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Date: 09/08/2011 16:48Endodontic Considerations in Dental Trauma

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Endodontic Considerations in Dental Trauma - MARTIN TROPE

Introduction

Traumatic injuries to the teeth result in damage to many dental and periradicular structures. Therefore, the management and

consequences of these injuries are multifactorial, and knowledge of the interrelating healing patterns of these tissues is essential.

The focus of this chapter is the dental pulp and how damage to the dentinopulpal complex can contribute to complications after a

traumatic injury and how correct diagnosis and treatment can result in favorable healing after an injury. More information on

management of dental trauma can be obtained by going on the Web site of the International Association of Dental Traumatology:

<http://www.iadt-dentaltrauma.org>.

Unique Aspects of Dental Trauma

Most dental trauma occurs in the 7- to 10-year-old age group owing to falls and accidents near home or school.1,2 It occurs primarily

in the anterior region of the mouth, affecting the maxilla more than the mandible.3

Thus, in many cases after a dental traumatic injury, endodontic therapy is provided to caries-free, single-rooted, young permanent

teeth. Therefore, maintenance of the tooth is particularly important in these young individuals. Luckily, the potential for a successful

endodontic outcome is very good if timely and correct treatment is provided soon after the injury.

Crown Fractures

INTRODUCTION

The primary aim from an endodontic point of view is to maintain pulp vitality after fractures involving the crowns of teeth.

Crown Infractions — "Incomplete fracture or crack of enamel without loss of tooth structure"4 and Uncomplicated Crown Fractures —

"Fractures of the enamel only or enamel and dentin without pulp exposure"4 are injuries that have little danger of resulting in pulp

necrosis. In fact, the biggest danger to the health of the pulp is through iatrogenic causes during the esthetic restoration of these teeth.Therefore, meticulous follow-up over a 5-year period is an important endodontic preventive measure in these cases. Endodontic

intervention should be considered at any follow-up time when reactions to sensitivity tests change, apical periodontitis develops, the

root appears to have stopped development, or the pulp is obliterating.

COMPLICATED CROWN FRACTURES

By definition, complicated crown fractures involve enamel, dentin, and pulp4 and occur in 0.9 to 13% of all dental injuries.5-7 A

crown fracture involving the pulp, if left untreated, will always result in pulp necrosis.8 However, the manner and time sequence in

which the pulp becomes necrotic allow a great deal of potential for successful intervention in maintaining pulp vitality. The first

reaction after an injury is

[Figure 1. Histologic appearance of the pulp within 24 hours of a traumatic exposure. The pulp proliferates over the exposed dentinal

tubules. There is approximately 1.5 mm of inflamed pulp below the surface of the fracture.]

hemorrhage and local inflammation. Subsequent inflammatory changes are usually proliferative but can be destructive. A proliferative

reaction is favored in traumatic injuries since the fractured surface is usually flat, allowing salivary rinsing with little chance of

impaction of contaminated debris. Therefore, unless impaction of contaminated debris is obvious, it is expected that within the first 24

hours after the injury, a proliferative response with inflammation will extend no more than 2 mm into the pulp (Figure 1).9-11 In time,

however, bacterial infection will result in local pulp necrosis and a slow apical spread of pulpal inflammation.

Figure 1. Histologic appearance of the pulp within 24 hours of a traumatic exposure. The pulp proliferates over the exposed dentinal



tubules. There is approximately 1.5 mm of inflamed pulp below the surface of the fracture.0

TREATMENT

Treatment options are (1) vital pulp therapy comprising pulp capping, partial pulpotomy, and full pulpotomy or (2) pulpectomy. The

choice of treatment depends on the stage of development of the tooth, time between the accident and treatment, concomitant

periodontal injury, and the restorative treatment plan.

STAGE OF DEVELOPMENT OF THE TOOTH

Loss of vitality in an immature tooth can have catastrophic consequences. Root canal treatment on a tooth with a "blunderbuss" canal

is time consuming and difficult. Of more importance, however, is the fact that necrosis of an immature tooth leaves it with thin

dentinal walls that are susceptible to fracture both during and after an apexification procedure.12 Therefore, every effort must be made

to keep the pulp vital at least until the apex and cervical root have completed development. Pulpectomy in a mature tooth has a high

success rate,13 but vital pulp therapy (rather than removal) on a mature tooth performed under optimal conditions can also be carried

out successfully.14,15 Therefore, vital pulp therapy can be an option under certain circumstances, even though a pulpectomy is the

treatment affording the most predictable success. In an immature tooth, vital pulp therapy should be attempted, if at all feasible,

because of the tremendous advantages of maintaining the vital pulp.

TIME BETWEEN THE ACCIDENT AND TREATMENT

For 48 hours after a traumatic injury, the initial reaction of the pulp is proliferative, with a depth of no more than 2 mm of pulpal

inflammation (see Figure 1). After 48 hours, chances of direct bacterial contamination of the pulp increase as the zone of inflammation

progresses apically.16 Thus, with time, the chance of success in maintaining a healthy pulp decreases.

CONCOMITANT ATTACHMENT DAMAGE

A concomitant periodontal injury will compromise the nutritional supply of the pulp. This fact is particularly important in mature

teeth, in which the chance of pulp survival is not as good as for immature teeth.17,18

RESTORATIVE TREATMENT PLAN

In a mature tooth, pulpectomy is a viable treatment option, unlike an immature tooth, in which the benefits of maintaining vitality of

the pulp are great. However, if performed under optimal conditions, vital pulp therapy after traumatic exposures can be successful.

Thus, if the restorative treatment plan is simple, and a composite resin restoration will suffice as the permanent restoration, this

treatment option should be given serious consideration. If a more complex restoration is to be placed (eg, a crown), pulpectomy would

be the more predictable treatment method.

Vital Pulp Therapy for Traumatic Dental Injuries

REQUIREMENTS FOR SUCCESS

Vital pulp therapy in traumatically injured teeth has a very high success rate if the following requirements are adhered to:

1. Treatment of a healthy pulp has been shown to be an essential requirement for successful therapy.19,20 Vital pulp therapy of the

inflamed pulp, on the other hand, affords a lower success rate.19,20 Therefore, the optimal time for treatment is within the first 24

hours, when pulp inflammation is superficial. As time increases between the time of injury and therapy, pulp removal must be

extended apically to ensure that noninflamed pulp tissue has been reached.

2. A bacteria-tight seal is the most critical factor for successful treatment.20 Challenge by bacteria during the healing phase will cause

failure.21 On the other hand, if the exposed pulp is effectively sealed from bacterial access, successful healing of the pulp with a hard

tissue barrier will occur, independent of the dressing placed on the pulp.21

3. A proper pulp dressing is important, and, presently, calcium hydroxide is the most common dressing used for vital pulp therapy. Its

advantages are that it is antibacterial22,23 and will disinfect the superficial pulp. Pure calcium hydroxide (pH 12.5) will cause necrosis

of about 1.5 mm of the pulp tissue24,25 involving the superficial layers of inflamed pulp if present (Figure 2). The toxicity of thecalcium hydroxide appears to be neutralized as the deeper layers of pulp are affected, causing coagulative necrosis at the junction of

the necrotic and vital pulp, resulting in only a mild irritation. This mild

[Figure 2. Pulp necrosis (1.5 mm) as a result of the high pH of calcium hydroxide.]

[Figure 3. Hard tissue barrier developed after calcium hydroxide partial pulpotomy. Histologic appearance of replacement

odontoblasts and a hard tissue barrier.]



irritation will initiate an inflammatory response and in the absence of bacteria24 will heal with a hard tissue barrier (Figure 3).25,26

Hard-setting calcium hydroxide does not cause necrosis to the superficial layers of pulp but has been shown to initiate healing with a

hard tissue barrier as well.27,28 A major disadvantage of calcium hydroxide is that it does not seal the fractured surface. Therefore, an

additional material must be used to ensure that the pulp is not challenged by bacteria, particularly during the critical healing phase.

Other materials, such as zinc oxide-eugenol,20 tricalcium phosphate,29 and composite resin,30 have been proposed as materials for

vital pulp therapy. They have not afforded the predictability of calcium hydroxide used in conjunction with a well-sealed coronal

restoration.

Mineral trioxide aggregate (MTA) has been reported to show promise as a pulp capping agent.31 It has a high pH, similar to calcium

hydroxide, when unset32 and after setting will create an excellent bacteria-tight seal.33 It also sets hard enough to act as a base for a

final restoration.34 MTA has not as yet gained popularity as a pulp capping agent, probably because of its need for a moist

environment for 6 hours to set. Thus, what is normally a one-step procedure for other medicaments becomes a two-step procedure

with MTA since a wet cotton pellet should be placed over it until it is set, and then later the permanent restoration can be fabricated.

Figure 2. Pulp necrosis (1.5 mm) as a result of the high pH of calcium hydroxide.0

Figure 3. Hard tissue barrier developed after calcium hydroxide partial pulpotomy. Histologic appearance of replacement odontoblasts

and a hard tissue barrier.0

Treatment Methods

PULP CAPPING

Pulp capping implies placing a dressing directly onto the pulp exposure. As indicated by the success rate of this procedure (80%)

compared with that of partial pulpotomy (95%),34 it appears that a superficial pulp cap should not be considered after traumatic pulp

exposures. The lower success rate is not difficult to understand since superficial inflammation develops soon after the traumatic

exposure. Thus, if the treatment is at the superficial level, a number of inflamed (rather than healthy) pulps will be treated, lowering

the potential for success. In addition, a bacteria-tight coronal seal is much more difficult to achieve in superficial pulp capping since

there is no cavity depth to create this bacteria-tight seal, as there is with a partial pulpotomy.

PARTIAL PULPOTOMY

Partial pulpotomy implies the removal of coronal pulp tissue to the level of healthy pulp tissue. In traumatic injuries, this level can be

accurately determined owing to the knowledge of the reaction of the pulp after a traumatic injury. This procedure is commonly called

the "Cvek pulpotomy."

