Review Article
Internal Root Resorption: A Review
Shanon Patel, BDS, MSc, MClinDent,* Domenico Ricucci, MD, DDS,† Conor Durak, BDSc, MFDS
RCS (Eng),* and Franklin Tay, BDSc (Hons), PhD‡
Abstract
Introduction: Internal root resorption is the progressive
destruction of intraradicular dentin and dentinal tubules
along the middle and apical thirds of the canal walls as
a result of clastic activities. Methods: The prevalence,
etiology, pathogenesis, histologic manifestations, differ-
ential diagnosis with cone beam computed tomography,
and treatment perspectives involved in internal root
resorption are reviewed. Results: The majority of the
documentation that exists in the literature is in the
form of case reports, and there are only a limited number
of studies that attempted to examine the histologic
manifestations and biologic aspects of the disease.
This might be due, in part, to the relatively rare occur-
rence of this type of resorption and the lack of an in
vivo model, apart from the previous attempt on the
use of diathermy, to predictably reproduce the condition
for study. From a histologic perspective, internal root
resorption is manifested in one form that is purely
destructive, internal (root canal) inflammatory resorp-
tion, and another that is accompanied by repair, internal
(root canal) replacement resorption that is featured by
the deposition of metaplastic bone/cementum-like
tissues adjacent to the sites of resorption. Conclusions:
From a differential diagnosis perspective, the advent of
cone beam computed tomography has considerably
enhanced the clinician’s capability of diagnosing
internal root resorption. Nevertheless, root canal treat-
ment remains the treatment of choice for this pathologic
condition to date. (J Endod 2010;36:1107–1121)
Key Words
Bone metaplasia, cone beam computed tomography,
internal root resorption, pulp histology, pulp inflamma-
tion
From the *Endodontic Postgraduate Unit, King’s College,
London Dental Institute, London, United Kingdom; †Private
practice, Rome, Italy; and ‡Department of Endodontics, School
of Dentistry, Medical College of Georgia, Augusta, Georgia.
Address requests for reprints to Dr Domenico Ricucci,
Piazza Calvario, 7, 7022 Cetraro (CS), Italy. E-mail address:
dricucci@libero.it.
0099-2399/$0 - see front matter
Copyright ª 2010 American Association of Endodontists.
doi:10.1016/j.joen.2010.03.014
JOE — Volume 36, Number 7, July 2010
R oot resorption is the loss of dental hard tissues as a result of clastic activities (1). It
might occur as a physiologic or pathologic phenomenon. Root resorption in the
primary dentition is a normal physiologic process except when the resorption occurs
prematurely (2, 3). The initiating factors involved in physiologic root resorption in the
primary dentition are not completely understood, although the process appears to be
regulated by cytokines and transcription factors that are similar to those involved in
bone remodeling (4, 5). Unlike bone that undergoes continuous physiologic
remodeling throughout life, root resorption of permanent teeth does not occur
naturally and is invariably inflammatory in nature. Thus, root resorption in the
permanent dentition is a pathologic event; if untreated, this might result in the
premature loss of the affected teeth.
Root resorption might be broadly classified into external or internal resorption by
the location of the resorption in relation to the root surface (6, 7). Internal root
resorption has been reported as early as 1830 (8). Compared with external root
resorption, internal root resorption is a relatively rare occurrence, and its etiology
and pathogenesis have not been completely elucidated (9). Nevertheless, internal
root resorption poses diagnostic concerns to the clinician because it is often confused
with external cervical resorption (ECR) (10–12). Incorrect diagnosis might result in
inappropriate treatment in certain cases (13).
The aim of this work is to review the etiology and pathogenesis of internal root
resorption as well as the problems encountered in the diagnosis and treatment planning
of this condition. In addition, the epidemiology, classification, and histologic features of
internal root resorption will be discussed.
Prevalence
Internal root resorption has been described as intraradicular or apical according
to the location in which the condition is observed (9). Intraradicular internal resorp-
tion is an inflammatory condition that results in progressive destruction of intraradic-
ular dentin and dentinal tubules along the middle and apical thirds of the canal walls.
The resorptive spaces might be filled by granulation tissue only or in combination with
bone-like or cementum-like mineralized tissues (14). The condition is more frequently
observed in male than female subjects (15, 16). Although intraradicular internal root
resorption is a relatively rare clinical entity even after traumatic injury (17, 18), a higher
prevalence of the condition has been associated with teeth that had undergone specific
treatment procedures such as autotransplantation (19). Cabrini et al (20) amputated
the coronal pulps of 28 teeth and dressed the radicular pulp stumps with calcium
hydroxide mixed with distilled water. Eight of the 28 teeth extracted between 49 and
320 days after the procedure demonstrated histologic evidence of internal resorption.
Çalisxkan and Türkün (16) examined the prognosis of endodontic treatment on 25 teeth
with nonperforating and perforating internal resorption. The authors reported that the
most commonly affected teeth were maxillary incisors. The small sample sizes in these
studies precluded definitive conclusions to be drawn on the prevalence of internal root
resorption. Moreover, diagnosis of internal resorption in most of the earlier studies was
based solely on 2-dimensional radiographic evidence, without complementary 3-
dimensional radiographic and/or histologic support. Further epidemiologic studies
are required to identify whether there are racial predilections in the manifestation of
intraradicular internal resorption.
Compared with intraradicular internal resorption, apical internal resorption is
a fairly common occurrence in teeth with periapical lesions (21). The authors exam-
ined the extent of internal resorption in 75 roots (69 roots with radiolucent periapical
Internal Root Resorption 1107
Review Article
lesions and 6 vital control roots) and graded the severity of resorption
on a 4-point scale. They concluded that 75% of teeth associated with
periapical lesions had internal apical resorption and that vital teeth
had statistically less apical internal resorption than teeth with periapical
lesions. Severe internal resorption could be identified in 48% of those
cases with periapical lesions. Conversely, only 1 root in the control
group displayed mild internal resorption, which was speculated to be
transient in nature as a result of trauma. Because apical internal resorp-
tion is invariably associated with apical inflammatory external resorp-
tion of the cementum from partially resorbed root apices (22, 23),
only the intraradicular forms of internal root resorption will be
discussed in the rest of this article and will be simply referred to as
internal root resorption.
Etiology and Pathogenesis
Osteoclasts are motile, multinucleated giant cells that are respon-
sible for bone resorption. They are formed by the fusion of mononu-
clear precursor cells of the monocyte-macrophage lineage derived
from the spleen or bone marrow, as opposed to osteoblasts and oste-
ocytes that are derived from skeletal precursor cells (24–26). They are
recruited to the site of injury or irritation by the release of many
proinflammatory cytokines. To perform their function, osteoclasts
must attach themselves to the bone surface. Recent studies indicated
that the polarity of osteoclasts is regulated by their actin cytoskeleton
(27, 28). On contact with mineralized extracellular matrices, the
actin cytoskeleton of an actively resorbing osteoclast is reorganized
to produce an organelle-free zone of sealing cytoplasm (clear zone)
associated with the osteoclast’s cell membrane to enable it to achieve
intimate contact with the hard tissue surface (29). The clear zone
surrounds a series of finger-like projections (podosomes) of cell
membrane known as the ruffled border. It is underneath this ruffled
border that bone resorption occurs. The resorptive area within the clear
zone, therefore, is isolated from the extracellular environment, creating
an acidic microenvironment for the resorption of hard tissues (30).
Odontoclasts are the cells that resorb dental hard tissues (Fig. 1)
and are morphologically similar to osteoclasts (31). Odontoclasts differ
from osteoclasts by being smaller in size and having fewer nuclei and
smaller sealing zones possibly as result of differences in their respective
resorption substrata (32). Osteoclasts and odontoclasts resorb their
target tissues in a similar manner (29). Both cells possess similar enzy-
matic properties (33), and both create resorption depressions termed
Howship’s lacunae on the surface of the mineralized tissues (Fig. 1)
(29). Although mononuclear dendritic cells share a common hemato-
poietic lineage with the multinucleated osteoclasts, they have previously
been regarded solely as immunologic defense cells. Recent studies indi-
cated that immature dendritic cells function also as osteoclast precur-
sors that have the potential to transdifferentiate into osteoclasts (34,
35). Because dendritic cells are present in the dental pulp, it is
possible they might function also as precursors of odontoclasts.
From a molecular signaling perspective, the OPG/RANKL/RANK tran-
scription factor system (36) that controls clastic functions during bone
remodeling has also been identified in root resorption (37). The system
is responsible for the differentiation of clastic cells from their precursors
via complex cell-cell interactions with osteoblastic stromal cells. Similar to
periodontal ligament cells that are responsible for external root resorp-
tion (38), the human dental pulp has recently been shown to express os-
teoprotegerin (OPG) and receptor activator of nuclear factor kappa B
ligand (RANKL) mRNAs (39). Osteoprotegerin, a member of the tumor
necrosis factor superfamily, has the ability to inhibit clast functions by
acting as decoy receptors that bind to RANKL and reduce the affinity of
the latter to RANK receptors on the surface of clastic precursors. This
1108 Patel et al.
results in inhibition of the regulation of clastic cell differentiation. Thus,
it is possible that the OPG/RANKL/RANK system might be actively involved
in the differentiation of odontoclasts during internal root resorption.
It is known that osteoclasts do not adhere to nonmineralized
collagen matrices (40). It has been suggested that the presence of a non-
collagenous, organic component within dentin (odontoblast layer and
predentin) prevents resorption of the root canal wall (41, 42). Similar
to osteoclasts, odontoclasts might bind to extracellular proteins
containing the RGD (arginine-glycine-aspartic acid) sequence of
amino acids via integrins (43). The latter are specific surface adhesion
glycoprotein membrane receptors containing different a and
b subunits. In particular, avb3 integrin plays a key role in the adhesion
of clastic cells (44). Extracellular matrix proteins containing the RGD
peptide sequence present on the surface of mineralized tissues, in
particular osteopontin, serve as binding sites of clastic cells (45).
The osteopontin molecule contains different domains, with one domain
binding to apatites in the denuded dentin and another domain binding
to integrin receptors in the plasma membranes of clastic cells. Thus,
osteopontin serves as a linker molecule that optimizes the attachment
of a clastic cell to mineralized tissues, mediating the rearrangement
of its actin cytoskeleton (46). It has been speculated that the lack of
RGD peptides in predentin reduces the binding of odontoclasts, thereby
conferring resistance of the canal walls to internal root resorption.
For internal root resorption to occur, the outermost protective
odontoblast layer and the predentin (Fig. 1) of the canal wall must be
damaged, resulting in exposure of the underlying mineralized dentin to
odontoclasts (40, 47). The precise injurious events necessary to bring
about such damages have not been completely elucidated. Various
etiologic factors have been proposed for the loss of predentin,
including trauma, caries and periodontal infections, excessive heat
generated during restorative procedures on vital teeth, calcium
hydroxide procedures, vital root resections, anachoresis, orthodontic
treatment, cracked teeth, or simply idiopathic dystrophic changes
within normal pulps (18, 20, 48–55). In a study of 25 teeth with
internal resorption, trauma was found to be the most common
predisposing factor that was responsible for 45% of the cases
examined (16). The suggested etiologies in the other cases were inflam-
mation as a result of carious lesions (25%) and carious/periodontal
lesions (14%). The cause of the internal resorption in the remaining teeth
was unknown. Other reports in the literature also support the view that
trauma (18, 42, 56) and pulpal inflammation/infection (11, 56) are the
major contributory factors in the initiation of internal resorption.
Wedenberg and Lindskog (47) reported that internal root resorp-
tion could be a transient or a progressive event. In an in vivo primate
study, the root canals were accessed in 32 incisors with the predentin
intentionally damaged. The access cavities in half of the teeth were
sealed; the other half were left open to the oral cavity. The teeth were
extracted at intervals of 1, 2, 6, and 10 weeks. The authors noted
only a transient colonization of the damaged dentin by multinucleated
clastic cells in the teeth that had been sealed (ie, transient internal
root resorption). Those teeth were free from bacterial contamination,
and no signs of active hard tissue resorption occurred. In the teeth
that were left unsealed during the experimental period, there were signs
of extensive bacterial contamination of pulpal tissue and dentinal
tubules. Those teeth demonstrated extensive and prolonged coloniza-
tion of the damaged dentin surface by clastic cells and signs of miner-
alized tissue resorption (progressive internal root resorption). Damage
to the odontoblast layer and predentin of the canal wall is a prerequisite
for the initiation of internal root resorption (42). However, the advance-
ment of internal root resorption depends on bacterial stimulation of the
clastic cells involved in hard tissue resorption (Fig. 2). Without this
stimulation, the resorption will be self-limiting (42).
JOE — Volume 36, Number 7, July 2010
 Review Article

