CHAPTER

31 Root Resorption

Chapter Outline
‰ Definition ‰ Diagnosis of Resorption
‰ Classification of Resorption ‰ Internal Resorption
‰ Protective Mechanism against Resorption ‰ External Root Resorption
‰ Cells Involved in Root Resorption ‰ Cervical Root Resorption (Extracanal
‰ Mechanism of Root Resorption Invasive Resorption)

Introduction Etiology of Root Resorption

Resorption is a condition associated with either physi-
ologic or a pathologic process resulting in a loss of dentin, Local Systemic Idiopathic
cementum, and/or bone. It causes loss of the tooth struc- • Trauma • Paget’s disease
ture either internal or external which may lead to extraction • Periapical pathology • Hormonal imbalance:
of the tooth if not treated well at the time. There are many • Cysts and tumors – Hyperthyroidism
• Impacted tooth – Hypothyroidism
classifications and terms coined for resorption defects
• Intracoronal – Hypo and hyper
depending upon their location and etiology. Etiology of any bleaching pituitarism
resorption defect is inflammation which starts from injury
in form of dental trauma, surgical procedures, chemical
injury from bleaching agents or excessive pressure from
impacted tooth. Tooth can be saved if treatment is given
Classification of Resorption
at initial stage but if resorption continues without treat- (Flowchart 31.1)
ment, it may lead to extraction of the tooth. Identification Cohen’s classification of root resorption
of stimulating factors and removal of the etiology are the ‰ According to nature
main requirements to render proper treatment to the tooth • Physiologic [(in deciduous teeth during eruption of
undergoing resorption. permanent teeth (Figs. 31.1A to C)]
• Pathologic (in teeth due to underlying pathology)
Definition ‰ According to anatomic region of occurrence

According to American Association of Endodontics in 1944 • Internal

(Glossary—Contemporary Terminology for Endodontics), • External
‰ Based on cause
resorption is defined as “A condition associated with either
a physiologic or a pathologic process resulting in the loss of • Local
dentin, cementum or bone.” – Inflammatory
Root resorption is the resorption affecting the cemen- a. External
tum or dentin of the root of tooth. Resorption is a perplexing b. Internal
problem for which etiologic factors are vague. – Pressure
External resorption: When resorption is initiated in a. Orthodontic tooth movement
periodontium and initially affects the external surface of b. Impacted tooth
the tooth. – Dentoalveolar ankylosis
Internal resorption: When resorption is initiated within • Systemic
the pulp space affecting the internal dentin surface. • Idiopathic

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Flowchart 31.1 Lindskog classification of root resorption.

A B C
Figs. 31.1A to C Primary tooth is lost naturally due physiological root resorption caused by pressure of erupting permanent tooth.
(A) Permanent tooth bud under primary tooth; (B) eruption of permanent tooth with simultaneous root resorption of primary tooth; (C) loss
of primary tooth with eruption of permanent tooth.

Andreasen classification of root resorption Protective Mechanism Against

‰ Internal resorption Resorption
• Root canal replacement resorption There are few hypotheses which tell the protective mecha-
• Internal inflammatory resorption nism against resorption. These are as follows.
‰ External resorption
• Surface resorption Remnant of Epithelial Root Sheath
• Inflammatory resorption Remnants of epithelial root sheath surround the roots like
• Replacement resorption a net and impart resistance to resorption and subsequent
• Dentoalveolar ankylosis ankylosis

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Intrinsic Factors
Intrinsic factors found in predentin and cementum act as
inhibitor of resorption

Presence of Osteoprotegerin (OPG)

OPG a member of tumor necrosis factor (TNF) binds to recep-
tor activator of NF- B ligand and reduces its concentration
and further inhibits its ability to stimulate osteoclast produc-
tion (osteoclastogenesis) and subsequently inhibits resorption

Anti-Invasion Factors
Low-molecular-weight proteolytic activity inhibitor is pre-
sent in cartilages, blood vessel walls and teeth. It causes loss
of ruffled border, attachment ability of osteoclasts to bone
and thus bone resorption Fig. 31.2 Diagram showing giant cells.

Intermediate Cementum
Presence of hyaline layer of Hopewell-Smith (intermediate
cementum) is hypercalcified in relation to adjacent dentin
and cementum. It prevents development of inflammatory
resorption in replanted teeth with pulpal pathosis, possibly
by forming a barrier against egress of noxious agents from
the dentinal tubules to the PDL

Anti-Resorptive Factors
Like estrogen, calcitonin, platelet-derived growth factor,
calcium, tumor growth factor, interlukin,-17 etc.

