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Calcium hydroxide-induced resorption of

deciduous teeth: A possible explanation

Article in Bioscience Hypotheses · November 2012

DOI: 10.4103/2155-8213.103910

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ORIGINAL HYPOTHESIS

Calcium hydroxide–induced resorption of

deciduous teeth: A possible explanation
G. R. Ravi, R. V. Subramanyam1
Departments of Pedodontics, and 1Oral Pathology, Drs Sudha and Nageswara Rao Siddhartha Institute of Dental Sciences, Chinoutapally,
Gannavaram, Andhra Pradesh, India

A B S T R A C T

Introduction: Calcium hydroxide (CaH) is customarily used for permanent teeth but not for deciduous dentition because it is known
to cause internal resorption in the latter. Though this has been attributed to chronic inflammation and odontoclasts, the exact
mechanism has not been elucidated. The Hypothesis: The authors propose an explanation that CaH-induced odontoclastogenesis
could be multifactorial. Odontoclasts may result from fusion of cells of monocyte/macrophage series either due to inflammatory
mediators or through stimulation by stromal odontoblasts /fibroblasts. Pre-existing progenitor cells of primary tooth pulp because
of their inherent propensity may transform into odontoclasts. Evaluation of the Hypothesis: The hypothesis discusses the role
of various inflammatory cytokines that may be responsible for CaH-induced transformation of pre-odontoclasts to odontoclasts.
Alternatively, pre-existing progenitor cells with proclivity to change into odontoclasts may cause internal resorption. The loss of
protective layer of predentin over mineralized dentin may also make the primary tooth more susceptible to resorption.

Key words: Calcium hydroxide, deciduous, internal resorption, odontoclast, progenitor

Introduction the development of chronic pulpal inflammation and

Calcium hydroxide (CaH) was originally introduced to
the field of endodontics by Herman in 1920 as root canal
filling and antimicrobial agent.[1,2] Since then, CaH has
been used for various endodontic procedures including
pulp capping, pulpotomy, intracanal medication,
apexification, root perforation, and is found in some
root canal sealants.[3-5]
The two most important reasons for using CaH in
endodontics are its antimicrobial effect and the
potential to stimulate mineralized repair of pulp and
periapical tissues.[6-9] However, the usage of calcium
hydroxide is not routinely recommended for primary
dentition because its application frequently results in
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DOI:
10.4103/2155-8213.103910
internal root resorption.[10-15]
When CaH is placed in permanent teeth, it results in
calcific (dentin) bridge formation, but in primary teeth
it is likely to cause internal resorption. Though various
theories have been proposed and suggested to elucidate
this phenomenon, the exact mechanism continues to
be obscure. Therefore, the authors present a hypothesis
that could possibly provide an explanation.
The Hypothesis
We hypothesize that odontoclasts cause resorption
of primary teeth on the placement of CaH and this
odontoclastogenesis could be as a result of:
• CaH-induced chronic inflammatory response which
could influence the macrophages to fuse and form
odontoclasts
 either through direct stimulation,
 or indirectly by stimulating stromal odontoblasts/
fibroblasts.
• A pre-existing predilection of progenitor cells in
deciduous tooth pulp to form odontoclasts. In

Corresponding Author: Dr. R. V. Subramanyam, Department of Oral Pathology, Drs Sudha and Nageswara Rao Siddhartha Institute of Dental
Sciences, Chinoutapally, Gannavaram–521 286, Andhra Pradesh, India. E-mail: subrarv@gmail.com