TECHNIQUE

Anesthesia, rubber dam placement, and superficial disinfection are performed. A 1 to 2 mm deep cavity is prepared into the pulp using

a sterile diamond bur of appropriate size with copious water coolant (Figure 4).35 A slow-speed bur or spoon excavator should be

avoided unless cooling of the high-speed bur is not possible. If bleeding is excessive, the pulp is amputated deeper until only moderate

hemorrhage is seen. Excess blood is carefully removed by rinsing with sterile saline or anesthetic solution and dried with a sterile

cotton pellet. Care must be taken not to allow a blood clot to develop as this will compromise the prognosis.26,34 If the pulp is of

sufficient size to allow 1 to 2 mm of additional pulp necrosis, a thin layer of pure calcium hydroxide is mixed with sterile saline or

anesthetic solution and carefully placed. If

[Figure 4. Cvek partial pulpotomy. A, The fractured teeth are cleaned and disinfected and a rubber dam is placed. B, Cavities are

prepared at high speed with a round diamond bur that includes 1 to 2 mm of superficial pulp tissue. C, Calcium hydroxide is placed on

a plugger and D, placed on the soft tissue of the pulp (only). E, Calcium hydroxide is removed from the walls of the cavities. F, The

cavity preparations are filled with glass ionomer cement. G, The exposed dentin is etched, and H, the dentin is covered with composite

resin. I, The radiograph taken 6 months later shows the formation of hard tissue barriers in both teeth.]

the pulp size does not permit additional loss of pulp tissue, a commercial hard-setting calcium hydroxide can be used.36 The prepared

cavity is filled with a material with the best chance of a bacteria-tight seal (zinc oxide-eugenol or glass ionomer cement) to a level

flush with the fractured surface. The material in the pulpal cavity, and all exposed dentinal tubules are covered with hard-setting

calcium hydroxide. The enamel is then etched and restored with bonded composite resin, as in pulp capping. The use of MTA for pulpcapping and pulpotomies is described in Chapter 35, "Vital Pulp Therapy."

Follow-up places the emphasis on maintenance of positive sensitivity tests and radiographic evidence of continued root development.

Partial pulpotomy affords many advantages over pulp capping. Superficial inflamed pulp is removed in the preparation of the pulpal

cavity. Calcium hydroxide disinfects dentin and pulp and removes additional pulpal inflammatory tissue. Most importantly, space is

provided for a material that will provide a bacteria-tight seal to allow pulpal healing with hard tissue development under optimal

conditions. Additionally, coronal pulp tissue remains that allows sensitivity testing to be carried out at the follow-up visits. The

prognosis is excellent (94-96%).34,37



Figure 4. Cvek partial pulpotomy. A, The fractured teeth are cleaned and disinfected and a rubber dam is placed. B, Cavities are

prepared at high speed with a round diamond bur that includes 1 to 2 mm of superficial pulp tissue. C, Calcium hydroxide is placed on

a plugger and D, placed on the soft tissue of the pulp (only). E, Calcium hydroxide is removed from the walls of the cavities. F, The

cavity preparations are filled with glass ionomer cement. G, The exposed dentin is etched, and H, the dentin is covered with composite

resin. I, The radiograph taken 6 months later shows the formation of hard tissue barriers in both teeth. Courtesy of Dr. Allessandra

Ritter.0

FULL PULPOTOMY

This procedure involves removal of the entire coronal pulp to the level of root orifices. This level of pulp amputation is chosen

arbitrarily because of its anatomic convenience. Therefore, since the inflamed pulp sometimes extends past the canal orifices into the

root pulp, many "mistakes" are made, resulting in treatment of an inflamed rather than a noninflamed pulp. This procedure is indicated

when it is predicted that the pulp is inflamed to deeper levels of the coronal pulp. Traumatic exposures after 72 hours and a carious

exposure are two examples in which this type of treatment may be indicated. Because of the fairly good chance that the dressing will

be placed on an inflamed pulp, full pulpotomy is contraindicated in mature teeth. However, the benefits outweigh the risks for this

treatment in immature teeth with incompletely formed apices and thin dentinal walls.

TECHNIQUE

Anesthesia, rubber dam placement, and superficial disinfection are done as described with pulp capping and partial pulpotomy. The

coronal pulp is removed to the level of the root orifices. Calcium hydroxide dressing, a bacteria-tight seal, and coronal restoration area part of the technique as described with partial pulpotomy. The follow-up is done as described with pulp capping and partial

pulpotomy. A major disadvantage of this treatment method is that sensitivity testing is not possible owing to the loss of coronal pulp.

Therefore, radiographic follow-up is extremely important to monitor for continuation of root formation and signs of apical

periodontitis.

Since the cervical pulpotomy is performed on pulps that are expected to have deep inflammation, and the site of pulp amputation is

arbitrary, more "mistakes" are made, leading to treatment of the inflamed pulp. Consequently, prognosis in the range of 75% is poorer

than partial pulpotomy.38 Because of the inability to evaluate pulp status after a full pulpotomy, some authors have recommended

routine pulpectomy after the roots have fully formed (Figure 5). This philosophy is based on the fact that the pulpectomy procedure

has a success rate in the range of 95%, whereas if apical periodontitis develops following pulpotomy, the prognosis of root canal

treatment drops significantly to about 80%.13,39

[Figure 5. Successful pulpotomy followed by a pulpectomy at 18 months.]

Figure 5. Successful pulpotomy followed by a pulpectomy at 18 months. Courtesy of Dr. Leif Tronstad.0

PULPECTOMY

Pulpectomy implies removal of the entire pulp to the level of the apical foramen. The indications are for complicated crown fracture of

mature teeth (if conditions are not ideal for vital pulp therapy). This procedure is not different from root canal treatment of a vital,

nontraumatized tooth.

Treatment of Nonvital Pulps

IMMATURE TOOTH: APEXIFICATION

Apexification is indicated for teeth with open apices and thin dentinal walls in which standard instrumentation techniques cannot

create an apical stop to facilitate effective root canal filling.

BIOLOGIC CONSEQUENCES

A nonvital immature tooth presents a number of difficulties for adequate endodontic therapy. The canal is (often) wider apically than

coronally, necessitating the use of a filling material that conforms to the shape of the apical part of the canal. Since the apex is

extremely wide, no barrier exists to stop this material from moving into and traumatizing the apical periodontal tissues. Also, the lack

of an apical stop and extrusion of material might result in a canal that is susceptible to leakage. An additional problem in immatureteeth with thin dentinal walls is their susceptibility to fracture both during and after treatment. These problems are overcome by

stimulating the formation of a hard tissue barrier to allow for optimal filling of the canal and reinforcing the weakened root against

fracture both during and after apexification.12,40

TECHNIQUE

Since in the vast majority of nonvital teeth are infected,41,42 the first phase of treatment is to disinfect the root canal system to ensure

periapical healing.16,22 The canal length is estimated with a parallel preoperative radiograph and confirmed radiographically with the

first endodontic instrument. Preparation of the canal (owing to the thin dentinal walls) is performed very lightly and with copious

irrigation using 0.5% sodium hypochlorite.43,44 A lower strength and increased volume of NaOCl are used because of the increased



danger of extruding sodium hypochlorite through the open apex in immature teeth. An irrigation needle that can passively reach close

to the apical level is used in disinfecting the canals. The canal is dried with paper points, and a creamy mix of calcium hydroxide is

spun into the canal with a lentulo-spiral. The calcium hydroxide is left in the canal for at least 1 week to be effective in accomplishing

disinfection.23 The continuation of treatment can take place any time after 1 week. Further treatment should not be delayed more than

1 month since the calcium hydroxide could be washed out by tissue fluids through the open apex, leaving the canal susceptible to

reinfection.

Hard Tissue Apical Barrier

TRADITIONAL METHOD

The formation of a hard tissue barrier at the apex requires an environment similar to that required for hard tissue formation in vital

pulp therapy, that is, a mild inflammatory stimulus, to initiate healing and a bacteria-free environment to ensure that inflammation is

not progressive. As with vital pulp therapy, calcium hydroxide is used for this procedure.45-47 Pure calcium hydroxide powder is

mixed with sterile saline (or anesthetic solution) to a thick (powdery) consistency. Ready-mixed commercial calcium hydroxide can

also be used. The calcium hydroxide is packed against the apical soft tissue with a plugger or thick point to initiate hard tissue

formation. This step is followed by backfilling with calcium hydroxide to completely fill the canal, thus ensuring a bacteria-free canal

with little chance of re-infection during the 6 to 18 months required for hard tissue formation at the apex. The calcium hydroxide is

meticulously removed from the access cavity to the level of the root orifices, and a well-sealing temporary filling is placed in the

access cavity. A radiograph is taken, and the canal should appear to have become calcified, indicating that the entire canal has been

filled with the calcium hydroxide. Because calcium hydroxide washout is evaluated by its relative radiodensity in the canal, it is

prudent to use a calcium hydroxide mixture without the addition of a specific material to enhance the radiopaque property of themedicament such as barium sulfate. These additives do not wash out as readily as calcium hydroxide, so if they are present in the

canal, evaluation of washout is not possible.

At 3-month intervals, a radiograph is taken to evaluate whether a hard tissue barrier has formed and if the calcium hydroxide has

washed out of the canal. This is assessed to have occurred if the canal can again be seen radiographically. If calcium hydroxide

washout is seen, it is replaced as before. If no washout is evident, it can be left intact for another 3 months. Excessive calcium

hydroxide dressing changes should be avoided if at all possible since the initial toxicity of the material is thought to delay healing.48

When completion of a hard tissue barrier is suspected, the calcium hydroxide should be washed out of the canal with sodium

hypochlorite and a radiograph taken to evaluate the radiodensity of the apical stop. A file that can easily reach the apex can be used to

gently probe for a stop at the apex. When a hard tissue barrier is indicated radiographically and can be probed with an instrument, the

canal is ready for filling (Figure 6).

Figure 6. Successful apexification. The patient presented with an acute abscess. The canal was disinfected, and the wide apical lumen

was closed with a long-term calcium hydroxide application. When a barrier was felt, the canal was filled with a permanent root

filling.0

MTA BARRIER

The creation of a physiologic hard tissue barrier using calcium hydroxide, although quite predictable, takes anywhere from 3 to 18

months. The disadvantage of this long time period is that the patient is

[Figure 6. Successful apexification. The patient presented with an acute abscess. The canal was disinfected, and the wide apical lumen

was closed with a long-term calcium hydroxide application. When a barrier was felt, the canal was filled with a permanent root

filling.]

required to present for treatment multiple times; also, the tooth may fracture during treatment, before the thin weak roots can be

strengthened. In addition, one study has indicated that long-term treatment with calcium hydroxide may weaken the dentin of the roots

and make them even more susceptible to fracture.49

MTA has been used to create a hard tissue barrier quickly after the disinfection of the canal. Calcium sulfate can be pushed through

the apex to provide a resorbable extraradicular barrier against which to pack the MTA. The MTA is mixed and placed into the apical 3

to 4 mm of the canal in a manner similar to the placement of calcium hydroxide. A wet cotton pellet is placed against the MTA and

left for at least 6 hours, and then the entire canal is filled with a root filling material. The filling can also be placed immediately since

the tissue fluids of the open apex will probably provide enough moisture to ensure that the MTA will set sufficiently. The cervicalcanal is then reinforced with composite resin to below the marginal bone level as described below.