Figure 1. Light microscopy images of a case with early internal (root canal) inflammatory resorption. (a) Maxillary canine with caries penetrating the pulp. The
tooth was tender to percussion. There was no response to sensitivity tests. (b) Sections were taken along the buccolingual plane. Overview image shows carious
perforation and necrotic tissue in the root canal (Taylor’s modified Brown & Brenn [TBB]; original magnification, !2). (c) Coronal third of the root canal shown
in (b). Dense bacterial biofilm was present on the canal walls. Necrotic tissue can be identified in the canal lumen (TBB; original magnification, !16). (d) High
magnification of the area indicated by the arrow in (c). Dense aggregation of bacteria can be seen along the canal wall (TBB; original magnification, !400. Inset;
original magnification, !1000). (e) Apical third of the root. Contrary to the histologic condition present in the coronal two thirds, the tissue was vital (hematoxylin-
eosin [H&E]; original magnification, !25). (f) Magnification of the left root canal wall. The odontoblast layer was absent, with only some remaining predentin.
Resorption lacunae can be observed along the canal wall (H&E; original magnification, !100). (g) Higher magnification of the upper lacuna in (f). Large multi-
nucleated resorbing cell (odontoclast) and granulation tissue consisting of fibroblasts and chronic inflammatory cells can be seen (H&E; original magnification,
!400). (h) High magnification view of the odontoclast showing multiple nuclei. The empty space is a shrinkage artifact (H&E; original magnification, !1000).

JOE — Volume 36, Number 7, July 2010 Internal Root Resorption 1109
Review Article
For internal resorption to occur, the pulp tissue apical to the
resorptive lesion must have a viable blood supply to provide clastic cells
and their nutrients, whereas the infected necrotic coronal pulp tissue
provides stimulation for those clastic cells (7) (Fig. 2). Bacteria might
enter the pulp canal through dentinal tubules, carious cavities, cracks,
fractures, and lateral canals. In the absence of a bacterial stimulus, the
resorption will be transient and might not advance to the stage that can
be diagnosed clinically and radiographically. Therefore, the pulp apical
to the site of resorption must be vital for the resorptive lesion to prog-
ress (Fig. 1). If left untreated, internal resorption might continue until
the inflamed connective tissue filling the resorptive defect degenerates,
advancing the lesion in an apical direction. Ultimately, if left untreated,
the pulp tissue apical to the resorptive lesion will undergo necrosis, and
the bacteria will infect the entire root canal system, resulting in apical
periodontitis (57) (Fig. 2).
Histologic Manifestations
Our knowledge of the histologic manifestations of internal root
resorption in humans is based largely on the work of Wedenberg and
Zetterqvist (56). In that study, internal root resorption lesions in
both primary and permanent teeth were examined with light micros-
copy, scanning electron microscopy, and enzyme histochemistry. The
study examined 6 primary and 7 permanent teeth that were extracted
as a result of progressive internal resorption. The histologic appear-
ance and histochemical profiles of the primary and permanent teeth
were identical, but the resorption process generally occurred at
a faster rate in the primary teeth. Pulpal tissues in all the teeth
were inflamed to varying degrees, with the inflammatory infiltrate
consisting predominantly of lymphocytes and macrophages, with
some neutrophils. The inflammation was associated with dilated
blood vessels, and in 11 of the cases, bacteria were evident either
in the necrotic coronal pulp tissue or within the dentinal tubules
adjacent to the lesion. The granulation tissue in the pulp cavities con-
tained fewer blood vessels than in normal pulp tissue and resembled
periodontal connective tissues, with comparatively more cells and
fibers. Indeed, the periodontal membrane was continuous with the
tissue in the pulp cavities in all but 2 teeth through either the apical
foramen or perforations of the external root surfaces as a result of
the resorption process. A distinguishing feature of all the lesions

Figure 2. Light microscopy images of a case with early internal (root canal) inflammatory resorption followed by necrosis and infection. (a) Periapical radiograph
shows a mandibular second premolar with gross caries and enlargement of the periodontal ligament. There was no response to sensitivity tests, and the tooth was
extremely sensitive to percussion. The buccal gingival tissues were swollen and fluctuant. The diagnosis was pulpal necrosis with acute apical abscess. After dis-
cussing the various treatment options, the patient opted for extraction. (b) Sections were taken along the mesiodistal plane. Overview image shows that the distal
caries had penetrated the pulp space. Pulp tissue was necrotic (TBB; original magnification, !2). (c) Apical third. Main canal and ramifications were filled with
a bacterial biofilm (TBB; original magnification, !16). (d) Higher magnification of the main canal in (c). Numerous resorptive defects were present on the right
root canal walls and filled with bacteria (TBB; original magnification, !100). (e) High magnification of the upper lacuna in (d). Predentin was absent, and the
cavity was occupied by a bacterial biofilm. Some polymorphonuclear leukocytes can be observed (TBB; original magnification, !400). (f) Resorption lacuna apical
to that shown in (e) (TBB; original magnification, !400). (g) High magnification taken from the left canal wall of the apical canal. Despite the presence of necrotic
pulp tissue along the root canal wall, predentin was intact at this level, and no resorption can be seen (H&E; original magnification, !400).