Cells Involved in Root Resorption

Clast Cells
Odontoclasts, Dentinoclasts, Osteoclasts, Fig. 31.3 Structure of bone showing osteoclasts and osteoblasts.
and Cementoclasts bone tumors. Though macrophages have structure (Fig.
All these cells belong to the group of clast cells and they 31.3) similar to osteoclasts and like osteoclasts, can become
have a common origin, that is, circulating monocytes which multinucleated giant cells, macrophages lack a ruffled bor-
form macrophages. When the inflammation gets out of der, that is, attached to hard tissue substrates during resorp-
control, these monocytes/macrophages join to form giant tion and do not create lacunae on the dentinal surface.
cells (Fig. 31.2). These are highly vacuolated and contain
numerous mitochondria. Majority of odontoclasts have 10 Mechanism of Root Resorption
or fewer nuclei, that is, 96% are multinucleated and rest 4%
are mononucleated. Resorption of hard tissue takes place in two events:
Oligonuclear odontoclasts are cells with <5 nuclei. They 1. Degradation of inorganic crystal structures—hydroxyapatite
resorb more dentin per nucleus when compared with cells 2. Degradation of the organic matrix—principally Collagen
with higher number of nuclei. Type 1

Monocytes and Macrophages Degradation of the Inorganic Crystal Structures

Monocytes and macrophages along with osteoclasts are The degradation of inorganic structures initiates when pH
found in tissue surfaces adjacent to bone, for example, in is 3–4.5 at the site of resorption. This is created by the polar-
resorpting surfaces of rheumatoid arthritis, periodontal ized proton pump formed in ruffled border of the clast cells.
diseases, periradicular granulomas, cysts and in metastatic Below the pH of 5, the dissolution of hydroxyapatite occurs.

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Enzymes carbonic anhydrase II which catalyzes the If tooth is nonvital: External inflammatory root resorption
conversion of CO2 and H2CO3 intracellularly also maintains with infected pulp or internal root resorption with necrotic
an acidic environment at the site of resorption which is a coronal pulp.
readily available source of H+ ions. The enzyme acid phos-
phatase also favors the resorption process.
Internal Resorption
CO2 + H2O H2CO3
According to Shafer, “internal resorption is an unusual form
H2CO3 H+ + HCO3− of tooth resorption that begins centrally within the tooth,
apparently initiated in most cases by a peculiar inflamma-
tion of the pulp.” It is characterized by oval-shaped enlarge-
Degradation of the Organic Matrix ment of root canal space (Fig. 31.4).
Three main enzymes involved in this process are colla-
genase, matrix metalloproteinases (MMP) and cysteine
Synonyms of internal resorption
proteinases. • Chronic perforating hyperplasia of the pulp
Collagenase and MMP act at a neutral or just below • Internal granuloma
neutral pH—7.4. They are found more toward the resorb- • Odontoblastoma
ing bone surface where the pH is near neutral, because • Pink tooth of mummery
of the presence of the buffering capacity of the resorbing
bone salts. MMP is more involved in odontoblastic action.
Cysteine proteinases are secreted directly into the osteo- Etiology
clasts into the clear zone via the ruffled border. Cysteine
proteinases work more in an acidic pH and near the ruffled Though etiology is unknown but it is most often seen in the
border, the pH is more acidic. following cases:
‰ Long-standing chronic inflammation of the pulp
‰ Caries-related pulpits
Factors regulating resorption
‰ Traumatic injuries
Systemic Local
• Luxation injuries
• PTH favors resorption by • Interleukin 6 ‰ Iatrogenic injuries
stimulating osteoclasts and • Interleukin 1 • Preparation of tooth for crown
formation of multinucleated • Tumor necrosis • Deep restorative procedures
giant cells factor-α
• Application of heat over the pulp
• 1,2,5-dihydroxy vitamin D3 • Prostaglandin
increases resorption activity of • Bacterial toxins • Pulpotomy using Ca(OH)2
‰ Idiopathic
osteoblasts • Macrophage stimulat-
• Calcitonin inhibits resorption ing factor
by suppressing osteoclastic
cytoplasmic mobility of ruffled
border
PTH: parathyroid hormone.

Diagnosis of Resorption
Clinically: Pink spot in case of internal resorption
Imaging
‰ Conventional radiograph
‰ Digital radiographs
‰ CT scan
‰ Rapid prototyping tooth model
‰ Cone beam computed tomography (CBCT)

Vitality testing
If tooth is vital: Internal root resorption or subepithelial Fig. 31.4 Internal resorption showing oval-shaped enlargement
external root resorption. of root canal space.

