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Year : 2012  |  Volume : 3  |  Issue : 3  |  Page : 90-94

Calcium hydroxide-induced resorption of deciduous teeth: A possible explanation

1 Department of Pedodontics, Drs Sudha and Nageswara Rao Siddhartha Institute of Dental Sciences, Chinoutapally, Gannavaram, Andhra Pradesh, India
2 Department of Oral Pathology, Drs Sudha and Nageswara Rao Siddhartha Institute of Dental Sciences, Chinoutapally, Gannavaram, Andhra Pradesh, India

Date of Web Publication27-Nov-2012

Correspondence Address:
R V Subramanyam
Department of Oral Pathology, Drs Sudha and Nageswara Rao Siddhartha Institute of Dental Sciences, Chinoutapally, Gannavaram-521 286, Andhra Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2155-8213.103910

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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.

Keywords: Calcium hydroxide, deciduous, internal resorption, odontoclast, progenitor

How to cite this article:
Ravi G R, Subramanyam R V. Calcium hydroxide-induced resorption of deciduous teeth: A possible explanation. Dent Hypotheses 2012;3:90-4

How to cite this URL:
Ravi G R, Subramanyam R V. Calcium hydroxide-induced resorption of deciduous teeth: A possible explanation. Dent Hypotheses [serial online] 2012 [cited 2023 Jan 31];3:90-4. Available from:

  Introduction Top

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],[4],[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],[7],[8],[9] However, the usage of calcium hydroxide is not routinely recommended for primary dentition because its application frequently results in the development of chronic pulpal inflammation and internal root resorption. [10],[11],[12],[13],[14],[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 Top

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 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].
    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)

    Click here to view

  Evaluation of the Hypothesis Top

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, 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],[23],[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],[11],[12] Various inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukins (IL)-1α, IL-β, IL-6, IL-11, and IL-17, prostaglandin E2 (PgE2), and tumour growth factor-β (TGF-) are all known to stimulate osteoclast differentiation and activation. [26],[27],[28],[29] Similarly, in the case of primary teeth, CaH-induced inflammation could activate preodontoclasts and transform them into odontoclasts.

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-1β 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-1β. [30] Such cytokines can recruit more monocytes and macrophages, which may fuse to form odontoclasts and cause resorption [Figure 1]a.

The second and more likely pathway involves the RANK (Receptor Activator of Nuclear factor Kappa β-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 1]b The binding of RANKL to RANK is an essential step in the promotion of odontoclast differentiation and resorption. [29],[31],[32],[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-α and interleukins (IL-1α, IL-β, 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 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 1]c.

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 1]d.

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 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.

  References Top

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