1110 Patel et al. JOE — Volume 36, Number 7, July 2010


examined was the presence of numerous, large, multinucleated
odontoclasts occupying resorption lacunae on the canal walls. The
odontoclasts displayed evidence of active resorption and were
accompanied by mononuclear inflammatory cells in the adjacent
connective tissue. Both types of cell displayed tartrate-resistant acid
phosphatase activity. There were no predentin or odontoblasts on
the dentinal walls.
Of interest was the presence of a metaplastic mineralized tissue
that resembled bone or cementum. The metaplastic mineralized tissues
incompletely lined the pulp cavity in all cases, and islands of calcified
tissues were identified from the pulp in 3 teeth. Similar metaplastic
mineralized tissues were reported by Cvek (58) and Cvek et al (59),
with ‘‘ankylosis of the canal walls’’ similar to what was observed along
the external root surfaces. On the basis of those results, 2 types of
internal root resorption were described by Ne et al (60) and Heithersay
(61), internal (root canal) inflammatory resorption and internal (root
canal) replacement resorption. The prefixes ‘‘internal’’ and ‘‘root
canal’’ were used to delineate these entities from similar observations
in external root resorption.
Review Article
Internal (Root Canal) Inflammatory Resorption
This type of resorption might occur in any area of the root canal
system. It is characterized by the radiographic appearance of an oval-
shaped enlargement within the pulp chamber (Fig. 3). The condition
might go unnoticed until the lesion has advanced significantly, result-
ing in a perforation (62) or symptoms of acute or chronic apical pe-
riodontitis after the entire pulp has undergone necrosis and the pulp
space has become infected. If resorption occurs in the coronal
portion of the tooth, the latter might exhibit a pinkish hue that is clas-
sically described as the pink tooth of Mummery after the 19th century
anatomist James Howard Mummery (63), who first reported the
phenomenon.
Internal root canal inflammatory resorption involves a progressive
loss of intraradicular dentin without adjunctive deposition of hard
tissues adjacent to the resorptive sites (Figs. 1–3). It is frequently
associated with chronic pulpal inflammation, and bacteria might be
identified from the granulation tissues when the lesion is progressive
to the extent that it is identifiable with routine radiographs (47)
(Fig. 3). Although chronic inflammation is commonly present in pulpal

Figure 3. Light microscopy images of a case with internal (root canal) inflammatory resorption. (a) Radiograph of a nonrestorable grossly carious mandibular
molar. A radiolucent area can be seen in the distal root at the transition between the middle and the apical thirds of the root canal. (b) Longitudinal section of the
distal root, taken from a mesiodistal plane. The defect appears empty, except for some debris present in its apical extension (H&E; original magnification, !16). (c)
High magnification of the area from the right wall indicated by the arrow in (b). Resorption lacunae appear empty; no multinucleated cells are visible (H&E; original
magnification, !400). (d) Section taken approximately 60 sections after that shown in (b). Necrotic tissues can be seen at the transition between the resorption
area and the apical canal followed by a concentration of cells (TBB; original magnification, !50). (e) High magnification of the area demarcated by the rectangle in
(d), showing the transition between necrotic tissue with bacterial colonies and an area of acute inflammation (TBB; original magnification, !400). (f) High magni-
fication of the area indicated by the arrow at the center of the cellular accumulation in (d). Dense aggregation of polymorphonuclear leukocytes can be identified
(TBB; original magnification, !400). (Reprinted with permission from Ricucci D. Patologia e Clinica Endodontica. Edizioni Martina, Bologna, Italy, 2009).

JOE — Volume 36, Number 7, July 2010 Internal Root Resorption 1111
Review Article
infections, it alone does not provide the conditions necessary for medi-
ating root canal inflammatory resorption. Other conditions must be
present simultaneously to initiate the event; for example, conditions
must prevail for the recruitment and activation of odontoclast precur-
sors within the dental pulp, and the adjacent odontoblast layer and pre-
dentin must be disrupted (64) for those activated clastic cells to adhere
to the intraradicular mineralized dentin (Fig. 1). This probably explains
why root canal inflammatory resorption is less frequently observed than
external inflammatory root resorption (EIRR). The coronal part of the
pulp is usually necrotic, whereas the apical part of the pulp must remain
vital for the resorptive lesion to progress and enlarge (Fig. 1). One
hypothesis suggests that the necrotic coronal part of the infected pulp
provides a stimulus for inflammation in the apical part of the pulp.
An alternative hypothesis is based on the recent understanding that oste-
ocytes participate in bone homeostasis by inhibiting osteoclastogenesis
(65). In the presence of living osteocytes, osteoclasts fail to produce
actin rings, which are the hallmark of active resorbing cells. Conversely,
apoptosis of osteocytes induces the secretion of osteoclastogenic cyto-
kines that trigger bone resorption (66, 67). Similar to osteocytes, dental
pulp cells and odontoblasts undergo apoptosis during tooth
development as well as in response to certain types of injury (68–
71). Thus, it is possible that odontoblasts or pulpal fibroblasts
undergoing apoptosis as a result of trauma or caries produce
cytokines that initiate an internal resorptive response in the apical
part of the pulp. Internal resorption only occurs when the predentin
adjacent to the site of chronic inflammation is lost as a result of
trauma (56) or other unknown etiologic factors.
Internal (Root Canal) Replacement Resorption
Internal root canal replacement resorption is characterized by an
irregular radiographic enlargement of the pulp chamber, with discon-
tinuity of the normal canal space (72). Because the resorption process
is initiated within the root canal, the defect includes part of the canal
space, and hence the outline of the original canal appears distorted.
The enlarged canal space appeared radiographically to be obliterated
by a fuzzy-appearing material of mild to moderate radiodensity
(Fig. 4). This form of resorption is typically asymptomatic, and the
affected teeth might respond normally to thermal and/or electric pulp
testing unless the resorptive process results in crown or root perfora-
tion (60). Root canal replacement resorption appears to be caused by
a low-grade inflammation of the pulpal tissues such as chronic irrevers-
ible pulpitis or partial necrosis. Similar to root canal inflammatory
resorption, the chronic inflammatory process must occur along a region
of the canal wall in which the odontoblast layer and the predentin are
disrupted or damaged before the resorption component of the condi-
tion commences (56), because odontoblasts have to bind to extracel-
lular proteins containing the RGD amino acid sequence.
Histologically, resorption of the intraradicular dentin is accompanied
by subsequent deposition of a metaplastic hard tissue that resembles
bone or cementum instead of dentin (Fig. 4). Metaplasia refers to
a reversible change in which one adult cell type (epithelial or
mesenchymal) is replaced by another cell type (73). In the present
context, the metaplastic tissue appears lamella-like, with entrapped
osteocyte-like cells that resemble osteons of compact bone (Fig. 4).
A variant of internal root canal replacement resorption has previ-
ously been reported as ‘‘internal tunnelling resorption’’ (74). This entity
is usually found in the coronal portion of root fractures but might also
be seen after luxation injuries. The resorption process tunnels into the
dentin adjacent to the root canal, with concomitant deposition of bone-
like tissues in some regions. These bone-like tissues have the appear-
ance of cancellous bone instead of compact bone (Fig. 5). The process
1112 Patel et al.
might subsequently arrest and might be followed by complete oblitera-
tion of the canal space by cancellous bone.
Different hypotheses have been proposed regarding the origin of
the metaplastic hard tissues that are formed within the canal space.
The first hypothesis suggests that the metaplastic tissues are produced
by postnatal dental pulp stem cells (75, 76) present in the apical,
vital part of the root canal as a reparative response to the resorptive
insult. This is analogous to the formation of tertiary reparative dentin
by odontoblast-like cells after the death of the primary odontoblasts
(77). Unlike reactionary dentinogenesis, dentin repair studies have
shown that the matrix deposited during reparative dentinogenesis
demonstrates a high degree of heterogeneity. Following the depletion
of epithelial-mesenchymal interactions that occur in primary dentino-
genesis, the matrix deposited in reparative dentinogenesis often resem-
bles osteoid instead of tubular dentin (78–80). Odontoblasts are
postmitotic cells that are incapable of cell division following their
terminal differentiation. Despite the advances in our understanding of
the molecular signaling that determines cell fate during tooth
morphogenesis and regeneration (81, 82), the precise cross-talk mech-
anisms that determine the commitment of mesenchymal progenitor cells
to a definitive odontoblast lineage (as opposed to the osteoblast lineage)
remain ambiguous at large (83, 84). In the absence of highly specific
epigenetically derived signals required for lineage diversification and
differentiation of ’’true’’ odontoblasts in an adult tooth, multipotent
stem cells engaged in the process of reparative dentin formation
retain the osteoblastic phenotype and secrete a matrix that more
resembles bone than dentin. These histologic observations appear to
be supported by the results of a recent article that involved the use of
gene therapy to introduce a growth factor into dental pulp stem cells
(85). In that study, the newly formed hard tissue resembled bone rather
than dentin, with concentric lamellae of mineralized matrix entrapping
osteocyte-like cells. In addition, a bone marrow–like hematopoietic
tissue could be identified within the newly formed hard tissues. Thus,
it is possible that a similar phenomenon occurs during the formation
of metaplastic tissues in root canal replacement resorption.
The second hypothesis proposes that both the granulation tissues
and metaplastic hard tissues are of nonpulpal origin. Those tissues might
be derived from cells that transmigrated from the vascular compartments
or originated from the periodontium (86). This hypothesis suggests that
in internal resorption, the pulpal tissues are replaced by periodontium-
like connective tissues. Such a scenario is analogous to what occurs
during ingrowth of connective tissues into the pulp space when a blood
clot became available (87–89) or, more recently, after pulpal
revascularization procedures (90, 91). Indeed, the histologic features
of heavy inflammatory infiltrates and bone/cementum-like metaplastic
tissues formation in root canal replacement resorption are highly reminis-
cent of similar unresolved lymphocyte infiltration and intracanal
cementum-like hard tissue deposition in experimental revascularization
procedures conducted in immature dog teeth with apical periodontitis
(92). Similar to the challenge posed by the authors of that article (92),
it is not clear whether internally resorbed roots filled with bone/
cementum-like tissues are as strong as teeth with canal walls supported
by intact intraradicular tubular dentin. Although root fracture associated
with internal resorption had been reported (93), the absence of histologic
backup and the paucity of such reports preclude evidence-based conclu-
sions to be drawn regarding the correlation between teeth with histories of
root canal replacement resorption and their fracture resistance.
Differential Diagnosis
The manner in which internal root resorption presents clinically
depends, to a degree, on the nature and position of the lesion within
JOE — Volume 36, Number 7, July 2010
 Review Article

