root resorption due to dental trauma - endoexperience resorption due to dental trauma... · root...

Endodontic Topics 2002, 1, 79–100 Copyright C Blackwell MunksgaardPrinted in Denmark. All rights reserved ENDODONTIC TOPICS 2002

1601-1538

Root Resorption due to DentalTraumaMARTIN TROPE

General principles

Protective mechanisms against resorption

Unlike deciduous teeth, permanent teeth rarely un-dergo root resorption (1). Even in the presence ofperi-radicular inflammation, resorption will occur pri-marily on the bone side of the attachment apparatusand the root will be resistant to it (Fig. 1) (2). Al-though many theories have been put forward, the rea-son for the resistance of the root to resorption is notfully understood. One theory maintains that the rem-nants of the epithelial root sheath surround the rootlike a net, therefore imparting a resistance to resorp-

Fig 1. A, B, C. Teeth with extensive peri-radicular periodontitis due to pulpal infection. Note the resorption of bone;however, the roots remain intact.

79

tion and subsequent ankylosis (3, 4). However, thistheory has failed to gain support, and a second hy-pothesis that has been put forward is more likely (5).

This theory is based on the premise that the ce-mentum and predentin covering on dentin are essen-tial elements in the resistance of the dental root toresorption. It has long been noted that osteoclastswill not adhere to or resorb unmineralized matrix.Major mediators of osteoclast binding are RGD-pep-tides that are bound to calcium salt crystals on min-eralized surfaces. Since the most external aspect ofcementum is covered by a layer of cementoblasts overa zone of non-mineralized cementoid, a surface thatprovides satisfactory conditions for osteoclast binding

Trope

is not present. Internally, the dentin is covered by pre-dentin matrix, which possesses a similar organic sur-face. Unlike the first theory, there are numerousstudies which lend support to this idea (1, 5, 6, 7, 8,9).

Another function of the cemental layer is related toits ability to inhibit the movement of toxins if presentin the root canal space into the surrounding peri-odontal tissues (10). The consequence of an infectedroot canal space is, therefore, most likely to be apicalperiodontitis, as the toxins can only communicatewith the periodontal tissues through the apical foram-ina or large accessory canals. However, if the ce-mental layer is lost or damaged, the inflammatorystimulators can pass from an infected pulp spacethrough the dentinal tubules into the surroundingperiodontal ligament, which, in turn, sets up an in-flammatory response. Since the cementum is lost, thisinflammatory response will result in both bone re-sorption and root resorption.

Requirements for the presence of rootresorption

Due to the previously described inhibitory effects oforganic pre-cementum and predentin, even in thepresence of inflammation, an intact root is resistantto resorption. However, if an injury removes or altersthe (protective) pre-dentin or pre-cementum, inflam-mation of the pulp or periodontium will induce rootresorption with multinucleated clastic cells similar tothose seen in bone resorption (11). (For a review ofosteoclast function see Levin L and Trope M (12))

Thus, in order for root resorption to occur, twothings must happen:

1. The loss or alteration of the protective layer(pre-cementum or pre-dentin)

2. Inflammation must occur to the unprotectedroot surface.

1. Loss or alteration of the protective layer

Damage to the protective layer can occur either di-rectly, due to the trauma of a dental injury, or in-directly, when an inflammatory response occurs as aresult of a dental injury. Most traumatic injuries, how-ever, cause surprisingly little damage to the cementallayer. Even in an avulsion injury, the greatest damagethat occurs is the tearing of the periodontal ligament

80

(Fig. 2), with only slight damage caused to the ce-mental layer. Physical damage to the cemental layerwill only occur at the specific points where the forceof the trauma pushed the tooth directly against thebony socket (13, 14). The only exception to this ruleis an intrusive injury, where the forcing of the conicalroot apically into a similarly shaped socket will causetremendous damage to the protective layer over theentire root surface.

Inflammation in reaction to the traumatic injuryvaries according to the stimulus it is exposed to afterthe injury, and has the potential to cause extensivedamage to the protective layer. For example, the ini-tial damage to the protective cementum after an avul-sion injury, as described above, is limited (13, 14).However, if the periodontal ligament cells remainingon the root are allowed to dry out before re-plantation, they will provide the stimulus for an in-

Fig.2. Histologic appearances the attachment apparatus ofa recently avulsed tooth. The periodontal ligament is tornbut the root surface is intact.

Root resorption due to dental trauma

flammatory response over the entire root surface,which, in turn, results in extensive damage to the pro-tective layer (13, 14).

Little is known about the causes of pre-dentin pro-tective damage. In most cases, the pulp will necrosevery quickly, which removes the blood supply to theresorbing cells and, this, in turn, protects the rootagainst extensive resorption (15). Therefore, as evi-denced by the extremely low incidence of internalroot resorption in permanent teeth, the conditions re-quired to create an inflamed pulp adjacent to a dam-aged root surface are extremely rare (15).

2. The inflammatory response

A. The destructive phase. The inflammatory responsecaused by the dental injury can be divided into twocritical phases. The first is the destructive phase whereactive resorption between the dried-out cells withmultinucleated giant cells takes place (Fig. 3). Thisdestruction will continue as long as there is stimuluspresent to allow the inflammation to develop. In mostcases, the conditions necessary to the creation of the

Fig.3. Histolologic appearance of multinucleated giantcells resorbing the root.

81

stimulus are due to either mechanical damage to theroot surface, or foreign materials or bacteria pickedup the accident site on the root surface; therefore,the stimulus can only exist for a short period of time.Healing will, therefore, take place without inter-vention by the dentist.

However, if the inflammatory stimulus is long-standing, the destructive root resorption will con-tinue until either no root structure remains or thestimulus is removed by the intervention of the den-tist. The destructive phase of root resorption is diag-nosed primarily by the radiolucent appearance of theroot and adjacent bone on X-rays (Fig. 4). Diagnosisis a major challenge as resorptive defects, facial or lin-gual/palatal, are most often missed during examina-tion, although newer radiographic techniques, suchas Tuned Aperture Computed Tomography (TACT)(16), display significant promise in improving ourability to identify these defects in the future. The di-agnosis is also occasionally assisted by the presence ofclinical symptoms which are similar to apical peri-odontitis. Once active root resorption has been diag-nosed, the challenge to the practioner is to determinewhether it will spontaneously heal, i.e. the stimulus isof short duration, or whether intervention is necess-ary due to the presence of a long-standing stimulus.

Since most of the root destruction occurs due tothe inflammatory response rather than direct physicaldamage, it seems logical that, if we could in some waylimit this inflammation, we would also limit the root

Fig.4. A, B. Radiographic appearance of root resorption inthe destructive phase. Note the radiolucencies in the rootand bone. (B. Courtesey Drs. J. O. and F. Andreasen)

Trope

Fig.5. Favorable healing with cementum (cemental healing,surface resorption). A previous resorptive defect is filledwith new cementum (NC) and new periodontal ligament(NPdl).

destruction and expect a more favorable outcome interms of healing (see below).

B. Healing phase The critical factor in determiningthe outcome after a dental traumatic injury has oc-curred is the type of cells that repopulate the rootsurface during the healing phase. If cementoblasts areable to cover the damaged root surface, a type of heal-ing termed cemental healing or surface resorption(17, 18) (Fig. 5) will occur and the outcome will befavorable.

If, on the other hand, bone producing cells are ableto cover the root surface, the conditions for healingwill be unfavorable, as direct contact with bone androot will occur over some areas of the root surface; aphenomenon termed as ankylosis (19). Bone resorbsand forms physiologically throughout life. Thus, theroot is resorbed by the osteoclasts but, in the re-forming stage, bone is laid down instead of dentin.The root is, therefore, slowly replaced with bone.This process is termed as replacement resorption orosseous replacement (17, 18) (Fig. 6).

The type of tissue that will cover the root surface isdependent on the surface area of the root damageand the relative proximity of the cells to the root; i.e.

