Entrance of the canal E Middle one third of the canal.

B C

150 Endodontics 7 - Pulpal Pathology 151

ve symptoms in 96%, and the absence of radiolucen- cies in 100%.

The success of pulpotomy with Cresatin depends on two factors:

1. The correct diagnosis of “pure” pulpitis, that is, without a component of periodontitis (lack of pain on palpation and percussion).

2. The presence of vital tissue within the root canal (positive response to vitality tests).

If the two circumstances are confirmed, the patient can live with the medicated tooth for as long as a month without any bother. There is thus plenty of time to plan the necessary appointments to complete the the- rapy. It is absolutely mistaken to give in to the temp- tation to also remove the pulp of the canals, if there is insufficient time to complete the cleaning and shaping of these canals. As will be seen later, the instruments must and can be placed inside the root canals only if they can be cleaned and shaped completely.

If the situation is not consistent with pure pulpitis – that is, if the tooth, in addition to responding to heat stimulation, is also sensitive to percussion – this indi- cates that a component of periodontitis is already pre- sent. Therefore, the treatment with Cresatin can be performed only after the canals have been cleansed and shaped. The removal of their contents prevents the development of an acute alveolar abscess.

However, since the tooth with pulpitis presents urgen- tly, it is unlikely that one will have the necessary time to prepare the canals. In these cases, once the pulpotomy has been performed, it is advisable to leave the pulp chamber completely open, without any medication, so that it may drain. The tooth will remain open until the date scheduled for the completion of the therapy. The diagnosis of pulpitis with concomitant periodon- tal involvement (pulpitis with acute apical periodonti- tis) is easy to make, since the patient can localize the tooth, which is sensitive to pressure and thus to per- cussion. This is due to involvement of the propriocep- tive nerves in the periodontal ligament.

Whether a “closed” treatment is performed or the tooth is left “open,” in the therapy of pulpitis, one must not forget to remove the tooth from the occlusion.

Necrosis

The irreversible inflammation of the pulp that occurs in pulpitis may persist for a certain period of time, but eventually it causes total necrosis of the pulp tissue. Necrosis, or death of the pulp tissue, is thus the di-

rect consequence of pulpitis, but it may also arise im- mediately after trauma that damages the vascular pe- duncle.

As a result of an inflammatory process, the pulp tissue continues to disintegrate, forming a slowly enlarging zone of liquefactive necrosis. The lack of collateral cir- culation and the presence of the inextensible walls of dentin aggravate and accelerate the process that leads to total necrosis of the tissue. Indeed, there is no drai- nage whatsoever of the inflammatory exudate, with a consequent increase of the tissue pressure that causes the destruction to proceed, until the entire pulp has become necrotic.74

The rapidity of the progression of the liquefactive ne- crosis varies, depending on whether the inflammatory fluids can drain, and thus on the rate of increase of in- trapulpal pressure.

Pulpitis in a tooth with a completely closed pulp chamber leads more rapidly to total necrosis of the entire pulp, with the almost miraculous resolution of all symptoms. In contrast, pulpitis in a tooth with pe- netrating caries or, especially, an open pulp chamber leads to slower destruction, with degeneration of the coronal pulp and the presence of vital tissue at the ra- dicular level.10

The zone of necrosis contains irritants that arise from both tissue destruction and aerobic and anaerobic bacteria. These irritants come into contact with the adjacent vital tissue and continue to cause damage in an apical direction.

When the pulp has become completely necrotic, the irritant substances may begin their destructive action on the periapical tissues. This occurs in most cases, but is not the rule.

On occasion, there are already symptoms and radio- graphic signs of periapical inflammation in the pre- sence of vital, albeit inflamed, pulp in the pulp cham- ber and histologically normal pulp in the root canals.19 It is believed that this is due to the passage of irritants arising from the coronal tissue through the radicular pulp, with a consequent periapical inflammatory re- sponse and resorption of the bony trabeculae. This cli- nical situation is more often found in young patients (Fig. 7.15).