Figure 4. Light microscopy images of a case with internal (root canal) replacement resorption. The tooth was derived from a 44-year-old male patient who was
referred to the first author for management of a perforated root. The tooth was asymptomatic on examination, but there was a history of previous trauma. (a)
Radiograph of a maxillary central incisor with a radiolucent lesion in the mid-third of the root canal. The radiolucent lesion appears to be mottled, which is sugges-
tive of internal root resorption with metaplasia. (b) Radiograph of the tooth after extraction taken at 90-degree angle to the clinical radiograph showing the conti-
nuity of the resorptive lesion with the canal space. (c) Cross section taken approximately at the level of line 1 in (b). Low magnification overview shows that the
dentin around the root canal had been replaced by an ingrowth of bone tissue, and the root appears to have been perforated on the distopalatal aspect (H&E;
original magnification, !8). (d) Higher magnification of (c) (H&E; original magnification, !16). (e) High magnification of the area demarcated by the rectangle
in (d). The intraradicular dentin has been resorbed (H&E; original magnification, !100). (f) High magnification taken from the right part of (c) showing that the
resorbed dentin has been substituted by lamellar bone. Osteocytes are present in lacunae between the lamellae. A characteristic cross section of an osteon can be
seen on the right (open arrows), with concentric lamellae surrounding a vascular structure (H&E; original magnification, !100). (g) High magnification of the
area indicated by the left open arrow in (e). A multinucleated resorbing cell (odontoclast) can be seen in a dentinal lacuna, indicating active resorption of the
dentinal wall (H&E; original magnification, !1000). (h) High magnification view of the bone surface indicated by the right arrow in (e). The large cells are
osteoblast-like cells. Once they produced mineralized tissue, they were embedded in the bone lacunae, assuming the characteristics of osteocytes (H&E; original
magnification, !1000). (i) Cross section taken approximately at the level of line 2 in (b). The root canal was still large at this level and surrounded by a relatively
thin layer of newly formed bone (H&E; original magnification, !16). (j) Cross section taken approximately at the level of line 3 in (b). At this level the root canal
appears consistently narrowed by a dense layer of newly formed bone (H&E; original magnification, !16).

JOE — Volume 36, Number 7, July 2010 Internal Root Resorption 1113
Review Article
Figure 4. (continued).
the tooth. If the pulp is still partially vital, the patient might experience
symptoms of pulpitis. However, if the resorption is no longer active and
the entire pulp has become necrotic, the patient might eventually
develop symptoms of apical periodontitis. Sinus tracts might be detected
clinically, which might be indicative of root perforation or chronic
apical abscess. A pink discoloration might be visible through the crown
of the tooth as a result of internal root resorption in the coronal third of
the root canal. The pink spot is caused by granulation tissue undermin-
ing the necrotic area of coronal pulp. Traditionally, the pink spot of
Mummery has been thought to be pathognomonic of internal root
resorption. However, these pink spots are more commonly associated
with ECR (12). Thus, differential diagnosis of internal root resorption
cannot be based solely on the observation of pink spots. In many
instances, there are no clinical signs, and the teeth that exhibit internal
root resorption are asymptomatic. Given the varied manner in which
internal root resorption might present clinically, the diagnosis of the
condition is primarily based on radiographic examination, with supple-
mentary information gained from history and clinical findings (10).
The difficulty in distinguishing internal resorption from ECR has
been highlighted in the literature (7, 10, 94). The problem in
diagnosis occurs when the ECR lesion is not accessible by probing
and is projected radiologically over the root canal. Both lesions
might have a similar radiographic appearance (Fig. 6). Gartner et al
(95) described guidelines that enable clinicians to differentiate the 2
processes radiographically. The authors reported internal root resorp-
tion lesions to be smooth and generally symmetrically distributed over
the root. They described the radiolucency of the internal root resorption
as having a uniform density. The pulp chamber or root canal outline
could not be followed through the lesion, because the canal walls essen-
1114 Patel et al.
tially balloon out. Internal root resorption lesions might also be oval,
circumscribed radiolucencies in continuity with the canal walls (60).
Lesions caused by ECR, by contrast, have borders that are ill-defined
and asymmetrical, with radiodensity variations in the body of the lesion.
The canal wall should be traceable through the ECR lesion because the
latter is superimposed over the root canal (95–98).
The use of parallax radiographic techniques is advocated for differ-
entiating internal from external resorption defects (10, 94, 95). A
second radiograph taken at a different angle often confirms the nature
of the resorptive lesion. ECR lesions will move in the same direction
as the x-ray tube shift if they are lingually/palatally positioned. They
will move in the opposite direction to the tube shift if they are
buccally positioned. Conversely, internal root resorption lesions
should remain in the same position relative to the canal in both
radiographs (Fig. 7). Radiologically, internal (root canal) replacement
resorption presents as a cloudy, mottled, radiopaque lesion with irreg-
ular margins (Fig. 8) as a result of the presence of metaplastic hard
tissue deposits within the canal space. Differentiating internal (root
canal) replacement resorption from ECR might be clinically challenging,
especially if the metaplasia has occupied the entire resorptive cavity.
Diagnostic accuracy based on conventional and digital radio-
graphic examination is limited by the fact that the images produced
by these techniques only provide a 2-dimensional representation of
3-dimensional objects (94, 99, 100). In addition, the anatomic
structures being imaged might be distorted (101). This might lead to
misdiagnosis and incorrect treatment in the management of internal
root resorption and ECR.
The advent of cone beam computed tomography (CBCT) has
enhanced radiographic diagnosis (102, 103). The use of CBCT
JOE — Volume 36, Number 7, July 2010
 Review Article

Figure 5. Light microscopy images of a variant of internal (root canal) replacement resorption with tunneling resorption. Lower right lateral incisor was derived
from a 39-year-old former boxer who suffered from jaw fracture during a boxing match in his early twenties and was placed in intermaxillary fixation. The patient
developed symptoms 20 years later and complained of pain associated with his lower incisors. (a) Radiograph of the mandibular right incisors. Lower right central
incisor had asymptomatic apical periodontitis associated with a necrotic and infected pulp. Lower right lateral incisor showed a large area of internal root resorp-
tion. The tooth did not respond to sensitivity tests. (b) Sagittal CBCT slice shows some calcified tissue in the resorptive defect. (c) Cross section taken at the level of
line 1 in (a, b). Overview shows that the canal was apparently empty at this level (H&E; original magnification, !6). (d) High magnification of the area indicated by
the arrow in (c). Lamellar bone fills an area of previous resorption. Note the osteon structure (arrow) (H&E; original magnification, !100). (e) Cross section
taken at the level of line 2 in (a, b). Overview shows that the canal lumen was partly occupied by necrotic remnants, partly by bone-like tissue (H&E; original
magnification, !8). (f) High magnification of the lower part in (e) (H&E; original magnification, !50). (g) Higher magnification of (f). Bone trabeculae sur-
rounded by necrotic debris (H&E; original magnification, !100). (h) Cross section taken from the same area as that in (e) (TBB; original magnification, !16). (i)
High magnification of the area indicated by the arrow in (h). Fragment of bone-like tissue can be seen surrounded by bacteria-colonized necrotic tissues (TBB;
original magnification, !100. Inset; original magnification, !1000). (j) Longitudinal section passing approximately through the center of the root apex. Dentin
walls had been resorbed and substituted by a bone-like tissue (H&E; original magnification, !16).