82

Fig.6. Osseous replacement. A. Histologic slide showingbone directly attached to the root and areas of both boneand root undergoing active resorption. Both areas will laterbe replaced with new bone; in this way, the entire root willeventually be replaced by bone. B. Radiographic appear-ance. The root is being replaced by bone, and the laminadura becomes lost around the root as it becomes incorpor-ated in the bone.

how far and how fast the cells can travel in order tocover the damaged root surface. A localized injuryover a small surface area favors cemental healing.Conversely, a diffuse injury over a large area will favorankylosis with osseous replacement. It has been re-ported that destruction of over 20% of the root sur-face is required for osseous replacement to occur(20). As described above, the surface area of rootdamage is dependent on the scale of the initial injurywhich cannot be reversed. More importantly, it is de-pendent on the extent of the destructive inflamma-tory response. There is the opportunity here for theinitial inflammation to be minimized by actions takenboth immediately after the injury, where the way inwhich the tooth is handled is of crucial importance,and by the pharmacological manipulation of the in-flammatory response.

External root resorptionAs the name implies, the root resorption occurs onthe outer surface of the root. Luxation injuries arethe most likely injury where root resorption may re-sult, and, as previously stated in this article, the long-


term outcome is dependent on whether the healingresponse is favorable or unfavorable. Figure 7 showsthe order of likelihood of favorable to unfavorablehealing following the different categories of luxationinjuries occurring.

Resorption due to stimulus lasting a shortduration (transient stimulus)

Short-acting stimulus is usually due to the mechanicaldamage of the traumatic injury alone without thepresence of an additional stimulus. Very little can bedone to reverse this initial attachment damage, there-fore the main focus of treatment is to do everythingpossible to limit the destructive inflammatory processthat occurs immediately after the injury. If the inflam-mation is minimized, the surface area of damagedroot surface will also be kept to a minimum. It is,therefore, hypothesized that a smaller damaged rootsurface will result in a more favorable healing out-come.

Treatment strategies are therefore directed at avoid-ing or minimizing the severity of the initial inflamma-tory response. These can be listed more specificallyas:1. Prevention of the initial injury.2. Minimizing additional damage after the initial in-

jury.3. Pharmacological manipulation (shut down) of the

initial inflammatory response.4. Possibly stimulating cemental, rather than bone,

healing.

Fig.7. Order of likelihood, from favorable to unfavorablehealing outcomes, following the different categories of lux-ation injuries.

83

5. Slowing down the osseous replacement when it isinevitable.

1. Prevention

Nothing can be done about the initial damage causedby the primary traumatic injury. However, there isevidence that preventative measures successfully limitthese injuries. In athletics, for instance, the mouth-guard is a proven protective device against traumaticdamage to the teeth (21). Education at all levelsshould be aim to increase the usage of mouth-guardsand other protective devices.

2. Minimizing Additional Damage after theInjury.

Steps must be taken to minimize additional avoidabledamage to the periodontal ligament. As with thetechniques for prevention outlined above, decisiveand correct action taken at the site of injury is prob-ably the most critical step in minimizing additionalattachment damage after an injury. Reports indicatethat the personnel typically present at the site of atraumatic dental injury are generally poorly educatedin the appropriate handling of these injuries (22). It,therefore, remains a huge challenge to the dentalcommunity to educate these people in the correctemergency treatment of a traumatic injury.

Initially, the tooth should be gently repositionedback into its original position as soon as possible. Thepatient should then be sent to the emergency roomor dentist immediately. If splinting is necessary itshould be performed with a functional splint for 7–10 days (11, 17, 23) (Fig. 8). Most importantly, thesplint should be constructed to allow adequatecleaning, thereby minimizing the wicking of bacteriafrom dental plaque into the blood clot between thetooth and the socket wall.

In the case of an avulsed tooth, replanting the toothas soon as possible is the preferable treatment. If thetooth cannot be replanted for any reason, the extra-oral dry time must be minimized by placing the toothin an appropriate storage medium. Milk, for instance,is a practical storage medium (24) as it is found nearmost accident sites, is relatively free of bacteria andhas an osmolarity that is not excessively harmful tothe periodontal ligament cells. Other practical alter-natives include sterile saline or saliva (vestibule of the

Trope

mouth). Water, on the other hand, is an unsuitablemedium for the storage of avulsed teeth.

However, newer specialized media such as Hank’sBalanced Salt Solution, which is a common culturemedium, or ViaSpan, a liver transplant medium, maybe able to sustain the viability of periodontal ligamentcells for considerably longer periods than milk can(24). The use of these specialized storage media hasbeen deemed impractical as they are seldom foundnear the accident site. However, if we consider thatmore than 60% of accidents occur close to the homeor school, it should be possible to educate the publicto have these media available at these sites. Media,such as ViaSpan, could also be placed in ambulanceswhere they could be used for severe injuries in life-threatening situations that do not allow immediatereplantation (22).

3. Pharmacological manipulation of theinflammatory response

An additional approach might be to pharmacologi-cally manipulate the inflammatory response in orderto minimize destruction and facilitate repair of thedamaged root surface by new cementum and peri-odontal ligament. Tetracycline has been widely usedin the treatment of periodontal disease because of itssustained antimicrobial effects. Recently, tetracyclinehas been shown to possess anti-resorptive, as wellanti-microbial, properties; specifically, it has a directinhibitory effect on osteoclasts and collagenase (25,26). Thus, if these drugs were found to be as effectiveas penicillin drugs in limiting bacterial contaminationafter a traumatic injury and, in addition to this, theypossessed an anti-resorptive, they might replace peni-cillin as the systemic antibiotic of choice after this typeof injury has occurred.

Our group has tested the effectiveness of systemictetracycline in an ‘infection’ model in dogs and foundthe results to be similar to penicillin (26). In addition,when used in an osseous remodeling model, tetracy-cline was found to result in significantly more ce-mental healing than penicillin, which did not helphealing at all (25). Provided the patient is not suscep-tible to tetracycline staining, we therefore recom-mend replacing systemic penicillin with tetracyclineafter a traumatic injury.

While tetracycline affects osteoclasts that are pres-ent at the site of resorption, drugs are also available

84

that affect the recruitment of osteoclasts to the injurysite, meaning that the combination of the two typesof drugs might have a synergistic effect on the inhi-bition of root resorption. Glucocorticoids have beenwidely used to reduce the deleterious effects of in-flammatory responses; more specifically, they havebeen shown to reduce osteoclastic bone resorption byaffecting cell recruitment using a plethora of mechan-isms. Therefore, they could potentially also be usefulin manipulating the initial inflammatory responseafter attachment damage, thereby encouraging repairby cementoblasts rather than bone-derived cells.

We tested the effect of local and systemic dexa-methasone in a dog model that has been shown toproduce a peak of inflammatory root resorption. Top-ical dexamethasone was found to be useful while sys-temic usage was not. Our group has recently testedLedermixA, a drug combining tetracycline and corti-costeroids (27), placed in the root canals of dogs im-

Fig.8. Examples of functional splits. A. TTS splint. Thissplint allows space for adequate cleaning, thereby minimiz-ing infection due to plaque and food debris. It is flexible ina horizontal and vertical direction. B. Resin splint that,whilst allowing functional movement, is too thick, thusmaking it impossible for patients to keep it clean.


mediately after tooth replantation. Thus, a tetracy-cline/corticosteroid combination is deposited in acontrolled released fashion to the periodontal liga-ment through the dentinal tubules. The results wereextremely promising compared to standard controls(Fig. 9). We therefore feel confident that in severetraumatic injuries, where a large surface area of peri-odontal inflammation is expected, removing the pulpand placing LedermixA into the canal at the emer-gency visit will become standard practice.

4. Stimulate Cemental Healing

If it were possible to stimulate periodontal cellgrowth, we may be able to limit the number of oss-eous cells able to attach to the denuded root surface,thus decreasing osseous replacement and slowingdown the loss of the tooth. Fibroblast-like cells in cul-ture secrete factors that have been shown to be sig-nificantly active in tissue repair processes. We hypo-thesized that the supernatant of cultured gingivalfibroblasts, if used as a storage medium, might con-tain a number of biologically-active factors that mightpromote periodontal ligament regeneration and re-pair. We tested this ‘conditioned medium’ as a storagemedium in dogs’ teeth for extended periods. The re-sults were extremely promising, as the ‘conditionedmedium’ appeared superior to Hanks’ Balanced SaltSolution and Viaspan after 96 h storage (28). How-ever, when tested as a periodontal ligament-stimulat-ing medium on roots with various extended drytimes, the results for this medium were disappointingas ViaSpan was the only medium which had a benefi-cial result (29). Therefore, work needs to continueto promote periodontal stimulation after a traumaticinjury.