A number of case reports have been published using this MTA apical barrier technique,50,51 and it has steadily gained popularity

with clinicians. Presently, no prospective long-term outcome study is available comparing its success rate with the traditional calcium

hydroxide technique.

FILLING OF THE ROOT CANAL

Since the apical diameter is larger than the coronal diameter in most of these canals, a softened filling technique is indicated. Care



must be taken to avoid excessive lateral force during filling owing to the thin root walls. If the hard tissue barrier was "produced" by

long-term calcium hydroxide therapy, it consists of irregularly arranged layers of coagulated soft tissue, calcified tissue, and

cementum-like tissue. Included also are islands of soft connective tissue, giving the barrier a "Swiss cheese" consistency.52,53

Because of the irregular nature of the barrier, it is not unusual for cement or softened filling material to be extruded into the apical

tissues (see Figure 6). Formation of the hard tissue barrier may also be some distance short of the radiographic apex. This is because it

forms wherever the calcium hydroxide comes in contact with vital tissue. In teeth with wide open apices, vital tissue can survive and

proliferate from the periodontal ligament a few millimeters into the root canal. The root canal filling should be completed to the level

of the hard tissue barrier and not forced toward the radiographic apex.

REINFORCEMENT OF THE THIN DENTINAL WALLS

The apexification procedure has become a predictably successful procedure. However, the thin dentinal walls present a clinical

problem. Should secondary injuries occur, teeth with thin dentinal walls are more susceptible to fractures, rendering them

nonrestorable.54,55 It has been reported that approximately 30% of these teeth will fracture during or after endodontic treatment.56

Consequently, some clinicians have questioned the advisability of the apexification procedure and have opted for more radical

treatment procedures, including extraction followed by extensive restorative procedures such as dental implants. Recent studies have

shown that intracoronal bonded restorations can internally strengthen endodontically treated teeth and increase their resistance to

fracture.12,57 Thus, after root filling, the material should be removed to below the marginal bone level and a bonded resin filling

placed.

Routine follow-up evaluation should be performed to monitor the outcome. Restorative procedures should be assessed to ensure that

they do not promote root fractures. Periapical healing and the formation of a hard tissue barrier occur predictably with long-termcalcium hydroxide treatment (79-96%).47,56 However, long-term survival is jeopardized by the fracture potential of the thin dentinal

walls. It is expected that internal strengthening of teeth as described above will increase their long-term survivability.

Pulp Revascularization

INTRODUCTION

Regeneration of a necrotic pulp has been considered possible only after avulsion of an immature permanent tooth. The advantages of

pulp revascularization are the possibility of further root development, reinforcement of dentinal walls by deposition of hard tissue, and

thus strengthening the root against fracture. After replantation of an avulsed immature tooth, a unique set of circumstances exists that

allows regeneration to take place. The young tooth has an open apex and is short, which allows new tissue to grow into the pulp spacerelatively quickly. The pulp is necrotic but usually not degenerated and infected, so it will act as a matrix into which the new tissue

can grow. It has been experimentally shown that the apical part of a pulp may remain vital and after replantation proliferate coronally,

replacing the necrotized portion of the pulp.58-60 In addition, the fact that, in most cases, the crown of the tooth is intact and caries

free ensures that bacterial penetration into the pulp space through cracks61 and defects will be a slow process. Thus, the race between

the new tissue and infection of the pulp space favors the new tissue.

Regeneration of pulp tissue in a necrotic infected tooth with apical periodontitis has been thought until now to be impossible.

However, if it were possible to create a similar environment as described above for the avulsed tooth, regeneration should occur. Thus,

if the canal is effectively disinfected, a matrix into which new tissue could grow is provided, and the coronal access is effectively

sealed, regeneration should occur as in an avulsed immature tooth. A report by Banchs and Trope reproduced results in cases reported

by others that indicate that it may be possible to replicate the unique circumstances of an avulsed tooth so as to revascularize the pulp

in infected necrotic immature roots62 (Figure 7). The case presented describes the treatment of a maxillary central incisor with

radiographic and clinical signs of apical periodontitis after a failed partial pulpotomy. The canal was disinfected without mechanical

instrumentation but with copious irrigation with 5.25% sodium hypochlorite and the use of a mixture of antibiotics.62 A blood clot

was produced to the level of the cementoenamel junction to provide a matrix for the ingrowth of new tissue, followed by a deep

coronal restoration to provide a bacteria-tight seal. Clinical and radiographic evidence of healing was seen after 6 months; the large

radiolucency had disappeared, and at the 12-month follow-up, it was obvious that the root walls were thickening. Recent studies have

confirmed the potent antibacterial properties of the triantibiotic paste used in this case,63,64 and studies are under way to find a

synthetic matrix that will act as a more predictable scaffold for new ingrowth of tissue than the blood clot used in these previous cases.

The procedure described in this section can be attempted in most cases, and if after 3 months no signs of regeneration are present, the

more traditional treatment methods should be initiated.

[Figure 7. A, Immature tooth with a necrotic infected canal with apical periodontitis. The canal is disinfected with copious irrigation

with sodium hypochlorite and triantibiotic paste. After 4 weeks, the antibiotic is removed and a blood clot is created in the canal

space. The access is filled with a mineral trioxide aggregate (MTA) base and bonded resin above it. B, At 7 months, the patient is

asymptomatic and the apex shows some signs of healing of the apical periodontitis and closure of the apex. C, At 12 months, apical

healing is obvious and root wall thickening has occurred, indicating that the root canal has been revascularized with vital tissue.]

Figure 7. A, Immature tooth with a necrotic infected canal with apical periodontitis. The canal is disinfected with copious irrigation

with sodium hypochlorite and triantibiotic paste. After 4 weeks, the antibiotic is removed and a blood clot is created in the canal

space. The access is filled with a mineral trioxide aggregate (MTA) base and bonded resin above it. B, At 7 months, the patient is

asymptomatic and the apex shows some signs of healing of the apical periodontitis and closure of the apex. C, At 12 months, apical

healing is obvious and root wall thickening has occurred, indicating that the root canal has been revascularized with vital tissue.

Courtesy of Dr. Blayne Thibodeau.0



MATURE TEETH

Traumatized mature teeth are routinely treated endodontically in the same manner as non-traumatized teeth.

Crown-Root Fractures

These fractures are first treated periodontally to ensure that a good margin for restoration is possible. If the tooth can be maintained

from a periodontal point of view, the pulp is treated as a crown fracture.

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Re: Endodontic Considerations in Dental Trauma

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Horizontal Root Fractures

INTRODUCTION

This injury implies fracture of the cementum, dentin, and pulp. They are relatively infrequent injuries, occurring in less than 3% of all

dental injuries.65 Incompletely formed roots with vital pulps rarely fracture horizontally.66 When a root fractures horizontally, the

coronal segment is displaced to a varying degree, but, generally, the apical segment is not displaced. Because the apical pulpal

circulation is not disrupted, pulp necrosis in the apical segment is extremely rare. Pulp necrosis develops in the coronal segment owing

to its displacement but occurs in only about 25% of cases.67 The clinical presentation is similar to that of luxation injuries. The extent

of displacement of the coronal segment is usually indicative of the location of the fracture and can vary from none, simulating a

concussion injury (apical fracture), to severe, simulating extrusive luxation (cervical fracture). Radiographic examination for root

fractures is extremely important. Since root fractures are usually oblique (facial to palatal), one periapical radiograph can easily missits presence. It is imperative to take at least three angled radiographs (45, 90, and 110 degrees) so that at least at one angulation the x-

ray beam will pass directly through the fracture line to make it visible on the radiograph (Figure 8).

[Figure 8. Radiographs showing the importance of an angled x-ray beam for diagnosis of root fracture. Three different vertical angled

radiographs produce different radiographic images.]

Figure 8. Radiographs showing the importance of an angled x-ray beam for diagnosis of root fracture. Three different vertical angled

radiographs produce different radiographic images.0

TREATMENT

Emergency treatment involves repositioning of the segments in as close proximity as possible and splinting to adjacent teeth for 2 to 4

weeks with a functional splint.68 This splinting protocol has recently changed from the 2 to 4 months of rigid splinting that had been

recommended for many years.69 If a long time has elapsed between the injury and treatment, it will likely not be possible to reposition

the segments close to their original position, compromising the long-term prognosis of the tooth.

Treatment of Root Fracture Complications

CORONAL ROOT FRACTURES

Historically, it had been thought that fractures in the cervical segment had a poor prognosis, and extraction of the coronal segment was

recommended. Research does not support such treatment, and, in fact, if the coronal segment is below the attachment level and

adequately splinted, the chances of healing do not differ from those of midroot or apical fractures.67

MIDROOT AND APICAL ROOT FRACTURES

Pulp necrosis occurs in 25% of root fractures.67,70 In the vast majority of cases, the necrosis occurs in the coronal segment only with

the apical segment remaining vital. Therefore, endodontic treatment is indicated in the coronal root segment only unless a periapical

lesion is seen in the apical segment. In most cases, the canal lumen is wide at the apical extent of the coronal segment, so long-term

calcium hydroxide treatment or an MTA apical plug is indicated. The coronal segment is root-filled after a hard tissue barrier has

formed apically in the coronal segment and periapical healing has taken place (Figure 9). If MTA is used, the root filling will be

placed before healing is seen, making follow-up visits essential in these cases.

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In rare cases, when both the coronal and apical pulp areas are necrotic, treatment is more complicated. Endodontic treatment through

the fracture is extremely difficult and should be avoided. Endodontic manipulations, medicaments, and filling materials all have a

detrimental effect on healing of the fracture site. In more apical root fractures, necrotic apical segments can be surgically removed.

This is a viable treatment if the remaining root is long enough to provide adequate periodontal support. Removal of the apical segment

in midroot fractures leaves the coronal segment with a compromised attachment, and the crown to root ratio must be assessed before

the decision to maintain the tooth is made.

[Figure 9. The coronal segment (only) is root-filled after a hard tissue barrier has formed at the most apical part of the coronal

segment.]

After the splinting period is completed, follow-up is conducted at the same intervals as all dental traumatic injuries: at 3, 6, and 12

months and yearly thereafter.

Figure 9. The coronal segment (only) is root-filled after a hard tissue barrier has formed at the most apical part of the coronal

segment.0

FACTORS INFLUENCING REPAIR

1. The degree of dislocation and mobility of the coronal fragment are extremely important in determining outcome.71-73 Increased

dislocation and coronal fragment mobility result in a decreased prognosis.

