.

ETIOLOGY Until now there is no convincing etiology for erosion. As expected many authorities theorize causes and pathogenesis erosion of these theories, the following are most popular.

•

INGESTED ACID o E.G citric acid.

•

Salivary citrates

•

Secreted acids Acids exist in gingival crevice Due to occlusal traumatism cause cervical erosion •

Chelating microbial metabolic products e.g pyrophosphate

•

Acid fumes

•

Excessive tensile stresses at the tooth clinical cervix Non-elastically defining tooth

contacts Which could be premature of heavy centric, immense working of balancing •

Refused acid As a result of chronic frevcient

Regurgitation The stomach HCl Can hit the teeth at specific locations Creating a very characteristic type of erosion lingual surface of the upper teeth • •

SIGNS & SYMPTOMS There is no demarcation between the lesion and the adjacent tooth surface

i.e an explore can be passed without any interception from the lesion to the tooth surface.

•

The lesion surface is glazed

•

Erosion usually does not affect occlusal surface

Excepts in very advanced situations Then only indirectly.

•

Sauucized cupping of palatal surfaces of maxillary incisors, occlusal and OR palatal surfaces of posterior teeth buccal surface of anterior or posterior teeth.

•

Teeth appear shiny when erosion is active

•

Metal Restorations stand proud of tooth tissue]

•

Tooth sensitivity to physical, chemcial, and mechanical stimuls is always evident. and main complaint of the patient •

Adjacent gingiva and periodontium are almost always sound and healthy.

The rate of erosion in active lesion estimated to be

1. Perforation of the pulp chamber of Root canal is very rare. as the stimulated secondary and tertiary dentin is usually produced at a faster Rate than that 1.5.4 mic/day ABFRACTION Defn: Defined as non carious cervical tooth ce. It is believed to be due to concentration of occlusal forces on the cervical margins of teeth and is frequently seen on teeth with high cuspal angles Such as max premolar wedge shaped appearance at the CE junction A combination of factors is usually involved etiology of tooth weak is multifactorial and a number of reports have indicated that it is unusual to have tooth wear with a single cause.

TREATMENT] The treatment plan should take the patient and dentist to the point where diseases is controlled and the dentition functional and stable.

Management of the patient where teeth are

worn poses the

following questions •

Does the patient perceive that there is a problem?

•

In the weak currently active if so, is it rapid of slow?

•

Will the patient cooperate in a preventive approach to the management If so, how easy it will be to monitor its success?

•

Is the wear so severe that restoration is required?

•

If Restoration is required, is there sufficient crown height and do occlusal relationships allow reasonable from and stability to be achieved?

•

Are other teeth likely to require restoration in the short to middle term?

The answers determine the strategy for management.

They all require decisions and patient involvement, particularly with regard to their possible long term.

CERVICAL TOOTH WEAR Most common cause is abrasion After confirming diagnosis, If of abrasion should be carried out in following sequence.

•

Diagnose the cause There is no use in treating and Restoring the teeth If the cause of abrasion is still in action

•

Knowing the causative factors first correct OR replace the iatrogenic dental work

•

The objective of Restoration should be to prevent further destruction of the teeth.

•

Abrasive lesions at non occluding tooth surfaces should be critically evaluated for need for restoring them If the lesions are multiple, shallow (not extending 0.5 in dentin) 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 exculicated 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 flouride solution to improve its caries resistance.

If the lesion is Wedge (V) shaped and exceeds 0.5 mm into dentin it should be restored.

If the involved teeth are extremely sensitive.

It is preferable to desensitize exposed dentin Before restoration it is started As in many situation if the sensitive teeth are restored immediately They will remain sensitive to thermal changes for ever Desensitization can

Flouride application 8-30 if Na of

Snf be accomplished by

for 4.8

mm Ionophoresis using electrolyte containing F ions

•

Restorative treatment ( BDJ P.A KING et al vol 186 No.7 April 1999)

If the abrasive lesion involves an anterior tooth or facially conspicuous area of posterior teeth The restoration can be done in one of the direct tooth colored materials There is a plethora of tooth-colored restorative materials now available Materials can either be composite resin or Glass ionomer based, of a combination of both.

Either is a layeral technique with individual materials of as a resin modified GIC The dynamic bond of GIC to enamel and dentin through an ion exchange process.

Process an opportunity for continual repair of the adhesive bond at the cement tooth interface There also additional benefit of flouride in release Relieving the possibility of marginal caries.

A COMPARATIVE ANALYSIS OF TECHNIQUES OF RESTORING CERVICAL LESIONS (S.K. SIDHU QUINT INT. VOL 24 No.8/1993)

Reported the effectiveness of three different materials and techniques in restoring cervical lesions using marginal leakage as the means of comparisons.

Micro leakage can expected to be minimal in cavities restored with the “Sandwich” technique in which GIC liner and composite resin resotrations material are placed.

ANTERIOR TOOTH WEAR The primary cause of this wear pattern is usually erosion SPACE LIMITATIONS Despite the fact that both upper and lower anterior opposing surfaces are worn.

There is usually no or minimal space available for restorations to the placed.

This may be forward posturing of the mandible Compensatory eruption of the worn teeth as the wear progress.

The space available for palatal restorations may be obtained by restorative means.

•

Space may be gained by orthodontic # which involves realignment of ant teeth of opening of ibt posteriorly.

This concept was described by DAHL in 1975

The technique originally described consisted of removable Crowns covering palatal surface of upper anterior teeth.

It was made to provide even contact with lower teeth and separate the back teeth.

In that patient the back teeth re-established occlusal contract over a period of 8 months. .

DISADAVANTAGE •

Increased treatment time

•

Extra lab procedure

POSTERIOR TOOTH WEAR Tooth wear affecting only posterior teeth is usually part of a generalized condition. Affecting the whole dentition.

Treatment must involve several modalities, which will be chosen an initiated in the following sequences.

Pulpally involved teeth should undergo endodontic therapy or extraction according to the restorability and future role in stomatognathic system.

Parafunction activities notably bruxism, should be controlled with the proper discluding-protecting occlusal splints.

Myofunctiona, TMJ or any other symptoms in the stomatognathic system should be diagnosed and resolved.

Sometimes, simply modifying the discluding occlusal splint used can be the treatment modality resolving both the situations

•

Occlusal equilibration should be performed after all notable symptoms are relieved.

Occlusal equilibration might be the only treatment needed, if lost 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 smoothing the peripheries of the occlusal tables, •

During the last 3 procedures exposed sensitive dentinal areas should be protected and the actual carious lesion should be obliterated.

Protection can be accomplished using flouride solutions Obliteration is achieved by a proper temporary Restoration.

•

Restorative modalities can now be initiated Restoration are only need in the following situations.

Noticeable loss of vertical dimension that has not been compensated for and that should be regained to effect a physiologic status in stomato-gnathic system.

There is an extensive loss of tooth structure in a localized or generalized fashion necessitating restoring the tooth to form and function.

Restoring remaining tooth structure would not be in and of itself, be conducive to occluding inclined planes working in harmony in creating a physiologic mandibular movement.

Decay or any other cavitating lesion is superimposed on the attraction reducing of a tooth surface.

Worn out tooth contour (proximally) is not conducive to proper maintenance of the periodontium.

A tooth is cracked or endodontically treated.

RESTRORATIVE TREATMENT MODALITIES. •

Lost tooth structure due to attrition is at high stress concentration areas, the pattern of tooth wear is such that individual posterior teeth may require restoration.

Only metallic (metallic-based) restoration should be used to replace them, Resin bonded heat-treated gold alloy restorations can be advantages.

•

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 occured.

Therefore if the alveolar bone did grow occlusally brining the occlusally worn teeth to their customary occlusal location, any building-up restorations could impinge on free-easy spaces.

Eliciting /of aggravating bruxism or other parafunctional habits. •

Estimate how much vertical dimension was lost.

Determining the indicated vertical dimension for the patient in the same way it is determined for a full denture construction.

Gives us an estimate of how much we should increase the height of worn clinical crowns.

Estimate how much additional vertical dimension the stomato-gnathic system can accommodate without untoward effects.

It is well established fact that not all the lost dimension can be tolerated by the stomato gnathic systems, especially if attrition has occurred over a long period ( >15 years) because there is a certain permanent physiologic accommodation which should not be disturbed.

Therefore If a substantial increase in vertical is planned ( > 2mm), it is wise to build a temporary restoration or a removable occlusal splint, that can be easily adjusted through subsequent addition or removal of material.

Composite resin temporary restorations are most frequently used.

The permanent restoration should be done in a cast alloy material.

A fully adjustable articulator, hinge axis determinations and use of pantographic tracing and factors records essential.

•

In most situations, no vertical dimension-increase is needed.

Restoration may be still be needed for the other indications mentioned.

In these cases it is preferable to use cast alloy restorations to preserve the remaining tooth structure and to assure the integrity of the supporting tissues. because of short crowns in these cases it may be necessary to use intraradicular retention means, with or without devitalizing the teeth.

Also extra coronal retention may be one of the choice here to affect the change in contour and occluding surfaces, in addition to attaining sufficient retention.

Splinting of these crown teeth via cast restoration may be indicated in these situations to increase resistance and retention forms and to minimize displacement of teeth.

•

In case with a carious lesion or defects superimposed on attrition facts, if the dimension of the lesion is very limited and there is sufficient tooth structure around it to accommodate walls Amalgam or direct gold can be used to restore them.

The Question of an Equilibration

An

equilibration

of

the

human

dentition

is

a

modification of the occlusal surfaces of teeth in order to improve the way they touch each other in closure and function.

In

order

to

determine

the

need

for

an

equilibration the dentist must compare the patient’s present occlusion to a standard of excellence, Here in lies the problem: there is no concept of perfect or ideal occlusion agrees

in

upon,

ambiguity

contemporary so

comparison

regarding

the

dentistry is

not

subject

that

everyone

possible.

of

The

occlusion

and

unresolved questions concerning its liability to oralfacial

pain

and

temporomandibular

(TMJD) are well documented.

joint

disorders

What is it about the

subject of occlusion that defies easy comprehension?

How is it that you can read a text or take a course on occlusion and you are unable to walk away with that: Now I understand the best way to do it:� factor? In fact we are often reminded that there are many ways to do it when we hear that not one occlusal scheme will serve all patients.

What is it about occlusion that is not clear?

A

major

source

definition itself.

of

the

confusion

lies

in

the

Originally, the definition was simply

the closure of teeth (Dorland, 1898).

If Occlusion were

suspect in a problem, one would naturally examine the manner

in

which

closure/function.

the

teeth

touched

each

other

in

Over the years however, the meaning

of the word was broadened and occlusion became a synonym

for

a

detailed

description

of

the

stomatognathic system. The expanded definition: The relationship between all the components of the masticatory dysfunction,

system and

in

normal

parafunction,

function,

including

the

morphological and functional features of contacting surfaces

of

opposing

teeth

and

restorations,

occlusal trauma and dysfunction, neuromuscular physiology, muscle

the

temporamandibular

function,

swallowing

psychophsiological

status,

joint

and

and

and

mastication,

the

diagnosis

prevention, and treatment of functional disorders of the masticatory system (Jablonski, 1982) The change was unfortunate because it clouded the issues. For example, how can we have a serious debate about the role of occlusion in the etiology of TMJD when, if you use Jablonski’s definition, dysfunction and the temporomandibular joint (TMJ) are part of that definition?

Occlusion and the stomatognathic system are two distinct entities and should be described separately.

It

restores order to the ambiguity.

Aside

from

contemporary

the

definition,

texts

on

what

occlusion

is

missing

in

(thestomatognathic

system)?

The

restorative

three basic tenets:

dentist

needs

to

understand

1.

The

most

desirable

way

the

stomatognathic

system should function 2. The most ideal morphology and occlusion of the dentition that allows the system to function ideally.

3. How to recognize and correct when the system is not functioning ideally.

What is missing is an understanding of engineering principles which can not only predict when the system is in a failure mode, but also can render the most optimum design of the occlusion (dentition) for success.

This paper takes

the position

that the majority of

problems that we are seeing today such as TMJD, oralfacial pain, and damaged dentition are the result of compression

of

teeth

which

can

easily

exceed

250

pounds/inches squared. Therefore, it is to our patient’s benefit that we learn as much as possible on the diagnosis and management of this powerful force.