In the meantime, recent studies have found thatEmdogainA (enamel matrix protein; Biora, Malmo,Sweden) may be extremely beneficial in teeth with

Favorable healing (%) Unfavorable healing (%)

Ledermix 69 41Control 14 86

P∞0.001 Ledermix vs. control

Fig.9. Favorable vs. unfavorable healing when LedermixAwas used immediately after the replantation of dried dogteeth. In controls when LedermixA was not used, favorablehealing occurred at a much lower rate.

85

extended extra oral dry times, as it not only makesthe root more resistant to resorption but also stimu-lates the formation of new periodontal ligament fromthe socket (30, 31) (Fig. 10). Up until this point,most studies with EmdogainA have tested the medic-ament in the most extreme cases where no peri-odontal ligament is expected to be present on theroot at the time of repositioning. Recent reports indi-cate, however, that it may be particularly beneficial inthose less extreme cases where small areas of osseousreplacement are expected or are present (30).

Fig.10. EmdogainA placed A. on the root surface and B.in the socket before the tooth is replanted.

Trope

5. Slow down ‘inevitable’ osseous replacement

When the periodontal ligament on the root surface isdefinitely destroyed and osseous replacement is inevi-table, the focus of the treatment is to slow down thereplacement of the root with bone. Injuries wheresuch a situation might occur are intrusive injuries oravulsion injuries with extended extra-oral dry times.Presently, in intrusive injuries, the tooth is reposi-tioned and the inevitable osseous replacement ac-cepted, a philosophy which should be re-examined inlight of improved treatment methods described insection 4 and below. For avulsion injuries with ex-tended dry times, the methods described below arepresently appropriate and accepted:1. All remaining periodontal ligament debris is re-

moved from the root by thorough curettage orwith the use of acid.

2. Fluoride has been shown to effectively slow downremodeling of the root to bone and the root issoaked in fluoride for 5 min before replantation(32, 33).

3. Bisphosphonates are drugs that have been foundto slow down osteoporosis in post-menopausal fe-males. We tested the topical use of bisphosphon-ates in extracted dog’s teeth which had been driedfor an extended period (34). The use of the bi-sphosphonate slowed down the osseous replace-ment but, at this stage, we do not know if its effectis superior to the proven effect of topical fluoride,a much cheaper drug.

4. It appears from preliminary studies that bothfluoride and bisphosphonate will be replaced byEmdogainA as the drug of choice for this appli-cation (30, 31).

Resorption due to a long-lasting(progressive) stimulus

As described previously, destructive inflammation androot resorption will continue as long as a stimulus forthe inflammation is present. Pressure, pulpal infectionand sulcular infection are common, long-lasting stim-uli for progressive root resorption. The presence of along-lasting stimulus does not imply that a short-acting stimulus was not initially present due to the ini-tial injury. While it is comfortable to separate out thesestimuli for the sake of explanation, it must be remem-

86

Fig.11. Pressure resorption due to orthodontic treatment.A. Teeth at the start of orthodontic treatment. B. Severeroot resorption on the left central incisor after orthodontictreatment. Note that, even though considerable resorptionhas taken place, favorable healing at the apex with ce-mentum can be seen. (Courtesy Dr IB Bender)

bered that they, and the consequences that result fromthem, are often superimposed on each other.

PressurePressure damage can be caused by many differentsources, but the most common causes tend to be eitherorthodontic tooth movement or impacted teeth or tu-mors. Different theories of the mechanism of ortho-dontic tooth resorption have been put forward butpresently it is considered to be a ‘sterile’ inflammation,with all the expected inflammatory cytokines presentduring active resorption. In most cases, orthodontictooth movement can be considered a ‘controlled’trauma where pressure is spread evenly over a root area,therefore minimizing the inflammatory response,which, in turn, favors resorption of the bone ratherthan the root. However, in rare cases where the press-ure is localized to the apical region, it can be intenseenough to cause cemental damage and apical root re-sorption. The resorption can result in considerableshortening of the root that, in some cases, will compro-mise the crown:root ratio of the tooth (Fig. 11).

Root resorption due to orthodontic pressure has al-ways been considered to be external root resorption.However, this is not necessarily true. Damage takesplace at the apex of the tooth near the cemental-den-tinal junction due to the orthodontic pressure. There-fore, protective damage can be either cementum orpredentin. Because the predentin can also be affected,


it is not unusual to see radiographic evidence of inter-nal apical resorption during the active stage of theprocess. In 1997, Bender et al. suggested the termperiapical replacement resorption (PARR) for describ-ing this type of resorption (35).

For impacted teeth or tumors, the resorption willoccur wherever the pressure from the impaction/tu-mor occurs. Treatment is relatively easy, in that re-moval of the source of the pressure will result in thecessation of resorption in the majority of cases. Repairand re-countouring of the root will occur after thepressure has been removed and this can result in someadditional root loss for a limited time after the press-ure has been removed. Interestingly, even though aconsiderable amount of root structure may be lostdue to orthodontic pressure, favorable healing withcementum is always expected. The reason for this isexplained by the fact that the resorption takes placeover a cross-section of the root in an apical to coronaldirection. Thus, even when a large amount of rootstructure has been lost from the root surface to berepaired, the area to be repaired stays relatively small,and cells with the potential to produce cementum cansurround the area on the remaining healthy root.Therefore cemental healing is favored (Fig. 11).

Pulp space infection

Apical periodontitis with apical rootresorption

The pulp of the tooth can become necrotic for manyreasons but the predominant cause is a bacterial chal-lenge through caries. When the pulp defenses areovercome and the pulp is necrotic and infected, theinflammatory stimulators will contact the surround-ing periodontal attachment through openings fromthe pulp to the periodontium. In most routine cases,the root surface is protected by the intact cementumon the root surface and the communications will beconducted primarily through the apical foramina or,occasionally, through accessory canals.

Invariably, the periodontal inflammation is ac-companied by slight resorption of the root at the ce-mento-dentinal junction. This resorption is usuallynot apparent radiographically but is routinely ob-served in a histologic evaluation. For a review of treat-ment strategies, please see the article in this issue byTrope M. and Bergenholtz G.: The microbiological

87

basis for endodontic treatment: can a maximal out-come be achieved in one visit?

Lateral periodontitis with root resorption

When the root loses its cemental protection, lateralperiodontitis with root resorption can result (Figs 3,4). In order for a pulp space infection to develop,the pulp must first become necrotic. This processwill occur after all except the most minor luxationinjuries because displacement of the tooth results insevering of the apical blood vessels. In matureteeth, pulp regeneration cannot occur and, usuallyby three weeks, the necrotic pulp will become in-fected (15, 36, 37). Because a serious injury is re-quired for pulp necrosis, it is usual that areas of ce-mental covering of the root are also affected, result-ing in its protective, insulating quality being lost.This means that bacterial toxins can now passthrough the dentinal tubules and stimulate an in-flammatory response in the corresponding peri-odontal ligament (38).

The result of this is the resorption of the root andbone. The periodontal infiltrate consists of granu-lation tissue with lymphocytes, plasma cells, and poly-morphonuclear leukocytes. Multinucleated giant cellsresorb the denuded root surface and this continuesuntil the stimulus (pulp-space bacteria) is removed(36) (Fig. 3). Radiographically, the resorption is ob-served as progressively radiolucent areas of the rootand adjacent bone (Fig. 4).