2. Immature teeth are seldom involved in root fractures, but when they are, the prognosis is good.72,74

3. Quality of treatment: prognosis increases with early treatment, close reduction of the root segments, and semi-rigid splinting for 2 to

4 weeks.68

Complications are as follows: (1) pulp necrosis that can be treated successfully67,70 by treating the coronal segment with adequate

disinfection and long-term calcium hydroxide or MTA and filling when a hard tissue barrier has formed; (2) root canal obliteration

[Figure 10. Examples of root canal obliteration in root-fractured teeth. It is common for the segments that maintain vitality to

obliterate.]

is not uncommon if the root segment (coronal or apical) remains vital (Figure 10) .

Figure 10. Examples of root canal obliteration in root-fractured teeth. It is common for the segments that maintain vitality to

obliterate.0

ENDODONTIC ESSENTIALS

If the coronal segment is reduced quickly and a functional splint is placed for 2 to 4 weeks, pulp necrosis is remarkably low. It will

occur only 25% of the time, and in the vast majority of cases, the necrosis will occur only in the coronal segment. Root canal

obliteration of both segments is very common. When necrosis does occur, disinfection of the coronal segment only should be initiated,

followed by initiation of a physiologic barrier with long-term calcium hydroxide or a physical barrier with MTA. Root canal

obliteration is usually not treated endodontically.

Luxation Injuries

DEFINITIONS

1. Concussion implies no displacement, normal mobility, sensitivity to percussion.

2. Subluxation implies sensitivity to percussion, increased mobility, no displacement.

3. Lateral luxation implies displacement labially, lingually, distally, or incisally.

4. Extrusive luxation implies displacement in a coronal direction.



5. Intrusive luxation implies displacement apically into the alveolus.

Definitions 1 through 5 describe injuries of increasing magnitude in terms of the intensity of the injury and subsequent sequelae.

Luxation injuries result in damage to the attachment apparatus (periodontal ligament and cemental layer), the severity of which is

dependent on the type of injury sustained (concussion least, intrusion most). The apical neurovascular supply to the pulp is also

affected to varying degrees, resulting in altered or total loss of pulp vitality in the tooth. If the luxation injury is mild, the inflammatory

response to the external root surface will be small and the pulp will maintain vitality. Inflammation owing to the trauma will thus be

self-limiting, and cemental (favorable) healing will result.

If, on the other hand, the luxation injury is severe, the damage to the external root surface may be so diffuse that healing with new

cementum alone may not be possible. If bone attaches directly to the root (ankylosis), the root will eventually be replaced by bone

through physiologic resorption and apposition of the bone (osseous replacement). In addition and of special interest to the endodontist,

with a severe luxation injury, the neurovasculature tissues of the pulp may be severed, resulting in a necrotic pulp. If this necrotic pulp

becomes infected, the microbial toxins will pass through the tubules and the damaged cemental covering of the root, resulting in

potentially catastrophic periradicular inflammation with bone and root resorption.

There are two types of trauma-related resorption in which the pulp plays an essential role:

1. In external inflammatory root resorption, the necrotic, infected pulp provides the stimulus for periodontal inflammation. If the

cementum has been damaged and the intermediate cementum penetrated, as when the tooth undergoes a severe traumatic injury, the

inflammatory stimulators in the pulp space are able to diffuse through the dentinal tubules and stimulate an inflammatory response

over large areas of the periodontal ligament. Owing to the lack of cemental protection, periodontal inflammation will include root

resorption and the expected bone resorption.

2. In internal inflammatory root resorption, the inflamed pulp is the tissue involved in resorbing the root structure. The pathogenesis of

internal root resorption is not completely understood. It is believed that coronal necrotic infected pulp provides a stimulus for pulpal

inflammation in the more apical parts of the pulp. If in "rare" cases, the inflamed pulp is adjacent to a root surface that has lost its

predentin protection, internal root resorption will result. Thus, both the necrotic infected pulp and the inflamed pulp contribute to this

type of root resorption.

Consequences of Apical Neurovascular Damage

PULP CANAL OBLITERATION

Pulp canal obliteration is common after luxation injuries, if not severe enough to sever the neurovascular supply apically. The

frequency of pulp canal obliteration appears inversely proportional to that of pulp necrosis. The exact mechanism of pulp canal

obliteration is not known. It is theorized that the sympathetic or parasympathetic control of blood flow to odontoblasts is altered,

resulting in uncontrolled reparative dentin formation.66,75 Another theory is that hemorrhage and blood clot formation in the pulp

after injury are a nidus for subsequent calcification if the pulp remains vital.66,75 Pulp canal obliteration can usually be diagnosed

within the first year after injury76 and was found to be more frequent in teeth with open apices (>0.7 mm radiographically), in teeth

with extrusive and lateral luxation injuries, and in teeth that have been rigidly splinted.76

PULP NECROSIS

The factors most important for the development of pulp necrosis are the type of injury (concussion least, intrusion most) and the stage

of root development (mature apex > immature apex).77 Pulp necrosis can lead to infection of the root canal system, with external

inflammatory root resorption as the consequence. To develop pulp space infection, the pulp must first become necrotic. In trauma,

necrosis is usually due to displacement of the tooth, resulting in severing of the apical blood vessels. In mature teeth, pulp regeneration

cannot occur, and usually by 3 weeks, the necrotic pulp will become infected. For details of the typical bacterial contents of a

traumatized necrotic pulp, see Chapter 7, "Microbiology of Endodontic Disease." Because serious injury is required for pulp necrosis,

it is usual that areas of cemental covering of the root are also affected, resulting in the loss of its protective (insulating) quality. Now

microbial toxins can pass through the dentinal tubules and stimulate an inflammatory response in the corresponding periodontal

ligament. The result is 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 (pulp space bacteria) is removed (Figure 11).78 Radiographically, the resorption is

[Figure 11. Histologic appearance of multinucleated osteoclasts (dentinoclasts) resorbing the dentin of the root.]

[Figure 12. Inflammatory root resorption owing to pulp space infection. Note the radiolucencies in the root and surrounding bone.]

observed as progressive radiolucent areas of the root and adjacent bone (Figure 12).

Figure 11. Histologic appearance of multinucleated osteoclasts (dentinoclasts) resorbing the dentin of the root.0



Figure 12. Inflammatory root resorption owing to pulp space infection. Note the radiolucencies in the root and surrounding bone.

Courtesy of Dr. Fred Barnett.0

TREATMENT

The attachment damage owing to the traumatic injury is often the focus of an emergency visit that, unfortunately, rarely involves the

endodontist. The clinician's attention to pulp space infection should ideally be within 7 to 10 days after the injury.79,80 Root canal

therapy either removes the necrotic pulp as a nidus for microbes or removes the stimulus (microbes already present) to the periapical

inflammation. Without microbial stimulation, resorption will not occur or will heal.33-35 In most cases, a new cemental attachment

will form, but if a large area of root is affected, osseous replacement (ankylosis) can result by the mechanism already described.

Treatment principles include prevention of pulp space infection or elimination of the bacteria if they are present in the pulp space.

1. Prevention of pulp space infection

a. Reestablish the vitality of the pulp. If the pulp stays vital, the canal will be free of bacteria, and external inflammatory root

resorption will not occur. In severe injuries in which vitality has been lost, it is possible under some circumstances to promote

revascularization of the pulp. Revascularization is possible in young teeth with incompletely formed apices if the teeth are replaced in

their original position within 60 minutes of the injury.81,82 However, even under the best conditions, revascularization will fail to

occur on many occasions. Thus, a diagnostic dilemma results. If the pulp revascularizes, external root resorption will not occur and the

root will continue to develop and strengthen. However, if the pulp becomes necrotic and infected, the subsequent externalinflammatory root resorption that develops could result in the loss of the tooth in a very short time. At present, the diagnostic tools

available cannot detect a vital pulp in this situation before approximately 6 months after successful revascularization. This period of

time is obviously unacceptable since by that time, the teeth not revascularized could be lost to the resorption process. Recently, the

laser Doppler flowmeter has been shown to be an excellent diagnostic tool for the detection of revascularization in immature teeth (see

Chapter 14C, "Laser Doppler Flowmetry" . These devices appear to accurately detect the presence of vital tissue in the pulp space

by 4 weeks after the traumatic injury.83

b. Prevent root canal infection by root canal treatment at 7 to 10 days. In teeth with closed apices, revascularization cannot occur.

These teeth should be endodontically treated within 7 to 10 days of the injury before the ischemically necrosed pulp becomes

infected.79,80 This is also a convenient time because this is the time period in which the functional splint is removed and

chemotherapeutic medicaments to limit the initial inflammatory response are stopped.79 From a theoretical point of view, the teeth

treated at this time can be considered equivalent to the treatment of a tooth with a vital pulp. Therefore, the endodontic treatment couldbe completed in one visit. However, efficient treatment is extremely difficult so soon after a serious traumatic injury, and it is

beneficial to start the endodontic treatment with pulpectomy and canal preparation followed by an intracanal dressing with a creamy

mix of calcium hydroxide.79,80 The practitioner can now fill the canal at his or her convenience, after periodontal healing of the

injury is complete, approximately 1 month after the instrumentation visit. There appears to be no necessity for long-term calcium

hydroxide treatment in cases in which the endodontic treatment is started within 10 days of the injury. Notwithstanding, in a compliant

patient, the calcium hydroxide can be applied for a long term (up to 6 months) to ensure periodontal health prior to final root canal

filling.80

2. Elimination of pulp space infection

When root canal treatment is initiated later than 10 days after the accident, or if active external inflammatory resorption is observed,

the preferred antibacterial protocol consists of microbial control followed by a long-term dressing with densely packed calcium

hydroxide.80 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 the microbial control phase with instrumentation of the canal and placement with a lentulo-spiral of a creamy

mix of calcium hydroxide as an intracanal antibacterial agent. The patient is seen in approximately 1 month, at which time, the canal is

filled with a dense mix of calcium hydroxide. Once filled, the canal should appear radiographically to be calcified since the

radiodensity of calcium hydroxide in the canal is usually similar to that of the surrounding dentin (Figure 13). A radiograph is then

taken at 3-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 (ie, calcium hydroxide washout) are 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 permanently root-filled (Figure 14). If it is felt

that additional healing would be beneficial before root filling, the need for replacing the calcium hydroxide in the canal is assessed. If

the canal still appears calcified radiographically, 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 repacked and reassessed in another 3 months.

[Figure 13. Root canal that "disappears" after placement of a thick mix of pure calcium hydroxide.]

Figure 13. Root canal that "disappears" after placement of a thick mix of pure calcium hydroxide. Courtesy of Dr. Fred Barnett.0

Figure 14. The root canal is filled when the adjacent bone has healed, indicating that root resorption has stopped. Left, Active root

resorption with lucencies in the root and bone. Middle, After long-term calcium hydroxide treatment, the adjacent bone has healed.