DENTAL COMPRESION SYNDROME A New Look at an Old Problem Historical Background The flattened teeth in the skulls of our ancestors are dramatic evidence that the untoward condition of clenching and

grinding

of

one’s

teeth

has

been

in

existence since the beginning of time.

Clay tablets from the royal library of the Assyrian King Ashurbanipal reveal that grinding of ones teeth was considered both dangerous and pathogonomonic as far fact as the seventh century B.C. described

abnormal

wear

of

teeth

In 1886, Black associated

with

nonfunctional activity, but it was Karolyi (1901) who introduced condition.

most

of

the

current

concepts

of

this

Since that time it has been known by many

names� The Karolyi Effect (1901), Neuralgia Traumatica (1906),

La Bruxumania

(1907),

Traumatic

Occlusion

(1917), Occlusal Habit Neurosis (1928), Traumatogenic Occlusion (1930), Bruxism (1931), Bruxomania (1936), Parafunction (1958), and Dental Compression Syndrome (1993).

Dental Compression Syndrome or DCS was coined to achieve a better patient understanding and to include a wider range of parafunctional activities such as nail biting, tongue thrusting and chewing of oral tissues.

Etiology

There are many reasons why people are affected with DCS and patients have to be informed to raise their awareness.

DCS Triggers: I. Exercise/Sports Rowing,

water-skiing,

lifting

weights,

wrestling,

boxing, riding a motorcycle or any sport where there is a bracing of the body.

II.

Psychological Anxiety, fear, tension, pleasure, aggression, anger, dreaming, stress

III.

Medical

Sleep apnea, oral pain, pain in other parts of the body IV.

Drugs Caffeine, amphetamines, cocaine, ecstasy

V.

Bio-engineering factors DCS

can

be

easily

bioengineering

initiated

principles

in

by the

a

violation

of

stomatognathic

system such as prematurities, off-loading of teeth, horizontal distraction of mandible upon closure, and misalignment of TMJ components.

It

is

important

to

realize

while

interviewing

the

patient that there may be more that one or even several factors contributing to the problem.

Diagnosis

One reason DCS has been so successful over the centuries

is

that

it

works

well

within

one’s

subconscious. Since few patients affected with DCS are cognizant, it is imperative that the visual signs of compression to be recognized so that the problem can be addressed.

Besides the obvious signs of a flattened

dentition and hypertrophied muscles of mastication, there are certain deformations that appear in the oral environment that are barely recognized as to their cause or significance. They are affect the dentition, bone, and restorative materials.

Deformations of the Dentition Classified

as

non-carious

lesions

(NCLs)

these

defects typically are site specific in that they appear at the tips of functional cusps and the gingival area of teeth where the susceptibility to stress is high. (Fig. 1.2) a finite element analysis of a tooth model confirms that stress is highest in these areas.

There are two distinct mechanisms responsible for the loss of tooth structure during compression: tensil forces and positive ion egress.

Engineers tell us that

these high stresses may be responsible for the pain experienced by patients who have restorations in this area where tensile forces are powerful enough to pull apart the enamel prisms.

Although NCSs can be caused by a variety of agents

such

as

low

pH

and

mechanical

abrasion,

compression NCLs distinguish themselves by a glassy sheen.

Kornfeld published on the phenomenon in 1932

when he observed that these defects were hard, smooth, and almost glass-like in appearance.

It is suggested

that the glassy effect is due to the exit of positive ions from these focal points of high stress. produced

by

the

compression

of

The ions are

collagen

in

the

dentition and alveolar bone (piezzo electric effect.)

It is to be noted that compression NCLs do not appear on every patient who clenches their teeth for a variety

of

reasons:

variations

in

the

intensity

and

frequency of DCS, but primarily genetics. They seem to be more prevalent and dramatic in patients with dense alveolar bone compared

to patients with periodontally

compromised teeth. What we are actually seeing are multi-shaped examples of hard tissue fatigue.

Fatigue applies to changes in the properties of a material due to repeated applications of stresses or strains in this case, compression failure from DCS J.E Gordon, a professor of materials at Reading University, describes fatigue: “ one of the most insidious causes of loss of strength in a structure.�

If a subject, such as a tennis ball, rebounds to its original shape after repeated applications, it is said to be elastic in nature.

However, if a subject exhibits

residual defects or sets after repeated applications it is said to be of a plastic nature.

Biological structures,

such as teeth and bone, are termed viscoelastic.

Compression failure of an object occurs at its most vulnerable site. gingival area.

Teeth are most susceptible at the

If alveolar bone recedes, the failure site will also be lowered. in

Fig 15 and 16 demonstrate defects appearing

tandem

as

the

supporting

changing the fulcrum point.

bone

atrophies,

thus

Also note in fig. 15 that

the only occlusal contact is on the incline plane forcing the bicuspid to be flexed toward the lingual when the patient clenches.

Deformations in Restorative Materials Fatigue easily manifests itself in prostheses and restorative materials such as amalgam and acrylic.

In

engineering these wavy patterns are termed ‘Lines of Luder or molecular slip bands.

The explanation is that

molecules in the alloy are rearranging themselves under the

influence

of

compressive

strain.

One

candemonstrate the effect by bending a metal coat hanger

back

and

forth

configuration

that

is

and

examining

produced.

Figures

the 17

stress &

18

demonstrate Luder Lines in amalgam and figures 19 & 20 in acrylic.

Epidemiology A survey was taken of 100 patients (50 female, 50 male, age range 17-76)

Management of DCS

Management of DCS begins with awareness and proceeds with a three-step treatment plan that consist of: I. Education II. Equilibration III. Guard Therapy

Step I: Education The dental healthcare provider must educate the patient as to everything he or she knows about DCS in the simplest terms.

Patients need to understand that

teeth should only touch upon swallowing and should know the resting position of the mandible (lips together, teeth apart.) The list of etiological agents should be reviewed. Patients should be asked to monitor their jaw position

during

waking

hours

and

be

sensitive

to

headaches and tension in muscles of mastication upon waking.

Step II: Equilibration In order to determine the need for an equilibration, the patient’s present occlusion must be compared to a standard of excellence, ie, ideal occlusion.

Based upon

nature’s original design the most ideal occlusion is where the occlusal contact is confined to the tip of the functional cusp.

There are two noteworthy observations. One is the minimal contact confined t the tip of the functiona cusp

and the other is the generous space between the incline planes of the cusps termed theintro-incline space. From these observations it is interesting to note that teeth d not require large areas of contact inorder to maintain their position work efficiently, and be comfortable.

But

what was nature’s intention in providing such clearance between the incline planes?

From an engineering point

of view, there are several advantages.

Vertical Loading The intro-incline space (between the incline-planes) ensures vertical loading.

Misch and Bidez describe

vertical compression forces as normal and explain that they act perpendicular to and maintain the integrity of the alveolar bone.

Neutralization This is the desired buccal-lingual position of the tooth by reciprocal action of the muscles of the tongue and cheek.

When the incline planes do not touch, the

tooth is free to assume a neutral position.

Prevention of Off-Loading When

the

incline

planes

of

the

cusps

are

in

contact, bending or off-loading of the tooth is likely during

mastication

and

compression

resulting

in

destructive shearing forces, which act parallel to the alveolar bone

Step-III: Occlusal Guards Proper management of the patient who is affected with

DCS

entails

separate levels.

addressing

the

problem

on

three

The sharpening procedure satisfies the

engineering requirements and educating the patient can certainly help in stress management during waking hours, but only a guard can insure protection while sleeping.

It is often referred to as a deprogrammer or mandibular repositioner. A common question regarding this design is, “Do the posterior teeth supererrupt?� No, it is not like the Hawley retainer that is worn a majority of the time.

Posterior teeth do not supererrupt overnight

consider the mouth breather.

Generally, studies agree that there is an overall reduction of oral-facial pain (78%) when DCS is treated with

any

type

of

guard.

But

the

smaller

anterior

deprogrammer seems to work best.

For proper management of DCs, the Dentist should monitor for signs of compression and wear, educate the patient abut the problem, and provide treatment, While every patient with a flattened dentition should not have their teeth dramatically altered or reconstructed, there should be consensus in the dental profession that the natural, sharp morphology of teeth is superior to a flattened dentition and should be preserved throughout one’s lifetime.

Tooth discolouration and staining:

Colour and colour perception Basic colour

is

understanding important

of

of

many

the

elements

aspects

of

of

tooth

restorative

dentistry.

The science of colour is important in dentistry with regard to colour perception and description, and can be improved with training. The appearance of tooth colour is dependent on the quality of the reflected light and is also as a consequence, dependent on the incident light.

Tooth discolouration and staining Historically,

tooth

discolouration

has

been

classified according to the location of the stain, which may be either intrinsic or extrinsic.

It may also be of

merit to consider a further category of internalized stain or discolouration

Intrinsic discolouration Intrinsic discolouration occurs following a change to the structural composition or thickness of the dental hard tissues.

The normal colour of teeth is determined

by the blue, green and pink tints of the enamel and is reinforced by the yellow through to brown shades of dentine beneath.

A number of metabolic diseases and

systemic factors are known to affect the developing dentition and cause discolouration as a consequence.

Local factors such as injury are also recognized.

1. Alkaptonuria 2. Congenital erythropoietic porphyria 3. Congenital hyperbilirubinaemia 4. Amelogenesis imperfecta 5. Dentinogenesis imperfecta 6. Tetracycline staining 7. Fluorosis 8. Enamel hypoplasia 9. Pulpal haemorrhagic products 10. Root resorption 11. Ageing

Extrinsic discolouration Extrinsic

discolouration

is

outside

the

tooth

substance and lies on the tooth surface or in the acquired pellicle. The origin of the stain may be: 1. Metallic 2. Non-Metallic

Internalised discolouration Internalised discolouration is the incorporation of extrinsic stain within the tooth substance following dental development.

It occurs in enamel defects and

in the porous surface of exposed dentine. The routes by which pigments may become internalized are: 1. Developmental defects

2. Acquired defects a) Tooth wear and gingival recession b) Dental caries c) Restorative materials

LOCAL FACTORS The mechanisms of tooth discolouration Intrinsic tooth discolouration The

formation

of

intrinsically discoloured

teeth

occurs during tooth development and results in an alteration of the light transmitting properties of the tooth structure.

As mentioned in the classification

section, there are a number of metabolic disorders which affect the dentition during its formation, unlike the inherited disorders in which only the hard tissue forming at the time may be involved.

These disorders

will now be discussed individually.

1. Alkaptonuria: This inborn error of metabolism results

in

incomplete

phenylalanine, homogentistic

which acid.

metabolism promotes This

of

the

affects

tyrosine build

the

up

and of

permanent

dentition by causing a brown discolouration.

2. Congenital erythropoietic porphyria: This is a rare,

autosomal recessive, metabolic disorder in which

there is an error in porphyrin metabolism leading to the accumulation of porphyrins in bone marrow, red blood cells,

urine,

faeces

and

teeth.

A

red-brown

discolouration of the teeth is the result and the affected teeth show a red fluorescence under ultra-violet light.

King George III was said to have suffered with acute intermittent porphyria but with the later onset of this disorder, his teeth are unlikely to have been affected.

3. Congenital hyperbilirubinaemia: The breakdown produces

haemolysis

discolouration. common,

will

cause

a

yellow-green

Mild neonatal jaundice is relatively

but

in

rhesus

incompatibility

massive

haemolysis will lead to deposition of bile pigments in the calcifying dental hard tissues, particularly at the neonatal line.

4.

Amelogenesis

imperfecta:

In

this

hereditary

condition, enamel formation is disturbed with regard to mineralization or matrix formation and is classified accordingly. majority dominant

of

There are 14 different sub types; the them

or

expressivity. amelogenesis

are

X-linked

inherited

trait

with

as

an

varying

autosomal degrees

of

The appearance depends upon the type of imperfecta,

varying

from

the

relatively

mild hypomature ‘snow-capped’ enamel to the more severe hereditary hypoplasia with thin, hard enamel which has a yellow to yellow brown appearance. (Fig.2) 5.

syndromes :

Systemic

Defects

in

enamel

formation may also occur in a number of systemically involved

clinical

syndromes

such

as

Vitamin

D-

dependent rickets, epidermolysis bullosa and pseudohypoparathyroidism.

