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REVIEW
External cervical resorption-part 1: histopathology,distribution and presentation
S. Patel1,2 , A. M. Mavridou3, P. Lambrechts3 & N. Saberi1
1Department of Endodontology, King’s College London Dental Institute, London; 2Specialist Practice, London, UK; and3Department of Oral Health Services, University of Leuven, Leuven, Belgium
Abstract
Patel S, Mavridou AM, Lambrechts P, Saberi N.
External cervical resorption-part 1: histopathology, distribution
and presentation. International Endodontic Journal, 51, 1205–
1223, 2018.
External cervical resorption (ECR) is the loss of dental
hard tissue as a result of odontoclastic action. It is a
dynamic process that involves periodontal, dental and
in later stages pulpal tissues. Over the last two dec-
ades, ECR has attracted increased interest; this is in
part due to novel micro-CT and histopathological
techniques for its assessment and also improved radio-
graphic detection using CBCT. This literature review
will cover the aetiology, potential predisposing factors,
histopathology and diagnosis of ECR. Part 2 will
cover the management of ECR.
Keywords: cone beam computed tomography,
external cervical resorption, histology, nano-CT.
Received 9 March 2018; accepted 22 April 2018
Introduction
Root resorption is the loss of dental hard tissue (i.e.
cementum, dentine and/or enamel) as a result of
odontoclastic action (Patel et al. 2009a). Root resorp-
tion is desirable in primary teeth (physiological root
resorption) as it facilitates their exfoliation, and subse-
quent eruption of the underlying permanent successor
tooth. Root resorption in adult teeth is undesirable as
it leads to irreversible damage, which may necessitate
dental treatment, or even extraction.
Root resorption may be simply classified by its loca-
tion on the root surface as external or internal resorption.
External root resorption may be further subclassified
into surface resorption, external inflammatory resorp-
tion, external cervical resorption, external replacement
resorption and transient apical resorption (Patel & Pitt
Ford 2007, Patel & Saberi 2018). External cervical
resorption (ECR) usually manifests in the cervical aspect
of teeth; it develops as a result of damage to, and/or defi-
ciency of the periodontal ligament (PDL) (Andreasen &
Andreasen 2007) and the subepithelial cementum.
External cervical resorption (ECR) is a dynamic pro-
cess that involves periodontal, dental and in later
stages pulpal tissues (Luso & Luder 2012, Mavridou
et al. 2016a) and has attracted increased interest in
the last two decades (Th€onen et al. 2013, Mavridou
et al. 2017a). This is due to a combination of
improved radiographic detection with CBCT (Patel
et al. 2007, 2009b, Durack et al. 2011), and novel
micro-CT and histopathological assessment of ECR
(Mavridou et al. 2016a,b, 2017b).
An electronic literature search was carried out and
included the databases Medline (Ovid), PubMed and
Embase. The cut-off date was set to October 2017.
However, complementary searches were also carried
out in November and December 2017. The searches
used controlled vocabulary and free-text terms. These
included the terms ‘root resorption’, ‘tooth resorption’,
‘external cervical resorption’, ‘invasive cervical resorp-
tion’, ‘peripheral cervical resorption’, ‘extracanal invasive
resorption’, ‘odontoclastoma’, ‘peripheral inflammatory
Correspondence: Shanon Patel, Department of Endodontol-
ogy, King’s College Dental Institute, Floor 25 – Tower Wing,
Guy’s Hospital, London SE1 9RT, UK (e-mail: shanonpatel@
gmail.com).
International Endodontic Journal, 51, 1205–1223, 2018© 2018 International Endodontic Journal. Published by John Wiley & Sons Ltd
doi:10.1111/iej.12942
1205
root resorption’, ‘supraosseous extracanal invasive resorp-
tion’, ‘idiopathic external resorption’ and ‘ECR’. In addi-
tion to database searches, the ‘early view’ and
prepublication online sections of major international
journals were also individually checked.
The articles were reviewed independently by two
evaluators (NS and SP) for their relevance in terms of
overall scientific evidence for ECR. In addition, the ref-
erence lists of these articles were reviewed to identify
any relevant studies that had not been identified via
previous electronic or hand searches. Overall, 147
articles were assessed.
The review of literature revealed the lack of original
basic scientific research papers on the subject of ECR.
Whilst there are many published articles on the topic,
the majority of these are case reports, case series,
treatment demonstrations or narratives (Table 1),
which lack adequate scientific quality as described by
Centre for Evidence-based Medicine (CEBM) and their
hierarchical system. Although it has been generally
recognized that the best clinical and scientific evi-
dence is a combination and amalgamation of clini-
cally relevant research and individual clinical
expertise (Sackett et al. 1996), in the case of ECR, the
evidence of the former is sparse.
This lack of evidence may be attributed to treat-
ment-focused nature of many of the previous publica-
tions, as opposed to an enquiry-based practice. This
has resulted in the lack of understanding of the true
nature of ECR, which could potentially lead to misdi-
agnosis (and potential under-reporting) and misman-
agement of ECR.
This review would ideally take the form of a sys-
tematic review of randomized controlled trials. How-
ever, this is not possible as majority of literature on
this topic, as explained and demonstrated above, con-
sists of case (series) reports, review papers and ex vivo
studies, thus, making such a review impossible to per-
form. The aim of part 1 of this literature review is to
present the relevant literature on the aetiology,
pathogenesis and diagnosis; part 2 will describe the
management of ECR.