Right, The canal is now filled.0



Treatment of Established External Root Resoption in a Young Patient

Arresting external inflammatory root resorption owing to pulp space infection is achieved by disinfecting the pulp space. This is

particularly difficult after a luxation injury since the cemental covering is also damaged. This results in the microbes and their by-

products moving deep into the dentinal tubules to stimulate and maintain the inflammation in the surrounding periapical tissues.

Recently, a triantibiotic paste introduced by Hoshino et al.84 has been used in the revascularization

[Figure 14. The root canal is filled when the adjacent bone has healed, indicating that root resorption has stopped. Left, Active root

resorption with lucencies in the root and bone. Middle, After long-term calcium hydroxide treatment, the adjacent bone has healed.

Right, The canal is now filled.]

process of necrotic teeth with open apices and apical periodontitis.85 The antibiotic paste comprising metronidazole, ciprofloxacin,

and minocycline has been shown to have an excellent antimicrobial spectrum for pulp space microbes and an excellent ability to

penetrate the dentinal tubules. Since many cases of external inflammatory resorption owing to pulp space infection occur in immature

teeth or teeth with apical resorption, the same procedure for the healing of external resorption and revascularization should work in

these cases also. With this antibacterial medicament, the potential exists to arrest the external inflammatory root resorption and

revascularize the root canal (Figure 15).

[Figure 15. Immature tooth with a necrotic infected pulp, apical periodontitis, and external inflammatory root resorption. Treatment is

as described in Figure 7. Note the healing of the external root resorption and the continued root development.]

The canal is disinfected without mechanical instrumentation but with copious irrigation with 5.25% sodium hypochlorite and the use

of a mixture of antibiotics for at least 4 weeks.64,85 A blood clot is produced by mechanically irritating the periradicular tissues to the

level of the cementoenamel junction to provide a matrix for the ingrowth of new tissue followed by a deep coronal restoration to

provide a bacteria-tight seal. The patient is followed every 3 months until evidence of healing of the external root resorption and

thickening of the dentinal walls are seen (see Figures 7 and 15).

Recent studies have confirmed the potent antibacterial properties of the triantibiotic paste used in this case,64 and studies are underway to find a synthetic matrix that will act as a more predictable scaffold for new ingrowth of tissue than the blood clot that was used

in these previous cases. The procedure described here can be attempted in most cases, and if after 3 months no signs of resorption

repair and regeneration are present, the more traditional treatment methods can be initiated.

Figure 15. Immature tooth with a necrotic infected pulp, apical periodontitis, and external inflammatory root resorption. Treatment is

as described in Figure 7. Note the healing of the external root resorption and the continued root development. Courtesy of Dr. Linda

Levin.0

Endodontic Essentials

CONCUSSION AND SUBLUXATION

Since both of these injuries imply no noticeable displacement of the tooth in its socket, pulp consequences should not be expected.

However, baseline and follow-up diagnostic tests are essential to pick up late complications such as pulp canal obliteration (most

likely) or pulp necrosis.

Teeth that give a positive pulp test response at the initial examination cannot be assumed to be healthy and continue to give a positive

response over time. Teeth that yield a negative response or no response, however, cannot be assumed to have necrotic pulps because

they may give a positive response at later follow-up visits. It has been demonstrated that it may take as long as 9 months for normal

blood flow to return to the coronal pulp of a traumatized fully formed tooth. As circulation is restored, the responsiveness to pulp

testing returns.85

The transition from a negative to a positive response at a subsequent test may be considered a sign of a healthy pulp. The repetitiousfinding of positive responses may also be taken as a sign of a healthy pulp. The transition from a positive to a negative response may

be taken as an indication that the pulp is probably undergoing degeneration. The persistence of a negative response would suggest that

the pulp has been irreversibly damaged, but even this is not absolute.86 Thermal and electric pulp tests of all anterior teeth (canine to

canine) of the maxillary and mandibular jaws should be performed at the time of the initial examination and carefully recorded to

establish a baseline for comparison with subsequent repeated tests in later months. These tests should be repeated at 3 weeks; 3, 6, and

12 months; and yearly intervals following the accident. The purpose of the tests is to establish a trend as to the physiologic status of

the pulps of these teeth. Particularly in traumatized teeth, carbon dioxide snow (-78°C) or dichlordifluoro-methane (-40°C) placed on

the incisal third of the facial surface gives more accurate responses than does a water ice pencil.87,88 The intense cold seems to

penetrate the tooth and splints or restorations and reach the deeper areas of the tooth. In addition, dry ice does not form ice water,

which could disperse over adjacent teeth or gingiva to give a false-positive response. The electric pulp test relies on electric impulses

directly stimulating the nerves of the pulp. These tests have limited value in young teeth but are useful in cases in which the dentinal



tubules are closed and do not allow dentinal fluid to flow in them. This situation is typical of teeth in elderly patients or in traumatized

teeth that are undergoing premature sclerosis. In these situations, the thermal tests that rely on fluid flow in the tubules cannot be used

and the electric pulp test becomes important.

LATERAL LUXATION, EXTRUSIVE LUXATION

The tooth should be repositioned as soon as possible and a functional splint placed. The endodontic focus takes place at 7 to 10 days

after the emergency visit. The endodontist must evaluate the potential for revascularization of the pulp and therefore not initiate root

canal treatment, or if revascularization is not likely, root canal treatment should be initiated at this 7- to 10-day time period.

The potential for revascularization depends primarily on the width of the apical constriction at the time of repositioning. If the width is

1.0 mm or more, revascularization is considered a possibility. The wider the apical opening is, the higher the likelihood of

revascularization.89 If revascularization is considered possible, a regular follow-up regimen must be scheduled. Since pulp testing is

so erratic in these types of teeth, radiographic follow-up at short intervals with similar angulations is undertaken. A small amount of

radiographically appearing root resorption should be expected owing to the initial inflammation. This should be self-limiting and not

increase in size after 3 weeks. If the radiographic resorption increases or any other signs of pulp infection are present, root canal

therapy should be quickly initiated. If the apical opening is < 1 mm, root canal treatment should be started immediately. If the patient

does not present to the clinician within 7 to 10 days postinjury, or if radiographic evidence of active external resorption is present,

long-term calcium hydroxide treatment or a triantibiotic regimen should be initiated.

INTRUSIVE LUXATION

Intrusive luxation is the most destructive traumatic injury. Attachment damage is diffuse, and pulp survival is considered impossible.

It is possible that in immature roots, spontaneous re-erupt and revascularization may occur, but in mature teeth, pulp necrosis is a

certainty.4 Thus, at the fist chance of accessing the pulp space, root treatment should be initiated.

The Avulsed Tooth

The conditions at the emergency visit will have an important effect on the steps taken at the second visit. Ideally, the tooth should be

replanted as soon as possible after the avulsion and functionally splinted. If unable to replant the tooth, it should be placed in a

physiologic storage solution to allow for an extended extraoral time with fewer resorption complications after reimplantation. At the

emergency visit, the root is prepared depending on the maturity of the tooth (open versus closed) and the extraoral dry time. A dry

time of 60 minutes is considered the point at which survival is unlikely for periodontal ligament cells.

Extraoral Dry Time < 60 Minutes

CLOSED APEX

The root should be rinsed of debris with water or saline and replanted in as gentle a fashion as possible. If the tooth has a closed apex,

revascularization is not possible,89 but because the tooth was dry for less than 60 minutes (replanted or placed in appropriate

medium), the chance for periodontal healing exists. Most importantly, the chance of a severe inflammatory response at the time of

replantation is lessened. A dry time of less than 15 to 20 minutes is considered optimal where periodontal healing would be

expected.90-92

A continuing challenge is the treatment of the tooth that has been dry for more than 20 minutes (periodontal cell survival is ensured)

but less than 60 minutes (periodontal survival unlikely). In these cases, logic suggests that the root surface consist of some cells with

the potential to regenerate and some that will act as inflammatory stimulators. Exciting new strategies are under investigation that may

be extremely valuable in these cases. The use of Ledermix placed in the canal space at the emergency visit has been found to be

valuable in cases that were considered hopeless in the past93 (see below), and this medicament may prove extremely valuable in the

20- to 60-minute dry time period. Studies are ongoing to evaluate its potential.

Egydentist

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Posts: 64

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Date: 09/08/2011 16:52

Re: Endodontic Considerations in Dental Trauma

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OPEN APEX

Soak in doxycycline or cover with minocycline for 5 minutes, gently rinse off debris, and replant. In an open-apex tooth,

revascularization of the pulp and continued root development are possible (Figure 16). Cvek et al.94 found in monkeys that soaking

the tooth in doxycycline (1 mg in approximately 20 mL of physiologic saline) for 5 minutes before replantation significantly enhanced




http://www.4endo.net/forum_quote_63_64.html





revascularization. This result was confirmed in dogs by Yanpiset et al.95 A recent study found that covering the root with minocycline

that attaches to the root for approximately 15 days further increased the revascularization rate in dogs.96 Although these animal

studies do not provide us with a prediction of the rate of revascularization in humans, it is reasonable to expect that the same

enhancement of revascularization that occurred in two animal species will occur in humans as well. As with the tooth with the closed

apex, the open-apex tooth is then gently rinsed and replanted.

Figure 16. Revascularization of an immature root. A tooth with an open apex was replanted soon after the avulsion. The follow-up

radiograph 1 year later confirmed that revascularization had taken place. In this case, it appears that new periodontal tissue has formed

with a lamina dura within the pulp canal. Courtesy of Dr. Russell Stock.0

Exraoral Dry Time > 60 Minutes

CLOSED APEX

Remove the periodontal ligament by placing it in etching acid for 5 minutes, soak it in fluoride, and replant. When the root has been

dry for 60 minutes or more, survival of the periodontal ligament cells is not expected.90,97 In these cases, the root should be prepared

to be as resistant to resorption as possible (attempting to slow the ankylotic osseous replacement process). These teeth should be

soaked in an acid for 5 minutes to remove all remaining periodontal ligament

[Figure 16. Revascularization of an immature root. A tooth with an open apex was replanted soon after the avulsion. The follow-up

radiograph 1 year later confirmed that revascularization had taken place. In this case, it appears that new periodontal tissue has formed

with a lamina dura within the pulp canal.]

and thus remove the tissue that will initiate the inflammatory response on replantation. The tooth should then be soaked in 2%

stannous fluoride for 5 minutes and replanted.98,99 Alendronate was found to have resorption slowing effects similar to those of

fluoride when used topically,100 but further studies need to be carried out to evaluate whether its effectiveness is superior to fluoride

and if this justifies its added cost. Some studies have found that Emdogain (enamel matrix protein) may be beneficial in teeth with

extended extraoral dry times, not only to make the root more resistant to resorption but also possibly to stimulate the formation of new

periodontal ligament from the socket.101,102 More recent studies have not confirmed the beneficial effect of Emdogain.103

If the tooth has been dry for more than 60 minutes and no consideration is given to preserving the periodontal ligament, theendodontics may be performed extraorally. In the case of a tooth with a closed apex, no advantage exists to this additional step at the

emergency visit. However, in a tooth with an open apex, the endodontic treatment, if performed after replantation, involves a long-

term apexification procedure. In these cases, completing the root canal treatment extraorally, where a seal in the "blunderbuss" apex is

easier to achieve, may be advantageous. When endodontic treatment is performed extraorally, it must be performed aseptically with

the utmost care to achieve a root canal system free of bacteria.