On the other hand, it should not be surprising to find vital – and therefore sensitive – pulp within a root canal in a tooth whose pulp chamber was com- pletely necrotic, whose pulp tests were all negati- ve, and whose access cavity was created without the need for anesthesia. The more the necrosis nears the blood supply and the tissue is far from the exposure

nals requires the intra-operative use of anesthesia, but this changes nothing in terms of the aims of therapy. More rarely, true diagnostic problems may present themselves, such as when the pulp chamber is com- pletely divided into two sectors by the presence of a calcification and, depending on where the tests are

initially degenerates without progressing to liquefacti- ve necrosis, but transforms into a homogeneous mass varying from pink to deep red in color (Fig. 7.19). This can easily be extirpated with the help of a bar- bed broach, obviously without the need for any ane- sthesia.

D

E

Fig. 7.19. A. Preoperative radiograph of the upper left central incisor. The tooth had sustained trauma se- veral weeks previously. B. Clinical appearance of the dental crown. Note the change of colour. The tooth does not respond to any of the pulp vitality tests, including the cavity test. C. Without anesthesia, the ac- cess cavity has been made and the pulp has been extirpated. D. Postoperative radiograph. E. The same tooth after bleaching of the crown.

A

B

152 Endodontics 7 - Pulpal Pathology 153

Symptomatology

The tooth with a necrotic pulp is completely asymp- tomatic. The patients may give a history of pulpitis, from which they may believe they just recovered, or a history of trauma. Sometimes, the patients may be suspicious only because of the discoloration of the

crown of the tooth (Fig. 7.20). On occasion, the pa- tient’s history is completely unremarkable, and the- re is no apparent explanation of the pulp necrosis, which is identified on routine check-ups or possi- bly by the development of a mucosal fistula (Fig. 7.21).

Pain associated with pulp necrosis arises from the pe-

C D

Fig. 7.21. A. Preoperative radiograph of the upper left canine with a necrotic pulp and intact crown, free of caries, with no apparent reason to explain the pulp necrosis. The patient was referred because of the presence of a mucosal fistula. B. Postoperative radiograph. Some sealer has been pushed into the fistulous tract. C. Seven months later. D. Two years later.

A B

Fig. 7.20. A, B. The chief complaint was the discoloration of the tooth. The radiograph shows a lesion involving the periapical and mesial areas of the cu- spid and the distal aspect of the lateral incisor. C. Postoperative radiograph. The lateral incisor tests vital.

B C

present (Fig. 7.22).

Pulp tests

The tooth with a necrotic pulp does not respond to the heat or cold test, to the cavity test, or to the electric test. Nonetheless, in some cases, a very slight response may occur at the highest levels of the electric pulp tester. This happens when the current is transmit- ted to the surrounding vital periodontal tissues by the products of liquefactive necrosis in the canal. This is therefore not a false positive response, but rather the minimal sensation that the patient feels only when the instrument achieve its maximal output of electri- cal current.

Therapy

Treatment consists of endodontic therapy, which, in the absence of symptoms, can be planned normally.

to perform proper endotontic therapy and the success rate was higher after pulp capping as compared to pulpectomy and canal treatment.

Today, however, given the abundant research that has been performed, such an attitude is no longer accep- table. The exposed pulp horn must no longer produ- ce the same fear that it did almost one hundred years ago.

Herman 23 _{first introduced the use of calcium hydroxi-} de in such cases, and Teuscher and Zander 64 _{first de-} scribed the formation of the dentin bridge below the treatment. Using labeled radioactive calcium, Pisanti and Sciaky 46 _{demonstrated that calcium hydroxide} does not participate actively in the formation of the dentin bridge, and concluded that the calcium of the dentin bridge came from the bloodstream only. Via 73 _{noted that after 24 months 68.9% of the cases} that he had treated with calcium hydroxide had failed, primarily as a result of internal resorption.

Ostrom and Lyon 44 _{and Quigley} 49 _{also reported high} failure rates, in addition to the observation of zones of pulp degeneration below the dentinal bridges.