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Clinical Features
‰ Internal root resorption is usually asymptomatic until
root is perforated. It is detected coincidentally by routine
radiographs
‰ Patient may complain of pain when the lesion perforates
and tissue is exposed to oral fluids (Fig. 31.5)
‰ Most commonly affected teeth are maxillary central
incisors
‰ Usually single tooth is involved but sometimes multiple
teeth are also involved
‰ It occurs in permanent as well as in deciduous teeth. In
primary teeth, it spreads more rapidly
‰ Granulation tissue can clinically manifest itself as a “pink
spot” where crown dentin destruction is severe leading
to pink tooth appearance (Fig. 31.6).
Fig. 31.7 Radiograph showing oval radiolucent enlargement of
pulp space in mandibular lateral incisor with internal resorption.

Radiographic Features
Outline of lesion: Lesion appears as uniform, round-to-
oval radiolucent enlargement of the pulp space (Fig. 31.7).
Outline of root canal: There is distortion of original root
canal outline.
Radiographs are taken from different angles to show the
resorptive lesion in the central location.

Types of Internal Resorption

‰ Internal replacement resorption
‰ Internal inflammatory resorption

Internal Replacement Resorption

Fig. 31.5 Line diagram showing internal resorption with root
perforation. (Metaplastic Resorption)
Resorption of dentin and subsequent deposition of hard
tissues are found that resembles bone or cementum or oste-
odentin, but not dentin. They represent areas of destruction
and repair. This occurs mainly due to low grade irritation
of pulpal tissue.

Etiology
‰ Trauma
‰ Extreme heat to the tooth
‰ Chemical burns
‰ Pulpotomy procedures

Radiographic Features
Radiographically, the tooth shows enlargement of the
canal space. This space latter gets engorged with a mate-
Fig. 31.6 Photograph showing internal resorption of right rial of radiopaque appearance giving the expression of
maxillary central incisor resulting in pink tooth appearance. hard tissue.

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Histopathology ‰ According to Heithersay, the internal resorption may

Histological studies of internal resorption demonstrate result from collateral blood supply via an interconnect-
replacement of normal pulp tissue by a periodontal-like con- ing large accessory canal, which provides a vascular bed
nective tissue with both osteogenic and resorptive potential. for the process

Origin of metaplastic hard tissue Clinical Features

‰ Metaplastic hard tissue formed in replacement resorp-
Clinical characteristics of internal root resorption are depend-
tion is produced by postnatal dental pulp stem cells
ent on the development and location of the resorption.
present in apical part of root canal as reparative response ‰ It is asymptomatic in most of the cases, but when resorp-
to restorative insult
tion is actively progressing, it may present symptoms of
‰ Both granulation tissue and metaplastic hard tissue are
pulpitis
nonpulpal in origin and might be derived from cells ‰ If it occurs in or near the crown, a pinkish or reddish color
that transmigrated from vascular compartment from
is seen through the crown and appears gray/dark gray if
periodontium.
the pulp becomes necrotic
‰ In advance cases of resorption, perforation of the root
Internal Inflammatory Resorption
is usually followed by the development of a sinus tract
This is that form of internal resorption in which progressive ‰ Internal resorption is active only in teeth where a part of
loss of dentin is present without deposition of any form of the pulp remains vital. Therefore, pulp tests may show
hard tissue in the resorption cavity. different responses, a positive pulp test if the coronal
pulp is vital, or a negative pulp test if the coronal pulp
Pathophysiology (Fig. 31.8) becomes necrotic while the apical pulp is vital
‰ Long-standing injury leads to chronic pulp inflammation
and circulatory changes within the pulp. Active hyper- Radiographic Features
emia with high oxygen pressure supports and induces It presents round or ovoid radiolucent area in the central
the osteoclastic activity portion of the tooth with smooth well-defined margins. The
‰ Electric activity: Piezoelectricity arising due to increased defect does not change its relation to the tooth, when the
blood flow adds to the resorptive process rays are projected from an angulation.
‰ Sudden trauma leads to intrapulpal hemorrhage, which
latter organizes to form clot and forms the granulation
Histology
tissue. Proliferating granulation tissues compresses the
dentinal walls and stimulate the formation of odonto- Pulp tissue shows chronic inflammation reaction and
blasts which differentiate from the connective tissue. resorption lacunae irregularly occupied by “dentinoclasts”
Thereby, the resorption process starts. similar to osteoclasts. The granulation tissue present in this
type of resorption is highly proliferating in nature.