OPEN APEX

Replant? If yes, treat as described with a closed-apex tooth. Endodontic treatment may be performed out of the mouth. Since these

teeth are in young patients in whom facial development is usually incomplete, many pediatric dentists consider the prognosis to be so

poor and the potential complications of an ankylosed tooth so severe as to recommend that these teeth not be replanted. However,

considerable debate exists as to whether it would be beneficial to replant the root even though it will inevitably be lost owing to

osseous replacement. If the patients are followed carefully and the root is submerged at the appropriate time,104,105 the height and,

more importantly, the width of the alveolar bone will be maintained. This allows for easier permanent restoration, when the facial

development of the child is complete. Studies are ongoing to evaluate whether the present recommendations should be changed.

Adjunctive Therapy

INTRODUCTION

Systemic antibiotics given at the time of replantation and prior to endodontic treatment are effective in preventing bacterial invasion of

the necrotic pulp and therefore subsequent inflammatory resorption.106 Tetracycline has the additional benefit of decreasing root

resorption by affecting the motility of the osteoclasts and reducing the effectiveness of collagenase.107 The administration of system

antibiotics is recommended beginning at the emergency visit and continuing until the splint is removed.108 For patients not

susceptible to tetracycline dentin staining, doxycycline twice daily for 7 days at an appropriate dose for patient age and weight107,108is the antibiotic of choice. Penicillin V 1,000 mg and 500 mg every 6 hours for 7 days has also been shown to be beneficial. The

bacterial content of the sulcus also should be controlled during the healing phase. In addition to stressing to the patient the need for

adequate oral hygiene, chlorhexidine rinses for 7 to 10 days are useful.

In a recent study by our group, great benefit was seen in removal of the pulp contents at the emergency visit and placing Ledermix

(not available in the United States) into the root canal.93 This product contains a tetracycline corticosteroid combination that has been

shown to move through the dentinal tubules. Based on the results of the study, the use of the medicament was able to shut down the

inflammatory response after replantation to allow for more favorable healing compared with those teeth that did not have the

medicament.



The need for analgesics should be assessed on an individual case basis. Mild analgesics are usually adequate, or a nonsteroidal anti-

inflammatory drug may be recommended. The patient should be sent to a physician for consultation regarding a tetanus booster within

48 hours of the initial visit.

SECOND VISIT

This visit should take place 7 to 10 days after the emergency visit. At the emergency visit, emphasis is placed on the preservation and

healing of the attachment apparatus. The focus of this visit is the prevention or elimination of potential irritants from the root canal

space. These irritants, if present, provide the stimulus for the progression of the inflammatory response and bone and root resorption.

Also at this visit, the course of systemic antibiotics is completed, the chlorhexidine rinses can be stopped, and the splint is removed.

Endodontic Treatment

EXTRAORAL TIME < 60 MINUTES

Closed Apex

Initiate endodontic treatment at 7 to 10 days. In cases in which endodontic treatment is delayed or signs of resorption are present, treat

with calcium hydroxide until evidence of healing is present, such as redevelopment of the periodontal ligament space. The root canal

can then be filled and the crown restored.

Open Apex

Avoid endodontic treatment and look for evidence of revascularization. At the first indication of an infected pulp, initiate the

apexification procedure.

EXTRAORAL TIME > 60 MINUTES

Closed Apex

These teeth are treated endodontically in the same way as those teeth that had an extraoral time of < 60 minutes.

Open Apex

If endodontic treatment was not performed out of the mouth, initiate the apexification procedure. In these teeth, the chance of

revascularization is extremely poor.80,109 Therefore, no attempt is made to revitalize these teeth. An apexification procedure is

initiated at the second visit if root canal treatment was not performed at the emergency visit. If a root canal filling was placed at the

emergency visit, the second visit is a recall visit to assess initial healing only.

Temporary Restoration

Effectively sealing the coronal access is essential to prevent infection of the canal between visits. Recommended temporary

restorations are reinforced zinc oxide-eugenol cement, acid-etch composite resin, or glass ionomer cement. The depth of the temporary

restoration is critical to its sealing ability. A depth of at least 4 mm is recommended and a cotton pellet need not be placed; the

temporary restoration is placed directly onto the calcium hydroxide in the access cavity. Calcium hydroxide should first be removed

from the walls of the access cavity because it is soluble and will wash out when it comes in contact with saliva, leaving a defective

temporary restoration. After initiation of the root canal treatment, the splint is removed. If time does not permit complete removal of

the splint at this visit, the resin tacks are smoothed so as not to irritate the soft tissues and the residual resin is removed at a later

appointment. At this appointment, healing is usually sufficient to perform a detailed clinical examination on the teeth surrounding the

avulsed tooth. The sensitivity tests, reaction to percussion and palpation, and periodontal probing measurements should be carefully

recorded for reference at follow-up visits.

Root Filling Visit

INTRODUCTION

The root canal can be filled at the practitioner's convenience or, in the case of long-term calcium hydroxide therapy, when an intact

lamina dura can be traced. If the endodontic treatment was initiated 7 to 10 days after the avulsion and clinical and radiographic

examinations do not indicate pathosis, filling of the root canal at this visit is acceptable, although the use of long-term calcium

hydroxide is a proven option for these cases. On the other hand, if endodontic treatment was initiated more than 7 to 10 days after the

avulsion or if active resorption is visible, the pulp space must first be disinfected before root filling. Traditionally, the reestablishment

of a lamina dura (see Figure 14) is a radiographic sign that the canal bacteria have been controlled. When an intact lamina dura can be

traced, root filling can take place. The canal is cleaned, shaped, and irrigated under strict asepsis. After completion of the

instrumentation, the canal can be filled by any acceptable technique, with special attention to an aseptic technique and the best

possible seal of the filling material.



PERMANENT RESTORATION

Much evidence exists that coronal leakage caused by defective temporary and permanent restorations results in a clinically relevant

amount of bacterial contamination in the root canal after root filling.110 Therefore, the tooth should receive a permanent restoration at

or soon after the time of filling of the root canal. As with the temporary restoration, the depth of restoration is important for its seal;

therefore, the deepest restoration possible should be made. A post should be avoided if possible. Because most avulsions occur in the

anterior region of the mouth, where esthetics is important, composite resins with the addition of dentin bonding agents are usually

recommended in these cases. They have the additional advantage of internally strengthening the tooth against fracture if another

traumatic event should occur.

FOLLOW-UP CARE

Follow-up evaluations should take place at 3 months, at 6 months, and yearly for at least 5 years. If osseous replacement (ankylosis) is

identified (Figure 17),

[Figure 17. Radiographic appearance of osseous replacement. The root acquires the radiographic appearance of the surrounding bone

(without a lamina dura). Note that radiolucencies typical of active inflammation are not present.]

timely revision of the long-term treatment plan is indicated. In the case of inflammatory root resorption (see Figure 12), a new attempt

at disinfection of the root canal space by standard retreatment can reverse the process. Teeth adjacent to and surrounding the avulsed

tooth or teeth may show pathologic changes long after the initial accident. Therefore, these teeth should be tested at recall and theresults compared with those collected soon after the accident.

Figure 17. Radiographic appearance of osseous replacement. The root acquires the radiographic appearance of the surrounding bone

(without a lamina dura). Note that radiolucencies typical of active inflammation are not present.0

Internal Root Resorption

INTRODUCTION

Internal root resorption is rare in permanent teeth. Internal resorption is characterized by an oval-shaped enlargement of the root canal

space.4 External resorption, which is much more common, is often misdiagnosed as internal resorption. Internal root resorption is

characterized by resorption of the internal aspect of 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. There are different theories on the

origin of the pulpal granulation tissue involved in internal resorption. The most logical explanation is that it is pulp tissue that is

inflamed owing to an infected coronal pulp space. Communication between the coronal necrotic tissue and the vital pulp is through

appropriately oriented dentinal tubules.78 In addition to the requirement of granulation tissue, root resorption takes place only if the

odontoblastic layer and predentin are lost or altered.78

Reasons for the loss of predentin adjacent to the granulation tissue are not obvious. Trauma frequently has been suggested as a

cause.111,112 Some report that trauma may be recognized as an initiating factor in internal resorption.113 They are divided into a

transient type and a progressive type, the latter requiring continuous stimulation by infection. Another reason for the loss of predentin

might be extreme heat produced when cutting on dentin without an adequate water spray. The heat presumably would destroy the

predentin layer, and if later the coronal aspect of the pulp 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. Internal root resorption

has been produced experimentally by the application of diathermy.113

Internal root resorption is usually asymptomatic and is first recognized clinically through routine radiographs. Pain may be a

presenting symptom if perforation of the crown occurs and the metaplastic tissue is exposed to the oral fluids. For internal resorption

to be active, at least part of the pulp must be vital, so a positive response to pulp sensitivity testing is possible. The coronal portion of

the pulp is often necrotic, whereas the apical pulp that includes the internal resorptive defect remains vital. Therefore, a negative

sensitivity test result does not rule out active internal resorption. It is also possible that the pulp becomes nonvital after a period of

active resorption, giving a negative sensitivity test, radiographic signs of internal resorption, and radiographic signs of apical

inflammation. Traditionally, the pink tooth has been thought pathognomonic of internal root resorption. The pink color is due to the

granulation tissue in the coronal dentin undermining the crown enamel (Figure 18). The pink tooth can also be a feature of cervical

subepithelial external inflammatory root resorption that must be ruled out before a diagnosis of internal root resorption is made.

[Figure 18. Pink spot associated with internal root resorption.]

Figure 18. Pink spot associated with internal root resorption.0

RADIOGRAPHIC APPEARANCE

The usual radiographic presentation of internal root resorption is a fairly uniform radiolucent enlargement of the pulp canal (Figure



19). 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. Only on rare occasions, when the internal resorptive defect penetrates the root and

impacts the periodontal ligament, does the adjacent bone show radiographic changes.