Barabas has reported areas of

hypoplastic enamel, irregularities in the region of the amelo-dentinal and the cemento-dentinal junctions in Ehlers-Danlos there

is

Syndrome.

pitting

of

the

In

epidermolysis

enamel

possibly

bullosa

caused

by

vesiculation of the ameloblast layer. However, the effect

of these conditions depends on disease activity during the development of the dentition and is usually a minor element.

6. Dentinogenesis imperfecta: Dentine defects may occur genetically or through environmental influences.

The genetically determined dentine defects may be in isolation or associated with a systemic disorder. main condition related to the dentine alone

The

ENAMEL HYPOPLASIAS AND HYPOCALCIFICATION Enamel is ectodermally derived and is produced by ameloblasts.

Which differentiate from inner enamel epithelial cells of enamel organ

Dental enamel is formed in 2 stages

Deposition of organic matrix

Mineralization &

Secretary phase

Disturbance

of

Maturation phase

either

stage

may

cause

abnormalities of tooth structure,

A disturbance of matrix of deposition produces hypoplasia Characterized

by

thickness or deficient

enamel

that

is

irregular

in

in structure

The defects may range from small pits or grooves in the enamel surface to gross deficiency of tissue.

Disturbance during the second stage of developed causes Hypocalcification: although the enamel is of normal thickness, parts of it, at least, are poorly mineralized.

CAUSES REPORTED

TO

AND BE

FACTORS

ASSOCIATED

COMMONLY

WITH

ENAMEL

HYPOPLASIAS Table (1) Causes and factors commonly reported to be associated with enamel hypoplasias of human teeth.

I. Chronological enamel defect Local Causes Systemic causes Local acute mechanical trauma • Neonatal Mechanical Ventilation (Moylan et.al.1980) • Falls and Similar Injuries (Andreasen et al.1971) • Gunshot (Pindborg, 1970) • Surgery (Williamson, 1966) • Ritual Mutilation (Pindborg, 1969) Electric burn (Alexander, 1964)

II Hereditary enamel defect `Genetic Causes

Inborn errors of metabolism • Galactosaemia (Benusis et al. 1978) • Phenylketonuria (Meyers et al, 1968) • Alkaptonuria (Siekert and Gibilisco, 1970, Link, 1973) Amelogenesis imperfecta • Erythropoietic (AI) as isolated phenomenon Porphyria (Rayne, 1967) (Table:2) • Primary Hyperoxaluria (Glass, 1967)

Chromosomal anomalles • Trisomy 21 (Down syndrome). (Cohen, 1971) Irradiation (Doline Congenital defects Amelopgenesis imperfecta et al. 1980) • Heart disease (Hakala, (AI) associated with other lesions 1967) • Unilateral Facial • Epidermolysis bullosa.

Hypoplasia (Gibbard and (Anwill et al. 1965) Winter, 1972) • Pseudohypoparathyroidi • Unilateral Facial sm (Jensen, 1981) Hypertrophy, (Benusis et al.

1978) • Taurodontism, curly hair, scierotic bones, (Tricho-dentoLocal infection Neonatal disturbances • Periapical • Premature birth osseous syndrome).

• (Gorlin et al. 1976) Osteitis (Rosentein, 1974) (McCormick and • Hypocalcaemia (Purvis et Filostrat, 1968) al. 1973) • Acute Neonatal • Haemolytic anaemia Maxillitis (Poley (Solyga, 1970) and Wegner, 1967) • Allergy (Rattner and Meyers, 1962) Infection diseases • Viral Rubella (Guggenheim et al. 1971) • Bacterial Syphilis, Tetanus Neurological disturbances

•

Tuberous sclerosis 9Hoff et al. 1975) Endocrinopathies • Hypothyroidism • Hypoparathyroidism (APECS).

(Myllarniemi et.al. 1978) • Diabetes (Grahnen et al.

1968) Regional Nutritional deficiencies Odontodysplasia (Enwonwu, 1973) (Gardner and Sapp, 1973) Nephropathies • Nephrotic syndrome Other genetically (Oliver et.al. 199963) determined diseases • Infections of urinary • Ehlers-Danlos system (Freden et.al.

Syndrome (Barabas, 1980) 1969) Enteropathies • Coeliac disease (Smith et al. 1979) • Lymphangiectasia (Dummer, 1977) Liver disease, (Pindborg, 1970) Intoxications • Tetracyclines (Baker, 1975) • Thalidomide (Axrup et al. 1966) • Vitamin D (Pindborg, 1970) • Pica (Lawson et al.

1971)

Thoma and Goldman believe that hypoplasia is due to an alteration in ameloblastic activity of the enamel organ. This alteration is probably inhibitory in nature and causes atrophy and lack of unction of ameloblastic cells. These cells do not recover their vitality and when

the alteration disappears, neighboring cells continue to form normal enamel, leaving behind a line of ill-formed enamel.

The exact cause of enamel defect is often not obvious from the clinical history, but a number of potential causes have been identified (Table1) Hereditary

enamel

defects

(amelogenesis

imperfecta) affect all areas of the enamel in permanent and deciduous teeth, in contrast to the ordinary type of ‘chronological’ enamel hypoplasia.

The frequency of enamel hypoplasia is greatest in the anterior dentition, is intermediate in premolars, and lowest inmolars.

On average, maxillary central incisors

are most often hypoplastic

and

canines,

lower

lateral

incisors, and second molars are least often hypoplastic.

Within

the

dental

literature

one

hypothesis

is

repeatedly given to explain variations in frequencies of defects

by

tooth

type.

According

to

this

‘time

of

development’ hypothesis, the frequency of defects is dependent on which tooth crowns are developing at the time which insults are most active.

Earlier occurring

insults will affect only the earlier developing tooth crowns,

whereas

subsequently

later-occuring

developing

tooth

insults

crowns.

will

affect

Analysis

of

tooth crowns by developmental period clearly shows that time of development is not the sole determinant of hypoplasia. (fig.1) While time of development provides an explanation for part of the difference in frequency of hypoplasias, it clearly does not explain all of the differences, as teeth

developing at the same time do not all have a similar frequency should

of

enamel hypoplasia.

also

be

considered

susceptibility

to

hypoplasias

Therefore,

which

might

such

as

factors govern

biological

gradients.

Hypoplasias are not randomly distributed within tooth crowns.

Furthemore, the distribution is similar

for all tooth crowns, regardless of time of development.

Overall,

there

frequency

of

is

a

consistent

defects

in

the

pattern

middle

of

thirds

increased of

tooth

crowns, while the cervical third is more hypoplastic than the incisal third in all tooth classes, there is some evidence that this difference increases as one moves toward the posterior teeth.

The

process,

which

controls

within

tooth

differential susceptibility to hypoplasias, is yet to be considered.

However study by Goodman and Amelagos

(1985) suggested four factors to considered.

First, the

number of secretary (matrix-forming) ameloblasts may decrease towards the cervical half of the crown. Second, there is some evidence that rate of crown development increases in the middle and cervical third of tooth crowns.

In this situation ameloblasts are forming more

enamel in a given unit of time and may, therefore, be rendered more vulnerable to disruption when their rate of development is rapid.

A third explanation holds that

the expression of a hypoplasia is a function of enamel prism

direction.

Enamel

prisms

are

most

nearly

perpendicular to the surface at the zone just cervical to the midpoint.

This orientation may increase the ease

with which one can discern variation in prism lengths.

Fourth,

longer

prism

might

be

more

sensitive

to

disruption.

When long-term ingestion of excessive fluoride is the cause of hypoplasia, the affected enamel can be expected to be distributed over the part of the crowns of teeth developing during that period.

LOCALIZED NON HEREDITARY ENAMEL HYPOPLASIA TREATMENT MODALITIES Since these defects varying in extent and locations, there will be also be a range of treatment modalities.

If Defects are of minimum size (narrow lines or isolated pits or shallow depressions.

Selective odontomy can be performed blending the defects with the remaining tooth surfaces.

If odontotomy and esthetic reshaping of the tooth enamel cannot produce a pleasing functional effect;

It is necessary to resort to direct-tooth colored material It should be clear that acid etching of the fluoride hypoplastic

enamel

is

extremely

conducive to efficient retention.

difficult

and

non-

Therefore several applications of conditioning acids should be used.

If the defect is at the adjusting or contacting area, it is necessary to resort to metallic or cast restorations.

However it should be clear that fluoride hypoplastic enamel is very brittle and chips very easily during tooth preparations and restorations 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.

Such vital bleaching can be accomplished in the following way.

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 choice

They can be applied according to the following 1. Loss of Vertical dimension 2. Check biting 3. Gingival irritation/loss of occlusal table 4. Attrition/decay 5. Attrition /sensitivity 6. Bruxism / occlusal splints 7. TMJ / disoccluding splint 8. Vertical dimension measurement 9. Tooth brush abrasion 10. Pipe stem abrasion 11. Sewing thread abrasion 12.

Pica syndrome

13.

Iatrogenic ablation

14.

Iontophorosis

LASER THERAPY: Lasers are now more actively used for oral hard and soft tissue treatment Hashimoto reported that after irradiation of defective enamel of rats with an laser, the surface became smooth and small defects disappeared

LOCALIZED 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 grey.

TREATMENT MODALITIES No attempt should be made for localized odontotomy, etching

restorations,

or

non-veneering

types

of

restoration.

If a diagnosis is made in 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

iontophoresis,

and

strict

prevention of plaque accumulation in these areas.

In many situations mineralization of these decalcified of unmineralized areas will take place to some extent.

Usually o VITAL BLEACHING o LAMINATED VEENERING o COMPOSITE VEENERING o PFM OR CAST CERAMICS Are the treatment used.

AMELOGENESIS IMPERFECTA Amelogenesis imperfecta (AI) is a group of inherited abnormalities of dental enamel

It

may

hypoplastic,

be

differentiate

hypocalcified,

into and

3

main

groups

hypomaturative,

depending on the clinical presentation of the defects and likely stage of enamel formation.

Each main group of AI may be further divided into several

subgroups

depending

on

the

mode

of

inheritance, as well as the clinical appearance of the defective enamel

Table (2) Classification of Amelogenesis Imperfecta (AI) according to Witkop (1989) Clinical and radiographic appearance

Inheritance

Type

Subtype

Hypoplastic (HAI)

I IA IB

Pitted Local

ID

Smooth

IF

Rough

IC

Local

IG

Rough

X-linked dominant

IE

Smooth Male

Hypomaturation (HMAI) Autosomal-recessive

II IIA

Pigmented

X-linked recessive

IIB

Male

Autosomal-dominant

Autosomal-recessive

Colour

Enamel Enamel Clinical appearance Thickness Hardness Enamel does not develop to normal thickness Yellow-white Normal Normal Pin-points in random, multiple teeth Yellow-white Normal Normal Pits or depressions, usually buccally, linear horizontal White to yellow- ¼ to 1/8th of Normal but Thin,glossy,general;teeth do not contact, brown normal may abrade Anterior Open Bite (AOB) occurs in about 50% Yellow-white to ¼ of normal Chips from Rough,granular surface’teeth do not contact white dentine (AOB) occurs in about 50%

Radiographic Appearance Mild lucency in deep pits Mild lucency in deep pits Thin,opaue enamel;normal contrast to dentine Thin,opaque enamel;normal contrast to dentine

More severe than the dominant type

Hypocalcified enamel may occur in the hypoplastic areas Yellow Nearly absent Rough,granular surface;occasionally enamel not evident missing teeth, (AOB) occurs frequently 11/13 Yellow-brown Thin Abrades Smooth,shiny,thin;teeth do not contact Thin,opaque enamel easily (AOB) most common presentation for outline;normal contrast affected males to dentine Enamel is of normal thickness but has a mottled appearance Brown-stains deep White;darkens with age

Normal

Female

Yellow

Normal

White to honey Normal

Near normal

Chips easily

Shiny,smooth,dark enamel (AOB) occurs infrequently Soft; abrades Mottled enamel,which darkens;posterior cervical less affected

Enamel same radiodensity as dentine Enamel same radiodensity as dentine

Autosomal-dominant

IIC

Hypocalcification (HCAI) Autosomal-dominant

III

Vertical bands of normal enamel between Enamel same radiodensity abnormal;posterior cervicalless affected as dentine Snow-caped teeth Opaque white Involve ¼ to 1/3 of the crowns of teeth, it may be mistaken for fluorosis but does not have the accented perichymata linear patternseen influorosis Enamel initially develops normal thickness, but consists of poorly calcified matrix,which is rapidly lost leaving dentine cores.