Treatment

The attachment damage due to the traumatic injuryand minimizing the subsequent inflammation wasthe focus of the emergency visit. The practitioner’sshould ideally pay attention to pulp space infection7–10 days after the injury (36, 37). Root canal dis-infection removes the stimulus for the peri-radicularinflammation and the resorption will stop (36, 37).In most cases, favorable healing with cementum willoccur but, if a large area of root is affected, osseousreplacement may result by the mechanism describedearlier. In cases where the peri-radicular inflam-mation is stimulated by pulpal infection, bone re-sorption is usually extensive. This may be con-sidered to be a protective reaction since this exten-sive bone resorption will slow down the ability of

Trope

bone producing cells from attaching directly to thedamaged root surface, allowing for healing with ce-mentum.

Treatment principles include the prevention orelimination of the stimulus for the peri-radicular in-flammation, i.e. prevention or elimination of the pulpspace bacteria.

1. Prevention of pulp space infection

A. Maintain the vitality of the pulp. If the pulp is vital,the canal will be free of bacteria and, thus, this typeof external inflammatory root resorption will not oc-cur. In severe injuries where vitality has been lost it ispossible, under some circumstances, to promote re-vascularization of the pulp space (39) (Fig. 12). Thevital tissue that is present in the pulp space has beenreported to be either new pulp or even periodontalligament that has grown into the space. Revascul-arization is possible in young teeth with incompletelyformed apices (. 1.1 mm wide radiographically) ifthey are replaced close to their original position soonafter the injury (39, 40, 41). In the case of an avulsedtooth, revascularization is considered possible if re-plantation occurs before 60 min of dry time haselapsed. For avulsed teeth, soaking it in doxycyclinefor 5 min before replantation has been shown todouble the revascularization rate (40, 41). It is hypo-thesized that this is because doxycycline will kill bac-teria on the root surface and, importantly, at the pulplumen, thus allowing for the new tissue to grow into

Figure 12. Revascularization of an immature tooth. A. Thestage of root development soon after repositioning. B. Oneyear later, it can be seen that the root has continued to de-velop and thicken.

88

the pulp space without challenge from bacteria. How-ever, even under the best conditions revascularizationwill occur only about 50% of the time.

Revascularization after a traumatic dental injury is arace between the new tissue replacing the ischemicallynecrotic pulp and the bacteria moving into the unpro-tected pulp space. The new tissue will take about onemonth to revascularize a young pulp and, if bacteriado not populate the area before that time, revascul-arization will take place. Theoretically, if in an in-fected case with peri-radicular inflammation, the pulpcould be effectively disinfected and reinfection pre-vented by an adequate coronal seal, it should be poss-ible to revascularize a pulp space after it has becomeinfected. This theory is confirmed by isolated casesthat have started to appear within the last few years(42).

B. Prevent root canal infection by root canal treatmentat 7–10 days. In teeth with closed apices, revascul-arization cannot occur. These teeth should be endo-dontically treated within 7–10 days of the injury be-fore the ischemically necrosed pulp becomes infected(36, 37). From a theoretical point of view, the teethtreated during this time period can be considered asif this were equivalent to the treatment of a toothwith a vital pulp and, therefore, the endodontic treat-ment could be completed in one visit. However, ef-ficient treatment is extremely difficult soon after aserious traumatic injury and, in the author’s opinion,it is beneficial to start the endodontic treatment withchemomechanical preparation, after which an intra-canal dressing with a creamy mix of calcium hydrox-ide is placed (43, 44). The practitioner can now obtu-rate the canal at his/her convenience after the peri-odontal healing of the injury is complete approxi-mately one month after the intrumentation visit (43,44). There appears to be no necessity for long-termcalcium hydroxide treatment in cases where the endo-dontic treatment is started within 10 days of the in-jury. Notwithstanding, in a compliant patient, the cal-cium hydroxide can be applied long-term (up to 6months) to ensure periodontal health prior to fillingthe root canal with gutta-percha (37).

C. The elimination of pulp space infection. When rootcanal treatment is initiated later than 10 days after theaccident or if active external inflammatory resorptionis observed, the preferred antibacterial protocol con-


Fig.13. Canal filled with thick mix of calcium hydroxide.A. Wide radiolucent canal. B. Canal appears to be calcifiedwhen filled with calcium hydroxide.

sists of a chemomechanical preparation, followed bylong-term dressing with densely packed calcium hy-droxide (37). Calcium hydroxide can affect an alka-line pH in the surrounding dentinal tubules, kill bac-teria and neutralize endotoxin, a potent inflammatorystimulator.

The first visit consists of thorough chemo-mechan-ical instrumentation of the canal and the placementof a creamy mix of calcium hydroxide with a lentulo-spiral as an intracanal antibacterial agent. The patientis seen at approximately one month, at which timethe canal is filled with a dense mix of calcium hydrox-ide. Once filled, the canal should appear radiographi-cally to be calcified, since the radiodensity of calciumhydroxide in the canal is usually similar to the sur-rounding dentin (Fig. 13). A radiograph is then takenat three month intervals. At each visit, the tooth istested for symptoms of periodontitis. In addition,healing of the resorptive process and the presence orabsence of the calcium hydroxide i.e calcium hydrox-ide washout is also assessed.

Since the root surface is so radiodense as to makethe assessment of healing difficult, the adjacentbone healing is assessed. If the adjacent bone hashealed, it is assumed that the resorptive process hasstopped in the root as well and the canal can be ob-turated with gutta-percha (Fig. 14). If it is felt thatadditional healing would be beneficial before obtu-

89

Fig.14.. A. Destructive resorption is seen soon after thetraumatic injury. B. After long-term Ca(OH)2 treatment, theresorptive defects have healed, and an intact lamina dura canbe traced around the root. The tooth is ready for obturation.

ration, the need for replacing the calcium hydroxidein the canal is assessed. If the canal still radiographi-cally appears calcified, there is no need to replacethe calcium hydroxide. If, on the other hand, thecanal has regained its lucent appearance, the cal-cium hydroxide should be re-packed and reassessedin another three months.

Sulcular infectionThis progressive external root resorption, which is ofinflammatory origin, occurs immediately below theepithelial attachment of the tooth, usually but not ex-clusively in the cervical area of the tooth. This type ofresorption is most often referred to as cervical root re-sorption (17). However, the periodontal attachment ofteeth is not always at the cervical margin, leading to thesame process occurring more apically on the root sur-face. The anatomic connotation of its name has led toconfusion and misdiagnosis of this condition. Becauseof this confusion, attempts have been made to renamethis type of external resorption (18, 45, 46), and it isreferred to as subepithelial external root resorptionthroughout this paper. Its exact pathogenesis is notfully understood (15) but, since its histological appear-ance and progressive nature is identical to other formsof progressive inflammatory root resorption, it appearslogical that the pathogenesis would be the same (i.e. anunprotected or altered root surface attracting re-sorbing cells and an inflammatory response maintainedby infection). Causes of the root damage immediatelybelow the epithelial attachment of the root include or-

Trope

thodontic tooth movement, trauma, non-vital bleach-ing and other less definable cause (47). The pulp playsno role in cervical root resorption and is mostly normalin these cases (15).

Because the source of stimulation (infection) is notthe pulp, it has been postulated that it is the bacteriain the sulcus of the tooth that stimulate and sustain aninflammatory response in the periodontium at theattachment level of the root (15). This theory isstrengthened by the fact that bone resorption similar tomarginal periodontitis will always accompany this typeof root resorption and it is universally accepted thatmarginal periodontitis has a bacterial cause (Fig. 15).

Classification

Progression of the resorptive defect once the dentinhas been penetrated is variable and unpredictable, andHeithersay has classified this type of resorption intofour classes in order of severity (48) (Fig. 16). Resorp-tive defects in the root coronal or just below the attach-

Fig.15. Radiographic appearance of sub-epithelial externalroot resorption. Note the small opening and the ballooningof the defect inside the root. The pulp is not penetrated.Bone resorption similar to an angular bony defect is seen.

90

ment level are relatively easy to treat but, on the otherhand, if the defect extends below the bone level, it isvery complicated and sometimes impossible to treat.

Histological Appearance

Histologically, the defect appears similar to any exter-nal inflammatory root resorptive defect. There isusually a small opening into the root, with largeamounts of granulomatous tissue inside the defectand multinucleated giant cells resorbing the dentinalstructure. In extensive defects, osseous tissue may beseen inside the granulomatous tissue, indicatingquiescent periods in the process where healing withreformation of an attachment may have beenattempted. Even in the most extensive defects, thepredentin/odontoblastic layer is unaffected, demon-strating the resistant nature of this tissue (Fig. 17).