Figure 19. Uniform radiolucency observed in teeth with internal root resorption.0

HISTOLOGIC APPEARANCE

Similar to other inflammatory resorptive defects, the histologic picture of internal resorption is granulation tissue with multinucleated

giant cells. An area of necroticpulp is found coronal to the granulation tissue. Dentinal tubules containing microorganisms and

communicating between the necrotic zone and the granulation tissue can sometimes be seen.78,80,113,114 Unlike external root

resorption, the adjacent bone is not affected with internal root resorption.

[Figure 19. Uniform radiolucency observed in teeth with internal root resorption.]

ENDODONTIC TREATMENT

Treatment of internal root resorption is conceptually very easy. Since the resorptive defect is the result of the inflamed pulp and the

blood supply to the tissue is through the apical foramina, endodontic treatment that effectively removes the blood supply to theresorbing cells is the treatment approach. After adequate anesthesia is obtained, 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 completion of the root canal instrumentation, it should be possible to obtain a blood-free and

dry canal with paper points. Calcium hydroxide is 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 with a soft root filling technique (Figure 20). With modern dental

techniques, this treatment alternative should be weighed against the advantages of implant dentistry.

[Figure 20. An internal root resorption defect is filled with a softened gutta-percha filling technique.]

Figure 20. An internal root resorption defect is filled with a softened gutta-percha filling technique.0

References

1. Andreasen JO, Ravn JJ. Epidemiology of traumatic dental injuries to primary and permanent teeth in a Danish population sample.

Int J Oral Surg 1972;1:235.

2. Skaare AB, Jacobsen I. Dental injuries in Norwegians aged 7-18 years. Dent Traumatol 2003;19:67.

3. Bastone EB, Freer TJ, McNamara JR. Epidemiology of dental trauma: a review of the literature. Aust Dent J 2000;45:2.

4. Andreasen JO, Andreasen FM. Textbook and color atlas of traumatic injuries to the teeth. 3rd ed. Copenhagen and St. Louis:

Munksgaard and CV Mosby; 1994.

5. Canakci V, Akgul HM, Akgul N, Canakci CF. Prevalence and handedness correlates of traumatic injuries to the permanent incisors

in 13-17-year-old adolescents in Erzurum, Turkey. Dent Traumatol 2003;19:248.

6. Saroglu I, Sonmez H. The prevalence of traumatic injuries treated in the pedodontic clinic of Ankara University, Turkey, during 18

months. Dent Traumatol 2002;18:299.

7. Tapias MA, Jimenez-Garcia R, Lamas F, Gil AA. Prevalence of traumatic crown fractures to permanent incisors in a childhood

population: Mostoles, Spain. Dent Traumatol 2003;19:119.

8. Kakehashi S, Stanley HR, Fitzgerald RJ. The effect of surgical exposures on dental pulps in germ-free and conventional laboratory

rats. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1965;20:340.

9. Cvek M, Cleaton-Jones PE, Austin JC, Andreasen JO. Pulp reactions to exposure after experimental crown fractures or grinding in

adult monkeys. J Endod 1982;8:391.

10. Cvek M. A clinical report on partial pulpotomy and capping with calcium hydroxide in permanent incisors with complicated

crown fracture. J Endod 1978;4:232.



11. Heide S, Mjor IA. Pulp reactions to experimental exposures in young permanent monkey teeth. Int Endod J 1983;16:11.

12. Katebzadeh N, Dalton BC, Trope M. Strengthening immature teeth during and after apexification. J Endod 1998;24:256.

13. Sjogren U, Hagglund B, Sundqvist G, Wing K. Factors affecting the long-term results of endodontic treatment. J Endod

1990;16:498.

14. Masterton JB. The healing of wounds of the dental pulp. An investigation of the nature of the scar tissue and of the phenomena

leading to its formation. Dent Pract Dent Rec 1966;16:325.

15. Weiss M. Pulp capping in older patients. N Y State Dent J 1966;32:451.

16. Cvek M, Hollender L, Nord CE. Treatment of non-vital permanent incisors with calcium hydroxide. VI. A clinical,

microbiological and radiological evaluation of treatment in one sitting of teeth with mature or immature root. Odontol Revy

1976;27:93.

17. Andreasen JO. Luxation of permanent teeth due to trauma. A clinical and radiographic follow-up study of 189 injured teeth. Scand

J Dent Res 1970;78:273.

18. Eklund G, Stalhane I, Hedegard B. A study of traumatized permanent teeth in children aged 7-15 years. Part III. A multivariate

analysis of post-traumatic complications of subluxated and luxated teeth. Sven Tandlak Tidskr 1976;69:179.

19. Swift EJ Jr, Trope M. Treatment options for the exposed vital pulp. Pract Periodontics Aesthet Dent 1999;11:735.

20. Tronstad L, Mjor IA. Capping of the inflamed pulp. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1972;34:477.

21. Cox CF, Keall CL, Keall HJ, et al. Biocompatibility of surface-sealed dental materials against exposed pulps. J Prosthet Dent

1987;57:1.

22. Bystrom A, Claesson R, Sundqvist G. The antibacterial effect of camphorated paramonochlorophenol, camphorated phenol and

calcium hydroxide in the treatment of infected root canals. Endod Dent Traumatol 1985;1:170.

23. Sjogren U, Figdor D, Spangberg L, Sundqvist G. The antimicrobial effect of calcium hydroxide as a short-term intracanal

dressing. Int Endod J 1991;24:119.

24. Mejare I, Hasselgren G, Hammarstrom LE. Effect of formaldehyde-containing drugs on human dental pulp evaluated by enzyme

histochemical technique. Scand J Dent Res 1976;84:29.

25. Schroder U, Granath LE. Early reaction of intact human teeth to calcium hydroxide following experimental pulpotomy and its

significance to the development of hard tissue barrier. Odontol Revy 1971;22:379.

26. Schroder U. Reaction of human dental pulp to experimental pulpotomy and capping with calcium hydroxide [thesis]. Odont Revy

1973;24 Suppl 25:97.

27. Stanley HR, Lundy T. Dycal therapy for pulp exposures. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1972;34:818.

28. Tronstad L. Reaction of the exposed pulp to Dycal treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1974;38:945.

29. Heller AL, Koenigs JF, Brilliant JD, et al. Direct pulp capping of permanent teeth in primates using a resorbable form of

tricalcium phosphate ceramic. J Endod 1975;1:95.

30. Arakawa M, Kitasako Y, Otsuki M, Tagami J. Direct pulp capping with an auto-cured sealant resin and a self-etching primer. Am

J Dent 2003;16:61.

31. Deutsch AS, Musikant BL, Cavallari J, et al. Root fracture during insertion of prefabricated posts related to root size. J Prosthet

Dent 1985;53:786.



32. Torabinejad M, Hong CU, McDonald F, Pitt Ford TR. Physical and chemical properties of a new root-end filling material. J Endod

1995;21:349.

33. Torabinejad M, Rastegar AF, Kettering JD, Pitt Ford TR. Bacterial leakage of mineral trioxide aggregate as a root-end filling

material. J Endod 1995;21:109.

34. Cvek M. A clinical report on partial pulpotomy and capping with calcium hydroxide in permanent incisors with complicated

crown fracture. J Endod 1978;4:232.

35. Granath LE, Hagman G. Experimental pulpotomy in human bicuspids with reference to cutting technique. Acta Odontol Scand

1971;29:155.

36. Stanley HR, Lundy T. Dycal therapy for pulp exposures. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1972;34:818.

37. Fuks AB, Cosack A, Klein H, Eidelman E. Partial pulpotomy as a treatment alternative for exposed pulps in crown-fractured

permanent incisors. Endod Dent Traumatol 1987;3:100.

38. Gelbier MJ, Winter GB. Traumatised incisors treated by vital pulpotomy: a retrospective study. Br Dent J 1988;164:319.

39. Seltzer S, Bender IB, Turkenkopf S. Factors affecting successful repair after root canal therapy. J Am Dent Assoc 1963;52:651.

40. Teixeira FB, Teixeira EC, Thompson JY, Trope M. Fracture resistance of roots endodontically treated with a new resin filling

material. J Am Dent Assoc 2004;135:646.

41. Bergenholtz G. Micro-organisms from necrotic pulps of traumatized teeth. Odont Revy 1974;25:347-58.

42. Shuping G, {145}rstavik D, Sigurdsson A, Trope M. Reduction of intracanal bacteria using nickel-titanium rotary instrumentation

and various medications. J Endod 2000;26:751-5.

43. Cvek M, Nord CE, Hollender L. Antimicrobial effect of root canal debridement in teeth with immature root. A clinical and

microbiologic study. Odontol Revy 1976;27:1.

44. Spangberg L, Rutberg M, Rydinge E. Biologic effects of endodontic antimicrobial agents. J Endod 1979;5:166.

45. Heithersay GS. Calcium hydroxide in the treatment of pulpless teeth with associated pathology. J Br Endod Soc 1962;8:74.

46. Herforth A, Strassburg M. [Therapy of chronic apical periodontitis in traumatically injuring front teeth with ongoing root growth].

Dtsch Zahnarztl Z 1977;32:453.

47. Cvek M. Prognosis of luxated non-vital maxillary incisors treated with calcium hydroxide and filled with gutta-percha. A

retrospective clinical study. Endod Dent Traumatol 1992;8:45.

48. Lengheden A, Blomlof L, Lindskog S. Effect of delayed calcium hydroxide treatment on periodontal healing in contaminated

replanted teeth. Scand J Dent Res 1991;99:147.

49. Andreasen JO, Farik B, Munksgaard EC. Long-term calcium hydroxide as a root canal dressing may increase risk of root fracture.

Dent Traumatol 2002;18:134.

50. Giuliani V, Baccetti T, Pace R, Pagavino G. The use of MTA in teeth with necrotic pulps and open apices. Dent Traumatol

2002;18:217.

51. Maroto M, Barberia E, Planells P, Vera V. Treatment of a non-vital immature incisor with mineral trioxide aggregate (MTA). Dent

Traumatol 2003;19:165.

52. Binnie WH, Rowe AH. A histological study of the periapical tissues of incompletely formed pulpless teeth filled with calcium

hydroxide. J Dent Res 1973;52:1110.



53. Cvek M. Treatment of non-vital permanent incisors with calcium hydroxide. IV. Periodontal healing and closure of the root canal

in the coronal fragment of teeth with intraalveolar fracture and vital apical fragment. A follow-up. Odontol Revy 1974;25:239.