Classification
Internal inflammatory resorptions may be classified accord-
ing to location as
• Apical
• Intraradicular

Apical internal inflammatory resorption

‰ Seen in teeth with inflammatory periapical pathologies
‰ Management: There are two approaches to the endodon-
tic management of apical internal resorption:
• To extend instrumentation only to the position of
the resorption with the expectation that removal of
microorganisms followed by root canal filling, hard
tissue repair will occur in the resorbed apical region
of the tooth
Fig. 31.8 Chronic irritation of pulp can induce osteoclastic • To enlarge and prepare the apical region, either
activity in pulp, resulting in internal inflammatory resorption. with hand or rotary filing techniques, to include the

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 Root Resorption 489
resorbed region and then root fills to the root canal
“terminus”
Intraradicular inflammatory resorption
‰ Internal resorption fully contained within an otherwise
intact root will be referred to as intraradicular internal
inflammatory resorption
‰ This can be recognized as round- or oval-shaped radio-
lucencies contained within the root
‰ A common finding is a large accessory canal commu-
nicating from the periodontal ligament to the resorbed
area; this may have allowed the passage of a collateral
blood supply which probably played an important role
in the development and maintenance of the internal
resorptive process
‰ Treatment is endodontic therapy. The obturation of the A B
canal can be done by using vertically condensed gutta- Figs. 31.9A and B (A) Internal resorption; (B) external resorption.
percha, obtura, or microseal technique

Differences between internal and external resorption (Figs. 31.9A and B)

Internal resorption External resorption
Definition • Internal resorption is the resorption that begins • It is defined as loss of tooth substance from outer
centrally within the tooth, apparently initiated by a surface of the tooth, arising from a tissue reac-
peculiar inflammation of the pulp tion in periodontal or pericoronal tissue
Canal shape • It is characterized by oval-shaped enlargement of • Canal shape is not altered
root canal space • Defect is separate and is superficial on root
• Causes expansion of the canal lateral to the canal
Pink tooth of • Pathognomic feature • Pink tooth not seen
mummery • Hyperplastic vascular pulp tissue showing through • Pulp is nonvital consisting of granulation tissue
the tooth
Symmetry • Symmetric defect though may be eccentric • Usually asymmetrical
Margins • Smooth and well defined • Rough with moth eaten appearance
Radiographic • Ballooning of canal space • Scooped out areas on the root surface
appearance • Lesion appears close to canal even if angulation of • Lesion moves away from canal as the angulation
radiograph changes changes
• Root canal and resorptive defect appears contiguous • Root canal can be seen running through the
• Does not involve bone so radiolucency is confined to defect
root. Bone resorption is seen if lesion perforates the • It involves resorption of bone, so radiolucency
root appears both in root and bone
Pulp vitality test • Pulp is vital unless it gets involved • Pulp is nonvital as it commonly involves infected
pulp space

Management of Internal Root Resorption ‰ Teeth with perforation often need both surgical and non-
surgical procedures
‰ Early diagnosis is important to prevent the weaken-
ing of the remaining root structure by the resorptive Treatment options in teeth with internal resorption
process • Without perforation: Endodontic therapy
‰ Conventional root canal therapy should be instituted • With perforation
as soon as the diagnosis of internal resorption is – Nonsurgical: Ca(OH)2 therapy—obturation
made – Surgical:
‰ If the apical third is not involved, then the cases are Surgical flap
treated as usual and the resorbed area is filled with warm Root resection
Intentional replantation
gutta-percha technique

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Management of Nonperforating Resorption Various materials used include:

Pulp removal and canal preparation: Removal of all
‰ MTA
inflamed tissue from the resorptive defect is the basis of
‰ Glass ionomer cement
the treatment. But sometimes complete extirpation of the
‰ Super EBA
inflamed tissue may become difficult by hand instruments.
‰ Hydrophilic plastic polymer (2-hydroxyethyl meth-
Evidence shows that ultrasonic instruments can give better acrylate with barium salts)
results as compared to hand instruments. Ultrasonic vibra-
‰ Zinc oxide eugenol and zinc acetate cement
tion is unparalleled in its ability to enhance cleaning with
‰ Amalgam alloy
irrigant (Fig. 31.10).
‰ Thermoplasticized gutta-percha administered either by
injection or condensation techniques
Canal obturation: Because of the size, irregularity and
in accessibility of the resorption defects, obturation of the Management of Perforating Internal Resorption
canal may be technically difficult. When the internal root resorption has progressed through
Canal apical to the defect is filled with solid gutta-percha the tooth into the periodontium, there are additional
while the resorptive area is usually filled with material that problem of periodontal bleeding, pain and difficulty in
will flow in the irregularities. The warm gutta-percha tech- obturation. Presence of a perforation cannot be determined
nique, thermoplasticized gutta-percha technique and the radiographically unless a lateral radiolucent lesion is pre-
use of chemically plasticized gutta-percha are methods of sent adjacent to the lesion. Clinically in some cases, a sinus
obturation to be used (Figs. 31.11 to 31.15). tract may be present and there will be continued hemor-
rhage in the canal after the pulp is removed.
Nonsurgical repair
Indications of nonsurgical repair:
‰ When the defect is not extensive
‰ When defect is apical to epithelial attachment
‰ When hemorrhage can be controlled
In this technique, after thorough cleaning and shaping
of the canal, the intracanal calcium hydroxide dressing is
placed and over it a temporary filling is placed to prevent
interappointment leakage.
Patient is recalled after 3 months for replacement of cal-
cium hydroxide dressing and for radiographic confirmation
of the barrier formation at the perforation site. Afterwards,
2 months recall visits are scheduled until there is a radio-
graphic barrier at resorption defect. After the barrier is
formed, the canal is obturated with gutta-percha as in the
Fig. 31.10 Use of ultrasonics helps in better cleaning of canal. nonperforating internal resorption.

A B C D E
Figs. 31.11 A to D Management of internal resorption case of maxillary central incisor: (A) Preoperative radiograph of central incisor
showing internal resorption defect; (B) Working length radiograph; (C) Obturation of canal by Obtura II; (D and E) Confirmation of internal
resorption before and after on CBCT.

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Surgical repair
If it is not possible to get access to the lesion through the
canal, surgical repair of the defect should be considered.
Treatment options in surgical repair can be
‰ Surgical flap: Defect is exposed to allow good access.
The resorptive defect is curetted, cleaned and restored
A B
using an alloy, composite, glass ionomer cement, super
EBA, MTA, biodentine, etc. Final obturation is done using
gutta-percha
‰ Root resection: If the resorbed area is located in the
apical third, root may be resected coronal to the defect
and apical segment is removed afterwards. Following
root resection, retrofilling is done. If one root of a
multirooted tooth is affected, root resection may be
C D considered based on anatomical, periodontal and
restorative parameters
Figs. 31.12A to D Management of 36 with internal resorption. (A)
‰ Intentional replantation: If the perforating resorption
Preoperative radiograph; (B) Working length radiograph; (C) Master
cone radiograph; (D) Obturation by themoplasticized gutta-percha. with minimal root damage occurs in an inaccessible area,
Courtesy: Jaidev Dhillon intentional replantation may be considered.

A B C
Figs. 31.13A to C Management of internal resorption with MTA and obtura using cone beam computed tomography (CBCT):
(A) CBCT view of internal resorption; (B) MTA plug at apical part of root; (C) Postobturation radiograph.
Courtesy: Anil Dhingra

A B C
Figs. 31.14A to C Management of maxillary second premolar with internal resorption. (A) Preoperative radiograph;
(B) Working length radiograph; (C) Obturation by themoplasticized gutta-percha.
Courtesy: Punit Jindal

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A B C
Figs. 31.15A to C Management of mandibular lateral incisor with internal resorption: (A) Preoperative radiograph;
(B) Working length radiograph; (C) Obturation by themoplasticized gutta-percha.

External Root Resorption External resorption may be found in the following

conditions:
External root resorption is defined as loss of tooth substance ‰ Periodontal disease
from outer surface of the tooth, arising from a tissue reaction ‰ Luxation injuries
in periodontal or pericoronal tissue (Figs. 31.16A and B). ‰ Hypoparathyroidism
‰ Hyperparathyroidism
Classification ‰ Turner syndrome
According to Rita F Ne, Gutman et al. (Quintessence International, ‰ Paget disease
1999), external resorption is of three types: ‰ Gaucher disease
• Surface resorption ‰ Radiation therapy
• Inflammatory root resorption
• Replacement resorption Surface Resorption (Fig. 31.17)
External surface resorption is a transient phenomenon in
According to Cohen, on the basis of the location: which the root surface undergoes spontaneous destruction
• Cervical and repair. It is the least destructive form of external root
• Lateral resorption and is a self-limiting process; hence, it requires
• Apical
no treatment.

