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Introduction: The usage of Calcium hydroxide (CaOH2) has wide applications due to the property of osteo-inductive, protective, and antibacterial actions. However, it is not used in primary teeth, as it fails to form reparative dentin and the exact mechanism has not been explained. The hypothesis: The authors propose an explanation that lack of dentin bridge formation in response to (CaOH2) in primary teeth could be multifactorial: inability of the deciduous stem cells to generate complete dentin-pulp-like tissue; the absence of calcium-magnesium-dependent adenosine triphosphatase (Ca-Mg ATPase) in the odontoblasts; the pre-existing predilection of deciduous dentine pulp to form odontoclasts; the solubility of (CaOH2). Evaluation of the hypothesis: The hypothesis discusses the innate traits of the deciduous stem cells that lack the ability to form the dentin bridge, the absence of Ca-Mg ATPase enzyme and increased solubility of (CaOH2) together fail to stimulate the odontoblasts. Alternatively, pre-existing progenitor cells with proclivity to change into odontoclasts may cause internal resorption and hamper formation of reparative dentin.

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.