Calcium Hydroxide Induced Resorption of Deciduous Teeth A Possible Explanation
Calcium Hydroxide Induced Resorption of Deciduous Teeth A Possible Explanation
Calcium Hydroxide Induced Resorption of Deciduous Teeth A Possible Explanation
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ORIGINAL HYPOTHESIS
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.
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
addition, the loss of predentin could expose mineralized promoting pulp cells to differentiate into new
dentin to odontoclasts, making it more vulnerable to odontoblasts that place a mineralized dentin bridge on
resorption. Various mechanisms involved in triggering the pulp exposure.[20,21] This is probably because of the
resorption of deciduous teeth on placement of CaH are high alkaline pH (nearly 12.5) of CaH, which is employed
illustrated as a schematic flowchart in Figure 1. for obtaining the bactericidal action through the release
of hydroxyl ions in an aqueous environment.[22-24]
Evaluation of the Hypothesis Surprisingly, the very properties of CaH that produce
healing in permanent teeth, provoke untoward
When CaH was introduced, it was presented as an reactions in the pulps of primary teeth.[25] These intense
alternative to formocresol for vital pulp treatment in inflammatory responses to high alkaline pH of CaH in
primary teeth,[16] but it was later found that internal deciduous teeth could trigger macrophages to fuse and
resorption rather than dentine formation occurred in transform into odontoclasts.
primary teeth.[17] However, some researchers claim
that internal resorption following CaH pulpotomies of The role of inflammatory response to calcium
primary teeth could be caused by pre-existing pulpal hydroxide in odontoclastogenesis
inflammation prior to treatment[18] or the presence Chronic inflammatory reaction in deciduous teeth
of an extravascular blood clot intervening between is rapid, diffuse and often results in extensive tissue
the chemical and the pulp tissue.[19] Nevertheless, destruction.[10-12] Various inflammatory cytokines such
internal resorption of primary teeth was still observed as tumor necrosis factor- (TNF-), interleukins (IL)-1,
even though stringent conditions were taken to avoid IL-, IL-6, IL-11, and IL-17, prostaglandin E2 (PgE2), and
clotting.[12] tumour growth factor- (TGF-) are all known to stimulate
osteoclast differentiation and activation.[26-29] Similarly,
When CaH is applied directly to the pulp tissue, it in the case of primary teeth, CaH-induced inflammation
produces a limited necrotic zone of superficial could activate preodontoclasts and transform them into
liquefaction necrosis that causes a mild irritation, odontoclasts.
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)
Essentially, there are two pathways for odontoclastogenesis in pulpal tissues of permanent teeth, supporting the
to occur. The first involves activation of odontoclastic cells preferential resorption of primary teeth.[39]
through the ATPP2XR7 (a gene coding for a purinergic
ligand-gated ion channel)IL-1 inflammation modulation Hence, in the case of deciduous teeth, even before the
pathway. Local damage of tissue may result in ATP actual time for exfoliation of deciduous teeth, there is an
release, which can activate the receptor P2 R7 on inherent predilection for the formation of odontoclasts.
macrophages or other cell types leading to further release This pre-existing propensity for transformation could be
of cytokines including IL-1.[30] Such cytokines can recruit influenced or hastened by placement of CaH–probably
more monocytes and macrophages, which may fuse to through its high alkaline pH [Figure 1c].
form odontoclasts and cause resorption [Figure 1a].
The role high alkaline pH of calcium hydroxide
The second and more likely pathway involves the RANK The high pH of CaH has beneficial effects which include
(Receptor Activator of Nuclear factor Kappa –expressed the neutralization of acid products, antimicrobial
by odontoclasts)RANKL (RANK ligand–expressed property, and the activation of alkaline phosphatase.[40]
by odontoblasts, pulp, and periodontal ligament The pH of most calcium hydroxide pastes is
(PDL) fibroblasts, as well as by cementoblasts)OPG approximately 12. The exposure of CaH to blood results
(osteoprotegerin). RANK-RANKL stimulate odontoclast in crystalline precipitation due to the intensely differing
formation and the OPG, a secreted decoy receptor for pH values.[41,42] In the case of permanent dentition, when
RANKL, regulates negatively the odontoclastogenesis. CaH is applied in direct pulp capping, because of its high
[Figure 1b] The binding of RANKL to RANK is an essential alkaline pH, it promotes pulp cells to differentiate into
step in the promotion of odontoclast differentiation and new odontoblast-like cells that generate a mineralized
resorption.[29,31-33] dentin bridge on the area of pulp exposure.[21] This
happens because there is an inherent proclivity for
The two important factors that could positively impact odontoblasts to differentiate from undifferentiated
odontoclast differentiation are RANKL and macrophage mesenchymal cells in the case of permanent teeth.