JOE — Volume 36, Number 7, July 2010 Internal Root Resorption 1115
Review Article
Figure 6. (a) Clinical examination reveals that the mandibular left central
incisor tooth was discolored and nonresponsive to sensitivity testing. (b)
Two periapical radiographs taken at different horizontal angles confirm the
resorptive lesion is labially positioned by using the parallax principle; the
root canal outline is still visible through the lesion, indicating that the lesion
is ECR. (c, d) Sagittal and axial CBCT slices show that the lesion is actually
internal root resorption, which is located at the periphery of the root canal.
True nature of the resorptive lesion could only be assessed with CBCT. (Re-
printed with permission from Patel S. New dimensions in endodontic imaging:
part 2—cone beam computed tomography. Int Endod J 2009;42:463–75).
provides greater 3-dimensional geometric accuracy when compared
with conventional radiography (104). Several case reports and case
series have confirmed the usefulness of CBCT in diagnosing and
managing resorptive lesions (105, 106). Sensitivity and specificity,
which are defined as the number of true positive decisions/the
number of actually positive cases and the number of true negative
1116 Patel et al.
decisions/the number of actually negative cases, respectively, constitute
the basic measures of performance of diagnostic tests. The receiver
operating characteristic (ROC) curve, which is defined as a plot of test
sensitivity versus its specificity, is a well-accepted method of evaluating
the quality or performance of diagnostic tests. The area under an ROC
curve that has been fit by the conventional binormal model (Az) is widely
used as an index of diagnostic performance (107). Recently, Patel et al
(98) compared the accuracy of intraoral periapical radiography with
CBCT for the detection and management of root resorption lesions.
ROC Az values for correctly diagnosing internal root resorption with in-
traoral radiography were satisfactory (0.78). However, CBCT resulted in
a perfect diagnosis (Az 1.00). The authors concluded that the superior
accuracy of CBCT warrants reassessment of the use of conventional
radiographic techniques for assessing root resorption lesions.
The use of CBCT can be invaluable in the decision-making process.
The scanned data provide the clinician with a 3-dimensional apprecia-
tion of the tooth, the resorption lesion, and the adjacent anatomy. The
true nature of the lesion might be assessed, including root perforations
and whether the lesion is amendable to treatment (Figs. 7 and 8). In the
same study (98), the authors concluded that there was a significantly
higher prevalence in the choice of the correct treatment option when
CBCT was used compared with the use of intraoral radiographs for diag-
nosing resorptive lesions.
Treatment Perspectives
Once internal root resorption has been diagnosed, the clinician
must make a decision on the prognosis of the tooth. If the tooth is
deemed restorable and has a reasonable prognosis, root canal treatment
is the treatment of choice. The aim of root canal treatment is to remove
any remaining vital, apical tissue and the necrotic coronal portion of the
pulp that might be sustaining and stimulating the resorbing cells via their
blood supply, and to disinfect and obturate the root canal system (108).
Internal root resorption lesions present the endodontist with
unique difficulties in the preparation and obturation of the affected
tooth. Access cavity preparation should be conservative, preserving as
much tooth structure as possible, and should avoid further weakening
of the already compromised tooth. In teeth with actively resorbing
lesions, bleeding from the inflamed pulpal and granulation tissues
might be profuse and might impair visibility during the initial stages
of chemomechanical debridement. The shape of the resorption defect
usually renders it inaccessible to direct mechanical instrumentation.
Chemomechanical Debridement of the Root Canal
The principal cause of persistent apical periodontitis might be
attributed to microorganisms remaining within the canal after root canal
treatment (109–112). Root canals have complex morphology that
harbors bacteria. Despite advances in endodontic techniques,
instruments and irrigants fail to predictably access the restricted areas
of the canal space (113–116). The use of ultrasonic instruments to
agitate the irrigant has been shown to improve the removal of necrotic
debris and biofilms from inaccessible areas of the root canal (117).
Ultrasonic activation of irrigants after mechanical preparation of root
canals has been shown to reduce the number of bacteria. Given the inac-
cessibility of internal root resorption lesions to chemomechanical
debridement, ultrasonic activation of irrigants should be viewed as an
essential step in the disinfection of the internal resorption defect.
However, even with the use of ultrasonic instruments, bacteria might still
remain in confined areas (117). Chemomechanical debridement of
the root canal space fails to consistently render the root canal system
bacteria-free (118–122). Thus, an intracanal, antibacterial medica-
ment should be used to improve disinfection of the inaccessible root
JOE — Volume 36, Number 7, July 2010
 Review Article

Figure 7. (a, b) Parallax views of the maxillary left lateral incisor showing internal (root canal) resorption. A gutta-percha point has been used to track the sinus.
The reconstructed sagittal (c) and axial (d) slices from CBCT reveal that the lesion has extensively resorbed the palatal aspect of the root (arrows) and has nearly
perforated the root wall. (e) The tooth has been obturated with gutta-percha by using a thermoplasticized technique.
resorption defects (114). Calcium hydroxide is antibacterial and has adequately. To completely seal the resorptive defect, the obturation mate-
been shown to effectively eradicate bacteria that persist after chemome- rial should be flowable. Gutta-percha is the most commonly used filling
chanical instrumentation (123, 124). Calcium hydroxide has also been material in endodontics. Gencoglu et al (129) examined the quality of
shown to have a synergistic effect when used in conjunction with root fillings in teeth with artificially created internal resorptive cavities.
sodium hypochlorite to remove organic debris from the root canal They found that the Microseal (Sybron Endo, Orange, CA) and Obtura
(125, 126). Nevertheless, some case reports demonstrated the inability II (Spartan, Fenton, MO) thermoplastic gutta-percha techniques were
of calcium hydroxide to eliminate bacteria in ramifications because of significantly better in filling artificial resorptive cavities than Thermafil
its low solubility and inactivation by dentin, tissue fluids, and organic (Dentsply, York, PA), Soft-Core core systems (CMS Dental, Copenhagen,
matter (127, 128). Despite these limitations, the use of multiple Denmark), and cold lateral condensation (CLC). The CLC technique
calcium hydroxide dressings has been advocated to enhance produced slightly fewer voids than Obtura II, but a larger proportion
chemomechanical debridement of the internal root resorption defect. of the canal space was filled with sealer with this technique. Goldman
et al (130) also concluded that the Obtura II system performed statisti-
cally better in obturating resorptive defects than CLC, Thermafil, and
Obturation of the Root Canal a hybrid technique. Stamos and Stamos (131) reported 2 cases of internal
The primary objective of root canal treatment is to disinfect the root root resorption in which the Obtura II system was used to successfully
canal system. This is followed by obturation of the disinfected canal with obturate the canals. Similar conclusions were reached by others (132).
an appropriate root-filling material to prevent it from reinfection. By their In situations when the root wall has been perforated, mineral
very nature, internal root resorption defects can be difficult to obturate trioxide aggregate (MTA) should be considered the material of choice

JOE — Volume 36, Number 7, July 2010 Internal Root Resorption 1117
Review Article
Figure 8. (a, b) Radiographs reveal internal (root canal) replacement resorption of maxillary left central incisor; note the lesion remains centered with second
parallax view. (c) CBCT-reconstructed coronal (left) and axial (right) views of the tooth indicate that calcified tissue was present in the coronal part of the defect.
(d) The tooth was obturated with gutta-percha by using a thermoplasticized technique; note the irregular borders and varying radiodensity of the root filling asso-
ciated within the internal root resorption lesion. (e) 2-year review radiograph.
to seal the perforation. MTA is biocompatible (133) and has been
shown to be effective in repairing furcation perforations (134) and
lateral root perforations (135). The material is well-tolerated by peri-
radicular tissues and has been shown to support almost complete
regeneration of the periodontium (134). In addition, MTA has superior
sealing properties when compared with other materials (136). A hybrid
technique might also be used to obturate canals; the canal apical to the
resorption defect is obturated with gutta-percha, and then the resorp-
tion defect and associated perforation are sealed with MTA (137,
138). When internal resorption has rendered the tooth untreatable
or unrestorable, extraction is the only treatment option.
Concluding Remarks and Future Directions
To date, root canal treatment remains the only treatment of choice
with teeth diagnosed with internal root resorption. Because the resorp-
tive defect is the result of an inflamed pulp and the clastic precursor cells
are predominantly recruited through the blood vessels, controlling the
process of internal root resorption is conceptually easy, via severing
the blood supply to the resorbing tissues with conventional root canal
therapy. With that said, early detection and a correct differential diag-
nosis are essential for successful management of the outcome of internal
resorption to prevent overweakening of the remaining root structures
and root perforations. The advent of CBCT no doubt has improved the
clinician’s diagnostic capability for internal root resorption. Neverthe-
1118 Patel et al.
less, internal root resorption is often asymptomatic, and painful symp-
toms do not appear until an advanced stage of the lesion. Thus, the
clinician’s ability to detect this pathologic entity must rely heavily on
the use of radiographs in routine oral examinations. Although the advent
of CBCT provides an important adjunctive diagnostic tool for differenti-
ating between internal root resorption and ECR, it does not break new
ground from a treatment perspective. Irrespective of whether the lesion
is manifested histologically as the inflammatory or the replacement form
of the disease, the ultimate treatment of choice for those prognostically
favorable teeth is still nonsurgical root canal therapy.
Although this pathologic condition has been reported for more
than a century, our knowledge on the pathogenesis of this disease is,
unfortunately, surprisingly thin. The majority of the documentation
that existed in the literature is in the form of case reports, and there
are only a limited number of studies that examined the histologic mani-
festations and biologic aspects of the disease. In particular, the patho-
genesis aspects of this disease still contain a high degree of uncertainty,
with much of the information adapted from our understanding of
external root resorption. This might be due, in part, to the relatively
rare occurrence of this type of resorption and the lack of an in vivo
model, apart from the previous attempt on the use of diathermy, to
predictably reproduce the condition for study.
From a histologic perspective, it appears that the disease might be
manifested as one form that is purely destructive, caused by inflamma-
tion and elaborative clastic functions, and another form that is
JOE — Volume 36, Number 7, July 2010