Aetiology
Although several potential aetiological factors have
been associated with the development and progression
of the ECR, the aetiology and pathogenesis of ECR are
still poorly understood and as a result, many of these
resorptive defects are misdiagnosed, under-reported
and mismanaged.
Heithersay (1999b) assessed 257 teeth with ECR
and postulated that orthodontic treatment, traumatic
injury, internal bleaching, surgery and restorative
treatment were the principle potential predisposing
factors for ECR. Mavridou et al. (2017a) assessed 337
ECR cases and reported several additional potential
predisposing factors, several of which had previously
been identified in case (series) reports (Fig. 1). These
included extraction of a neighbouring tooth (Gunst
et al. 2013), malocclusion (Vossoughi & Takei 2007),
playing wind instruments (Gunst et al. 2011), peri-
odontitis (Beertsen et al. 2001), autotransplantation
(Kandalgaonkar et al. 2013), transmission of feline
viruses to humans (Von Arx et al. 2009), herpes zos-
ter (Solomon et al. 1986, Ramchandani & Mellor
2007, Patel et al. 2016a), systemic and genetic fac-
tors (Moskow 1989, Llena-Puy et al. 2002, Edwards
& McVaney 2005, Neely & Gordon 2007, Arroyo-
Bote et al. 2017), the use of bisphosphonates (Patel &
Saberi 2015), impacted teeth (mandibular third
molars affecting mandibular second molars, sponta-
neous resorption of impacted teeth), cysts, tumours
(Fuss et al. 2003) and pressure of erupting canines
applied to lateral incisors (Ericson et al. 2002, Alqer-
ban et al. 2009, Hadler-Olsen et al. 2015).
Orthodontic treatment as a potential predisposing
factor increased from 28.4% (Heithersay 1999b) to
45.7% (Mavridou et al. 2017a). This increased inci-
dence may be partly attributed to increased aware-
ness of ECR (Chen et al. 2010), and increased uptake
of orthodontic treatment (RIZIV 2017).
The decreased incidence of internal bleaching as a
potential predisposing factor as reported by Mavridou
et al. (2017a) may be due to milder bleaching prod-
ucts being used nowadays compared to concentra-
tions of 30% H2O2 used in the past (Friedman et al.
1988, Rotstein et al. 1991, Attin et al. 2003). How-
ever, even with this reduced concentration of bleach-
ing agents, diffusion of hydroxyl radicals can damage
Table 1 Publications on ECR, including type of study
Type of study Number Comments
Case report/series 112 Aetiology, diagnosis and/or
treatment
Basic research
(Biological and
technical laboratory
studies)
15 Ex vivo radiological,
histopathological and
microbiological studies
(including animal studies)
Clinical research 7 Observational and
interventional studies
Review article 13 Narrative descriptive papers
External cervical resorption-part 1 Patel et al.
© 2018 International Endodontic Journal. Published by John Wiley & Sons LtdInternational Endodontic Journal, 51, 1205–1223, 20181206
the PDL fibroblasts (Rotstein et al. 1993, Chapple &
Matthews 2007, Lou et al. 2016). Therefore, it is
essential to advise patients of potential risk for ECR,
especially when performing bleaching on younger
patients, as the diameter of their dentinal tubules is
larger and the risk for diffusion is greater (Camps
et al. 2007).
Mavridou et al. (2017a) reported only a 1.2% asso-
ciation with restorative procedures, compared to
14.4% reported by Heithersay (1999b).
In the veterinary literature, ECR is referred to as
feline odontoclastic resorptive lesions (FORL) or
tooth esorption (TR). The prevalence has been
reported to vary significantly from 14.3% to 85%,
depending on the examined cat populations and
the different experimental methodology used (Pet-
tersson 2010). Von Arx et al. (2009) first sug-
gested that the transmission of feline herpes virus
(FHV) can result in multiple human ECR lesions. It
has been suggested that FORL is a multifactorial
condition in which bacterial and/or viral infections
trigger an inflammatory process that subsequently
leads to FORL initiation (Booij-Vrieling 2010). The
possibility of virus transmission from cats to
humans and its impact on ECR initiation needs
further investigation.
Traumatic injuries in particular luxation and avul-
sion result in localized damage and/or rupture of
PDL; this has also been suggested as a cause of ECR
(Heithersay 1999b, Trope 2002, Andreasen &
Andreasen 2007, Mavridou et al. 2017a).
Other researchers have also suggested that bacte-
ria-induced inflammation may be involved in ECR
(Beertsen et al. 2001, Lin et al. 2013).
In the majority (59%) of clinical cases (199/337
teeth), more than one potential predisposing factor
was identified, indicating that ECR is multifactorial
and not idiopathic (Mavridou et al. 2017a). Some
combinations of potential predisposing factors, such as
orthodontics with traumatic injury (17.6%) (19 of
108 teeth), with parafunctional habits (13%) (14 of
108 teeth) or extraction of a neighbouring tooth
(12%) (13 of 108 teeth), have a much higher fre-
quency suggesting a multifactorial aetiology. It should
be mentioned that in previous reports, only 20% of
the ECR cases were identified as multifactorial (Hei-
thersay 1999b). This difference is believed to be due to
the establishment of a more systematic experimental
Figure 1 Comparison of percentage of appearance of potential predisposing factors, as reported in the work of Heithersay
1999a and Mavridou et al. 2017a.