54. Trabert KC, Caput AA, Abou-Rass M, et al. A histological study of the periapical tissues of incompletely formed pulpless teeth

filled with calcium hydroxide. J Dent Res 1973;52:1110.

55. Deutsch AS, Musikant BL, Cavallari J, et al. Root fracture during insertion of prefabricated posts related to root size. J Prosthet

Dent 1985;53:786.

56. Kerekes K, Heide S, Jacobsen I. Follow-up examination of endodontic treatment in traumatized juvenile incisors. J Endod

1980;6:744.

57. Goldberg F, Kaplan A, Roitman M, et al. Reinforcing effect of a resin glass ionomer in the restoration of immature roots in vitro.

Dent Traumatol 2002;18:70.

58. Barrett AP, Reade PC. Revascularization of mouse tooth isografts and allografts using autoradiography and carbon-perfusion.

Arch Oral Biol 1981;26:541.

59. Ohman A. Healing and sensitivity to pain in young replanted human teeth. An experimental, clinical and histological study.

Odontol Tidskr 1965;73:166.

60. Skoglund A, Tronstad L. Pulpal changes in replanted and autotransplanted immature teeth of dogs. J Endod 1981;7:309.

61. Love RM. Bacterial penetration of the root canal of intact incisor teeth after a simulated traumatic injury. Endod Dent Traumatol

1996;12:289.

62. Banchs F, Trope M. Revascularization of immature permanent teeth with apical periodontitis: new treatment protocol? J Endod2004;30:196.

63. Thibodeau B, Teixeira F, Yamauchi M, et al. Pulp revascularization of immature dog teeth with apical periodontitis J Endod

2007;33:680-9.

64. Yanpiset K, Trope M. Pulp revascularization of replanted immature dog teeth after different treatment methods. Endod Dent

Traumatol 2000;16:211-16.

65. Windley W III, Teixeira F, Levin L, et al. Disinfection of immature teeth with a triple antibiotic paste. J Endod 2005;31:439-43.

66. Zachrisson BU, Jacobsen I. Long-term prognosis of 66 permanent anterior teeth with root fracture. Scand J Dent Res 1975;83:345.

67. Andreasen FM. Pulpal healing after luxation injuries and root fracture in the permanent dentition. Endod Dent Traumatol

1989;5:111.

68. Jacobsen I, Kerekes K. Diagnosis and treatment of pulp necrosis in permanent anterior teeth with root fracture. Scand J Dent Res

1980;88:370.

69. Andreasen JO, Andreasen FM, Mejare I, Cvek M. Healing of 400 intra-alveolar root fractures. 2. Effect of treatment factors such

as treatment delay, repositioning, splinting type and period and antibiotics. Dent Traumatol 2004;20:203.

70. Rabie G, Barnett F, Tronstad L. Long-term splinting of maxillary incisor with intra-alveolar root fracture. Endod Dent Traumatol

1988;4:99.

71. Cvek M. Treatment of non-vital permanent incisors with calcium hydroxide. IV. Periodontal healing and closure of the root canal

in the coronal fragment of teeth with intraalveolar fracture and vital apical fragment. A follow-up. Odontol Revy 1974;25:239.

72. Jacobsen I, Zachrisson BU. Repair characteristics of root fractures in permanent anterior teeth. Scand J Dent Res 1975;83:355.



73. Andreasen JO, Andreasen FM, Mejare I, Cvek M. Healing of 400 intra-alveolar root fractures. 1. Effect of pre-injury and injury

factors such as sex, age, stage of root development, fracture type, location of fracture and severity of dislocation. Dent Traumatol

2004;20:192.

74. Andreasen FM. Pulpal healing after luxation injuries and root fracture in the permanent dentition. Endod Dent Traumatol

1989;5:111.

75. Jacobsen I. Root fractures in permanent anterior teeth with incomplete root formation. Scand J Dent Res 1976;84:210.

76. Andreasen JO. Review of root resorption systems and models. Etiology of root resorption and the homeostatic mechanisms of the

periodontal ligament.

77. Andreasen FM, Zhijie Y, Thomsen BL, Andersen PK. Occurrence of pulp canal obliteration after luxation injuries in the

permanent dentition. Endod Dent Traumatol 1987;3:103.

78. Andreasen FM, Pedersen BV. Prognosis of luxated permanent teeth — the development of pulp necrosis. Endod Dent Traumatol

1985;1:207.

79. Tronstad L. Root resorption — etiology, terminology and clinical manifestations. Endod Dent Traumatol 1988;4:241.

80. Trope M, Moshonov J, Nissan R, et al. Short vs. long-term calcium hydroxide treatment of established inflammatory root

resorption in replanted dog teeth. Endod Dent Traumatol 1995;11:124.

81. Trope M, Yesilsoy C, Koren L, et al. Effect of different endodontic treatment protocols on periodontal repair and root resorption of

replanted dog teeth. J Endod 1992;18:492.

82. Cvek M, Cleaton-Jones P, Austin J, et al. Effect of topical application of doxycycline on pulp revascularization and periodontal

healing in reimplanted monkey incisors. Endod Dent Traumatol 1990;6:170.

83. Yanpiset K, Vongsavan N, Sigurdsson A, Trope M. Efficacy of laser Doppler flowmetry for the diagnosis of revascularization of

reimplanted immature dog teeth. Dent Traumatol 2001;17:63.

84. Hoshino E, Kurihara-Ando N, Sato I, et al. In-vitro antibacterial susceptibility of bacteria taken from infected root dentine to a

mixture of ciprofloxacin, metronidazole and minocycline. Int Endod J 1996;29:125-30.

85. Gazelius B, Olgart L, Edwall B. Restored vitality in luxated teeth assessed by laser Doppler flowmeter. Endod Dent Traumatol

1988;4:265.

86. Bhaskar SN, Rappaport HM. Dental vitality tests and pulp status. J Am Dent Assoc 1973;86:409.

87. Fulling HJ, Andreasen JO. Influence of maturation status and tooth type of permanent teeth upon electrometric and thermal pulp

testing. Scand J Dent Res 1976;84:286.

88. Fuss Z, Trowbridge H, Bender IB, et al. Assessment of reliability of electrical and thermal pulp testing agents. J Endod

1986;12:301.

89. Kling M, Cvek M, Mejare I. Rate and predictability of pulp revascularization in therapeutically reimplanted permanent incisors.

Endod Dent Traumatol 1986;2:83-9.

90. Soder PO, Otteskog P, Andreasen JO, Modeer T. Effect of drying on viability of periodontal membrane. Scand J Dent Res1977;85:164.

91. Andreasen JO. Effect of extra-alveolar period and storage media upon periodontal and pulpal healing after replantation of mature

permanent incisors in monkeys. Int J Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1981;10:43.

92. Barrett EJ, Kenny DJ. Avulsed permanent teeth: a review of the literature and treatment guidelines. Endod Dent Traumatol

1997;13:153.



93. Bryson EC, Levin L, Banchs F, et al. Effect of immediate intracanal placement of Ledermix Paste® on healing of replanted dog

teeth after extended dry times. Endod Dent Traumatol 2002;18:316-21.

94. Cvek M, et al. Effect of topical application of doxycycline on pulp revascularization and periodontal healing in reimplanted

monkey incisors. Endod Dent Traumatol 1990;6:170-7.

95. Yanpiset K, Trope M. Pulp revascularization of replanted immature dog teeth after different treatment methods. Endod Dent

Traumatol 2000;16:211-17.

96. Ritter AL, Ritter AV, Murrah V, et al. Pulp revascularization of replanted immature dog teeth after treatment with minocyline and

doxycycline assessed by laser flowmetry, radiography and histology. Dent Traumatol 2004;5:75-84.

97. Andreasen JO, Kristerson L. The effect of limited drying or removal of the periodontal ligament. Periodontal healing after

replantation of mature permanent incisors in monkeys. Acta Odontol Scand 1981;39:1.

98. Bjorvatn K, Selvig KA, Klinge B. Effect of tetracycline and SnF2 on root resorption in replanted incisors in dogs. Scand J Dent

Res 1989;97:477.

99. Selvig KA, Zander HA. Chemical analysis and microradiography of cementum and dentin from periodontically diseased human

teeth. J Periodont 1962;33:103.

100. Levin L, Bryson EC, Caplan D, Trope M. Effect of topical alendronate on root resorption of dried replanted dog teeth. Dent


101. Filippi A, Pohl Y, von Arx T. Treatment of replacement resorption with Emdogain — preliminary results after 10 months. Dent


102. Iqbal MK, Bamaas N. Effect of enamel matrix derivative (EMDOGAIN) upon periodontal healing after replantation of

permanent incisors in beagle dogs. Dent Traumatol 2001;17:36.

103. Araujo M, Hayacibara R, Sonohara M, et al. Effect of enamel matrix proteins (Emdogain) on healing after re-implantation of

"periodontally compromised" roots. An experimental study in the dog. J Clin Periodontol 2003;30:855-61.

104. Flores MT, Andersson L, Andreasen JO, et al. Guidelines for the management of traumatic dental injuries. II. Avulsion of

permanent teeth. Dent Traumatol 2007;3:130-6.

105. Andersson L, Malmgren B. The problem of dentoalveolar ankylosis and subsequent replacement resorption in the growing

patient. Aust Endod J 1999;25:57.

106. Hammarstrom L, Pierce A, Blomlof L, et al. Tooth avulsion and replantation —

a review. Endod Dent Traumatol 1986;2:1.

107. Sae-Lim V, Wang CY, Choi GW, Trope M. The effect of systemic tetracycline on resorption of dried replanted dogs' teeth.

Endod Dent Traumatol 1998;14:127.

108. Sae-Lim V, Wang CY, Trope M. Effect of systemic tetracycline and amoxicillin on inflammatory root resorption of replanted

dogs' teeth. Endod Dent Traumatol 1998;14:216.

109. Trope M. Root resorption of dental and traumatic origin: classification based on etiology. Pract Periodontics Aesthet Dent

1998;10:515.

110. Ray HA, Trope M. Periapical status of endodontically treated teeth in relation to the technical quality of the root filling and the

coronal restoration. Int Endod J 1995;28:12.

111. Seltzer S. Endodontology. Philadelphia: Lea & Febiger; 1988.

112. Wedenberg C, Zetterqvist L. Internal resorption in human teeth — a histological, scanning electron microscopic, and enzyme

histochemical study. J Endod 1987;13:255.



113. Wedenberg C, Lindskog S. Experimental internal resorption in monkey teeth. Endod Dent Traumatol 1985;1:221.

114. Silverman S. The dental structures in primary hyperparathyroidism. Oral Surg Oral Med Oral Pathol Oral Radiol Endod

1962;15:426.

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