IIIA

Regular

Autosomal-dominant

IIIB

Regular

HypomaturatinIV Hypoplastic with taurodontism Autosomal-dominant IVA Autosomal-dominant

IVB

Soft;abrades

Soft;cheesy

Soft,cheesy enamel;can be removed with a Enamel same as or less prophylaxis radiodensity than dentine.

Same clinical findings as IIIA, but with a greater degree or severity

Enamel is a mottled white-yellow brown with pts most frequently on the labial face or in this with areas of Hypomaturation HM-HP with taurodontism HP-HM taurodentism

Near normal with

Thin

Enamel predominantly Hypomaturation Enamel same as with areas of Hypoplastic radiodensity than dentine Enamel predominantly Hypoplastic with Areas of Hypomaturation

DIFFRENTIAL DIAGNOSIS OF A.I The D.D. between enamel hypoplasia and A.I. must be based on clinical and laboratory data.

The diagnosis of A.I. should be based on the following criteria • Generalized enamel hypoplasia of both the primary and permanent dentitions.

• Family history of the condition • Absence

of

systemic

diseases

that

may

cause

generalized enamel hypoplasia

SIGNS AND SYMPTOMS • Thin enamel • Open contact • Small

teeth,

with

short

roots

very

limited

chambers and root canal dimensions.

• Delay in eruption • Sometimes enamel is glassy • There may be some discoloration usually yellow • The enamel would look unwrinkled • All signs of severe occlusal occur

pulp

Early diagnosis is the key to a relatively successful # Only two modulation can be used in most cases. • Selective teeth.

odontotomy

esthetically

reshaping

the

This is repeated procedure that is needed

throughout the lifetime of the tooth because of frequent changes in shape (attrition) • Full veenering includes procedures with metallic, metallic based or cast ceramic restorations.

At no

time should these restorations oppose a natural tooth

teeth should be restored at the same

time with same materials

Oral Rehabilitation of Young Adults with Amelogenesis Imperfecta Amelogenesis imperfecta (AI) is a rare developmental abnormality

of

the

tooth

enamel,

with

a

suitable

occurrence of approximately 1:4,000 to 14000 in Western populations.

A widely used classification system for AI is

based on genetic interference, histopathology, and specific clinical dental characteristics. A more recent classification system also includes limited molecular and biochemical information. In general, the inheritance pattern is equally autosomal dominant or recessive, or X-linked.

Within

affected families, there is an extremely variable clinical appearance of enamel hypoplasia, hypocalcification, or

hypomaturation, depending on which stages of enamel formation are involved.

Dental features associated with AI include quantities and qualitative enamel deficiencies, pulpal calcification, taurodontism,

and

root

malformations:

failed

tooth

eruption and impaction of permanent teeth; progressive root and crown resorption; congenitally missing teeth; and anterior and posterior open bite occlusions (fig) Children and young adolescents exhibit these general features of AI, which may not be the same in young adults, where caries and marked sensitivity may commonly result from widespread exposed dentin in the permanent teeth.

This

exposure may arise either from a deficiency in the enamel attachment to dentin or from extensive occlusal wear of defective enamel that may be also result in the loss occlusal vertical dimension (OVD) In younger patients especially,

they

may

be

compensation for the wear. may

also

occur

at

appreciable

dentoalveolar

Excessive tooth enamel wear

proximal

contacts

or,

conversely

interproximal tooth spacing may be present when the teeth are small and the enamel is inherently thin.

Factors

adversely

management associated

may

include

gingivitis

and

influencing poor gingival

oral

restoration hygiene

hyperplasia.

with Oral

hygiene is poor in some patients, often because of tooth hypersensitivity and the presence of an anterior open bite associated with mouth breathing.

Patient-1 A healthy 18-year old woman was referred by her general dental practitioner for the treatment of AI (Fig-2) She wanted to improve the appearance of her anterior teeth especially, which were discolored brown and had stained, pitted, hypoplastic enamel.

The patient stated

that her primary teeth were also discolored.

There was

minimal occlusal tooth wear, without exposed dentin. She also

had

poor

oral

hygiene,

caries

and

several

unsatisfactory restorations.

The oral hygiene of the patient was improved after intensive therapy, then porcelain veneers were bonded to enamel following preparation of all the anterior teeth. The patient was extremely pleased with the result, and she gained an additional incentive for

maintaining her oral

hygiene brown, discolored posterior teeth were restored sequentially, when the patient was 19 to 22 years with metal-ceramic and gold crowns all the OVD At a 5 year review, there was some gingival recession around the restored anterior teeth and the metal ceramic crowns on the maxillary interior teeth were replaced with all ceramic crown to further improve the appearance of the patient.

DISCUSSION Of practical importance for the restorative treatment of AI are the following parameters: • Size

of

the

pulp

chambers

and

amount

of

occlusal and interproximal tooth wear • Loss

of

OVD

and

degree

of

dentoalveolar

compensation • Number,

form,

color,

and

sensitivity

of

the

affected permanent teeth • Strength of attachment of the enamel to dentin and dentin quality • Thickness

of

enamel

and

degree

of

mineralization, and the ability of restorations to bond satisfactorily to the affected enamel.

Newer dentin bonding systems provide more reliable bonding to dentin than did earlier systems and, although the newer systems also infiltrate enamel prisms more effectively, they might provide more Durable dentin bonding than when attempting to an absence of typical etch patterns in enamel affected by hin, smooth, hypoplastic, and male X linked variants of AI. Hypocalcified and hypomatured enamel in particular also contain increased amounts of protein.

A major restorative problem can be the continued debonding of interim resin composite veneers, as occurred with patient 2. In this situation, adequate retention of the final

restorations

requires

crowns,

or

removal

of

the

overlying defective enamel is suggested Before bonding the veneers to the exposed dentin.

The general treatment sequence suggested for young adults presenting with AI is as follows

Preventive and initial phases; • Oral hygiene instruction, prophylaxis, and scaling • Fluoride and chlorhexidine mouthrinses, control of dentin hypersensitivity • Extraction

of

non-strategic

teeth,

initial

urgent

restorative treatments • Orthodontic and other consultations Restorative phase (over an extended period): • Maxillary overdenture or provisional occlusal splint • Resin

composite

buildups

for

anterior

and

other

selected teeth if the enamel is suitable for resin bonding • Thin gold crowns or resin-bonded cast onlays for posterior teeth

Complete-mouth rehabilitation • Crown

lengthening

of

worn

maxillary

and

other

selected teeth if required • Metal-ceramic crowns or than all ceramic polymer resin-bonded crowns and porcelain veneers if the enamel is suitable for bonding

Maintenance phase • Monitor oral hygiene, periodontal and pulpal status, and restorations Initial restorative treatment should be conservative, using direct adhesive materials. However infective enamel quantity and quality might require selective clinical crown lengthening

surgery

and

the

placement

of

crowns

lengthening surgery and the placement of crowns for adequate retention esthetics, and the reestablishment of OVD. OVD

can

be

reestablished

using

several

restorative

methods, but careful treatment planning is required before undertaking the occlusal rehabilitation. Overdentures are the least expensive and least invasive treatment approach and, should patients be able to adapt to an altered increased OVD the prostheses can be adjusted or remade.

The dentures also act as reservoirs for topical fluoride gels and de-sensitizing agents.

Although posterior resin composite onlays with cusp coverage may be functionally adequate to reestablish the

OVD

in

some

instances

of

AI,

bonded

cast

restorations are preferable when multiple restorations are required for occlusal stability. Preparations for thin gold crowns are also more conservative than those for metal ceramic crowns and gold crowns are preferred for restoring molars that have extensive interproximal and occlusal wear the creation of a tin oxide or silica layer on

the

sand

blasted

fitting

surfaces

of

metal-alloy

castings significantly improves the adhesion of luting cements.

Restoring

primary

molars

using

nickel-

chromium crowns, and then later the permanent molars with thin gold crowns, early in life will preserve the OVD and ceramic

prevent interproximal tooth

crowns

with

labial

porcelain

wear.

Metal

margins

are

considered a satisfactory esthetic option in adults for restoring defective anterior and posterior teeth.

The

preparations are more conservative than those required for all ceramic crowns with high-strength cores.

Conclusion The complexity of the management of patients with AI support

the

profession

suggestion

should

have

that a

rehabilitation of rare disorders. with

AI

should

start

with

the

key

prosthodontic

position

in

the

Treatment of patients early

diagnosis

and

intervention to

LOCALIZED NON-HEREDITARY DENTIN HYPOPLASIA The odontoblasts are also very specialized cells. function

and

products

(Dentin)

can

be

Their

disturbed

by

environmental irritation, leading to deficient or complete absence of matrix deposition.

The

ameloblasts

are

irreplaceable

cells,

and

their

disappearance means no enamel in this particular area.

However, the odonto blasts are replaceable cells

If they disappear there will be no dentin temporarily, but dentin deposition will be resumed as soon as after pulp cells start depositing it.

In these cases, the defect will be isolated within the dentin substance.

The causes are exactly the same as those for localized enamel hypoplasia.

As long as they are covered with the dentin and enamel, there will be no apparent destruction to be diagnosed of 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 situation, 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 of the lesions dimensions.

Treatment here could consist of intermediary busing, as it is an additional dimension to that part of the tooth preparation that is going to be restored.

LOCALIZED NON-HEREDITARY DEMIN HYPOCALCIFICATION

These defects have same causes as hypoplasia

Even though the dentin will be present in substances, 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

lesions.

The best hedge against problems from the presence of such

type

of

dentin

intermediary busing.

in

tooth

preparation

is

proper

DENINOGENESIS IMPERFECTA These are also genetically dictated classes of diseases affecting the formation or maturation of dentin matrix in the

absence

of

any

obvious

systemic

of

biochemical

changes

Most

of

them

are

autosomal

dominant.

The

most

frequently reported is the hereditary opalescent dentin.

SIGNS AND SYMPTOMS • The color may be grey, brown yellow, brown to violet • Most of them exhibit translucent hue • The enamel although intact, is easily d of defective D.E Junction • The crowns are overcontoured • The roots are short and slender • Signs and symptoms of extensive attrition • The

dentin

devoid

of

tubules,

contains

interglobular dentin • The decay if initiated spread laterally • Root enamel and pulp chamber is obliterated • Dentin hardness and residence is decreased.

lot

of

TREATMENT MODALITIES Any possible success for treatment depends upon early diagnosis and cure.

Only two possible # modalities can be used here namely

• Selective odontotomy • Permanent full veneering

There should not be any false security in preparing these teeth. root

canals,

Because of the absence of pulp chamber and as

these

teeth

are

very

susceptible

to

fracture.

There should not be any attempt to use intracoronal or intraradicular retention modes.

Therefore the only retention possible is an extracornal reinforcing protecting veneering restoration.

Splinting between these teeth is one way to avoid fracture.

TETRACYLINE DISCOLORATION It is a soft of permanent staining of the dentin and to some extent enamel.

Discoloration in enamel and dentin can be treated in the same way localized non-hereditary enamel

and

hypercalcification

DISCOLORATION IN THE PULP ROOT CANAL SYSTEM, This can result from pulpal neurosis in which the disintegration

products

diffuse

there

dentinal

tubules

from root canal-pulp chamber system.

Discoloring dentin and entire tooth

Such discoloration intensifies with time

Due to more disintegration products while in dentinal tubules

This discoloration is usually grayish to dark black

Internal resorption causes pinkish discoloration.

At the areas where pulp tissues come close to the tooth surface following resorption of pulp chamber of root canal cells.

Internal

hemorrhage,

due

to

excessive

instrumentation irritation during cavity preparation.