Patel et al. External cervical resorption-part 1
International Endodontic Journal, 51, 1205–1223, 2018© 2018 International Endodontic Journal. Published by John Wiley & Sons Ltd 1207
approach (Mavridou et al. 2016b) and to the consider-
ation of an updated list of potential predisposing fac-
tors (Mavridou et al. 2017a).
Histological and 3D characteristics of
ECR
External cervical resorption (ECR) cases share several
common features (Heithersay 1999a, Luso & Luder
2012, Mavridou et al. 2016a). These are (i) the initia-
tion point (portal(s) of entry), (ii) the resorption area
with its channels and external interconnections (por-
tals of exit), (iii) the pericanalar resorption-resistant
sheet (PRRS), (iv) the repair by substitution of the
resorbed tissues by reparative bone-like tissue and
finally, (v) the remodelling of this reparative tissue
(Mavridou et al. 2016a). In root filled teeth, there is
no PRRS area due to its removal during the mechani-
cal preparation of the root canal (Mavridou et al.
2017b).
Portal(s) of entry
Are located in the cementum below the gingival
epithelial attachment. This area has typically two his-
tological patterns (Mavridou et al. 2016a). Firstly, a
connective tissue with a dense inflammatory lympho-
plasmacytic infiltrate, epithelial tissue is often seen to
cover the granulation tissue (Fig. 2) (Lin et al. 2013,
Mavridou et al. 2016a). Secondly, an ingrowth of
reparative bone-like tissue occurs, whilst local fusion
of the adjacent alveolar bone with resorbed dentine
and even resorbed enamel occurs. In any case, the
localized destruction and/or removal of PDL at the
portal of entry are needed for ECR to occur (Karring
et al. 1980, Nyman et al. 1980, Mavridou et al.
2016a) (Fig. 3).
Resorption area containing channels and external
interconnections
Resorptive lesions expand in all three dimensions
away from portal(s) of entry encircling and/or pro-
gressing towards the root canal system, resulting in
the destruction of dental hard tissues (i.e. cementum,
dentine and enamel). Several resorption channels and
interconnections with the PDL (portals of exit) are
created. The advancing resorptive lesion is prevented
from perforating into the root canal by the Peri-
canalar resorption-resistant sheet (PRRS see below).
Resorption (clastic) cells located within resorption
lacunae (Von Arx et al. 2009) are identified as large
osteoclast-like multinucleated cells with a size of
approximately 20 9 30 lm (Mavridou et al. 2016a)
(Fig. 4). When the clastic cells are detached, other
types of cells (mononuclear phagocytes, or osteoblast-
like cells entrapped in osteoid) can repopulate the
lacunae area (Mavridou et al. 2016a).
Pericanalar resorption-resistant sheet (PRRS)
Is a nonuniform layer/area with a thickness of 70 up
to 490 lm depending on its location within the root
(Mavridou et al. 2016a) (Fig. 5). Histological and
micro-CT assessment has confirmed that the PRSS
consists of dentine and occasionally bone-like tissue
(Gunst et al. 2013, Mavridou et al. 2016b) (Fig. 6).
Although the term ‘resistant’ is used, pulp perforation
can occur especially in advanced cases. In areas with
small PRRS disruptions, the cellular consistency of
the pulp is modified and odontoblasts can be atrophic
(Fig. 6a). In other areas of the pulp, the odontoblastic
layer appears intact (Fig. 6a). Histological findings
also include the formation of pulp stones and diffuse
calcifications (Fig. 6b). Other observations included
hyalinosis (thickening of the walls) of the blood ves-
sels and an increase of the deposition of predentine
(Mavridou et al. 2016a).
Clastic cells
Clastic cells
Enamel
Dentine
Epithelial tissue
Figure 2 Histological image of the portal of entry, of tooth
26 with ECR showing the epithelial tissue ingrowth. Resorp-
tion is observed simultaneously at enamel and dentine. His-
tological staining was performed with a combination of
Stevenel’s blue and Von Gieson’s picrofuchsin, visualizing
mineralized tissue (red) and nonmineralized tissue (blue-
green).
External cervical resorption-part 1 Patel et al.
© 2018 International Endodontic Journal. Published by John Wiley & Sons LtdInternational Endodontic Journal, 51, 1205–1223, 20181208
Repair
Repair of the resorbed dental hard tissues occurs by
ingrowth and apposition of reparative bone-like tissue
through the portal(s) of entry into the tooth (Fig. 7a,
b). The reparative tissue appears as a lamellar trabec-
ular bone, with islands of woven bone formed in
regions of rapid bone repair-remodelling cycle. Histo-
logical findings show bone-like related cells (os-
teoblast-like cells, osteocytes) and osteoid tissue
(Mavridou et al. 2016a) (Fig. 3).
Remodelling of reparative bone-like tissue
Remodelling refers to the cyclic resorption and
reforming of the bone-like tissue involving clastic and
blastic cells. It is possible that in different areas of the
same tooth active resorption of dentine, active repair
by osteoid formation and remodelling of the bone-like
tissue take place simultaneously (Mavridou et al.
2016a) (Fig. 6).