colony stimulating factor (M-CSF).[34] M-CSF is known However, when CaH is placed in deciduous teeth, it is
to facilitate osteoclast differentiation by promoting very likely that the same high alkaline pH could trigger
cell survival and proliferation of osteoclast precursors, existing pre-odontoclasts (stromal undifferentiated
inducing RANK on hematopoietic cells so they can mesenchymal cells) to transform into odontoclasts.
respond to RANKL, and regulating cytoskeletal changes
associated with bone resorption.[35] In a similar fashion, it The role of predentin
could expedite odontoclast differentiation and resorption It has been well-established by previous studies that
in deciduous teeth. Thus, odontoclastic resorption could resorption can occur when the protective unmineralized
be directly related to CaH placement in primary dentition. tissues such as precementum and predentine are
breached or mechanically damaged, allowing
The role of pre-existing progenitor cells in osteoclasts/odontoclasts to gain access to calcified
odontoclastogenesis dental tissues.[43,44] It is known that the placement of
It is a known fact that all deciduous teeth are eventually CaH produces a superficial zone of necrosis because of
shed off by 12 years of age. Therefore, it is not surprising to its high alkalinity.[20,21] This could also cause damage to
expect predilection for formation of odontoclasts at the time the predentine, which in turn could lead to exposure
of exfoliation of deciduous teeth. However, it is astonishing of the underlying dentin to resting odontoclasts. These
to note that there is a high propensity for the formation odontoclasts, thus activated, could result in tooth
of odontoclasts well ahead of the eruption of deciduous resorption [Figure 1d].
teeth.[36,37] Even before the eruption of the deciduous
teeth into the oral cavity, probably under the influence Research implications
of various factors like tartrate-resistant acid phosphatase Resorption of primary teeth due to placement of
(TRAP), RANK, RANKL, M-CSF, cytokines such as TNF- CaH is multifactorial, which may or may not be
and interleukins (IL-1, IL-, IL-6, IL-11, IL-17), the mutually exclusive. Though it has been established
progenitor cells could be transformed into pre-odontoclasts that odontoclasts that form in response to CaH cause
which in turn transform into odontoclasts. [29,37,38] resorption of deciduous teeth, the exact process
Yildrim et al. observed that there is significant expression needs to be probed. Our hypothesis provides an
of RANKL and M-CSF in the primary dental pulp than explanation how these events could occur but these
40. Souza V, Bernabe PF, Holland R, Nery MJ, Mello W, Otoboni 44. Tronstad L. Root resorption—A multidisciplinary problem in
Filho JA. Tratamento naõ-cirurgico de dentes com lesões dentistry. In: Davidovitch Z, editor. Biological mechanisms in
periapicais. Rev Brasil Odont 1989;46:39-46. tooth eruption and resorption. Proceedings of the International
41. Nelson Filho P, Silva LA, Leonardo MR, Utrilla LS, Figueiredo F. Conference on Biological Mechanisms of Tooth Eruption and
Connective tissue responses to calcium hydroxide-based root Root Resorption; March 2-4, 1988; Columbus, Ohio: Columbus
canal medicaments. Int Endod J 1999;32:303-11. State University. Columbus, OH: The Ohio State University;
42. Shimizu T, Kawakami T, Ochiai T, Kurihara S, Hasegawa H. 1988; p. 298-302.
Histopathological evaluation of subcutaneous tissue reaction
in mice to a calcium hydroxide paste developed for root canal
fillings. J Int Med Res 2004;32:416-2. Cite this article as: Ravi GR, Subramanyam RV. Calcium hydroxide-induced
resorption of deciduous teeth: A possible explanation. Dent Hypotheses
43. Reitan K. Biomechanical principles and reactions. In: Graber
2012;3:90-4.
TM, Swain BF, editors. Orthodontics: current principles and
Source of Support: Nil, Conflict of Interest: No.
techniques. St Louis: C.V. Mosby; 1985. p. 101-92.
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