90 Dental Hypotheses Jul-Sep 2012 / Vol 3 | Issue 3

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Ravi and Subramanyam: Calcium hydroxide and internal resorption
addition, the loss of predentin could expose mineralized
dentin to odontoclasts, making it more vulnerable to
resorption. Various mechanisms involved in triggering
resorption of deciduous teeth on placement of CaH are
illustrated as a schematic flowchart in Figure 1.
Evaluation of the Hypothesis
When CaH was introduced, it was presented as an
alternative to formocresol for vital pulp treatment in
primary teeth,[16] but it was later found that internal
resorption rather than dentine formation occurred in
primary teeth.[17] However, some researchers claim
that internal resorption following CaH pulpotomies of
primary teeth could be caused by pre-existing pulpal
inflammation prior to treatment[18] or the presence
of an extravascular blood clot intervening between
the chemical and the pulp tissue.[19] Nevertheless,
internal resorption of primary teeth was still observed
even though stringent conditions were taken to avoid
clotting.[12]
When CaH is applied directly to the pulp tissue, it
produces a limited necrotic zone of superficial
liquefaction necrosis that causes a mild irritation,
Figure 1: Flowchart depicting the cascade of events and factors that could be responsible for CaH-induced resorption of deciduous teeth (See text for
explanation)
Jul-Sep 2012 / Vol 3 | Issue 3
promoting pulp cells to differentiate into new
odontoblasts that place a mineralized dentin bridge on
the pulp exposure.[20,21] This is probably because of the
high alkaline pH (nearly 12.5) of CaH, which is employed
for obtaining the bactericidal action through the release
of hydroxyl ions in an aqueous environment.[22-24]
Surprisingly, the very properties of CaH that produce
healing in permanent teeth, provoke untoward
reactions in the pulps of primary teeth.[25] These intense
inflammatory responses to high alkaline pH of CaH in
deciduous teeth could trigger macrophages to fuse and
transform into odontoclasts.
The role of inflammatory response to calcium
hydroxide in odontoclastogenesis
Chronic inflammatory reaction in deciduous teeth
is rapid, diffuse and often results in extensive tissue
destruction.[10-12] Various inflammatory cytokines such
as tumor necrosis factor- (TNF-), interleukins (IL)-1,
IL-, IL-6, IL-11, and IL-17, prostaglandin E2 (PgE2), and
tumour growth factor- (TGF-) are all known to stimulate
osteoclast differentiation and activation.[26-29] Similarly,
in the case of primary teeth, CaH-induced inflammation
could activate preodontoclasts and transform them into
odontoclasts.
Dental Hypotheses 91
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Ravi and Subramanyam: Calcium hydroxide and internal resorption
Essentially, there are two pathways for odontoclastogenesis
to occur. The first involves activation of odontoclastic cells
through the ATPP2XR7 (a gene coding for a purinergic
ligand-gated ion channel)IL-1 inflammation modulation
pathway. Local damage of tissue may result in ATP
release, which can activate the receptor P2  R7 on
macrophages or other cell types leading to further release
of cytokines including IL-1.[30] Such cytokines can recruit
more monocytes and macrophages, which may fuse to
form odontoclasts and cause resorption [Figure 1a].
The second and more likely pathway involves the RANK
(Receptor Activator of Nuclear factor Kappa –expressed
by odontoclasts)RANKL (RANK ligand–expressed
by odontoblasts, pulp, and periodontal ligament
(PDL) fibroblasts, as well as by cementoblasts)OPG
(osteoprotegerin). RANK-RANKL stimulate odontoclast
formation and the OPG, a secreted decoy receptor for
RANKL, regulates negatively the odontoclastogenesis.
[Figure 1b] The binding of RANKL to RANK is an essential
step in the promotion of odontoclast differentiation and
resorption.[29,31-33]
The two important factors that could positively impact
odontoclast differentiation are RANKL and macrophage
colony stimulating factor (M-CSF).[34] M-CSF is known
to facilitate osteoclast differentiation by promoting
cell survival and proliferation of osteoclast precursors,
inducing RANK on hematopoietic cells so they can
respond to RANKL, and regulating cytoskeletal changes
associated with bone resorption.[35] In a similar fashion, it