Pathogenesis
External cervical resorption is a dynamic and evolving
process, with destructive and reparative phases (Luso
& Luder 2012, Mavridou et al. 2016a). The patho-
genesis of ECR consists of three main stages:
Resorption initiation
This is the first stage of ECR and is characterized by a
localized destruction/disruption of the normal PDL
structure, including the unmineralized cementum
Portal of entry
PRRS
Bone-like tissue
Calculus
Blastic cells
Bone-liketissue
Area 1
Area 1
Figure 3 Histological image of tooth 46 with ECR showing a small portal of entry and ingrowth of bone-like tissue. Active
blastic cells are also found in the reparative bone-like tissue. Histological staining was performed with a combination of Steve-
nel’s blue and Von Gieson’s picrofuchsin, visualizing mineralized tissue (red) and nonmineralized tissue (blue-green).
Patel et al. External cervical resorption-part 1
International Endodontic Journal, 51, 1205–1223, 2018© 2018 International Endodontic Journal. Published by John Wiley & Sons Ltd 1209
leading to the formation of a blood clot and a local-
ized inflammatory response of the exposed dentine
(Polimeni et al. 2006). Macrophages then migrate to
the affected area and, in addition to wound debride-
ment, will result in the formation of granulation tis-
sue (Karring et al. 1980). The granulation tissue is
also able to contact the dentine through an exposure
in the cementum-enamel junction (CEJ). This ‘gap’
may be either due to a localized cementum removal,
caused by traumatic damage or a cemental tear (Lin
et al. 2011) or due to a natural incomplete closure of
cementum over enamel in this area (Schroeder &
Scherle 1988, Neuvald & Consolaro 2000). Thus, the
exposed dentine could be vulnerable to resorption
from the adjacent bone or to circulating immune cells
which are attracted to the underlying mineralized
dental hard tissue. Different types of the cells (bone,
PDL fibroblasts or epithelial gingival cells) can repopu-
late the wounded area, and different phenomena may
occur (Nyman et al. 1985). In the case of bone cells,
ankylosis can occur (Melcher 1970, Line et al. 1974,
Nyman et al. 1980). In the case of PDL cells, cemen-
tum formation and PDL regeneration will take place
(Melcher 1970, Line et al. 1974, Karring et al. 1980).
In case of epithelial gingival cells, no repair will take
place (Nyman et al. 1980). The stimulation of clastic
cells is mainly through the expression of ‘Receptor
Activator of Nuclear Factor k B Ligand’ (RANKL) by
clastic cells, damaged and compressed periodontal
ligament cells and/or certain bacterial species. RANKL
binds to RANK receptors of clastic precursor cells,
which will then become mature clastic cells by means
of fusion (Kanzaki et al. 2001, Fukushima et al.
2003, Belibasakis et al. 2007, Uchiyama et al. 2009).
Recent evidence suggests that hypoxia also might
play a role in the activation of osteoclastogenesis
(Knowles & Athanasou 2009), as it can disturb the
metabolism and impede the recovery of human peri-
odontal ligament fibroblasts (Zhang et al. 2013). The
synergetic effect of hypoxia and bacteria in the PDL
may also accelerate the inflammation (G€olz et al.
2015).
Clastic cellsReparative
bone-like tissue
Dentine
Resorption lacunae on dentine
Figure 4 Active resorption occurring in both dentine and
reparative bone-like tissue, observed in tooth 26 with ECR.
Resorption of the bone-like tissue is a part of the remodelling
process. Histological staining was performed with a combina-
tion of Stevenel’s blue and Von Gieson’s picrofuchsin, visual-
izing mineralized tissue (red) and nonmineralized tissue
(blue-green).
PRRS
Figure 5 Nano-CT imaging of tooth 13 and 3D modelling using CTan, CTvol and CTvox softwares, showing the thickness dis-
tribution of the pericanalar resorption-resistant sheet (PRRS).
External cervical resorption-part 1 Patel et al.
© 2018 International Endodontic Journal. Published by John Wiley & Sons LtdInternational Endodontic Journal, 51, 1205–1223, 20181210
Resorption progression
Several factors have been suggested as stimulating
factors for ECR to progress. These include infection
(bacteria) (G€olz et al. 2015, Mavridou et al. 2016a),
continuous mechanical force on the PDL (e.g. during
orthodontic treatment) (Niklas et al. 2013, Le et al.
2016), discontinuous mechanical unloading (Arnett
et al. 2003a,b) caused by chewing, parafunction or a
combination. All these factors may induce a hypoxic
microenvironment, which activates osteoclastogenesis
(Arnett et al. 2003a,b, Knowles & Athanasou 2009,
Arnett 2010) and subsequently helps in the pro-
gression of ECR (Mavridou et al. 2017a). Hypoxia as
a driving force of angiogenesis could influence the
continuous development of highly vascularized
Bone-like tissue
Bone-liketissue
Athrophic odontoblastic layer
Intact odontoblastic layer
Pulp stones
(a)
(b)
DentinePRRS
PRRS
Figure 6 (a) Structure of pericanalar resorption-resistant sheet and pulp tissue. PRRS is consisted of predentine, dentine and
occasionally bone-like tissue. (b) Calcification inside the pulp. Histological staining was performed with a combination of Steve-
nel’s blue and Von Gieson’s picrofuchsin, visualizing mineralized tissue (red) and nonmineralized tissue (blue-green).