accompanied by repair, albeit a ‘‘frustrated repair,’’ as a result of the
deposition of metaplastic bone/cementum-like tissues instead of true
dentin. In the general scheme of things, the reparative form of the
disease exhibits histologic manifestations that are not so much different
to the manifestation of similar frustrated repairs in reparative dentino-
genesis (eg, direct pulp capping; Ricucci et al, unpublished results,
2009) and revascularization of nonvital dental pulps (92). There
remains a wide gap of knowledge in our understanding of the condi-
tions that precipitate the 2 different forms of internal root resorption.
For example, it is not known whether one can alter the inflammatory
and microbial status of the involved pulp to shift the manifestation of
the disease from a purely destructive form to one that is accompanied
by at least some form of repair. Such a notion might sound philosoph-
ical to the practicing clinician. However, it might have an outreaching
appeal to the molecular biologists and stem cell scientists within our
profession in their quest for controlling the commitment of progenitor
cell types capable of recapitulating the embryonic events in primary
odontogenesis as a future endodontic treatment strategy.
As the concept of pulpal regeneration becomes a foreseeable
reality, it is prudent to elaborate on whether such a treatment strategy
might be adaptable for the management of teeth with internal root
resorption. There are similarities and differences between the currently
achievable status of pulpal revascularization and the replacement form
of internal root resorption. The similarities are evident in the manifes-
tations of frustrated repair by metaplastic hard tissues after the senes-
cence of primary odontoblasts. The dental pulp is equipped with the
potential of regenerating odontoblast-like cells from dental pulpal
stem cells through limited molecular signaling mechanisms after suc-
cumbing of ectomesenchymal crosstalks that occur during primary
dentinogenesis. Scientists are beginning to grasp the fundamentals of
these intricate signaling mechanisms; however, control is still lacking
in the ability to precisely delineate the odontoblastic lineage from the
osteoblastic lineage. Nevertheless, the advances achieved so far have
been phenomenal. After all, the creativity of evolution in which nature
explores all options and produces the best solution has taken millions
of years to bring to perfection. On the contrary, gene and stem cell ther-
apies have only been proactive for more than 2 decades. Unlike pulpal
revascularization procedures, however, the onset of internal root
resorption is hallmarked by the recruitment of clastic precursors, their
activation, and subsequent attachment to osteopontin-rich mineralized
matrices. Thus, even if precise controls of signaling mechanisms for the
differentiation of odontoblasts from their progenitor cells are available,
additional strategies must be targeted at pacifying the activities of clastic
cells at 1 of the 3 aforementioned stages (ie, recruitment, activation, and
attachment). Although these tasks might appear formidable, it is at the
molecular signaling level that one anticipates the greatest expansion of
horizons. Advances in different scientific disciplines will enrich the pool
of ideas for future therapeutic strategies, apart from conventional root
canal therapy, in the treatment of internal root resorption. The scope of
deepening this pool is tremendous.
Acknowledgments
The authors wish to thank Cavendish Imaging, London, UK,
and the Department of Dental & Maxillofacial Imaging, The Dental
Institute, Kings’ College London, London.
References
1. Patel S, Pitt Ford TR. Is the resorption external or internal? Dent Update 2007;34:
218–29.
2. Bille ML, Nolting D, Kvetny MJ, Kjaer I. Unexpected early apical resorption of
primary molars and canines. Eur Arch Paediatr Dent 2007;8:144–9.
JOE — Volume 36, Number 7, July 2010
Review Article
3. Bille ML, Kvetny MJ, Kjaer I. A possible association between early apical resorption
of primary teeth and ectodermal characteristics of the permanent dentition. Eur J
Orthod 2008;30:346–51.
4. Harokopakis-Hajishengallis E. Physiologic root resorption in primary teeth:
molecular and histological events. J Oral Sci 2007;49:1–12.
5. Yildirim S, Yapar M, Sermet U, Sener K, Kubar A. The role of dental pulp cells in
resorption of deciduous teeth. Oral Surg Oral Med Oral Pathol Oral Radiol Endod
2008;105:113–20.
6. Andreasen JO. Review of root resorption systems and models: biology of root
resorption and the homeostatic mechanisms of the periodontal ligament. In:
Davidovitch Z, ed. Proceedings of the International Conference on the Biological
Mechanisms of Tooth Eruption and Root Resorption. Birmingham, UK: Ebsco
Media; 1988:9–21.
7. Tronstad L. Root resorption: etiology, terminology and clinical manifestations. En-
dod Dent Traumatol 1988;4:241–52.
8. Bell T. The anatomy, physiology, and disease of the teeth. Philadelphia, PA: Carey
and Lee Publishing; 1830. 171–2.
9. Levin L, Trope M. Root resorption. In: Hargreaves KM, Goodis HE, eds. Seltzer and
Bender’s dental pulp. Chicago, IL: Quintessence Publishing Co Inc; 2002:425–48.
10. Gulabivala K, Searson LJ. Clinical diagnosis of internal resorption: an exception to
the rule. Int Endod J 1995;28:255–60.
11. Haapasalo M, Endal U. Internal inflammatory root resorption: the unknown
resorption of the tooth. Endod Topics 2006;14:60–79.
12. Patel S, Kanagasingham S, Pitt Ford T. External cervical resorption: a review. J En-
dod 2009;35:616–25.
13. Frank AL. External-internal progressive resorption and its nonsurgical correction.
J Endod 1981;7:473–6.
14. Lyroudia KM, Dourou VI, Pantelidou OC, Labrianidis T, Pitas IK. Internal root resorp-
tion studied by radiography, stereomicroscope, scanning electron microscope and
computerized 3D reconstructive method. Dent Traumatol 2002;18:148–52.
15. Goultschn J, Nitzan D, Azaz B. Root resorption: review and discussion. Oral Surg
Oral Med Oral Pathol 1982;54:586–91.
16. Çalisxkan MK, Türkün M. Prognosis of permanent teeth with internal resorption:
a clinical review. Endod Dent Traumatol 1997;13:75–81.
17. Andreasen JO, Andreasen FM. Root resorption following traumatic dental injuries.
Proc Finn Dent Soc 1992;88(Suppl 1):95–114.
18. Andreasen JO. Luxation of permanent teeth due to trauma: a clinical and radio-
graphic follow up study of 189 injured teeth. Scand J Dent Res 1970;19:273–86.
19. Ahlberg K, Bystedt H, Eliasson S, Odenrick L. Long term evaluation of autotrans-
planted maxillary canines with completed root formation. Acta Odontol Scand
1983;41:23–31.
20. Cabrini R, Maisto O, Manfredi E. Internal resorption of dentine: histopathologic
control of eight cases after pulp amputation and capping with calcium hydroxide.
Oral Surg Oral Med Oral Pathol 1957;10:90–6.
21. Vier FV, Figueiredo JA. Internal apical resorption and its correlation with the type
of apical lesion. Int Endod J 2004;37:730–7.
22. Malueg LA, Wilcox LR, Johnson W. Examination of external apical root resorption
with scanning electron microscopy. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod 1996;82:89–93.
23. Laux M, Abbott PV, Pajarola G, Nair PN. Apical inflammatory root resorption:
a correlative radiographic and histological assessment. Int Endod J 2000;33:
483–93.
24. Udagawa N, Takahashi N, Akatsu T, et al. Origin of osteoclasts: mature monocytes
and macrophages are capable of differentiating into osteoclasts under a suitable
microenvironment prepared by bone marrow-derived stromal cells. Proc Natl
Acad Sci U S A 1990;87:7260–4.
25. McHugh KP, Shen Z, Crotti TN, et al. Role of cell-matrix interactions in osteoclast
differentiation. Adv Exp Med Biol 2007;602:107–11.
26. Soltanoff CS, Yang S, Chen W, Li YP. Signaling networks that control the lineage
commitment and differentiation of bone cells. Crit Rev Eukaryot Gene Expr
2009;19:1–46.
27. Takahashi N, Ejiri S, Yanagisawa S, Ozawa H. Regulation of osteoclast polarization.
Odontology 2007;95:1–9.
28. Saltel F, Chabadel A, Bonnelye E, Jurdic P. Actin cytoskeletal organisation in oste-
oclasts: a model to decipher transmigration and matrix degradation. Eur J Cell Biol
2008;87:459–68.
29. Pierce AM. Experimental basis for the management of dental resorption. Endod
Dent Traumatol 1989;5:255–65.
30. Silver IA, Murrills RJ, Etherington DJ. Microelectrode studies on the acid micro-
environment beneath adherent macrophages and osteoclasts. Exp Cell Res
1988;175:66–76.
31. Furseth R. The resorption process of human teeth studied by light microscopy,
microradiography and electron microscopy. Arch Oral Biol 1968;12:417–31.
32. Lindskog S, Blomlöf L, Hammarström L. Repair of periodontal tissues in vivo and
vitro. J Clin Periodontol 1983;10:188–205.
Internal Root Resorption 1119
Review Article
33. Nilsen R, Magnusson BC. Enzyme histochemistry of induced heterotopic bone
formation in guinea pigs. Arch Oral Biol 1979;24:833–41.
34. Speziani C, Rivollier A, Gallois A, et al. Murine dendritic cell transdifferentiation
into osteoclasts is differentially regulated by innate and adaptive cytokines. Eur J
Immunol 2007;37:747–57.
35. Gallois A, Lachuer J, Yvert G, et al. Genome-wide expression analyses establish
dendritic cells as a new osteoclast precursor able to generate bone-resorbing cells
more efficiently than monocytes. J Bone Miner Res 2009 [Epub ahead of print]