A B
Figs. 31.16A and B External resorption: (A) Schematic representation of external root resorption; (B) Radiograph showing external root
resorption of distal root of mandibular first molar.

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Progressive surface resorption: In this type, the surface
resorption is the beginning of more destructive resorp-
tion, either inflammatory resorption or replacement
resorption.

Treatment
No treatment is indicated.

External Inflammatory Root Resorption

(Fig. 31.18)
It is the most common and most destructive type of resorp-
tion and is thought to be caused by presence of infected or
necrotic pulp tissue in the root canal. It is best described
as a bowl-shaped resorptive defect that penetrates dentin
Fig. 31.17 Surface resorption. (Fig. 31.19).

Etiology
‰ As part of the repair process
‰ Indirect physical injury, caused by physiologic function,
to localized areas of periodontal ligament or cementum
on root surface
‰ In trauma, it occurs because of direct mechanical contact
of the root surface and alveolar bone proper

Clinical Evaluation
No significant signs of external surface resorption are
detectable on the supragingival portion of the tooth.

Radiographic Evaluation
External surface resorption is usually not visible on radio-
graphs because of its small size. Later, it appears as small Fig. 31.18 External inflammatory resorption.
excavations on the lateral surface or at the root apex result-
ing in the appearance of shorter roots.

Histologic Evaluation
Small, superficial lacunae in the cementum and outermost
layer of dentin are seen which are simultaneously being
repaired with new cementum.

Classification
Surface resorption can be
‰ Transient
‰ Progressive

Transient surface resorption: In this type, the tooth has

a vital, healthy pulp that has recovered from traumatic
event. In such cases, the resorbed area will be restored
completely to normal surface contour by deposition of Fig. 31.19 Progression of inflammatory root resorption. It forms a
new cementum. bowl-shaped resorptive defect which penetrates dentin.

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Etiopathology Clinical Features

‰ Injury or irritation to the periodontal tissues where the ‰ Patient gives history of trauma
inflammation is beyond repair ‰ Signs of necrotic pulp/irreversible pulpitis
‰ Trauma leads to pulpal necrosis which may further ‰ Tooth is usually mobile
cause periodontal inflammation due to the passage of ‰ Inflammation of periodontal tissue
the toxins and microorganisms from the infected pulp, ‰ Percussion sensitivity is present
lateral canals, apical foramen, accessory canals, dentinal
tubules where there is a discontinuity of cementum Radiographic Features (Figs. 31.22A to C)
‰ Orthodontic tooth movement using excessive forces Bowl-like radiolucency with ragged irregular areas on the
(Fig. 31.20) root surface is commonly seen in conjunction with loss of
‰ Trauma from occlusion—leading to periodontal tooth structure and alveolar bone. Small lesion of external
inflammation root resorption usually go undetected.
‰ Avulsion and luxation injuries
‰ Pressure resorption occurring from pressure exerted by Histologic Evaluation
tumors, cysts and impacted teeth (Fig. 31.21)
Histologically, EIRR is represented by a bowl-shaped resorp-
‰ In the initial stages, bowl-shaped lacunae are seen in
tion area into cementum and dentin with inflammation of
cementum and dentin, if not controlled, it may resorb
adjacent periodontal tissue and infected or necrotic pulp
the entire root in latter stages
in the root canal.

Types of external inflammatory root resorption

Apical Lateral Cervical
Etiology Mainly trauma, Seen in luxation Injury to
inflammation and avulsion attachment
is confined to cases apparatus
apical area (Fig. below epithelial
31.23) attachment,
for example,
in orthdontic
tooth
movement,
bleaching of
nonvital tooth
Features Root resorption Cemental It is usually
at apical area loss is there, destructive,
Fig. 31.20 Orthodontic tooth movement resulting
bacterial toxins and there is
in inflammatory resorption.
pass through invasion of root
dentinal tubules by fibrovascular
and stimulate tissue from PDL
inflammatory
response in
periodontal
ligament
Clinical Symptoms Usually Asymptomatic,
features same as apical asymptomatic, probing may
periodontitis in later stages show profuse
tender on bleeding, in
percussion long-standing
cases pink tooth
appearance
which can
be confused
with internal
Fig. 31.21 External inflammatory root resorption resulting due to
resorption
pressure exerted by impacted 3rd molar.