Mitchell and Shankwalker 38 _{have described the inten-} se calcification that occurs in the pulp tissue following such treatment. This phenomenon has also been de- scribed by Baume.5 _{The quality and quantity of newly-} formed dentin is unpredictable.48 _{Other authors} 3,45 _ha- ve shown that the radiopaque zone observed beneath the site of exposure cannot always be related to the calcific barrier. Tziafas and Beltes 72 _{have also demon-} strated that many radiopaque zones are in fact zones of necrosis present beneath the capping material. The radiopaque quality of these zones can be attributed to impregnation with calcium salts, which derive at least in part from the capping agents.27,62

From these and other similar research, it is clear that, independent of the size of the exposure, pulp cap- ping, when performed in a desperate attempt to main- tain the vitality of a condemned pulp, is not only an unpredictable procedure with an uncertain prognosis, but it is also dangerous, since it may cause internal re- sorption, calcific pulp degeneration, or both. This may

Fig. 7.22. Upper left first molar with a necrotic pulp. Note the widening of the periodontal ligament space around the radicular apices.

154 Endodontics 7 - Pulpal Pathology 155

make possible the routine endodontic therapy which sooner or later will become necessary.37

Weine 75 _{states that calcium hydroxide is the material} of choice in direct pulp capping, but if such therapy fails and the tooth becomes symptomatic, it may be difficult, if not impossible, to treat it by traditional en- dodontics because of severe calcifications in the root canal, which are frequently associated with internal resorption, as described also by other authors.

Seltzer and Bender 59 _{concur with Weine in stating that} sometimes, notwithstanding the formation of the den- tinal bridge, the remaining pulp is chronically infla- med and can become necrotic. Internal resorption has been found in at least 33% of the teeth treated with pulpotomy and calcium hydroxide. In others, comple- te mineralization with the disappearance of the remai- ning pulp tissue has been reported. Such mineraliza- tion may obstruct the canal at such a point as to com- plicate its instrumentation if endodontic therapy beco- mes necessary in the future.

What makes pulpotomy or pulp capping with calcium hydroxide dangerous is that the pulp tissue is in so- me way stimulated to become isolated from commu- nication with the outside and thus form the dentinal bridge without knowing when to stop making these calcific depositions. The process of apposition, which is known to be associated with resorption, therefore continues.

Schultz et al.57 _{claim that “exposure of the pulp tis-} sue that occurs during the preparation of the cavi- ty requires a decision as to whether it is better to at-

tempt capping of the pulp or to treat the tooth endo-

dontically”.

In a histological assessment of the success of vital pulp therapies, Mullaney 41 _{emphasizes the importance} of examining serial sections, since the dentin bridge is often incomplete and areas of necrosis are frequen- tly present. He also notes the shortcoming of radio- graphic examination when used as the sole method of assessing success, since sufficient information re- garding the completeness of the dentinal bridge can- not be obtained.

Tronstad and Mjor 71 _{also state that, although the for-} mation of the dentinal bridge has been used as one of the criteria of the success of direct pulp capping, it can also occur in teeth with irreversible inflammation. Nevertheless, when the decision is made to undertake such therapy 75

– because of the poor endodontic skill of the dentist – because of the anatomical challenges presented by

the tooth and the dentist’s inability to overcome them

– because the patient is unable to afford the fee the following criteria must be carefully confirmed: a) the tooth must not be sensitive to heat or cold, nor

must there be spontaneous pain

b) there should be no pain on palpation or percus- sion

c) there should be no periapical radiographic change d) marked narrowing of the pulp chamber or root ca-

nal should not be present

e) there should be no calcifications in the pulp cham- ber

f) there should not be the slightest suspicion of bacte- rial infection, since asepsis is the most important factor in pulp healing following exposure.30

The indications for direct capping are therefore drasti- cally reduced to the following:

a) the patients should be young and well motivated, so that they will easily return for check-ups and ne- cessary radiographs

b) the exposure must be in healthy dentin and not be- low caries, and therefore not in infected dentin c) the maintenance of strict intra-operative asepsis is

mandatory

d) the pulp chamber must be free of calcifications, which occupy space and reduce the blood supply to the pulp tissue which must heal.

Finally, Langeland 35 _{is also clearly opposed to indirect} pulp capping, which he calls an unacceptable proce- dure. The reasons for its apparent success, as for di- rect capping or pulpotomy, are due to the removal of most of the disintegrated tissue, but the technique is destined to fail because of the presence of bacte- ria and sometimes a small zone of pulp necrosis that is left in contact with the capping agent. The success of any therapy depends on the total removal of all the disintegrated tissue.