Can also cause discoloration from pulp-root canal system

TREATMENT

If tooth non-vitality is the cause, endodontic therapy should be initiated After, successful treatment proceed with the following sequence of # a) NON VITAL BLEACHING (WALKING BLEACH)

STEPS b)

If

non-vital

bleaching

does

not

resort

to

end

with

pleasing results It veneer

may of

be

necessary

P.F.M.

of

to

cast

restorations as described before.

ceramic

laminated veneering

c) If internal resorption is the cause of discoloration Initiate endodontic therapy

After successful completion of endodontic#

Clean

out

concavities

in

the

pulp

chamber

expected by internal resorption.

Fill it with a suitable tooth-colored material, possibly, silicate cement.

d)

If

internal

hemorrhage

has

caused

the

discoloration The tooth should be covered with Z0E or a Z0E cemented temporary for a while

This will facilitate the resolution of hemorrhage

If discoloration does not disappear in time, if darkening

occurs

of

confronted

with

degenerative

pulpal symptoms

Endodontic therapy may be necessitated.

MALFORMATION Can be in either micro or macro forms, and is usually hereditary origin.

The most common type of malformation is one of 2 teeth (usually upper lateral) That is noticeably smaller in size than surrounding ones, with pointed incisal edges (PEG TEETH) Malformation should be differential from the illusion that can occur when there is a substantial discrepancy between tooth size and jaw size.

This

should

not

be

converted

by

restorative

procedures, but rather with orthodontic #.

TREATMENT MODALITIES If the affected tooth is properly aligned in the arch and has intact enamel and is not subjected to extensive occluding forces.

Conditioning of the enamel and building the tooth up with a direct tooth colored resinuous material will be the treatment of choice.

Correction of peg lateral

• If the affected tooth is malaligned Repositioning

should

be

performed

before

any

restorative treatment. • If the affected tooth does not have sufficient quality enamel to retain a restoration similar to that described.

OR if the tooth (after a restoration) can be subjected to excessive occluding forces.

It

is

preferable

to

select

P.F.M

of

cast

ceramic

veneering restorations as the treatment modality.

TRAUMA Separation and/or loss of tooth structure as a result of trauma.

Frequently occurs necessitating dental treatment Trauma that leads to these mishaps can be from substantial impact forces, as from a fall, a blow, or sudden biting on a hard unyielding substance, from long standing repetitious cyclic loading forces.

TREATMENT MODALITIES There

are

3

therapeutic

bases

for

the

#

of

should

be

traumatized teeth 1)

Accurate

and

detailed

diagnostic

data

collected.

In addition, data on the status of the root condition and development is necessary.

2) The patient should be awake of the fact that vitality of the tooth at the time of examination does not mean that tooth will be vital by the end of # of later in life.

As traumatic energy may start a degenerative process in P.D. organ that can lead to immediate pulp necrosis of a very delayed, slowly progressing one (sometimes over 10 years) 3) Sometimes, due to the incomplete tooth development and/or the extent of tooth involvement, or early stages of passive tooth eruption when the accidental tooth defect occurred.

The tooth will need 2 sets of restorative modalities.

The first one is a provisional restoration until the tooth completes its development Its

passive

eruption

is

stabilized

or

endodontic

therapy is successfully completed.

The second one is a permanent restorations.

4) The following is a scheme suggested for each class CLASS I • Smoothing the edges and peripheries of the defect is sufficient in most cases. • Esthetic reshaping of the involved area and similar areas on symmetrical teeth may be necessary. • If the defect involves a relatively large surface area of an anterior

teeth

not

correctable

by

either

of

the

step

considered above.

Surrounding enamel may be conditioned.

The area restored in a resinous direct tooth-colored material.

If it is posterior tooth, a metallic restoration should be used.

CLASS II In most cases, two sets of restorations are indicated The provisional teeth can be class IV for anterior teeth according to the extent and location of the defect.

For posterior teeth it can be an amalgam.

The permanent restoration is usually indicated after provisional one fulfills its objectives. i.e, after confirming a sound pulp dentin organ, or completion of passive eruption etc.

In many situations, the provisional restorations can actually serve as permanent ones.

CLASS III For these cases, the pulp and root canal therapy should be initiated immediately.

In most cases, for the purpose of esthetics, space maintenance and facilitating successful pulp and root canal therapy.

The

tooth

crown

should

be

built

up.

In

these

situations proceed according to the following sequence.

• Make initial pulp therapy e.g., pulp extirpation, pulpotomy, D.P.C In

extirpation

and

pulpotomy

situations,

leave

a

dry

cotton pellet in pulp chamber or its entry site, or inject an elastomeric important material into the pulp chamber and let it set.

Build

up

the

tooth

crown

with

a

provisional

#

restoration.

This can be pin-retained restoration, tooth colored restoration etc.

Follow the principles of building badly broken down tooth.

For further endodontic therapy steps make an access cavity preparation through the hardened restoration to the pulp chamber.

(The residual dry cotton pellet of elastomeric “plug� will guide, indicate and confirm the entry to the pulp chamber).

Proceed with indicated endodontic therapy When it is successfully completed

The created access cavity preparation through the restoration. Together with the involved pulp chamber and sometimes part of root canal, should be obliterated with the same material used to build up the crown with or without premade post. The choice of the post should be according to the need.

In this way, the provisional treatment restoration is converted

to

a

formulation

for

a

cast

alloy

based

reinforcing – protecting type of a restoration.

CLASS 4 Proceed according to the following sequence • If the tooth crown is intact, immediately initiate endodontic therapy.

• If the tooth crown is fractured proceed as described earlier.

• If the tooth crown is discoloured, especially in conspicuous teeth, and a veneering permanent restoration is not planned.

Use

non

vital

bleaching

procedures as described earlier.

of

laminated

veneering

Which is done after successful endodontic therapy. •

If

the

tooth

is

discoloured

beyond

any

possible

bleaching, laminated veneering is contraindicated and/or it has a provisional # restoration.

Tooth should be veneered with cast alloy based or east ceramic restorations.

CLASS 5 Accidental restorative

tooth

loss

capability

or

should

fracture be

beyond

replaced

any

with

a

prosthesis.

If

the

loss

occurred

early

in

life,

where

fixed

prosthesis is contraindicated, a provisional fired bridge can be used.

Pontic tooth can be a plastic denture tooth that should be chosen and adjusted to occupy the space and function of the lost tooth.

To facilitate attachment of the plastic tooth to the adjacent abutment teeth, it should accommodate two steel rods (0.050�). The steel rods are joined to the artificial

tooth through light or chemically cured resin in prepared cavities in the tooth embedding steel rods.

When conditions allow, a permanent fixed cast (cast alloy based) bridge should replace the provisional bridge.

CLASS 6 Root fractures can be classified therapeutically as cervically horizontal, midradicular horizontal, especially horizontal and vertical.

A) Cervically horizontal (slightly oblique) Root fractures are always accompanied by a complete loss of the crown looseness, necessitating its removal.

The treatment procedure here is endodontic therapy.

Preferably a one-visit procedure Then, the remaining tooth structure is handled some way as a badly broken shown tooth.

Any

indicated

periodontal

surgery,

intensional

extrusion etc., should be accomplished.

To bring the gingival margin of the defect occlusal to the attacking epithelium.

Proceeding with regular restoration of badly broken down, endodontically treated tooth.

B) MIDRADICULARLY HORIZONTAL (SLIGHTLY OBLIQUE) • If tooth vitality is assured, immobilization is the only treatment required until signs of repair are evident.

Splinting

could

be

permanent

as

healing

takes

several years.

REQUIREMENTS OF MODERN SPLINTS

Different

splinting

techniques

are

currently

recommended for stabilization.

Including • WIRE COMPOSITE SPLINT • ORTHODONTIC BRACKET SPLINT • RESIN SPLINT Each splinting option has its advantage and short comings.

A new splinting technique using a new device TTS (Titanium Trauma Splint) offers improved comfort and handling to the patient and dentist alike.

TTS

TTS splints (52 mm in length) in different colours depending upon the anodization process.

The TTS (Titanium Trauma Splint, patent pending) has been developed by the authors in close collaboration with Medartis AG, Basel, Switzerland. The main objective of

developing

a

new

device

was

to

optimize

current

splinting techniques.

After

repositioning

the

traumatized

maxillary

left

central incisor, minimal etching gel is applied according to the small openings of the TTS. Using bonding agent and light curing composite, resin, the TTS has been fixed to stabilize the injured tooth. At the time of splint removal, the TTS can just be “peeled� off from the tooth surface.

The TTS is made of pure titanium and is only 0.2 mm thick. Therefore, it can be easily adapted to the contour of the dental arch. Pliers or bending instruments are not necessary, since the TTS can be bent with the fingers. The TTS is available in two lengths, 52 mm and 100 mm. The TTS can be cut to the desired length with any cutting

instrument,

or

preferably

with

the

specially

designed

scissor-instrument.

The unique design of the TTS with its rhomboid mesh structure

makes

it

flexible

in

all

dimensions,

thus

allowing physiologic tooth mobility without transferring forces to the splinted teeth. On the other hand, the material and dimensional characteristics of the splint (width 2.8 mm) still guarantees a certain mechanical stiffness to withstand shearing forces.

Another

advantage

of

the

TTS

are

the

rhomboid

openings of the splint which facilitate its fixation. The size of the rhomboid openings (1.8 x 2.8 mm) clearly defines only a small area of bonding, thereby reducing the amount of composite to be used. It is no longer necessary to shape a bulk of composite around the splint. On the contrary, a thin layer of a (fluid), composite can be simply applied to fill the rhomboid openings with subsequent light-curing.

Case report – 1 A 26 year-old female patient, sustaining a tooth injury in a basketball game reported that her upper left incisor was displaced to the palate, and that she had

repositioned her mobile tooth immediately by pushing it forward with her tongue.

If tooth vitality is doubtful of the tooth, become nonvital,

endodontic

treatment

should

be

instituted

and

successfully completed.

Then a splinting, reinforcing stainless steel (chrome cobalt) rods should be cemented, joining two fragments together.

The tooth should be permanently splinted to adjacent teeth.

C) APICALLY HORIZONTAL (OR SLIGHTLY OBLIQUE ROOT FRACTURE) If the tooth vitality is assured, it should be left without any interferences.

However, if the tooth becomes non-vital or its utility is doubtful, endodontic therapy should be instituted and the apical root fragment is surgically removed.

Attempts to join and splint the apical fragment to main root, especially when surgery is not feasible, can interfere with the apical seal of the root canal.

D) VERTICAL ROOT # It is extremely difficult to diagnose this type of fracture Only through symptoms of • Isolated periodontal pocketing next to the # line • Tooth non-vitality • Loosened Retrograde filling.

• Reflecting a micro-gingival flap exposing a fracture line.

Then diagnosis can be accomplished

ETIOLOGY • Overcondensation during root canal filling • Overly energetic insertion of root canal posts and impact trauma.

TREATMENT Vertical fracture of the root has a very unfavourable prognosis.

As it always propagates quickly to the tooth crown

Thereby connecting the periodontium and pulp root canal tissues with the infected oral environment There will be no way to seal this created avenue.

Almost always, the root affected by this type pf fracture should be eradicated This means extraction of a single rooted teeth and hemisectioning

of

partial

amputation

of

multi-rooted

tooth.

CLASS VII In this class, after proper reduction of tooth and/or replacing in its socket If

its

replantation,

root

canal

debridement

and

obliteration should be done prior to reduction.

Tooth (teeth) should be splinted to the adjacent ones using one of the different methods described earlier.

CLASS VIII Cases falling under this category are usually reported immediately after the tooth #.

So the pulp is vital, even if it is exposed.

In these cases if the separated crown portion is retrieved and intact, the following should be done.

• Clean the retrieved tooth piece and keep in sterile solution.

•

If

the

pulp

is

involved,

initiate

and

complete

endodontic therapy in preferably one visit procedure.

• The enamel surface at the fracture line of the remaining tooth and intact broken portion should be conditioned and primed.

• If tooth is endodontically treated, the pulp chamber should be filled with composite resin.