could expedite odontoclast differentiation and resorption
in deciduous teeth. Thus, odontoclastic resorption could
be directly related to CaH placement in primary dentition.
The role of pre-existing progenitor cells in
odontoclastogenesis
It is a known fact that all deciduous teeth are eventually
shed off by 12 years of age. Therefore, it is not surprising to
expect predilection for formation of odontoclasts at the time
of exfoliation of deciduous teeth. However, it is astonishing
to note that there is a high propensity for the formation
of odontoclasts well ahead of the eruption of deciduous
teeth.[36,37] Even before the eruption of the deciduous
teeth into the oral cavity, probably under the influence
of various factors like tartrate-resistant acid phosphatase
(TRAP), RANK, RANKL, M-CSF, cytokines such as TNF-
and interleukins (IL-1, IL-, IL-6, IL-11, IL-17), the
progenitor cells could be transformed into pre-odontoclasts
which in turn transform into odontoclasts. [29,37,38]
Yildrim et al. observed that there is significant expression
of RANKL and M-CSF in the primary dental pulp than
92 Dental Hypotheses
in pulpal tissues of permanent teeth, supporting the
preferential resorption of primary teeth.[39]
Hence, in the case of deciduous teeth, even before the
actual time for exfoliation of deciduous teeth, there is an
inherent predilection for the formation of odontoclasts.
This pre-existing propensity for transformation could be
influenced or hastened by placement of CaH–probably
through its high alkaline pH [Figure 1c].
The role high alkaline pH of calcium hydroxide
The high pH of CaH has beneficial effects which include
the neutralization of acid products, antimicrobial
property, and the activation of alkaline phosphatase.[40]
The pH of most calcium hydroxide pastes is
approximately 12. The exposure of CaH to blood results
in crystalline precipitation due to the intensely differing
pH values.[41,42] In the case of permanent dentition, when
CaH is applied in direct pulp capping, because of its high
alkaline pH, it promotes pulp cells to differentiate into
new odontoblast-like cells that generate a mineralized
dentin bridge on the area of pulp exposure.[21] This
happens because there is an inherent proclivity for
odontoblasts to differentiate from undifferentiated
mesenchymal cells in the case of permanent teeth.
However, when CaH is placed in deciduous teeth, it is
very likely that the same high alkaline pH could trigger
existing pre-odontoclasts (stromal undifferentiated
mesenchymal cells) to transform into odontoclasts.
The role of predentin
It has been well-established by previous studies that
resorption can occur when the protective unmineralized
tissues such as precementum and predentine are
breached or mechanically damaged, allowing
osteoclasts/odontoclasts to gain access to calcified
dental tissues.[43,44] It is known that the placement of
CaH produces a superficial zone of necrosis because of
its high alkalinity.[20,21] This could also cause damage to
the predentine, which in turn could lead to exposure
of the underlying dentin to resting odontoclasts. These
odontoclasts, thus activated, could result in tooth
resorption [Figure 1d].
Research implications
Resorption of primary teeth due to placement of
CaH is multifactorial, which may or may not be
mutually exclusive. Though it has been established
that odontoclasts that form in response to CaH cause
resorption of deciduous teeth, the exact process
needs to be probed. Our hypothesis provides an
explanation how these events could occur but these
Jul-Sep 2012 / Vol 3 | Issue 3
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Ravi and Subramanyam: Calcium hydroxide and internal resorption
mechanisms need to be substantiated with scientific
evidence. Whether the high alkaline pH of CaH can
actually result in stimulation of progenitor cells (pre-
odontoclasts) to form odontoclasts or not, also requires
to be investigated.
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Ravi and Subramanyam: Calcium hydroxide and internal resorption

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Cite this article as: Ravi GR, Subramanyam RV. Calcium hydroxide-induced
resorption of deciduous teeth: A possible explanation. Dent Hypotheses
2012;3:90-4.
Source of Support: Nil, Conflict of Interest: No.

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