doi: 10.1359/jbmr.090829.
36. Boyce BF, Xing L. Functions of RANKL/RANK/OPG in bone modeling and remodel-
ing. Arch Biochem Biophys 2008;473:139–46.
37. Tyrovola JB, Spyropoulos MN, Makou M, Perrea D. Root resorption and the OPG/
RANKL/RANK system: a mini review. J Oral Sci 2008;50:367–76.
38. Wada N, Maeda H, Tanabe K, et al. Periodontal ligament cells secrete the factor that
inhibits osteoclastic differentiation and function: the factor is osteoprotegerin/os-
teoclastogenesis inhibitory factor. J Periodontal Res 2001;36:56–63.
39. Uchiyama M, Nakamichi Y, Nakamura M, et al. Dental pulp and periodontal liga-
ment cells support osteoclastic differentiation. J Dent Res 2009;88:609–14.
40. Trope M. Root resorption of dental and traumatic origin: classification based on
etiology. Pract Periodontics Aesthet Dent 1998;10:515–22.
41. Wedenberg C. Evidence for a dentin-derived inhibitor of macrophage spreading.
Scand J Dent Res 1987;95:381–8.
42. Wedenberg C, Lindskog S. Evidence for a resorption inhibitor in dentine. Eur J Oral
Sci 1987;95:205–11.
43. Schaffner P, Dard MM. Structure and function of RGD peptides involved in bone
biology. Cell Mol Life Sci 2003;60:119–32.
44. Nakamura I, Duong le T, Rodan SB, Rodan GA. Involvement of alpha(v)beta3 in-
tegrins in osteoclast function. J Bone Miner Metab 2007;25:337–44.
45. Ishijima M, Rittling SR, Yamashita T, et al. Enhancement of osteoclastic bone
resorption and suppression of osteoblastic bone formation in response to reduced
mechanical stress do not occur in the absence of osteopontin. J Exp Med 2001;
193:399–404.
46. Chung CJ, Soma K, Rittling SR, et al. OPN deficiency suppresses appearance of
odontoclastic cells and resorption of the tooth root induced by experimental force
application. J Cell Physiol 2008;214:614–20.
47. Wedenberg C, Lindskog S. Experimental internal resorption in monkey teeth. En-
dod Dent Traumatol 1985;1:221–7.
48. Rabinowitch BZ. Internal resorption. Oral Surg Oral Med Oral Pathol 1972;33:
2643–82.
49. Penido RS, Carrel R, Chialastri AJ. The anachoretic effect in root resorption: report
of case. ASDC J Dent Child 1980;47:53–5.
50. Ashrafi MH, Sadeghi EM. Idiopathic multiple internal resorption: report of case.
ASDC J Dent Child 1980;47:196–9.
51. Mandor RB. A tooth with internal resorption treated with a hydrophylic plastic
material: a case report. J Endod 1981;7:430–2.
52. Brady J, Lewis DH. Internal resorption complicating orthodontic tooth movement.
Br J Orthod 1983;11:155–7.
53. Walton RE, Leonard LA. Cracked tooth: an etiology for ‘idiopathic’ internal resorp-
tion? J Endod 1986;12:167–9.
54. Brooks JK. An unusual case of idiopathic internal root resorption beginning in an
unerupted permanent tooth. J Endod 1986;12:309–10.
55. Silveira FF, Nunes E, Soares JA, Ferreira CL, Rotstein I. Double ‘pink tooth’ asso-
ciated with extensive internal root resorption after orthodontic treatment: a case
report. Dent Traumatol 2009;25:e43–7.
56. Wedenberg C, Zetterqvist L. Internal resorption in human teeth: a histological,
scanning electron microscopic and enzyme histochemical study. J Endod 1987;
6:255–9.
57. Ricucci D. Apical limit of root canal instrumentation and obturation: part I—liter-
ature review. Int Endod J 1998;31:384–93.
58. Cvek M. Endodontic treatment of traumatized teeth. In: Andreasen JO, ed. Trau-
matic injuries of the teeth. Copenhagen: Munskaard Publishers; 1981:321–83.
59. Cvek M, Cleaton-Jones P, Austin J, Lownie J, Kling M, Fatti P. Effect of topical appli-
cation of doxycycline on pulp revascularization and periodontal healing in reim-
planted monkey incisors. Endod Dent Traumatol 1990;6:170–6.
60. Ne RF, Witherspoon DE, Gutmann JL. Tooth resorption. Quintessence Int 1999;30:
9–25.
61. Heithersay GS. Management of tooth resorption. Aust Dent J 2007;52:S105–21.
62. Frank AL, Weine FS. Nonsurgical therapy for the perforative defect of internal
resorption. J Am Dent Assoc 1973;87:863–8.
63. Mummery JH. The pathology of pink spots on teeth. Br Dent J 1920;41:301–11.
64. Masterton JB. Internal resorption of the dentine: a complication arising from
unhealed pulp wounds. Br Dent J 1965;118:241–9.
65. Heino TJ, Hentunen TA, Väänänen HK. Osteocytes inhibit osteoclastic bone resorp-
tion through transforming growth factor-beta: enhancement by estrogen. J Cell Bi-
ochem 2002;85:185–97.
1120 Patel et al.
66. Gu G, Mulari M, Peng Z, Hentunen TA, Väänänen HK. Death of osteocytes turns off
the inhibition of osteoclasts and triggers local bone resorption. Biochem Biophys
Res Commun 2005;335:1095–101.
67. Cardoso L, Herman BC, Verborgt O, Laudier D, Majeska RJ, Schaffler MB. Osteo-
cyte apoptosis controls activation of intracortical resorption in response to bone
fatigue. J Bone Miner Res 2009;24:597–605.
68. Franquin JC, Remusat M, Abou Hashieh I, Dejou J. Immunocytochemical detection
of apoptosis in human odontoblasts. Eur J Oral Sci 1998;106(Suppl 1):384–7.
69. Bronckers AL, Goei SW, Dumont E, et al. In situ detection of apoptosis in dental
and periodontal tissues of the adult mouse using annexin-V-biotin. Histochem
Cell Biol 2000;113:293–301.
70. Kitamura C, Ogawa Y, Morotomi T, Terashita M. Differential induction of apoptosis
by capping agents during pulp wound healing. J Endod 2003;29:41–3.
71. Mitsiadis TA, De Bari C, About I. Apoptosis in developmental and repair-related
human tooth remodeling: a view from the inside. Exp Cell Res 2008;314:869–77.
72. Oehlers FAC. A case of internal resorption following injury. Br Dent J 1951;90:
13–6.
73. Cotran RS, Kumar V, Collins T. Robbins: pathologic basis of disease. 6th ed. Phil-
adelphia, PA: WB Saunders; 1999. 36–7.
74. Andreasen FM, Andreasen JO. Resorption and mineralization processes following
root fracture of permanent incisors. Endod Dent Traumatol 1988;4:202–14.
75. Gronthos S, Brahim J, Li W, et al. Stem cell properties of human dental pulp stem
cells. J Dent Res 2002;81:531–5.
76. Huang GT, Gronthos S, Shi S. Mesenchymal stem cells derived from dental tissues
vs. those from other sources: their biology and role in regenerative medicine. J
Dent Res 2009;88:792–806.
77. Smith AJ, Patel M, Graham L, Sloan AJ, Cooper PR. Dentine regeneration: key roles
for stem cells and molecular signalling. Oral Biosci Med 2005;2:127–32.
78. Goldberg M, Six N, Decup F, et al. Application of bioactive molecules in pulp-
capping situations. Adv Dent Res 2001;15:91–5.
79. Aguiar MC, Arana-Chavez VE. Ultrastructural and immunocytochemical analyses of
osteopontin in reactionary and reparative dentine formed after extrusion of upper
rat incisors. J Anat 2007;210:418–27.
80. Hwang YC, Hwang IN, Oh WM, Park JC, Lee DS, Son HH. Influence of TGF-beta1 on
the expression of BSP, DSP, TGF-beta1 receptor I and Smad proteins during repar-
ative dentinogenesis. J Mol Histol 2008;39:153–60.
81. Kapadia H, Mues G, D’Souza R. Genes affecting tooth morphogenesis. Orthod Cra-
niofac Res 2007;10:237–44.
82. Mitsiadis TA, Graf D. Cell fate determination during tooth development and regen-
eration. Birth Defects Res C Embryo Today 2009;87:199–211.
83. James MJ, Järvinen E, Wang XP, Thesleff I. Different roles of Runx2 during early
neural crest-derived bone and tooth development. J Bone Miner Res 2006;21:
1034–44.
84. Chen S, Gluhak-Heinrich J, Wang YH, et al. Runx2, osx, and dspp in tooth devel-
opment. J Dent Res 2009;88:904–9.
85. Yang X, van der Kraan PM, Bian Z, Fan M, Walboomers XF, Jansen JA. Mineralized
tissue formation by BMP2-transfected pulp stem cells. J Dent Res 2009;88:
1020–5.
86. Stanley HR. Diseases of the dental pulp. In: Tieck RW, ed. Oral pathology. New
York: McGraw Hill; 1965.
87. Nygaard-Østby B. The role of the blood clot in endodontic therapy: an experi-
mental histologic study. Acta Odont Scand 1961;19:323–53.
88. Nygaard-Østby B, Hjortdal O. Tissue formation in the root canal following pulp
removal. Scand J Dent Res 1971;79:333–49.
89. Hørsted P, Nygaard-Østby B. Tissue formation in the root canal after total pulpec-
tomy and partial root filling. Oral Surg Oral Med Oral Pathol 1978;46:275–82.
90. Cvek M, Cleaton-Jones P, Austin J, Lownie J, Kling M, Fatti P. Pulp revascularization
in reimplanted immature monkey incisors - predictability and the effect of antibi-
otic systemic prophylaxis. Endod Dent Traumatol 1990;6:157–69.
91. Thibodeau B, Teixeira F, Yamauchi M, Caplan DJ, Trope M. Pulp revascularization
of immature dog teeth with apical periodontitis. J Endod 2007;33:680–9.
92. Wang X, Thibodeau B, Trope M, Lin LM, Huang GT. Histologic characterization
of regenerated tissues in canal space after the revitalization/revascularization
procedure of immature dog teeth with apical periodontitis. J Endod 2010;36:
56–63.
93. Anil S, Raji MA, Beena VT, Vijayakumar T. Fracture of tooth by internal resorption:
case report. Endod Dent Traumatol 1993;9:79–80.
94. Patel S, Dawood A, Whaites E, Pitt Ford T. The potential applications of cone beam
computed tomography in the management of endodontic problems. Int Endod J
2007;40:818–30.
95. Gartner AH, Mark T, Somerlott RG, Walsh LC. Differential diagnosis of internal and
external cervical resorption. J Endod 1976;2:329–34.
96. Heithersay GS. Clinical, radiographic, and histopathologic features of invasive
cervical resorption. Quintessence Int 1999;30:27–37.
97. Heithersay GS. Invasive cervical resorption. Endod Topics 2004;7:73–92.
JOE — Volume 36, Number 7, July 2010