In

both

treated

teeth

endodontically situations,

the

and two

non-endodontically pieces

are

brought

together, and kept under pressure until the primer and composite resin set.

The enamel surrounding the junctional line between two fragments is conditional and formed as usual, and composite resin is flowed there to further join the two fragments.

This type of restorative treatment modality should be considered

provisional

restoration,

especially

if

the

involved tooth is one that is laterally loading during functional movements.

However for immediate esthetic restoration This is an excellent # modality CASE REPORTS CASE REPORT – 1 – Enamel and dentin bonding agent used for repair.

CASE REPORT – 2 & 3 – use on adhesive luting system 1 & 2 – Gloss Pulp exposure. R.C.T. made necessary.

3

–

Small

exposure

was

treated

with

bonding/luting

system.

CLASS IX There

are

many

possible

reasons

for

the

high

incidence of cracked teeth in modern dentitions, eg., more people keep teeth in older age, with accompanying and more possible steep cusps, highly calcifying intermediary bases, use of high speed equipment in tooth preparation, use or posts in retaining restorations, etc.

There are numerous factors that encourage such incremental cracking of teeth. These include:

A. Premature occluding contacts, especially in lateral mandibular excursions. Balancing contacts are the most predisposing.

B. Very

wide

and

deep

intracoronal

restorations

(especially MOD restorations).

C. Disclusion

mechanism

including

posterior

teeth,

especially without any canine components.

D. Forced-in retention modes of a restoration, eg., pins, cements, etc.

E. Vibrating rotary instruments, especially high speed ones.

F. Posterior teeth cusp inclines and groove dimensions not compatible with the progressive and immediate side shifts of the mandibular movements.

G. Habits H. Severe thermal cycling in the oral environment.

I.

Non-vitality of tooth structures (totally and locally).

J. Hypermineralization

or

dehydration

of

tooth

structures.

K. Sharp deep surface fissures or grooves, extremely sharp line and point angles of a preparation in a

tooth, and any internal or external sharp details that may act as shear lines for a crack culminating in a fracture.

L. Loose intracoronal restorations. This situation will magnify the shear within the tooth.

The diagnosis of a cracked tooth in one of the most perplexing of all dental diseases. Usually the patient will show one or more of the following signs and symptoms.

Frequently,

the

chief

symptom

is

pain,

indicating

combinations of pulpitis and periodontitis at different levels, depending on the degree of periodontal and pulpal involvement with the crack. The same stimuli provoking these

types

of

pain

can

be

used

here

for

diagnosis

(thermal, osmotic pressure changes, etc.). usually, the tooth looks intact, without any restoration or with an apparently sound restoration. The patients almost always show evidence of good plaque control. The patient will frequently chewing,

complain since

that

posterior

the teeth

pain are

is

elicited

more

while

frequently

involved than anterior ones. The frequency of occurrences in posterior teeth is in the following order; second lower

molars, first lower molars, and maxillary premolars. The rest of the posterior teeth are seldom affected.

Upon applying pressure on segments of the tooth, one at a time, one application can start the painful episode.

Such pressure can be applied by wood sticks, mirror handles, inlay seaters, amalgam pluggers or asking the patient to bite on a rubber wheel.

If

the

tooth

contains

an

amalgam

restoration,

the

corrosion products of the amalgam might stain the crack.

The stained crack can be apparent from the tooth surface or

seen

only

after

removing

the

amalgam.

Also,

transillumination, using fiber optic or incandescent light, can show the crack when the light is brought close to it.

Furthermore, some coloring dyes can show up the crack by staining the accumulated plaque within it. Examples of these dyes are methylene blue or mercurochrome, etc.

In many situations the crack is apparent to the unaided eye without staining or transillumination, but usually accompanied with enamel crazing. So, whenever enamel crazing is discovered, further examination of the enamel

and dentin should be done to verify or negate the presence of a crack.

Any of the possible predisposing factors should be explored,

for

a

radiograph

can

show

an

apparently

completely sound tooth. However, infrequently, a crack might appear in it, if it is sizable enough and in the plane shown by the radiograph.

Periodontal break-down can be evident at the site of the crack (connected or disconnected pocket). This is due to the detachment of the periodontal membrane ligaments from the tooth at the site of the crack. In many situations, this could be the first sign of a crack. An orally apparent crack can be explored using a sharp explorer pressing it pulpally, as this might elicit the episode.

TREATMENT MODALITIES 1. Relieve the tooth from eccentric occluding contacts.

In some severe cases, it should also be released from centric ones.

2. Cement a circumferential band around the tooth (orthodontic or copper band).

In many situations the pain is completely alleviated by the two above mentioned treatment modalities.

3. If

the

signs

of

pulpitis

(or

pulpal

degeneration)

persist after (1) and (2), proceed with endodontic therapy. While in the pulp chamber and root canal system, look for any continuity of the crack with the root canal walls or subpulpal floor, because if the latter situations are verified, the tooth should be extracted or undergo hemisectioning or amputation.

If there is no crack continuity to these anatomical landmarks, complete endodontic treatment.

4. If the tooth contains an intracoronal restoration or a carious lesion, it should be removed and a temporary ZOE restoration should be inserted and kept there for at least two weeks (with the band on). Sometimes the temporary is mixed with a staining dye to verify the extent and propagation of the crack.

5. Any periodontal defect caused by the crack should be explored and corrected. If the crack involves the clinical root, the periodontal correction should be in such a way as to prevent the crack in these areas

from being continuous with the oral environment (clinical

crown).

Otherwise

the

tooth

should

be

extracted or the root amputated or hemisected.

The permanent restoration should be done only after: a. Cracked tooth, occurrence, and extent are verified. b. Endodontic

therapy,

if

indicated,

is

successfully

completed. c. The pulp dentin organ and the periodontium have recovered

from

the

degeneration

caused

by

the

presence of the crack.

The permanent restoration will be in the form of a reinforcing-protecting

type

of

cast

based

restoration,

usually accompanied by a foundation, so as to minimize the necessity for intracanal preparation for the reinforcing final restoration.

CLASS X To adequately treat this cyclic incomplete dislocation, the extent and cause of periodontal therapy should be instituted, which usually includes occlusal equilibration.

After eradicating the causes for the periodontal breakdown, sometimes the tooth needs to be immobilized, at

least for a while, to enhance and assure periodontal healing.

ROOT RESORPTION DUE TO DENTAL TRAUMA Protective mechanisms against resorption Unlike

deciduous

teeth,

permanent

teeth

rarely

undergo root resorption (1). Even in the presence of periradicular inflammation, resorption will occur primarily on the bone side of the attachment apparatus and the root will be resistant to it. Theory is based on the premise that the

cementum

essential

and

elements

predentin in

the

covering

resistant

of

on

dentin

dental

root

are to

resorption. It has long been noted that osteoclasts will not adhere to or resorb unmineralized matrix. Major mediators of osteoclast binding are RGD-peptides that are bound to calcium salt crystals on mineralized surfaces. Since the most external aspect of cementum is covered by a layer of cementoblasts over a zone of non-mineralized cementoid, a surface that provides satisfactory conditions for osteoclast binding is not present. Internally, the dentin is covered by pre-dentin

matrix,

which

possess

a

similar

organic

surface.

Another function of the cementum layer is related to its ability to inhibit the movement of toxins if present in

the root canal space into the surrounding periodontal tissues. The consequence of an infected root canal space is, therefore, most likely to be apical periodontitis, as the toxins can only communicate with the periodontal tissues through the apical foramina or large accessory canals.

However, if the cemental layer is lost or damaged, the inflammatory stimulators can pass from an infected pulp space

through

the

surrounding

periodontal

ligament,

which, in turn, sets up an inflammatory response. Since the cementum is lost, this inflammatory response will result in both bone resorption and root resorption.

Requirement for the presence of root resorption.

Due to the previously described inhibitory effects of organic pre-cementum and predentin, even in the presence of inflammation, an intact root is resistant to reorption.

However, if an injury removes or alters the (protective) pre-dentin

or

periodontium

pre-cementum, will

induce

inflammation root

of

pulp

resorption

or

with

multinucleated clastic cells similar to those seen in bone resorption.

Thus, in order for root resorption to occur, two things must happen: 1. The loss or alteration of the protective layer (precementum or pre-dentin) 2. Inflammation must occur to the unprotected root surface.

1. Loss or alteration of the protective layer Damage

to

the

protective

layer

can

occur

either

directly, due to trauma of a dental injury, or indirectly, when an inflammatory response occurs as a result of a dental injury. Most traumatic injuries, however, cause surprisingly little damage to the cemental layer. Even in an avulsion injury, the greatest damage that occurs is the tearing of the periodontal ligament. Physical damage to the cemental layer will only occur at the specific points where the force of the trauma pushed the tooth directly against the bony socket. The only exception to this rule is an intrusive injury, where the forcing of the conical root apically

into

a

similarly

shaped

socket

will

cause

tremendous damage to the protective layer over the entire root surface.

Inflammation

in

reaction

to

the

traumatic

injury

varies according to the stimulus it is exposed to after the injury, and has the potential to cause extensive damage to the protective layer. For example, the initial damage to the protective cementum after an avulsion injury, as described above, is limited. However, if the periodontal ligament cells remaining on the root are allowed to dry out before replantation,

they

will

provide

the

stimulus

for

an

inflammatory response over the entire root surface, which, in turn, results in extensive damage to the protective layer. In most cases, the pulp will necrose very quickly, which removes the blood supply to the resorbing cells and, this,

in

turn,

protects

the

root

against

extensive

resorption. Therefore, as evidence by the extremely low incidence of internal root resorption in permanent teeth, the

conditions

required

to

create

an

inflamed

pulp

adjacent to a damaged root surface are extremely rare.

2. The inflammatory response The

inflammatory

response

caused

by the

dental

injury can be divided into two critical phases. The first is the destructive phase where active resorption between the

dried-out cells with multinucleated giant cells takes place.

This destruction will continue as long as there is stimulus present to allow the inflammation to develop. In most cases, the conditions necessary to the creation of the stimulus are due to either mechanical damage to the root surface, or foreign materials or bacteria picked up the accident site on the root surface; therefore, the stimulus can only exist for a short period of time. Healing will, therefore, take place without intervention by the dentist.

However,

if

the

inflammatory

stimulus

is

longstanding, the destructive root resorption will continue until either no root structure remains or the stimulus is removed by the intervention of the dentist. The destructive phase of root resorption is diagnosed primarily by the radiolucent appearance of the root and adjacent bone on X-rays.

Diagnosis

is

a

major

challenge

as

resorptive

defects, facial or lingual/palatal, are most often missed during

examination,

techniques,

such

Tomography

(TACT),

although as

Tuned

display

newer Aperture

significant

radiographic Computed promise

in

improving our ability to identify these defects in the future.

Since most of the root destruction occurs due to the inflammatory

response

rather

than

direct

physical

damage, it seems logical that, if we could in some way limit this inflammation, we would also limit the root destruction and expect a more favorable outcome in terms of healing.

The critical factor in determining the outcome after a dental traumatic injury has occurred is the type of cells that repopulate the root surface during the healing phase.

If cementoblasts

are

able

to

cover the damaged

root

surface, a type of healing termed cemental healing or surface resorption will occur and the outcome will be favorable.

If, on the other hand, bone producing cells are able to cover the root surface, the conditions for healing will be unfavorable, as direct contact with bone and root will occur over some areas of the root surface; a phenomenon termed

as

ankylosis.

Bone

resorbs

and

forms

physiologically throughout life. Thus, the root is resorbed

by the osteoclasts but, in the reforming stage, bone is laid down instead of dentin. The root is, therefore, slowly replaced with bone. This process is termed as replacement resorption or osseous replacement.

The type of tissue that will cover the root surface is dependent on the surface area of the root damage and the relative proximity of the cells to the roof; i.e., how far and how fast the cells can travel in order to cover the damaged root surface. A localized injury over a small surface area favors cemental healing. Conversely, a diffuse injury over a large area will favor ankylosis with osseous replacement.

It has been reported that destruction of over 20% of the root surface is required for osseous replacement to occur.

More importantly, it is dependent on the extent of the destructive

inflammatory

response.

opportunity

here

initial

for

the

There

inflammation

is

the to

be

minimized by actions taken both immediately after the injury, where the way in which tooth is handled is of crucial importance.