Clinical Appearance

Resorption of this type is asymptomatic and usuallyonly detected through routine radiographs. Oc-casionally, if the resorption is extensive, symptoms ofpulpitis will develop. When the resorption is long-standing, the granulation tissue can be seen under-mining the enamel of the crown of the tooth, result-ing in a pinkish appearance. This ‘pink spot’ has tra-ditionally been used to describe the pathognomonicclinical picture of internal root resorption, resultingin many cervical root resorption cases being misdiag-nosed and treated as internal root resorption (Fig.18). Probing may result in profuse bleeding, indi-cating the presence of inflamed tissue rather than nor-mal attachment.

Radiographic Appearance

The radiographic appearance of subepithelial inflam-matory root resorption can be vary quite consider-

Fig.16. Heithersay’s classification of invasive cervical rootresorption.


ably. If the resorptive process occurs mesially or dist-ally on the root surface, it is common to see a smallradiolucent opening into the root. The radiolucencyexpands coronally and apically in the dentin, andreaches, but usually does not perforate, the root canal(Fig. 18). If the resorptive process is buccal or palatal-lingual, the radiographic picture depends on the ex-tent to which the resorptive process has spread in thedentin. It can be seen as a radiolucency at the attach-ment level or have spread a considerable way co-ronally or apically with a mottled appearance. Becausethe pulp is not involved, its outline can usually bedistinguished through the resorptive defect (Fig. 15).

Treatment

Treatment of this type of resorption poses manyproblems. In principle, it would be preferable to re-

Fig.17. Histologic appearance of extensive resorption.Areas of bone are seen with the resorptive defect, indicatingquiescent periods with an attempt to form an attachmentapparatus. Note that, even with extensive resorption, theodontoblast predentin layer remains intact. (Courtesy Dr.R. Watson)

91

move the cause of the inflammation, i.e. the sulcularbacteria. However, unlike pulpal infection that is pres-ent in a closed environment, the sulcus is difficult todisinfect over a long period of time. Therefore, inthese cases, with the hope that the damaged and sus-ceptible root surface will be altered to be resistant tofurther resorption after treatment, the resorptive de-fect is the focus of treatment strategies.

Aims of Treatment

The aim of treatment is two-fold:O Stop continuation of resorption. This may beachieved by removing all the granulomatous tissuefrom the root. In cases where removal of granulo-matous tissue would cause unacceptable damage tosupporting structures, an attempt is made to severethe blood supply to the granulomatous tissue, thuskilling the resorptive cells and inhibiting progressionof the resorptive process.O Replace the unprotected root surface with a foreignmaterial that clastic cells cannot be attached to or pen-etrate. Any well-sealing dental filling material can beused for this purpose. However, the problem existsthat, while placing a filling material in the root inhibitsattachment by clastic cells, it also does not allow attach-ment by those cells that provide for a normal peri-odontal ligament. Since most of these lesions are im-mediately below the attachment level, it is often notpossible to leave attachable root structure above thedefect while repairing it. The result is that root attach-ment will only occur apical to the filling material, leav-ing a periodontal pocket that is unacceptable.As mentioned previously, in subattachment root re-sorption the pulp is mostly healthy and, therefore,root canal therapy is not required. However, in clin-ical terms, the resorptive defect usually impinges onthe predentin (Fig. 16), making exposure of the pulpquite likely during removal of the granulomatoustissue. If the resorption is extensive the practitionermay choose to perform elective endodontic therapybefore treatment proceeds.

Treatment aims can be met from an internal or ex-ternal approach or by a combination of these two ap-proaches, and possible treatment approaches that ad-dress the different clinical situations associated withthis type of resorption are described below.

Trope

Localized defect entirely within the coronalthird of the tooth or close to the cervicalmargin. Heithersay Class 1 or 2 (48).

External Approach Angled radiographs are taken todetermine the exact location of the defect (buccal orlingual-palatal). Once the position has been deter-mined, a full thickness flap is raised and the granulo-matous tissue is removed from the root and the bonedefect (Fig. 19). It is also important to remove thegranulomatous tissue from sound, healthy bone sothat revascularization of the resorbing tissues will notoccur. The granulomatous tissue can be removedwith a curette or bur. The opening into the rootshould be as conservative as possible. The root defectis filled with a restorative material and the flap re-

Fig.18. A. ‘‘Pink spot’’ of external root resorption. The granulomatous tissue has spread coronally and undermined theenamel, resulting in the pink colour seen in the crown. B. Radiographic appearance of tooth showing external root resorptionwith a root-treated tooth. The tooth had been root-treated 3 years previously before signs of resorption were present.Therefore, the lesion cannot be internal root resorption.

92

placed in a way as to minimize the periodontal defectafter healing. For the small coronal defect, this ap-proach is preferable as, by raising the flap and curet-tage of the adjacent tissue, the blood supply to theresorbing cells is definitely severed. In addition, sincethe defect is small, a filling material can be placed inthe susceptible root without creating a periodontaldefect in the future.

Internal Approach It is also possible to remove thegranulomatous tissue and replace the space with a fill-ing material from an internal approach. Heathersayhas shown excellent results using trichloracetic acidinternally (49). The acid will chemically burn thegranulomatous tissue, thus necrosing it and providingspace for the filling material internally. This chemicalburning can also be achieved with the use of calcium


hydroxide but may take multiple applications toachieve the same results as trichloracetic acid. Theor-etically, a bur could be used but the chances of pulpexposure and/or extensive attachment damage arevery high with this approach.

Fig.19. Sub-epithelial root resorption treated by an exter-nal approach. A. The flap is raised, meaning the blood sup-ply to the granulomatous tissue in the root has been cut. B.The tissue is removed from the root and bone and C. theroot is filled with a composite resin filling.

93

Localized, medium-sized defect located in thecoronal and mid-root dentin with a smallsubepithelial opening on the root (Class 3) (47).

Treatment of these defects pose a very difficult chal-lenge. The practitioner should seriously considerwhether treatment would offer the patient a betterprognosis than leaving the tooth alone until symp-toms appear or the attachment of adjacent teeth isaffected. Extraction followed by an implant or fixedbridge should be seriously considered. Following aresome treatment ideas:

External Approach When the resorptive defect ex-tends apically, we have traditionally removed the en-tire root cementum surface adjacent to the granulo-matous tissue in the dentin. Thus, root surface withthe potential for periodontal ligament re-attachmenthas been removed. An alternative approach is to re-move the resorptive tissue from a small opening atthe most apical extent of the affected root, leavingcoronal root surface onto which a new attachmentmight develop (Fig. 20). After the tissue is removedand the opening repaired with an acceptable restora-tive material, the defect and denuded root surface iscovered with a spacer (freeze-dried bone), and theentire area covered with a Gore-Tex membrane (GoreTex, W. L. Gore, Flagstatt, AZ). Other approachesinclude:O Forced eruption. If the remaining root apical to theresorption defect is long enough to maintain thetooth forcefully erupting, the tooth is a very effectivetreatment method. The resorption defect is moved toa position coronal to the adjacent attachment. Theentrance of the defect into the root can now easily befound and the defect cleaned and restored. Reshapingof the ‘raised’ bony contour now allows an idealarchitecture to remain.O Forced eruption/re-intrusion. If the procedure de-scribed above is complete, but it is felt that the crownroot ratio is not ideal, after the repair is complete thetooth can be orthodontically moved into its originalposition (41). While biological width will always de-velop apical to the filling material, attachment wouldstill be superior to that attained with forced eruptiononly.O Intentional replantation. Intentional replantationshould achieve the same result as forced eruption,with or without re-intrusion, and can be considered

Trope

Fig.20. A. Radiograph showing the external resorptive defect extending past the mid-root level. B. The flap has been raised,with care taken to leave as much of the root structure intact as possible. C. Granulomatous tissue is removed from the bone.D. A barrier is used to stop new tissue from growing into the root or revascularizing the necrotic tissue left inside the root.E. After approximately one month, an external opening is made above the attachment, and the necrotic granulomatoustissue is removed and F. as viewed radiographically, replaced with a filling material.

if the practitioner is confident that the resorbed rootwill not fracture on extraction.