98. Patel S, Dawood A, Wilson R, Horner K, Mannocci F. The detection and manage-
ment of root resorption lesions using intraoral radiography and cone beam
computed tomography: an in vivo investigation. Int Endod J 2009;42:831–8.
99. Estrela C, Bueno MR, Leles CR, Azevedo B, Azevedo JR. Accuracy of cone beam
computed tomography and panoramic radiography for the detection of apical pe-
riodontitis. J Endod 2008;34:273–9.
100. Patel S, Dawood A, Whaites E, Pitt Ford T. New dimensions in endodontic imaging:
part 1—conventional and alternative radiographic systems. Int Endod J 2009;42:
447–62.
101. Gröndahl H-G, Hummonen S. Radiographic manifestations of periapical inflamma-
tory lesions. Endod Topics 2004;8:55–67.
102. Tyndall DA, Rathore S. Cone-beam CT diagnostic applications: caries, periodontal
bone assessment, and endodontic applications. Dent Clin North Am 2008;52:
825–41.
103. Dawood A, Patel S, Brown J. Cone beam CT in dental practice. Br Dent J 2009;207:
23–8.
104. Murmalla R, Wortche R, Muhling J, Hassfeld S. Geometric accuracy of the NewTom
9000 Cone Beam CT. Dentomaxillofac Radiol 2005;34:28–31.
105. Cohenca N, Simon JH, Marhtur A, Malfaz JM. Clinical indications for digital imaging
in dento-alveolar trauma: part 2—root resorption. Dent Traumatol 2007;23:
105–13.
106. Cotton TP, Geisler TM, Holden DT, Schwartz SA, Schindler WG. Endodontic appli-
cations of CBVT. J Endod 2007;9:1121–32.
107. Gatsonis CA. Receiver operating characteristic analysis for the evaluation of diag-
nosis and prediction. Radiology 2009;253:593–6.
108. European Society of Endodontology. Quality guidelines for endodontic treatment:
consensus report of the European Society of Endodontology. Int Endod J 2006;39:
921–30.
109. Lin LM, Pascon EA, Skribner J, Gangler P, Langeland K. Clinical radiographic, and
histologic study of endodontic treatment failures. Oral Surg Oral Med Oral Pathol
Oral Radiol Endod 1991;71:603–11.
110. Siqueira JF Jr. Aetiology of root canal treatment failure: why well treated teeth can
fail. Int Endod J 2001;39:249–81.
111. Fabricius L, Dahlén G, Sundqvist G, Happonen RP, Möller AJR. Influence of
residual bacteria on periapical tissue healing after chemomechanical treatment
and root filling of experimentally infected monkey teeth. Eur J Oral Sci 2006;
114:278–85.
112. Nair PNR, Henry S, Cano V, Vera J. Microbial status of apical root canal system of
human mandibular first molars with primary apical periodontitis after ‘one-visit’
endodontic treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;
99:231–52.
113. Ricucci D, Langeland K. Apical limit of root canal instrumentation and obturation:
part 2—a histological study. Int Endod J 1998;31:394–409.
114. Siqueira JF, Rôças IN, Santos SRLD, Lima KC, Magalhaes FAC, de Uzeda M. Efficacy
of instrumentation techniques and irrigation regimens in reducing the bacterial
population within root canals. J Endod 2002;3:181–4.
115. Nair PNR. On the causes of persistent apical periodontitis: a review. Int Endod J
2006;39:249–81.
116. Ricucci D, Siqueira JF Jr, Bate AL, Pitt Ford TR. Histologic investigation of root
canal-treated teeth with apical periodontitis: a retrospective study from 24 patients.
J Endod 2009;35:493–502.
117. Burleson A, Nusstein J, Reader A, Beck M. The in vivo evaluation of hand/rotary/
ultrasound instrumentation in necrotic, human mandibular molars. J Endod 2007;
33:782–7.
JOE — Volume 36, Number 7, July 2010
Review Article
118. Byström A, Sundqvist G. Bacteriologic evaluation of the efficacy of mechanical root
canal instrumentation in endodontic therapy. Scand J Dent Res 1981;89:321–8.
119. Byström A, Sundqvist G. Bacteriologic evaluation of the effect of 0.5 per cent
sodium hypochlorite. Oral Surg Oral Med Oral Pathol 1983;55:307–12.
120. Sjgören U, Figdor D, Sundqvist G. Influence of infection at the time of root filling on
the outcome of endodontic treatment of teeth with apical periodontitis. Int Endod J
1997;30:297–306.
121. McGurkin-Smith R, Trope M, Caplan D, Sigurdsson A. Reduction of intracanal
bacteria using GT rotary instrumentation, 5.25% NaOCl, EDTA and Ca(OH)2. J En-
dod 2005;31:359–63.
122. Siqueira JF Jr, Guimarães-Pinto T, Rôças IN. Effects of chemomechanical prepara-
tion with 2.5% sodium hypochlorite and intracanal medication with calcium
hydroxide on cultivable bacteria in infected root canals. J Endod 2007;33:800–5.
123. Byström A, Claesson R, Sundqvist G. The antibacterial effect of camphorated para-
monochlorophenol, camphorated phenol and calcium hydroxide in the treatment
of infected root canals. Endod Dent Traumatol 1985;1:170–5.
124. Sjgören U, Figdor D, Spångberg L, Sundqvist G. The antimicrobial effect of calcium
hydroxide as a short-term intracanal dressing. Int Endod J 1991;24:119–25.
125. Anderson M, Lund A, Andreasen JO, Andreasen FM. In vitro solubility of human
pulp tissue in calcium hydroxide and sodium hypochlorite. Endod Dent Traumatol
1992;1:170–5.
126. Türkün M, Cengiz T. The effects of sodium hypochlorite and calcium hydroxide on
tissue dissolution and root canal cleanliness. Int Endod J 1997;30:335–42.
127. Ricucci D, Siqueira JF Jr. Apical actinomycosis as a continuum of intraradicular
and extraradicular infection: case report and critical review on its involvement
with treatment failure. J Endod 2008;34:1124–9.
128. Ricucci D, Siqueira JF Jr. Anatomical and microbiological challenges to achieving
success with endodontic treatment: a case report. J Endod 2008;34:1249–54.
129. Gencoglu N, Yildrim T, Garip Y, Karagenc B, Yilmaz H. Effectiveness of different
gutta-percha techniques when filling experimental internal resorptive cavities.
Int Endod J 2008;41:836–42.
130. Goldman F, Massone EJ, Esmoris M, Alfie D. Comparison of different techniques
for obturating experimental internal resorptive cavities. Endod Dent Traumatol
2000;16:116–21.
131. Stamos DE, Stamos DG. A new treatment modality for internal resorption. J Endod
1986;12:315–9.
132. Wilson PR, Barnes IE. Treatment of internal root resorption with thermoplasticized
gutta-percha: a case report. Int Endod J 1987;20:94–7.
133. Torabinejad M, Hong CU, Pitt Ford TR, Kariyawasam SP. Tissue reaction to im-
planted Super EBA and Mineral Trioxide Aggregate in the mandible of guinea
pigs: a preliminary. J Endod 1995;21:569–71.
134. Regan JD, Gutmann JL, Witherspoon DE. Comparison of Diaket and MTA when
used as root-end filling materials to support regeneration of the periradicular
tissues. Int Endod J 2002;35:840–7.
135. Main C, Mirzayan N, Shabahang S, Torabinejad M. Repair of root perforations
using mineral trioxide aggregate: a long term study. J Endod 2004;30:80–3.
136. Jacobovitz M, Vianna ME, Pandolfelli VC, Oliveira IR, Rossetto HL, Gomes BP. Root
canal filling with cements based on mineral aggregates: an in vitro analysis of
bacterial microleakage. Oral Surg Oral Med Oral Pathol Oral Radiol Endod
2009;108:140–4.
137. Hsien H-C, Cheng Y-A, Lee Y-L, Lan W-H, Lin C- P. Repair of perforating internal
resorption with mineral trioxide aggregate: a case report. J Endod 2003;29:538–9.
138. Jacobowitz M, de Lima RK. Treatment of inflammatory internal root resorption with
mineral trioxide aggregate: a case report. Int Endod J 2008;41:905–12.
Internal Root Resorption 1121