External root resorption As the name implies, the root resorption occurs on the outer surface of the root. Luxation injuries are the most likely injury where root resorption may result, the long term outcome is dependent on whether the healing response

is

favorable

or

unfavorable.

The

order

of

likelihood of favorable to unfavorable healing following the different categories of luxation injuries occurring.

Resorption due to stimulus lasting a short duration (transient stimulus) Short-acting stimulus is usually due to the traumatic injury

alone

without

the

presence

of

an

additional

stimulus. Very little can be done to reverse this initial attachment damage, therefore the main focus of treatment is

to

do

everything

possible

to

limit

the

destructive

inflammatory process that occurs immediately after the injury. If the inflammation is minimized, the surface area of damaged root surface will also be kept to a minimum. It

is, therefore, hypothesized that a smaller damaged root surface will result in a more favorable healing outcome.

Treatment avoiding

or

strategies

minimizing

inflammatory

response.

are the

therefore severity

These

can

directed

of be

at

the

initial

listed

more

specifically as: 1. Prevention of the initial injury 2. Minimizing additional damage after the initial injury 3. Pharmacological

manipulation

(shut

down)

of

the

initial inflammatory response.

4. Possibly

stimulating

cemental,

rather

than

bone,

healing.

5. Slowing down the osseous replacement when it is inevitable.

Prevention: Nothing can be done about the initial damage caused by the primary traumatic injury. However, there is evidence that preventive measures successfully limit these injuries. In athletics, for instance, the mouth-guard is a proven protective device against traumatic damage to the teeth.

Minimizing Additional Damage after the Injury: Steps must be taken to minimize additional avoidable damage to the

periodontal

ligament.

Reports

indicate

that

the

personnel typically present at the site of a traumatic dental

injury

appropriate

are

generally

handling

of

poorly

these

educated

injuries.

It,

in

the

therefore,

remains a huge challenge to the dental community to educate these people in the correct emergency treatment of a traumatic injury.

Initially, the tooth should be gently repositioned back into its original position as soon as possible. The patient should then be sent to the emergency room or dentistry immediately.

If

splinting

is

necessary

it

should

be

performed with a functional splint for 7-10 days. Most importantly, the splint should be constructed to allow adequate

cleaning,

thereby

minimizing

the

wicking

of

bacteria from dental plaque into the blood clot between the tooth and the socket wall.

In the case of an avulsed tooth, replanting the tooth as soon as possible is the preferable treatment. If the tooth cannot be replanted for any reason, the extra oral

dry time must be minimized by placing the tooth in an appropriate storage medium.

However, newer specialized media such as Hank’s Balanced

Salt

Solution,

which

is

a

common

culture

medium, ViaSpan, a liver transplant medium, may be able to sustain the viability of periodontal ligament cells for considerably longer periods than milk can. The use of these

specialized

storage

media

has

been

deemed

impractical as they are seldom found near the accident site. However, if we consider that more than 60% of accidents occur close to the home or school, it should be possible

to

educate

the

public

to

have

these

media

available at these sites. Media, such as ViaSpan, could also be placed in ambulances where they could be used for severe injuries in life-threatening situations that do not allow immediate replantation.

3. Pharmacological manipulation of the inflammatory response:

An

additional

approach

might

be

to

pharmacologically manipulate the inflammatory response in order to minimize destruction and facilitate repair of the

damaged

root

surface

by

new

cementum

and

periodontal ligament. Tetracycline has been widely used in the

treatment

of

periodontal

disease

because

of

its

sustained antimicrobial effects. Recently, tetracycline has been shown to possess anti-resorptive , as well antimicrobial,

properties,

specifically,

it

has

a

direct

inhibitory effect on osteoclasts and collagenase.

While tetracycline affects osteoclasts that are present at the site of resorption, drugs are also available that affect the recruitment of osteoclasts to the injury site, meaning that the combination of the two types of drugs might have a synergistic effect on the inhibition of root resorption.

Glucocorticoids

have

been

widely

used

to

reduce the deleterious effects of inflammatory responses, more

specifically,

they

have

been

shown

to

reduce

osteoclastic bone resorption by affecting cell recruitment using a plethora of mechanisms.

Stimulate Cemental Healing :

If it were possible to

stimulate periodontal cell growth, we may be able to limit the number of osseous cells able to attach to the denuded root

surface,

thus

decreasing

the

loss

of

the

tooth.

Fibroblast like cells in culture secrete factors that have

been shown to be significantly active in tissue repair process.

In the meantime, recent studies have found that Emdogain (enamel matrix protein; Biora, Malmo, Sweden) may be extremely beneficial in teeth with extended extra oral dry times, as it not only makes the root more resistant to resorption but also stimulates the formation of new periodontal ligament from the socket.

5. Slow down ‘inevitable’ osseous replacement : When the periodontal ligament on the root surface is definitely destroyed and osseous replacement is inevitable, the focus of the treatment is to slow down the replacement of the root with bone. Injuries where such a situation might occur are intrusive injuries

or avulsion injuries with

extended extra-oral dry times. For avulsion injuries with extended dry times, the methods described below are presently appropriate and accepted: 1. All remaining periodontal ligament debris is removed from the root by thorough curettage or with the use of acid.

2. Fluoride has been shown to effectively slow down remodeling of the root to bone and the root is soaked in fluoride for 5 min before replantation.

3. Bisphosphonates are drugs that have been found to slow down osteoporosis in post-menopausal females. The topical use of bisphosphonates in extracted dog’s teeth which had been dried for an extended period. The use of the bisphosphonate slowed down the osseous replacement but, at this stage, we do not know if its effect is superior to the proven effect of topical fluoride, a much cheaper drug.

4. It appears from preliminary studies that both fluoride and bisphosphonate will be replaced by Emdogain as the drug of choice for this application.

Resorption

due

to

a

long

lasting

(progressive)

stimulus : Destructive inflammation and root resorption will continue as long as a stimulus for the inflammation is present. Pressure, pulpal infection and sulcular infection are

common,

resorption.

long-lasting

stimuli

for

progressive

root

PRESSURE Pressure damage can be caused by many different sources, but the most common causes tend to be either orthodontic tooth movement or impacted teeth or tumors.

Different theories of the mechanism of orthodontic tooth resorption have been put forward but presently it is considered to be a ‘sterile’ inflammation, with all expected inflammatory cytokines present during active resorption: In

most

cases,

orthodontic

tooth

movement

can

be

considered a ‘controlled’ trauma where pressure is spread evenly

over

a

root

area,

therefore

minimizing

the

inflammatory response, which, in turn, favors resorption of the bone rather than the root. However, in rare cases where the pressure is localized to the apical region, it can be intense enough to cause cemental damage and apical root resorption. The resorption can result in considerable shortening

of

the

root

that,

in

some

cases,

will

pressure

has

compromise the crown: root ratio of the tooth.

Root

resorption

due

to

orthodontic

always been considered to be external root resorption. For impacted

teeth

or

tumors,

the

resorption

will

occur

whenever the pressure from the impaction/tumor occurs.

Treatment is relatively easy, in that removal of the source of the pressure will result in the cessation of resorption in the

majority

of

cases.

Interestingly,

even

though

a

considerable amount of root structure may be lost due to orthodontic pressure, favorable healing with cementum is always expected. The reason for this is explained by the fact that the resorption takes place over a cross-section of the root in an apical to coronal direction. Thus, even when a large amount of root structure has been lost from the root surface to be repaired, the area to be repaired stays relatively small, and cells with the potential to produce cementum

can

surround

the

area

on

the

remaining

healthy root. Therefore cemental healing is favored.

PULP SPACE INFECTION Apical periodontitis with apical root resorption The pulp of the tooth can become necrotic for many reasons

but

the

predominant

cause

is

challenge through caries.

Lateral periodontitis with root resorption

a

bacterial

When the root loses its cemental protection, lateral periodontitis with root resorption can result. In order for a pulp

space

infection

to

develop,

the

pulp

must

first

become necrotic. Because a serious injury is required for pulp necrosis, it is usual that areas of cemental covering of the root are also affected, resulting its protective, insulating quality being lost. This means that bacterial toxins can now pass through the dentinal tubules and stimulate an inflammatory response in the corresponding periodontal ligament.

The result of this is the resorption of the root and bone. The periodontal infiltrate consists of granulation tissue

with

lymphocytes,

plasma

cells,

and

polymorphonuclear leukocytes. Multinucleated giant cells resorb the denuded root surface and this continues until the

stimulus

Radiographically,

(pulp-space the

bacteria)

resorption

is

is

removed.

observed

as

progressively radiolucent areas of the root and adjacent bone.

Treatment

The attachment damage due to the traumatic injury and minimizing the subsequent inflammation was the focus of the emergency visit. The practitioner’s should ideally pay attention to pulp space infection 7-10 days after

the

stimulus

injury. for

Root

the

canal

disinfection

peri-radicular

removes

inflammation

and

the the

resorption will stop.

In most cases, if a large area of root is affected, osseous

replacement

may

result

by

the

mechanism

described earlier.

Treatment elimination

of

principles the

include

stimulus

the

for

the

prevention

or

peri-radicular

inflammation, i.e., prevention or elimination of the pulp space bacteria.

1. Prevention of pulp space infection A. Maintain the vitality of the pulp. If the pulp is vital, the canal will be free of bacteria and, thus, this type of external inflammatory root resorption will not occur. In severe injures where vitality has been lost it is possible, under some circumstances, to promote revascularization

of the pulp space. The vital tissue that is present in the pulp space has been reported to be either new pulp or even periodontal ligament that has grown into the space.

Revascularization incompletely

is

formed

possible apices

in

young

(>

1.1

teeth

with

mm

wide

radiographically) if they are replaced close to their original position soon after the injury.

Revascularization after a traumatic dental injury is a race between the new tissue replacing the ischemically necrotic

pulp

and

the

bacteria

moving

into

the

unprotected pulp space. The new tissue will take about one month to revascularize a young pulp and, if bacteria do

not

populate

the

area

before

that

time,

revascularization will take place.

B. Prevent root canal infection by root canal treatment at 7-10 days. In teeth with closed apices, revascularization cannot

occur.

These

treated

within

7-10

teeth days

should of

the

be

endodontically

injury

before

the

ischemically necrosed pulp becomes infected.

C. The elimination of pulp space infection . When root canal treatment is indicated later than 10 days after the

accident or if active external inflammatory resorption is observed, the preferred antibacterial protocol consists of a chemomechanical

preparation,

followed

by

long-term

dressing with densely packed calcium hydroxide. Calcium hydroxide can affect an alkaline pH in the surrounding dentinal tubules, kill bacteria and neutralize endotoxin, a potent inflammatory stimulator.

The first visit consists of thorough chemo-mechanical instrumentation of the canal and the placement of a creamy mix of calcium hydroxide.

Once filled, the canal should appear radiographically to

be

calcified,

hydroxide

in

the

since canal

the is

radiodentsity usually

of

similar

calcium to

the

surrounding dentin. A radiograph is then taken at three month intervals. At each visit, the tooth is tested for symptoms of periodontitis. In addition, healing of the resorptive process and the presence or absence of the calcium hydroxide i.e. calcium hydroxide washout is also assessed.

Since the root surface is so radiodense as to make the assessment of healing difficult, the adjacent bone

healing is assessed. If the adjacent bone has healed, it is assumed that the resorptive process has stopped in the root as well and the canal can be obturated with guttapercha. If it is felt that additional healing would be beneficial before obturation, the need for replacing the calcium hydroxide in the canal is assessed. If the canal still radiographically appears calcified, there is no need to replace the calcium hydroxide. If, on the other hand, the canal has regained its lucent appearance, the calcium hydroxide should be re-packed and reassessed in another three months.

Sulcular infection This progressive external root resorption, which is of inflammatory

origin,

occurs

immediately

below

the

epithelial attachment of the tooth. This type of resorption is most often referred to as a cervical root resorption.

Causes

of

the

root

damage

immediately

below

the

epithelial attachment of the root include orthodontic tooth movement, trauma, non-vital bleaching and other less definable cause. The pulp plays no role in cervical root resorption and is mostly normal in these cases.