In conclusion, the dentist’s efforts to maintain the vi- tality of a pulp that has been exposed are not only ju- stified but obligatory in teeth with an immature apex especially if the exposure is a result of recent trau- ma. The treatment of choice in such cases is undou- btedly pulpotomy, which is preferable to direct pulp capping. This therapy should be considered a provi-

sional therapy, pending maturation of the apex and

root. The pulp must be kept vital, because it must still complete its primary, formative function. Seltzer and Bender 59 _{state that, once the development of the root} has been completed, the pulp has no reason to remain there. Since it represents only a threat because of the calcifications and internal resorption that may deve- lop, it must be removed, and the tooth must be trea-

Pulp capping with MT A

Recently, Dr. Mahmoud Torabinejad 67 _{of Loma Linda} University, California, has developed a new cement named Mineral Trioxide Aggregate (MTA; ProRoot MTA, Dentsply Tulsa Dental) (Figs. 7.23, 7.24), which appears to have all of the characteristics requested of the ideal cement to seal pathways of communica- tions between the pulp and the oral cavity (mecha- nical and carious pulp exposures), and between the root canal system and the periodontium (iatrogenic perforations, open apices, resorbed apices, root-end preparations).

MTA is an endodontic cement that is extremely bio- compatible, capable of stimulating healing and osteo- genesis, and is hydrophilic. MTA is a powder that con- sists of fine trioxides (Tricalcium oxide, Silicate oxi- de, Bismute oxide) and other hydrophilic particles (Tricalcium silicate, Tricalcium aluminate, responsi- ble for the chemical and physical properties of this aggregate), which set in the presence of moisture. Hydration of the powder results in formation of a col-

blasts, and the formation of dentin bridges when the material was used for direct pulp capping.

Several in vitro and in vivo experiments 4,43,66,68-70 _ha- ve shown that sealing ability and biocompatibility of MTA are superior to those of amalgam, Super-EBA and IRM; dye and bacterial leakage studies have confirmed the sealing ability of MTA; the citotoxicity of MTA was found to be less than that of Super-EBA or IRM. The characteristic that distinguishes MTA from other materials used to date in endodontics is its hydrophi- lic properties. Materials used to repair perforations, to seal the retro-preparation in surgical endodontics, to close open apices, or to protect the pulp in direct pulp capping, are inevitably in contact with blood and other tissue fluids. Moisture may be an important factor due to its potential effects on the physical pro- perties and sealing ability of the restorative materials.66 As shown by Torabinejad et al,66 _{MTA is the only ma-} terial that is not affected by moisture or blood conta- mination: the presence or absence or blood seems not to affect the sealing ability of the mineral trioxide ag- gregate. In fact, MTA sets only in the presence of wa- ter.67

156 Endodontics 7 - Pulpal Pathology 157

MTA has been used also as a pulp capping material in exposed pulps 47 _{(Fig. 7.25) and seems to be today the} material of choice.

Pulp capping is indicated for teeth with immature api- ces when the dental pulp is exposed, and there are no signs of irreversible pulpitis:65 _{in such cases the expo-} sures must be sealed to preserve vitality of the pulp tissue (Fig. 7.26). Recent studies have shown that MTA stimulates dentin bridge formation adjacent to the dental pulp. Dentinogenesis of MTA can be due to its sealing ability, biocompatibility, and alkalinity.47 Faraco and Holland,14 _{demonstrated that in teeth trea-} ted with MTA all bridges were tubular morphologi- cally, and in some specimens the presence of a slight layer of necrotic pulp tissue was observed in the su- perficial portion of these bridges. This suggested that the material, similarly to calcium hydroxide, initially causes necrosis by coagulation in contact with pulp connective tissue. This reaction may occur because of the product’s high alkalinity, whose pH is 10.2 du- ring manipulation and 12.5 after 3 hours.67 _{In a pre-} vious article, Holland et al.26 _{demonstrated the presen-} ce of calcite cristals in contact with MTA implanted in rat subcutaneous tissue. Those calcite cristals attract fibronectin, which is responsible for cellular adhe- sion and differentiation. Therefore we believe that the MTA mechanism of action is similar to that of calcium

hydroxide, but in addition, MTA provides a superior bacteria-tight seal.14

For all these reasons MTA is to be preferred to the use