Patel et al. External cervical resorption-part 1
International Endodontic Journal, 51, 1205–1223, 2018© 2018 International Endodontic Journal. Published by John Wiley & Sons Ltd 1211
(b)(a)
(d) (e)
(c)
Figure 7 (a) Clinical photograph of a symptomatic and discoloured tooth 11, (b) Periapical radiograph of tooth 11 which was
initially misdiagnosed as subgingival caries and temporally restored with a provisional restoration. The patient was referred to
an Endodontist who diagnosed ECR which was deemed unrestorable and subsequently extracted. (c) Coronal micro-CT image
of the tooth revealing bone-like tissue encompassing the root canal and extending beyond the mid-third of the root canal. Bot-
tom: Nano-CT image of tooth 36 showing ingrowth of bone-like tissue through the portal of entry. [Supplementary online only
Movies S1 and S2 (d) Micro-CT scan of tooth 36 with ECR, note the reparative nature of the resorptive lesion in the core of
the tooth, as well as the destructive nature on the distal aspect of the coronal third of the root. (e) Transaxial view of tooth 36
with ECR, note the reparative nature of the ECR.]
External cervical resorption-part 1 Patel et al.
© 2018 International Endodontic Journal. Published by John Wiley & Sons LtdInternational Endodontic Journal, 51, 1205–1223, 20181212
granulation tissue accompanying ECR (Mavridou
et al. 2016a, Rombouts et al. 2017).
In this phase, the resorptive process invades the
tooth structure by resorbing cementum, dentine and
enamel (Mavridou et al. 2016a). The resorptive lesion
extends in all planes (i.e. circumferentially and longi-
tudinally) within the dentine. The direction that clas-
tic cells move in is dependent on inflammatory
mediators (e.g. growth factors, cytokines, prostaglan-
dins etc.) and hormones (e.g. parathyroid hormone
(PTH), calcitonin, 1,25-dihydroxyvitamin D3 (cal-
citriol) (Manolagas 2002, V€a€an€anen 2005). The pres-
ence of the PRRS helps to prevent ECR from
perforating into the root canal; thus, the pulp tissue
retains its vitality (Mavridou et al. 2016a). It has
been suggested that the PRRS includes an inhibitory
resorptive factor (Wedenberg 1987) and lacks RGD
proteins (Levin 2012) which make it resistant to
resorption. However, in advanced cases of ECR, the
root canal may become perforated.
Reparative stage
This is the reversed stage of ECR, where repair takes
place by osteoblast-like cells that result in an
ingrowth of bone-like tissue into the resorption cavity
(Mavridou et al. 2016a). The reparative tissue and
the tooth structure eventually become part of the nor-
mal alveolar bone structure (Levin 2012). This is
regarded as a form of healing. After formation of the
bone-like tissue, active remodelling can occur asyn-
chronously at many sites. During this stage, repair
and remodelling evolve simultaneously at different
areas of the tooth (Mavridou et al. 2016a, 2017b).
This phenomenon is responsible for changes in the
CBCT image in long-term follow-up of ECR.
Distribution
External cervical resorption is most commonly
detected in maxillary central incisor teeth. Heithersay
(1999b) and Mavridou et al. (2017a) detected ECR in
29.2% and 28.8%, respectively, in 257 and 337 teeth
which were diagnosed with ECR (Fig. 8).
The next most affected teeth were maxillary canine,
maxillary lateral incisor, mandibular first molar and
maxillary first molar teeth. The incidence of ECR was
in the same order of magnitude in both studies (Hei-
thersay 1999b, Mavridou et al. 2017a). This similar
pattern of tooth distribution in these studies may be
associated with the high prevalence of traumatic
injuries (anterior teeth) (Bastone et al. 2000) and
parafunctional habits (molar tooth) in patients (Chat-
zopoulos et al. 2017). In another study which
assessed all ECR cases with radiographs and CBCT,
the incidence was similar for maxillary central incisor
teeth (30.4%), however, the next common teeth were
mandibular first molar, mandibular central incisor
and maxillary molar teeth (Patel et al. 2016b).
The increased incidence of ECR in premolar teeth
in the study of Mavridou et al. (2017a) may be asso-
ciated with the increased uptake of orthodontic treat-
ment (e.g. extraction of the first premolar and
orthodontic movement thereafter).
Mavridou et al. (2017a) detected ECR more fre-
quently in younger age groups than reported by Hei-
thersay (1999b). This may be due to a combination
of factors including increased uptake of orthodontic
treatment, increased visits to general dentists for
check-ups and more awareness of the clinical and
radiographic appearance of ECR (Proffit et al. 2013,
Van der Heyden 2013, RIZIV 2017). ECR does not
seem to be related to the gender of the patient (Hei-
thersay 1999b, Mavridou et al. 2017a).
Heithersay (1999b) and Mavridou et al. (2017a)
provided detailed and extensive descriptions of the
potential aetiological factors of ECR. However, it must
be stressed that no definitive cause-and-effect relation-
ship has been established. In the cases affected by a
combination of predisposing factors, it was impossible
to determine definitively whether ECR was the result
of one specific event or a combination of factors, or if
any of the potential causes identified were in fact con-
tributory. In 15% of the patient examined in Heither-
say’s study, no potential predisposing factor was
identified, furthermore, intracoronal restorations were
attributed as possible predisposing factors only when
no other potential cause could be identified (Heither-
say 1999b, Patel et al. 2016a).