External Approach/Internal Approach The need forroot canal therapy is assessed and depends on the ex-tent of the lesion. In these extensive lesions, electiveendodontic therapy is often the best choice as a pulpexposure at any time during the procedure compli-cates an already difficult treatment. A flap is raisedand the granulomatous tissue is aggressively removedfrom the bony defect only (Fig. 20). Care is taken toleave as much root-structure intact as possible. Sincethe source of the blood supply to the root defect isthe periodontal structures that have been severed dur-ing surgery, necrosis of the resorbing tissues in theroot results. To stop new tissue from growing intothe root or revascularizing the necrotic tissue left in-

94

side the root, a barrier membrane is used. After ap-proximately one month, an opening is made exter-nally above the attachment and the necrotic granulo-matous tissue is removed and replaced with a fillingmaterial (Fig. 20). If esthetics is not a major consider-ation, mineral trioxide aggregate (MTA) should be auseful filling material for this purpose.

With this approach, an attempt is made to preservethe ‘attachable’ root surface by not penetrating theroot with a bur during the initial surgical procedure.Since the defects are often in locations that are difficultto access, excessive amount of root is sacrificed, thusjeopardizing attachment after surgery. The success ofthis approach is dependent on the size of the openingof the defect into the root after the flap is raised. If theflap is raised with care, so that it does not put pressureon the root surface and break through the undermined


root surface, in most cases the opening into the root isvery small and the procedure can proceed as describedabove. If, on the other hand, the opening into the rootis large, the treatment plan should be re-assessed withextraction an option if a large periodontal defect is tobe expected after surgery.

Internal Approach In the author’s opinion, this ap-proach is not predictable enough in these extensivecases and should, therefore, not be considered.

Large defect extending apically. HeithersayClass 4.

In the author’s opinion, these cases offer such a poorprognosis that extraction and replacement with animplant or fixed bridge is the preferred approach.

Prevention Since we know some of the indirect causesof this type of root resorption, it is possible to pro-pose measures that may prevent it:O Nonvital bleaching. Research suggests that 30% hy-drogen peroxide activated with heat damages the ce-mentum layer through the dentinal tubules (50, 51).To minimize these factors the following protectivesteps are suggested.1. Protection of the dentinal tubules. Remove thegutta-percha apical to the cervical line to remove dis-colored dentin, but do not extend the preparationinto the root. Use the crestal bone as a guide. Placea layer of cement (IRM, Cavit, glass ionomer) to pre-vent ingress of the bleaching agent apically and intothe cervical dentinal tubules.2. Do not use heat. Walking bleaches have been ef-fective for over a quarter of a century. Repeated treat-ments produce results equal to a one-sitting thermo-catalytic procedure (51).3. Avoid etching the dentin. Some techniques sug-gest etching of the dentin before bleaching; however,a recent study showed similar bleaching results withand without etching (52).4. Do not use Superoxol as it is caustic. Some advocatesodium perborate (USP) and water for the walkingbleach and report excellent results with no history ofexternal resorption (51). Others showed in vitro the ef-fectiveness of sodium perborate and water as a bleach-ing agent, though it took longer to work (51, 52).

95

Orthodontic therapy All orthodontic forces, in par-ticular tipping forces, should be as light as possible inorder that they do not crush the attachment appar-atus while the tooth is being uprighted.

Surgical procedures Surgical procedures, including ex-cessive use of surgical elevators, theoretically damagethe attachment apparatus and should be avoided. Sur-gical procedures that could damage the cervical mar-gin, for example the canine wire lasso, before the or-thodontic movement of an impacted canine shouldnot be used; rather, surgical exposure and bandingwith acid etch and resin should be used to facilitatecoronal movement.

Periodontal procedures Procedures that leave the rootsurface denuded (i.e. without periodontal ligament orepithelium) should be avoided.

Future Strategies

A. Long-term disinfection of the sulcus. Advances inperiodontal therapeutic techniques include treat-ments that have the potential to disinfect the sulcusover a long period of time (53). If successful, the re-moval of the inflammatory stimulus would be a pref-erable way to treat these defects.

B. Manipulation of the inflammatory response. Localinjections of high doses of corticosteroids have beeneffective in treating giant cell bone lesions in a con-servative manner (15). Since the multinucleated re-sorbing cells are similar to the cells in root resorption,the use of similar steroid doses might stop the pro-gression of root resorption. The root canal could beused as a reservoir for the corticosteroids. Outcomesfrom this type of approach are being presently beingassessed.

Internal root resorptionInternal root resorption is rare in permanent teeth,and is characteristized by an oval-shaped enlargementof the root canal space (15) (Fig. 21). External re-sorption, which is much more common, is often mis-diagnosed as internal resorption.

Trope

Etiology

Internal root resorption is characterized by the resorp-tion of the internal aspect of the root by multinucleatedgiant 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 aredifferent theories on the origin of the pulpal granu-lation tissue involved in internal resorption. The mostlogical explanation is that pulp tissue becomes inflameddue to an infected coronal pulp space. Communicationbetween the coronal necrotic tissue and the vital pulp is

Fig.21. Radiographic appearance of internal root resorp-tion. A uniform oval radiolucency is seen in the root.

96

through appropriately oriented dentinal tubules (15).One investigator reports (9) that resorption of the den-tin is frequently associated with deposition of hardtissue resembling bone or cementum and not dentin.He postulates that the resorbing tissue is not of pulpalorigin but is ‘metaplastic’ tissue derived from the pul-pal invasion of macrophage-like cells (11). Others (54)concluded that the pulp tissue was replaced by peri-odontium-like connective tissue when internal resorp-tion was present. In addition to the requirement of thepresence of granulation tissue, root resorption takesplace only if the odontoblastic layer and predentin arelost or altered (45). Reasons for the loss of predentinadjacent to the granulation tissue are not obvious.Trauma frequently has been suggested as a cause (55).Some (9) report that trauma may be recognized as aninitiating factor in internal resorption. They are dividedinto a transient type and a progressive type, with thelatter requiring continuous stimulation by infection.Another reason for the loss of predentin might be theextreme heat produced when cutting on dentin with-out an adequate water spray. The heat presumablywould destroy the predentin layer and, if the coronalaspect of the pulp later became infected, the bacterialproducts could initiate the typical inflammation in con-junction with resorbing giant cells in the vital pulp ad-jacent to the denuded root surface. Internal root re-sorption has been produced experimentally by the ap-plication of diathermy (56).

Clinical manifestations

Internal root resorption is usually asymptomatic andis first recognized clinically through routine radio-graphs. If perforation of the crown occurs and themetaplastic tissue is exposed to the oral fluids, painmay be a presenting symptom. For internal resorp-tion to be active, at least part of the pulp must bevital, so that a positive response to pulp sensitivitytesting is possible. It should be remembered thatthe coronal portion of the pulp is often necroticwhereas the apical pulp, which includes the internalresorptive defect, can remain vital. Therefore, anegative sensitivity test result does not rule out ac-tive internal resorption.

It is also possible that the pulp becomes non-vitalafter a period of active resorption, giving a negativesensitivity test, and giving radiographic signs ofinternal resorption and apical inflammation. Tra-


ditionally, the pink tooth has been thought to bepathognomonic of internal root resorption. Thepink color is due to the granulation tissue in thecoronal dentin, undermining the crown enamel. Thepink tooth can also be a feature of subepithelial ex-ternal inflammatory root resorption, which must beruled out before a diagnosis of internal root resorp-tion is made.

Radiographic appearance

The usual radiographic presentation of internal rootresorption is a fairly uniform radiolucent enlargementof the pulp canal (Fig. 22). Because the resorption isinitiated in the root canal, the resorptive defect in-cludes some part of the root canal space. Therefore,the original outline of the root canal is distorted.Only on rare occasions, when the internal resorptivedefect penetrates the root and impacts the peri-odontal ligament, does the adjacent bone show radio-graphic changes.