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Treatment (Figs. 31.24 and 31.25)
Treatment of external inflammatory root resorption is
dependent on the etiology:
‰ If it is because of orthodontic treatment, remove the
pressure of orthodontic movement to arrest resorption
‰ In cervical resorption

• If pulp is vital and treatment of cervical resorption

is unlikely to cause pulpal injury, restore the defect
and carry on baseline thermal and electrical pulp
tests for records
• If treatment of the cervical resorption is likely to
cause pulpal injury, restore the defect and perform
endodontic treatment
‰ If pulp is nonvital, restore the defect and perform endo-
A B C
dontic treatment. If required, calcium hydroxide dressing
Figs. 31.22A to C External inflammatory root resorption: (A) In initial
is also given
stages, bowl-shaped resorption cavities are seen in root surface; (B)
‰ In case of infected gingival tissues, remove plaque and
More of resorption; (C) Complete resorption of root in later stages.
calculus and maintain periodontium
‰ Calcitonin can also be used as an interim root canal
medicament to assist in the inhibition of osteoclastic
bone and dentin resorption

Replacement Resorption/Dentoalveolar
Ankylosis (Fig. 31.26)
This is similar to ankylosis, but there is presence of an
intervening inflamed connective tissue, always progressive
and highly destructive. In this, tooth becomes a part of the
alveolar bone remodeling process and thus, progressively
resorbed. Ankylosis may be transient or progressive.
In the transient type, <20% of the root surface becomes
ankylosed. In such cases, reversal may occur, resulting in
re-establishment of a periodontal ligament connection
between tooth and bone.
Fig. 31.23 Radiograph showing apical root resorption in In the progressive type, tooth structure is gradually
maxillary central incisor. resorbed and replaced with the bone.

A B C D
Figs. 31.24A to D Management of external inflammatory root resorption of mandibular central incisors. (A) Preoperative radiograph
showing external root resorption involving roots of mandibular central incisors; (B) Working length radiograph; (C) Postobturation
radiograph; (D) Follow-up radiograph after 3 months.
Courtesy: Jaidev Dhillon

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A B C

D E
Figs. 31.25A to E Management of external root resorption of mandibular incisors: (A) Preoperative radiograph; (B) Working length
radiograph; (C) MTA plug at the apical third; (D) Postobturation radiograph; (E) Follow-up after 3 months.
Courtesy: Jaidev Dhillon

Etiopathogenesis
‰ Replacement resorption occurs after a severe dental
injury like intrusive luxation or avulsion resulting in dry-
ing and death of periodontal ligament cells
‰ An inflammatory process removes the necrotic debris
from the root surface which results in root surface devoid
of cementum
‰ To compensate this, cell in vicinity of root surface try to
repopulate it. Cells which form bone move across the socket
wall and colonize the damaged root wall. By this, bone
comes in direct contact with root without an intermediate
attachment apparatus resulting in dentoalveolar ankylosis

Histological Examination
‰ Direct fusion between dentin and bone without separat-
ing cemental or periodontal ligament layer
‰ Active resorption lacunae with osteoclasts are seen in con-
Fig. 31.26 Replacement resportion resulting in ankylosis. junction with apposition of normal bone laid by osteoblasts

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 Root Resorption 497
Clinical Features
‰ Replacement resorption is usually asymptomatic
‰ Infraocclusion, incomplete alveolar process develop-
ment (if the patient is young) and absence of normal
mesial drift
‰ Pathognomonic feature is immobility of affected tooth
and a distinctive metallic sound on percussion.

Radiographic Features
Moth eaten appearance with irregular border, absence of
periodontal ligament and lamina dura are seen in radio-
graphs of an ankylosed tooth.