Clinical presentation
Patients commonly are asymptomatic, and therefore,
ECR may be diagnosed purely as an incidental clinical
and/or radiographic finding. In more advanced cases,
when the resorption lesion has affected the pulp, the
patient may present with symptoms of (ir)reversible
pulpitis and/or apical periodontitis (Figs 9–11).The diagnosis of ECR defects can be challenging
(Gulabivala & Searson 1995, Schwartz et al. 2010,
Durack & Patel 2016, Patel et al. 2018). The clinical
presentation of ECR defects is determined by their
Patel et al. External cervical resorption-part 1
International Endodontic Journal, 51, 1205–1223, 2018© 2018 International Endodontic Journal. Published by John Wiley & Sons Ltd 1213
location and nature. Whilst early defects or those
located in interproximal aspects of teeth may not be
readily detected on clinical examination, extensively
cavitated cervical defects on the labial or lingual areas
may be diagnosed by direct vision or detected upon
probing with dental probes or periodontal scalers
(Bergmans et al. 2002, Patel et al. 2009a, 2016a,b,c).
These defects bleed profusely on probing as a result of
their vascularity (Trope 2002, Patel et al. 2009a).
Due to their location, ECR may be mistaken for buc-
cal caries, therefore, it is important to differentiate
these lesions by tactile feedback (probing). Depending
on its state, caries will feel soft or sticky on probing,
whereas ECR will be hard and scratchy (Bergmans
et al. 2002, Patel & Pitt Ford 2007, Patel et al.
2009a).
A ‘pink’ spot or banding in the cervical aspect of
the tooth is usually pathognomic of ECR (Heithersay
2004, Patel & Pitt Ford 2007). The discoloration is
due to the fibrovascular granulation tissue within the
resorptive defect being visible through the thinned-
out overlying enamel (Bergmans et al. 2002). As
described above, this highly vascular granulation tis-
sue is the reason behind its profuse bleeding on prob-
ing. Although pink spots may be easily detected by
the patient and/or clinician, they are more challeng-
ing to detect on posterior teeth, especially when they
are located on the interproximal or lingual/palatal
aspects of the tooth (Fig. 11). It must be stressed that
pink spots are relatively rare. Teeth with ECR may
Figure 8 Comparison of percentage of appearance of ECR in different tooth types, as reported in the work of Heithersay 1999a
and Mavridou et al. 2017a.
Figure 9 Periapical radiograph reveals a mesially impacted
unerupted 38 with signs of ECR of unidentifiable aetiology.
External cervical resorption-part 1 Patel et al.
© 2018 International Endodontic Journal. Published by John Wiley & Sons LtdInternational Endodontic Journal, 51, 1205–1223, 20181214
also be discoloured due to pulp necrosis; in these
cases, they will show a grey discolouration (Fig. 7).
As there is no classic presentation of ECR, many
defects may present as incidental signs on clinical or
radiographic examination or as a result of pulpal
involvement, that is symptoms of (ir)reversible pulpitis
(e.g. temperature sensitivity), or in more advanced
cases, they may be infected and display signs of apical
periodontitis (e.g. tenderness to percussion, presence
of a sinus) (Bergmans et al. 2002, Patel et al. 2009a,
Bhuva et al. 2011). Teeth affected by ECR respond
positively to sensibility testing as long as the root
canal has not been perforated and the pulp became
necrotic (Frank & Torabinejad 1998, Patel et al.
2009a).
In the co-author’s experience, early ECR lesions are
being more commonly detected by hygienists who
purposefully, as part of their treatment, visually assess
and gently probe and scale the circumference below,
and above the CEJ of their patient’s teeth.
Radiographic presentation
There is no ‘classic’ radiographic appearance of ECR.
Lesions may be symmetrical or asymmetrical; their
margins vary from being well defined and smooth to
(a)(b)
(c) (d)
Figure 10 A 65-year-old man presented complaining of a pimple on the inner aspect of his lower jaw; the only potential aetio-
logical factor was previous root canal treatment under rubber dam. (a) clinical photograph reveals a 2 mm abscess lingual to
tooth 41 (b) periapical radiograph reveals ECR of teeth 31 and 41. (c,d) The sagittal reconstructed CBCT images reveal that
the ECR is reparative in tooth 31 (yellow arrow) and resorptive in tooth 41 (red arrow) and that both teeth are unrestorable.
Note the completely different nature of the ECR in these neighbouring teeth.
(a)
(b) (c)
Figure 11 A 36-year-old man presented complaining of a pink discolouration on the labial aspect of tooth 21. (a) Clinical pho-
tograph confirms the patient’s complaint of a pink discolouration and also cavitation at the gingival margin, (b,c) parallax peri-
apical radiographs reveal ECR of tooth 21, note that the canal walls are visible through the resorptive lesions.
Patel et al. External cervical resorption-part 1
International Endodontic Journal, 51, 1205–1223, 2018© 2018 International Endodontic Journal. Published by John Wiley & Sons Ltd 1215
poor definition or ragged or even with no clear delin-
eation between ECR and healthy root structure (Dur-
ack & Patel 2016).
External cervical resorption in the ‘resorptive’ phase
will be radiolucent in nature, whereas ECR lesions in
the ‘reparative’ phase will be more radiopaque, that is
a mottled or cloudy appearance as a result of the ossi-
fication of the granulomatous resorptive tissue
(Fig. 12). In some cases, there may also be distinct,
radiopaque striations of hard tissue present (Iqbal
2007, Gunst et al. 2013).