Histologic appearance

Like that of other inflammatory resorptive defects,the histologic picture of internal resorption isgranulation tissue with multinucleated giant cells.An area of necrotic pulp is found coronal to thegranulation tissue. Dentinal tubules, which containmicroorganisms and communicate between the ne-crotic zone and the granulation tissue, can some-times be seen. Unlike external root resorption, theadjacent bone is not affected with internal root re-sorption.

Fig.22. Demonstration of the effect of angled X-rays oninternal vs. external root resorption. A. Internal root re-sorption stays centered in the root while B. external resorp-tion moves with the angled X-rays. (Courtesy Dr. ClaudiaBarthel).

97

Treatment

Treatment of internal root resorption is, conceptually,very easy. As the resorptive defect is the result of theinflamed pulp and the blood supply to the tissue isthrough the apical foramina, the correct approach totreatment is endodontic treatment that effectively re-moves the blood supply to the resorbing cells. Afteradequate anesthesia has been administered, the canalapical to the internal defect is explored and a workinglength short of the radiographic apex is used. Theapical canal is thoroughly instrumented to ensure thatthe blood supply to the tissue resorbing the root iscut off. By the completion of the root canal instrumen-tation it should be possible to obtain a blood free anddry canal with paper points.

Calcium hydroxide is then spun into the canal tofacilitate the removal of the tissue in the irregulardefect at the next visit. At the second visit, thetooth and defect are filled using a soft gutta-perchatechnique. In rare cases where extremely large inter-nal resorptive defects are found in the apical part ofthe canal, it is possible to surgically remove the de-fective root and place an endodontic implant in or-der to maintain stability of the tooth. With moderndental techniques, this treatment alternative shouldbe weighed against the advantages of implant den-tistry.

Diagnostic Features of External vs.Internal Root ResorptionIt is often very difficult to distinguish external frominternal root resorption, meaning that misdiagnosisand incorrect treatment result. What follows is a listof typical diagnostic features of each resorptive type.

Radiographic features

A change of angulation of X-rays should give a fairlygood indication of whether a resorptive defect isinternal or external. A lesion of internal origin appearsclose to the canal whatever the angle of the X-ray(Fig. 22). On the other hand, a defect on the externalaspect of the root moves away from the canal as theangulation changes (Fig. 22). In addition, by usingthe buccal-object rule, it is usually possible to distin-guish if the external root defect is buccal or lingual-palatal.

Trope

In internal resorption, the outline of the root canalis usually distorted and the root canal and the radio-lucent resorptive defect appear to be contiguous (Fig.21). When the defect is external, the root canal out-line appears normal and can usually be seen ‘runningthrough’ the radiolucent defect (Fig. 20A).

External inflammatory root resorption is alwaysaccompanied by the resorption of the bone in ad-dition to that of the root (Fig. 15B, 18B). There-fore, radiolucencies are apparent in the root and theadjacent bone. Internal root resorption does not in-volve the bone and, as a rule, radiolucency is con-fined to the root (Fig. 21). On the rare occasionsthat the internal defect perforates the root, thebone adjacent to it is resorbed and appears radio-lucent on the radiograph.

Vitality testing

External inflammatory resorption in the apical andlateral aspects of the root involves an infected pulpspace, so that a negative response to sensitivity testsis required to support the diagnosis. On the otherhand, since subepithelial external root resorptiondoes not involve the pulp (the bacteria are thoughtto originate in the sulcus of the tooth), a normal re-sponse to sensitivity testing is usually associated withthis type of resorption. Internal root resorptionusually occurs in teeth with vital pulps and gives apositive response to sensitivity testing. However, inteeth that exhibit internal root resorption, it is notuncommon to register a negative response to sensi-tivity testing, as the coronal pulp has often been re-moved or is necrotic and the active resorbing cells aremore apical in the canal. Also, the pulp might havebecome necrotic after active resorption has takenplace.

Pink spot

With apical and lateral external root resorption, thepulp is non-vital and therefore the granulation tissuethat produces the pink spot is not present in thesecases. A possible sign of subepithelial external andinternal root resorption is the pink spot, which iscaused by the granulation tissue undermining the en-amel.

98

Summary of possible diagnosticfeatures

External inflammatory root resorption dueto pulp infection

Apical. Negative pulp-sensitivity test, with or withouta history of trauma.

Lateral. History of trauma, negative pulp-sensitivitytest, lesion movement on angled X-rays, root canalvisualized radiographically overlying the defect. Bonyradiolucency is also apparent.

Sub-epithelial external inflammatory due tosulcular infection

History of trauma (often forgotten or not appreciatedby the patient), positive pulp sensitivity test, lesionlocated at the attachment level of the tooth, lesionmovement on angled X-rays, root canal outline is un-distorted and can be visualized radiographically,crestal bony defect associated with the lesion, pinkspot possible.

Internal Root Resorption

History of trauma, crown preparation or pulpotomy,positive pulp sensitivity test likely, may occur at anylocation along the root canal (not only attachmentlevel); lesion stays associated with the root canal onangled X-rays, radiolucency contained in the rootwithout an adjacent bony defect; pink spot possible.

The majority of misdiagnoses of resorptive defectsare made between subepithelial external and internalroot resorptions. The diagnosis should always be con-firmed while treatment is proceeding. If root canaltherapy is the treatment of choice for an apparentinternal root resorption, the bleeding within the canalshould cease quickly after pulp extirpation, as theblood supply of the granulation tissue is the apicalblood vessels. If bleeding continues during treat-ment––and particularly if it is still present at the sec-ond visit––the source of the blood supply is externaland treatment for external resorption should be car-ried out. It should also be possible to fill the entirecanal from within internal resorptionn during obdur-ation. Failure to achieve this should make the oper-ator suspicious of an external lesion. Finally, if theblood supply of an internal resorption defect is re-


moved on pulp extirpation, any continuation of theresorptive process on recall radiographs should alertthe dentist to the possibility that an external resorp-tive defect was misdiagnosed.

References1. Hammarstrom L, Lindskog S. General morphologic as-

pects of resorption of teeth and alveolar bone. Int EndodJ 1985: 18: 293–298.

2. Seltzer S. Endodontology. Philadelphia: Lea & Febiger,1988.

3. Loe H, Waerhaug J. Experimental replantation of teeth indogs and monkeys. Arch Oral Biol 1961: 3: 176–182.

4. Orban B. The epithelial network in the periodontal mem-brane. J Am Dent Assoc 1952: 44: 632–637.

5. Andreasen JO. Review of root resorption systems andmodels. Etiology of root resorption and the homeostaticmechanisms of the periodontal ligament. In: Davidovitched. The Biologic Mechanisms of Tooth Eruption and Resorp-tion. Birmingham, Alabama: EB-SCOP Media, 1989.

6. Karring T, Nyman S, Lindhe J. Healing following implan-tation of periodontitis affected roots into bone tissue. JClin Periodont 1980: 7: 96–103.

7. Polson AM, Caton JM. Factors influencing periodontal re-pair and regeneration. J Periodont 1982: 52: 617–623.

8. Stenvik A, Mjor IA. Pulp and dentin reaction to experi-mental tooth intrusion. Am J Orthodont 1970: 57: 370–376.

9. Wedenberg C, Lindskog S. Experimental internal resorp-tion in monkey teeth. Endod Dent Traumatol 1985: 1:221–226.

10. Selvig KA, Zander HA. Chemical analysis and microradio-graphy of cementum and dentin from periodontally dis-eased human teeth. J Periodontol 1962: 33: 303–310.

11. Andersson L, Friskopp J, Blomlof L. Fiberglass splintingof traumatized teeth. ASDC J Dent Child 1983: 3: 21.

12. Levin L, Trope M. Root Resorption . In: Seltzer S, BenderIB, Hargreaves K eds. The Dental Pulp. Carol Stream, IL:Quintessence Publishers, 2001.

13. Andreasen JO. The effect of extra-alveolar period and stor-age media upon periodontal and pulpal healing after re-plantation of mature permanent incisors in monkeys. Int JOral Surg 1981: 10: 43–51.