Because the source of stimulation (infection) is not the pulp, it has been postulated that it is the bacteria in the sulcus of the tooth that stimulate and sustain an inflammatory

response

in

the

periodontium

at

the

attachment level of the root. This theory is strengthened by the

fact that bone

resorption similar to

marginal

periodontitis will always accompany this type of root resorption and it is universally that marginal periodontitis has a bacterial cause.

Classification Progression of the resorptive defect once the dentin has been penetrated is variable and unpredictable, and Heithersay has classified this type of resorption into four classes in order of severity. Resorptive defects in the root coronal or just below the attachment level are relatively easy to treat; on the other hand, if the defect extends below the bone level, it is very complicated and sometimes impossible to treat.

Clinical Appearance Resorption of this type is asymptomatic and usually only detected through routine radiographs. Occasionally,

if the resorption is extensive, symptoms of pulpitis will develop.

When

the

resorption

is

longstanding,

the

granulation tissue can be seen undermining the enamel of the crown of the tooth, resulting in a pinkish appearance.

This ‘pink spot’ has traditionally been used to describe the pathognomonic clinical picture of internal root resorption, resulting in many cervical root resorption cases being misdiagnosed and treated as internal root resorption.

Radiographic Appearance The

radiographic

inflammatory

root

appearance

resorption

of

can

be

subepithelial varying

quite

considerably. If the resorptive process occurs mesially or distally on the root surface, it is common to see a small radiolucent

opening

into

the

root.

The

radiolucency

expands coronally and apically in the dentin, and reaches, but usually does not perforate, the root canal. If the resorptive

process

is

buccal

or

palatal-lingual,

the

radiographic picture depends on the extent to which the resorptive process has spread in the dentin.

Treatment

Treatment of this type of resorption poses many problems. In principle, it would be preferable to remove the cause of the inflammation, i.e., the sulcular bacteria.

However, unlike pulpal infection that is present in a closed environment, the sulcus is difficult to disinfect over a long period of time. therefore, in these cases, with the hope that the damaged and susceptible root surface will be altered to be resistant to further resorption after treatment, the resorptive defect is the focus if treatment strategies.

Aims of Treatment The aim of treatment is two-fold: •

Stop continuation of resorption . This may be achieved

by removing all the granulomatous tissue from the root. In cases where removal of granulomatous tissue would cause unacceptable damage to supporting structures, an attempt is made to severe the blood supply to the granulomatous tissue, thus killing the resorptive cells and inhibiting progression of the resorptive process. •

Replace the unprotected root surface with a foreign

material

that

clastic

cells

cannot

be

attached

to

or

penetrate. Any well-sealing dental filling material can be used for this purpose. However, the problem exists that, while

placing

a

filling

attachment

by

clastic

attachment

by

those

material cells,

cells

it

that

in also

the

root

does

provide

for

inhibits

not a

allow normal

periodontal ligament. Since most of these lesions are immediately below the attachment level, it is often not possible defect

to leave attachable while

repairing

it.

root structure The

result

is

above the that

root

attachment will only occur apical to the filling material, leaving a periodontal pocket that is unacceptable. If the resorption is extensive the practitioner may choose to perform

elective

endodontic

therapy

before

treatment

proceeds.

External approach Angled radiographs are taken to determine the exact location of the defect (buccal or lingual-palatal). Once the position has been determined, full thickness flap is raised and the granulomatous tissue is removed from the root and the bone defect.

It is also important to remove the granulomatous tissue from sound, healthy bone so that vascularization of the resorbing tissues

will not occur. The granulomatous tissue can be removed with a curette or bur. The opening into the root should be as conservative as possible. The root defect is filled with a restorative material and the flap replaced in a way as to minimize the periodontal defect after healing.

Internal Approach It is also possible to remove the granulomatous tissue and replace the space with a filling material from an internal approach.

Heathersay

has

shown

excellent

results

using

trichloracetic acid internally. The acid will chemically burn the granulomatous tissue, thus necrosing it and providing space for the filling material internally. This chemical burning can also be achieved with the use of calcium hydroxide but may take multiple applications to achieve the same results as trichloracetic acid.

Localized, medium-sized defect located in the coronal and midroot dentin with a small subepithelial opening on the root.

Treatment of these defects pose a very difficult challenge. The practitioner should seriously consider whether treatment would offer the patient a better prognosis than leaving the tooth alone until symptoms appear or the attachment of adjacent teeth is affected. Extraction followed by an implant or fixed bridge should be seriously considered.

External approach – An alternative approach is to remove the resorptive tissue from a small opening at the most apical extent of the affected root, leaving coronal root surface onto which a new attachment might develop. After the tissue removed and the opening repaired with an acceptable restorative material, the defect and denuded root surface is covered with a spacer (freeze-dried bone), and the entire area covered with a Gore-Tex membrane (Gore Tex, W. L. Gore, Flagstatt, AZ). Other approaches include: •

Forced eruption. If the remaining root apical to the resorption defect is long enough to maintain the tooth forcefully erupting, very effective treatment method. The resorption defect is moved to a position coronal to the adjacent attachment. The entrance of the defect into the root can now easily be found and the defect cleaned and restored. Reshaping of the ‘raised’ bony contour now allows an ideal architecture to remain.

•

Forced eruption/re-intrusion. If the procedure described above is complete the tooth can be orthodontically moved into its original position. While biological width will always develop apical to the filling material, attachment would still be superior to that attained with forced eruption only.

•

External approach/ Internal approach The need for root canal therapy is assessed and depends on the extent of the lesion. In these extensive lesions, elective endodontic therapy is often the best choice as a pulp exposure at any time during the procedure complicates an already difficult treatment. A flap is raised and the granulomatous tissue is aggressively removed from the bony defect only. Care is taken to leave as much rootstructure intact as possible. Since the source of the blood

supply

structures

to

that

the have

root been

defect

is

severed

the

periodontal

during

surgery,

necrosis of the resorbing tissues in the root results. To stop

new

tissue

from

growing

into

the

root

or

revascularising the necrotic tissue left inside the root, a barrier membrane month,

an

is

opening

used. is

After approximately

made

externally

above

one the

attachment and the necrotic granulomatous tissue is removed and replaced with a filling material. If esthetics is not a major consideration, mineral trioxide aggregate (MTA)

should

purpose.

be

a

useful

filling

material

for

this

Large defect extending apically. Heithersay Class 4.

These

cases

offer

such

a

poor

prognosis

that

extraction and replacement with an implant or fixed bridge is the preferred approach.

Future Strategies A. Long-term

disinfection

peridontal

of

therapeutic

the

sulus.

Advances

techniques

in

include

treatments that have the potential to disinfect the sulcus over a long period of time. If successful, the removal of the inflammatory stimulus would be a preferable way to treat these defects.

B. Manipulation

of

the

inflammatory

response.

Local

injections of high doses of corticosteroids have been effective in treating giant cell bone lesions in a conservative manner.

Since the multinucleated resorbing cells are similar to the cells in root resorption, the use of similar steroid doses might stop the progression of root resorption. The root canal could be used as a reservoir for the corticosteroids.

Outcomes from this type of approach are being presently being assessed.

INTERNAL ROOT RESORPTION Etiology Internal resorption

root

of

resorption

the

internal

is

characterized

aspect

of

the

by

the

root

by

multinucleated giant cells adjacent to granulation tissue in the pulp. Chronic inflammatory tissue is common in the pulp, but only rarely does it result in resorption. Trauma frequently been suggested as a cause. They are divided into a transient type and a progressive type, with the latter

requiring

continuous

stimulation

by

infection.

Another reason for the loss of predentin might be the extreme heat produced when cutting on dentin without an adequate water spray. The heat presumably would destroy the predentin layer and, if the coronal aspect of the pulp later became infected, the bacterial products could initiate the typical inflammation in conjunction with resorbing giant cells in the vital pulp adjacent to the denuded root surface.

Clinical manifestations Internally root resorption is usually asymptomatic and

is

first

recognized

clinically

through

routine

radiographs. If perforation of the crown occurs and the metaplastic tissue is exposed to the oral fluids, pain may be presenting symptom. For internal resorption to be active, at least part of the pulp must be vital, so that a positive response to pulp sensitivity testing is possible. It should be remembered that the coronal portion of the pulp is often necrotic whereas the apical pulp, which includes the internal resorptive defect, can remain vital. Therefore, a negative sensitivity test result does not rule out active internal resorption. Traditionally the pink tooth has been thought to be pathognomonic of internal root resorption.

The pink colour is due to the granulation tissue in the coronal dentin, undermining the crown enamel. The pink tooth can also be a feature of subepithelial external inflammatory root resorption, which must be ruled out before a diagnosis of internal root resorption is made.

Radiographic appearance The usual radiographic presentation of internal root resorption is a fairly uniform radiolucent enlargement of the pulp canal. Because the resorption is initiated in the root canal, the resorptive defect includes some part of the

root canal space. Therefore, the original outline of the root canal is distorted.

Treatment As the resorptive defect is the result of the inflamed pulp and the blood supply to the tissue is through the apical foramina, the correct approach to treatment is endodontic treatment that effectively removes the blood supply to the resorbing cells. After adequate anesthesia has been administered, the canal apical to the internal defect is explored and a working length short of the radiographic apex is used. The apical canal is thoroughly instrumented to ensure that the blood supply to the tissue resorbing the root is cut off. By the completion of the root canal instrumentation it should be possible to obtain a blood free and dry canal with paper points.

Calcium hydroxide is then spun into the canal to facilitate the removal of the tissue in the irregular defect at the next visit. At the second visit, the tooth and defect are filled using a soft gutta=percha technique.

Diagnostic Resorption

Features

of

External

vs.

Internal

Root

It is often very difficult to distinguish external from internal root resorption, meaning that misdiagnosis and incorrect treatment result. What follows is a list of typical diagnostic features of each resorptive type.

Radiographic features A change of angulation of X-rays should give a fairly good indication of whether a resorptive defect is internal or external. A lesion of internal origin appears close to the canal whatever the angle of the X-ray. On the other hand, a defect on the external aspect of the root moves away from the canal as the angulation changes. In addition, by using the buccal-object rule, it is usually possible to distinguish if the external root defect is buccal or lingualpalatal. In internal resorption, the outline of the root canal is usually distorted and the root canal and the radiolucent resorptive defect appear to be contiguous.

When the defect is external, the root canal outline appears normal and can usually be seen ‘running through’ the radiolucent defect.

External

inflammatory

root

resorption

is

always

accompanied by the resorption of the bone in addition to

that of the root. Therefore, radiolucencies are apparent in the root and the adjacent bone. Internal root resorption does not involve the bone and, as a rule, radiolucency is confined to the root. On the rare occasions that the internal defect perforates the root, the bone adjacent to it is resorbed and appears radiolucent on the radiograph.

Vitality testing External inflammatory resorption in the apical and lateral aspects of the root involves an infected pulp space, so that a negative response to sensitivity tests is required to support the diagnosis. On the other hand, since subepithelial external root resorption does not involve the pulp (the bacteria are thought to originate in the sulcus of the tooth), a normal response to sensitivity testing is usually associated with this type of resorption. Internal root resorption usually occurs in teeth with vital pulps and gives a positive response to sensitivity testing.

Pink Spot

With apical and lateral external root resorption, the pulp is non-vital and therefore the granulation tissue that produces the pink spot is not present in these cases.

The majority of misdiagnosis of resorptive defects is made between subepithelial external and internal root resorptions. The diagnosis should always be confirmed while treatment is proceeding. If root canal therapy is the treatment of choice an apparent internal root resorption, the bleeding within the canal should cease quickly after pulp extirpation, as the blood supply of the granulation tissue is the apical blood vessels. If bleeding continues during treatment and particularly if it is still present at the second visit the source of the blood supply is external and treatment for external resorption should be carried out. It should also be possible to fill the entire canal from within internal resorption during suspicious obturation.

Failure to achieve this should make the operator external lesion.

Finally,

if

the

blood

supply

of

an

internal

resorption defect is removed on pulp extirpation, any continuation

of

the

resorptive

process

on

recall

radiographs should alert the dentist to possibility that resorptive defect was misdiagnosed.