The outline of the root canal walls should be intact
and traceable through the lesion; this distinguishes it
from internal inflammatory resorption. The parallax
imaging technique may be used to distinguish
between internal resorption as well as confirm the
location of ECR lesions which are not clinically detect-
able. The canal walls will be visible with horizontal
parallax radiographs; however, the ECR lesion will
appear to move with the change of horizontal angle
of the X-ray tube. Lingually/palatally located ECR will
appear to move in the same direct as the parallax
shift, whereas labially/buccally located ECR will
appear to move in the opposite direction to the X-ray
tube shift. Internal root resorption lesions will always
stay centred with parallax radiographs (Durack &
Patel 2016).
Periapical radiographs (PRs) have several well-
established limitations in detecting radiographic signs
of endodontic disease (Bender & Seltzer 1961, Patel
et al. 2015). Firstly, unintentional geometric distor-
tion can result in PR under or overestimation of the
size of root resorption (Forsberg & Halse 1994, 1997),
Vaz de Souza et al. 2017). Secondly, anatomical noise
can result in PR missing or underestimating the size
of ECR (Kamburo�glu et al. 2011, Bernardes et al.
2012). Thirdly, as PRs are 2-dimensional shadow-
graphs, they only confirm the height and width of
ECR which is confined to the interproximal aspects of
the tooth, information on the depth, and/or
(a) (b) (c)
(d)(e) (f)
Figure 12 A 48-year-old man with symptoms of irreversible pulpitis localized to the 16. The potential aetiological factors were
previous dental treatment, including orthodontics and use of matrix bands. (a,b) Buccal and palatal views of the maxillary right
molar region, there are no obvious clinical or (c) radiographic signs of endodontic or periodontal disease. (d, e and f) coronal,
sagittal and axial reconstructed CBCT scans reveal clear signs of external cervical resorption (resorptive [red arrow] and repara-
tive [yellow arrow]). The CBCT scan has resulted in a change of diagnosis and management; this tooth was extracted as the
ECR defect was clearly unrestorable. This lesion cannot be classified with Heithersay classification as it cannot be visualized of
the periapical radiograph. However, it can be classified as ‘2Cp’ using the 3D Patel classification. (Patel & Saberi 2018).
External cervical resorption-part 1 Patel et al.
© 2018 International Endodontic Journal. Published by John Wiley & Sons LtdInternational Endodontic Journal, 51, 1205–1223, 20181216
circumferential (labial/buccal) spread of ECR is mini-
mal, that is the third dimension is missing (Patel et al.
2018).
The limitations of radiographs can result in misdi-
agnosis, inadequate assessment and/or poor manage-
ment of ECR (Gulabivala & Searson 1995, Patel et al.
2009b, Schwartz et al. 2010, Gunst et al. 2013). The
limitations of PR may be overcome with cone beam
computed tomography (Figs 10, 12, and 13).
CBCT overcomes the limitations of PR, allowing
ECR to be viewed in any plane without superimposi-
tion of overlying structures and geometric distortion
(anatomical noise); in addition, the reconstructed
CBCT images are also more accurate than PR
(Hashem et al. 2013, Patel et al. 2015). The radiation
dose of a CBCT scan is in the same order of magni-
tude as PRs (Loubele et al. 2009, Pauwels et al.
2012, Harvey & Patel 2016). It is now well estab-
lished that CBCT can improve the diagnosis and/or
management of complex endodontic problems (Brady
et al. 2014, Hashem et al. 2015, Patel & Vincer
2017, Rodriguez et al. 2017a,b).
The importance of CBCT in the management of
ECR is also highlighted in the European Society of
Endodontology [ESE] position statement (2014), and
the joint statement by the American Association of
Endodontists & American Academy of Oral & Maxillo-
facial Radiology [AAE/AAOMR] (2015).
CBCT has had a major impact on the diagnosis
and management of root resorption lesions. The true
nature and extent, that is the exact dimensions,
degree of circumferential spread and proximity to
the root canal, may be appreciated; the fine resorp-
tive extensions of the main resorptive lesion as well
as hard tissue deposits may be clearly visualized
(Mavridou et al. 2016b, Patel et al. 2018). This is
clinically relevant as these resorptive extensions may
extend apically and/or contain active resorptive tis-
sue allowing ECR to continue to progress if not
diagnosed and appropriately managed. It is possible
(a) (b) (c)
(d)
(e) (f)
(g)
Figure 13 A 64-year-old woman with no symptoms presented for a routine check-up. (a) Clinical examination reveals a pink
band of discolouration (green arrow) and a portal of entry lingually (purple arrow). (b,c) Periapical radiographs reveal exten-
sive ECR, note that the canal is visible through the radiolucency, confirming ECR. (d) Coronal, (e) sagittal and (f,g) axial recon-
structed CBCT slices reveal that the ECR-affected tooth is unrestorable. Note the apical extension of the resorptive lesion. The
lesion can be classified as a Heithersay class 3. However, the circumferential spread, depth and proximity to the pulp cannot
be determined on the periapical radiographs. A 3D Patel classification of ‘3Bp’ precisely describes the lesion and facilitates
reporting and communication between clinicians.
Patel et al. External cervical resorption-part 1
International Endodontic Journal, 51, 1205–1223, 2018© 2018 International Endodontic Journal. Published by John Wiley & Sons Ltd 1217
that the inability to identify and remove the repara-
tive resorptive tissue may also have a negative
impact on the outcome of treatment (Estevez et al.
2010).
The literature is replete with case (series) reports
confirming that PRs do not consistently reveal the
true nature of ECR compared to CBCT (Patel et al.