14. Soder PO, Otteskog P, Andreasen JO, Modeer T. Effectof drying on viability of periodontal membrane. Scand JDent Res 1977: 85: 167–172.

15. Tronstad L. Root resorption––etiology, terminology andclinical manifestations. Endod Dent Traumatol 1988: 4:241–249.

16. Nance RS, Tyndall D, Levin LG, Trope M. Diagnosis ofexternal root resorption using TACT (tuned-aperturecomputed tomography). Endod Dent Traumatol 2000:16: 24–28.

17. Andreasen JO, Andreasen FM. Textbook and Color Atlas ofTraumatic. Injuries to the Teeth, 3rd edn. Copenhagen andSt. Louis: Munksgaard and CV Mosby, 1994.

18. Trope M. Root resorption of dental and traumatic origin:Classification based on. etiology. J Pract Periodont AesthetDent, 1998: 10: 515–524.

99

19. Hammarstrom L, Pierce AM, Blomlof L, Feiglin B, Lind-skog S. Tooth avulsion and replantation: a review. EndodDent Traumatol 1986: 2: 1–9.

20. Lindskog S, Pierce AM, Blomlof L, Hammarstrom L. Therole of the necrotic periodontal membrane in cementumresorption and ankylosis. Endod Dent Traumatol 1985: 1:96–101.

21. Johnston T, Messer LB. An in vitro study of the efficacyof mouthguard protection for dentoalveolar injuries in de-ciduous and mixed dentitions. Endodontics DentalTraumatol 1996: 12: 277–285.

22. Sae Lim V, Lim LP. Dental trauma management awarenessof Singapore pre-school teachers. Dent Traumatol 2001:17: 71–60.

23. Trope M. Luxation injuries and external root resorption –etiology, treatment and prognosis. CDA Journal 2000:11: 860.

24. Trope M, Friedman S. Periodontal healing of replanteddog teeth stored in Viaspan, milk and Hanks Balanced SaltSolution. Endod Dent Traumatol 1992: 8: 183–188.

25. Sae-Lim V, Wang C-Y, Choi G-W, Trope M. The effect ofsystemic tetracycline on resorption of dried replanted dogs’teeth. Endod Dent Traumatol 1998: 14: 127–132.

26. Sae-Lim V, Wang C-Y, Trope M. Effect of systemic tetracy-cline and amoxicillin. on inflammatory root resorption ofreplanted dogs’ teeth. Endod Dent Traumatol 1998: 14:216–220.

27. Pierce A, Lindskog S. The effect of an antibiotic cortico-steroid combination on inflammatory root resorption. JEndod 1988: 14: 459–464.

28. Hupp JG, Trope M, Mesaros S, Aukhil I. Tritiated thymi-dine uptake in periodontal ligament cells of dogs’ teethstored in various media for extended time periods. EndodDent Traumatol 1997: 13: 223.

29. Pettiette M, Hupp J, Mesaros S, Trope M. Periodontalhealing of extracted dog teeth air dried for extendedperiods and soaked in various media. Endod DentTraumatol 1997: 13: 113–118.

30. Filippi A, Pohl Y, von Arx T. Treatment of replacementresorption with EmdogainA – preliminary results after 10months. Dent Traumatol 2001: 17: 3–10.

31. Iqbal MK, Bamaas N. Effect of enamel matrix derivative(EMDOGAINA) upon periodontal healing after re-plantation of permanent incisors in Beagle dogs. DentTraumatol 2001: 17: 36–34.

32. Bjorvatn K, Selvig KA, Klinge B. Effect of tetracycline andSnF2 on root resorption in replanted incisors in dogs.Scand J Dent Res 1989: 97: 477–482.

33. Selvig KA, Zander HA. Chemical analysis and microra-diography of cementum and dentin from periodonticallydiseased human teeth. J Periodont 1962: 33: 103–109.

34. Levin L, Bryson EC, Caplan D, Trope M. Effect of topicalalendronate on root resorption of dried replanted dogteeth. Dent Traumatol 2001: 17: 120–126.

35. Bender IB, Byers MR, Mori K. Periapical replacement re-sorption of permanent, vital, endodontically treated in-cisors after orthodontic movement: report of two cases. JEndod 1997: 23: 768–776.

36. Trope M, Yesilsoy C, Koren L, Moshonov J, Friedman S.Effect of different endodontic treatment protocols on peri-

Trope

odontal repair and root resorption of replanted dog teeth.J Endod 1992: 18: 492–497.

37. Trope M, Moshonov J, Nissan R, Buxt P, Yesilsoy C. Shortversus long term Ca(OH)2 treatment of established inflam-matory root resorption in replanted dog teeth. EndodonDent Traumatol 1995: 11: 124.

38. Andreasen JO. Periodontal healing after replantation oftraumatically avulsed human teeth. Assessment by mobilitytesting and radiography. Acta Odontol Scand 1975: 33:325–332.

39. Kling M, Cvek M, Mejare I. Rate and predictability of pulprevascularization in therapeutically reimplanted permanentincisors. Endodon Dent Traumatol 1986: 2: 83–89.

40. Cvek M, Cleaton-Jones P, Austin J, Lownie J, Kling M,Fatti P. Effect of topical application of doxycycline on pulprevascularization and periodontal healing in reimplantedmonkey incisors.. Endod Dent Traumatol 1990: 6: 170–177.

41. Yanpiset K, Trope M. Pulp revascularization of replantedimmature dog teeth after different treatment methods. En-dod Dent Traumatol 2000: 16: 211–217.

42. Iwaya S, Ikawa M, Kubota M. Revascularization of an im-mature permanent tooth with apical periodontitis and si-nus tract. Dent Traumatol 2001: 17: 185–187.

43. Bystrom A, Claesson R, Sundqvist G. The antibacterial ef-fect of camphorated paramonochlorphenol, camphoratedphenol and calcium hydroxide in the treatment of infectedroot canals. Endod Dent Traumatol 1985: 1: 170–177.

44. Sjogren U, Figdor D, Spangberg L, Sundqvist G. The anti-microbial effect of calcium hydroxide as a short term intra-canal dressing. Int Endod J 1991: 24: 119–125.

45. Frank AL, Bakland LK. Nonendodontic therapy for sup-raosseous extracanal invasive resorption. J Endod 1987: 7:348–355.

100

46. Gold SI, Hasselgren G. Peripheral inflammatory root re-sorption. J Periodontol 1992: 19: 523–527.

47. Heithersay GS. Invasive cervical resorption: an analysis ofpotential predisposing factors. Quintessence Int 1999: 30:83–95.

48. Heithersay GS. Clinical, radiographic and histopatholog-ical features of invasive cervical resorption. Quintessence Int1999: 30: 27–37.

49. Heithersay GS. Treatment of invasive cervical resorption:an analysis of results using topical application of trichlora-cetic acid, curettage and restoration. Quintessence Int1999: 30: 98–110.

50. Rotstein I, Lehr Z, Gedalia I. Effect of bleaching agents oninorganic components of human dentin and cementum. JEndod 1992: 18: 290–296.

51. Rotstein I, Mor C, Friedman S. Prognosis of intracoronalbleaching with sodium perborate penetration in vitro: 1year study. J Endodon 1993: 1: 10–12.

52. Weiger R, Kuhn A, Lost C. Radicular penetration of hy-drogen peroxide during intra-coronal bleaching with vari-ous forms of sodium perborate. Int Endodon J 1994: 6:313–317.

53. Fiorellini JP, Paquette DW. The potential role of con-trolled release delivery systems for chemotherapeuticagents in periodontics. Curr Opin Dent 1992: 2: 63–79.

54. Stanley HR. Diseases of the Dental Pulp. In: Tieck RW,ed. Oral Pathology. New York: McGraw Hill Co, 1965.

55. Wedenberg C, Zetterqvist L. Internal resorption in humanteeth/a histological, scanning electron microscope and en-zyme histo-chemical study. J Endod 1987: 13: 255–261.

56. Gottlieb B, Orban B. Veranderunngen in Periodontiumnach chirurgischer Diathermie. ZJ Stomatol 1930: 28:1208–1212.

root resorption due to dental trauma - endoexperience resorption due to dental trauma... · root...

Documents