Diagnosis
‰ Lack of mobility and high-pitched metallic sound on Fig. 31.27 Extracanal invasive resorption.
percussion
‰ Radiographically, loss of periodontal ligament space
with replacement by bone and uneven contour of root ‰ Bleaching of nonvital teeth
is indicative of ankylosis ‰ Periodontal treatment
‰ Bruxism
‰ Idiopathic
Treatment
Currently, there is no treatment for replacement resorption.
To slowdown the resorptive process, root surface is treated Etiopathogenesis
with fluoride solution prior to replantation if extraoral time Though it is a relatively common occurrence, it is not well
for tooth was >2 h and it was not kept moist to protect the recognized and often classified as idiopathic resorption
periodontal ligament. because of difficulty in establishing a cause and effect rela-
tion. It appears to originate in the cervical area of the tooth
Prevention below the epithelial attachment and often proceeds from
The following points should be considered in cases of a small surface opening to involve a large part of dentin
avulsion: between the cementum and the pulp.
‰ Immediate replantation without much of extraoral dry The resorption can proceed in several directions due to
time its invasive nature, hence the term invasive resorption. It
‰ Proper extraoral storage to prevent dehydration can extend coronally under the enamel, giving the tooth a
‰ In case of extended period of extraoral time, soak the pink spot appearance. Because cervical resorption is not
tooth in fluoride gel always associated with infected or necrotic pulp, the treat-
ment options vary accordingly.
Cervical Root Resorption
Theories of Cervical Root Resorption
(Extracanal Invasive Resorption)
‰ Some procedures like bleaching, trauma, or orthodontic
According to Cohen, it is the type of inflammatory root treatment cause alteration in the organic and inorganic
resorption occurring immediately below the epithelial cementum, finally making it more inorganic. This makes
attachment of tooth. Epithelial attachment need not be the cementum less resistant to resorption
always exactly at the cervical margin but can also be apical ‰ Immunological system senses the altered root surface,
to the cervical margin (Fig. 31.27). So the term “cervical” as a different tissue, attacks as a foreign body
is a misnomer.
Clinical Features
Etiology ‰ Initially, the cervical root resorption is asymptomatic in
According to Heithersay, etiology can be nature. Pulp is vital in most of the cases
‰ Orthodontic treatment ‰ It initially starts as a small lesion, progress and reaches
‰ Trauma the predentin. Predentin is more resistant to resorption,

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498 Textbook of Endodontics

spreads laterally in apical and coronal direction “envel- Frank’s Classification of Cervical Root
oping” the root canal Resorption (Figs. 31.29A to C)
‰ In long-standing cases, extensive loss of tooth structure
is replaced by granulation tissues which undermines the ‰ Supraosseous: Coronal to the level of alveolar bone
enamel in due course giving rise to pink spot appearance. ‰ Intraosseous: Not accompanied by periodontal breakdown
It is misdiagnosed as internal resorption, but confirmed ‰ Crestal: At the level of alveolar bone
with a radiograph. Rarely, it perforates into the tooth
causing secondary involvement of pulp Radiographic Features
Radiographically, one can see the moth eaten appearance with
Heithersay’s Classification (Fig. 31.28)
the intact outline of the canal. Because bone is often involved,
Class I: A small invasive resorptive lesion near cervical area resorption may give the appearance of an infrabony pocket.
with shallow penetration into dentin.
Class II: Well-defined resorptive defect close to coronal Treatment
pulp chamber, but little or no involvement of radicular
dentin. Main aim of the treatment is to restore the lost tooth struc-
Class III: Deep resorptive lesion involving coronal pulp and ture and to disrupt the resorptive process. Since pulp is
also coronal-third of the root. mostly vital, repair of resorbed area without removing the
Class IV: Resorptive defective extending beyond coronal- pulp is done. Heithersay recommended topical application
third of root canal. of 90% solution of trichloroacetic acid (to cause coagulation

Fig. 31.28 Heithersay’s classification of cervical root resorption.

A B C
Figs. 31.29A to C Frank’s classification of cervical root resorption: (A) Supraosseous; (B) Intraosseous;
(C) Crestal extracanal invasive resorption.

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 Root Resorption 499
and necrosis of necrotic tissue), curettage and then resto- 2. Classify external root resorption. Write in detail about
ration with glass ionomer cement. If symptoms of pulpitis replacement resorption.
develop later, endodontic treatment is done. 3. Write short notes on
• Differential diagnosis of internal and external
Conclusion resorption.
• Cervical root resorption.
Tooth resorption is a perplexing problem where the etio-
logic factors are vague and less clearly defined. For the best
treatment outcome, the clinician should have a very good
Bibliography
knowledge of the etiopathology of resorptive lesions. Early 1. AAE Glossary of Endodontic Terms. American Association of
diagnosis and prompt treatment in such cases are the key Endodontists website. 2014. Accessed July 29, 2016.
factors which determine the success of the treatment. More 2. Gartner AH, Mack T, Somerlott RG, Walsh LC. Differential
clinical studies and research with animal models are required diagnosis of internal and external root resorption. J Endod.
1976;2(11):329–334.
to explain more about this phenomenon scientifically.
3. Kuo T-C, Cheng Y-A, Lin C-P. Clinical management of severe
external root resorption. Chin Dent J. 2005;24(1):59–64.
Questions 4. Maria R, Mantri V, Koolwal S. Internal resorption: A review and
case report. Endodontology. 2010;22(1):100–108.
1. Define and classify root resorption. Write in detail about
internal resorption.

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