2007, 2016a, Estevez et al. 2010, Schwartz et al.
2010, Gunst et al. 2013, Salzano & Tirone 2015, Wu
et al. 2016). A clinical study compared PR and CBCT
for the detection and management of internal and
external cervical resorption lesions (Patel et al.
2009b). Receiver operator characteristic (ROC) curves
as well as the reproducibility of each technique were
determined for diagnostic accuracy and treatment
option chosen. The ROC value for PR and CBCT was
0.83 and 1, respectively. This study not only con-
firmed the superior accuracy of CBCT over PR but
also that the correct treatment plan was more likely
to be chosen when the clinician had access to CBCT.
Similar conclusions have been found in more recent
in vivo studies (Ee et al. 2014, Patel et al. 2016b,
Rodriguez et al. 2017a,b).
Using PRs, Heithersay (1999b) devised a PR classifi-
cation to categorize ECR according to its extension into
the root and proximity to the root canal. In summary,
class I, a small cervical lesion with shallow penetration
into dentine; class II, a well-defined lesion close to the
coronal pulp but with little or no extension into radicu-
lar dentine; class III, deeper invasion of the lesion into
the coronal third of the root; class IV, a lesion extend-
ing beyond the coronal third of the root (Heithersay
1999b). The limitation of this classification is that it is
only relevant if ECR is solely limited to the proximal
aspect of a tooth; this is impossible to confirm from a
2-dimensional radiograph. Heithersay’s classification
does not describe the true nature of ECR (resorptive
and reparative) as it does not describe the third dimen-
sion, that is buccolingual and/or circumferential
spread of ECR, nor does it describe the proximity of
ECR to the root canal.
In an ex vivo study, Vaz de Souza et al. (2017)
compared the diagnostic efficacy of two CBCT scan-
ners with PR for the detection and classification of
simulated external cervical resorption (ECR) lesions.
Simulated ECR lesions representing the four Heither-
say classes were created. Examiners were asked to
classify and identify the root surface(s) that ECR
extended to with PR and CBCT. The ECR lesions were
correctly identified according to the tooth surface in
87.8% Kodak CBCT, 89.1% Morita CBCT and 49.4%
PR cases. The ECR lesions were correctly classified
according to Heithersay classification in 71.4% Kodak
CBCT, 70% Morita CBCT and 32% PR of cases.
In a clinical study, Patel et al. (2016c) compared
the ability of PA and CBCT to detect, determine
the nature and plan the management of ECR. The
ROC analysis revealed that PR had a limited accu-
racy to detect the size (0.75), circumferential
spread (0.60) and location of ECR lesions compared
to CBCT. This resulted in the PA treatment plan
chosen to manage ECR varying significantly com-
pared to CBCT.
Patel et al. (2018) suggested a 3-dimensional classi-
fication for ECR based on the radiographic findings of
PR and CBCT (Table 2). This classification considers
the height of a lesion, its circumferential spread and
proximity to the root canal. The aim of the classifica-
tion is to ensure accurate diagnosis and communica-
tion of ECR between clinicians. In future, it should
allow an objective assessment of the outcome treat-
ment in relation to the nature and extent of ECR.
Table 2 The 3 dimensional classification for ECR
External cervical resorption-part 1 Patel et al.
© 2018 International Endodontic Journal. Published by John Wiley & Sons LtdInternational Endodontic Journal, 51, 1205–1223, 20181218
The score for the height of the lesion is recorded as
‘1’ for supracrestal defects, ‘2’ for subcrestal defects,
‘3’ for defects extending into the middle third of the
roots and ‘4’ for those invading the apical third of
the roots. The circumferential spread of ECR is
recorded as ‘A’ for lesions extending ≤90°, ‘B’ for
lesions extending >90° to ≤180°, ‘C’ for lesions
extending >180° to ≤270° and ‘D’ for those extend-
ing >270°. Finally, the proximity to the root canal
is noted; ECR is confined to dentine is graded as ‘d’,
and ‘p’ when there is (probeable) pulpal involve-
ment.
As with any X-ray image, CBCT scans must be jus-
tified and the principles of as low as reasonably
achievable (ALARA) followed (Pauwels et al. 2012,
European Society of Endodontology 2014).
Concluding remarks
• Several potential predisposing factors have been
identified for ECR; certain combinations of these
factors result in a higher frequency of ECR. More
research is required to confirm the cause-and-effect
relationship of these potential predisposing factors.
• The most commonly affected teeth appear to be
maxillary incisor, canine, first molar and mandibu-
lar first molar teeth.
• There are three stages in the process of ECR; initi-
ation, progression/resorption and reparative phase.
Resorption and repair/remodelling can progress in
parallel at different areas of the affected tooth.
• Periapical radiography has significant limitations
in the detection, assessment and treatment plan-
ning of ECR. The increased accuracy of CBCT
results in not only more accurate detection and
assessment of ECR but also selection of the most
appropriate treatment plan.
Conflict of interest
The authors have stated explicitly that there are no
conflict of interests in connection with this article.
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Supporting Information
Additional Supporting Information may be found in
the online version of this article:
Movie S1. Micro-CT scan of tooth 21 with ECR,
note the reparative nature of the resorptive lesion in
the core of the tooth, as well as the destructive nature
on the distal aspect of the coronal third of the root.
Movie S2. Transaxial view of tooth 36 with ECR,
note the reparative nature of the ECR.
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