Abstract
The findings from the recent literature on pulpal cell responses to the application of calcium hydroxide to exposed pulps are described. The effect of calcium hydroxide on healthy and inflamed pulp is discussed. The effect of incorporation of calcium hydroxide in various pulp-capping agents is presented.
The initial effect of calcium hydroxide applied to exposed pulp is the development of a superficial three-layer necrosis. The beneficial effect of calcium hydroxide is regarded as the result of the chemical injury caused by the hydroxyl ions, limited by a zone of firm necrosis against the vital tissue, and the toleration of calcium ions by the tissue. The firm necrosis causes slight irritation and stimulates the pulp to defense and repair. The observed sequence of tissue reactions is that which is expected when connective tissue is wounded. It starts with vascular and inflammatory cell migration and proliferation, to control and elimination of the irritating agent. This is followed by the repair process, including migration and proliferation of mesenchymal and endothelial pulp cells and formation of collagen. When the pulp is protected from irritation, odontoblasts differentiate, and the tissue formed assumes the appearance of dentin, i.e., the function of the pulp is normalized.
The mineralization of the collagen starts with dystrophic calcification of both the zone of firm necrosis and the degenerated cells in the adjacent tissue, leading to deposition of mineral in the newly-formed collagen. The presence of calcium ions stimulates precipitation of calcium carbonate in the wound area and thereby contributes to the initiation of mineralization.
Hard tissue formation in contact with some hard-setting calcium hydroxide cements has been reported, indicating a less-extensive initial chemical injury than that produced by calcium hydroxide alone. The differences in tissue response to various calcium hydroxide-containing cements are related to such factors as differences in pH and rates of release of hydroxyl ions and calcium ions. Other components of the cements, leading to different chemical reactions, may inactivate calcium hydroxide or be noxious to the pulp and thereby interfere with healing. Decisive factors for healing of the inflamed pulp are the degree of inflammation, the time of irritation and infection, and the location of the exposure. The effect of calcium hydroxide is not a factor.
Internal dentin resorption, observed in pulpotomized primary teeth capped with calcium hydroxide, occurs when chronically inflamed pulp is present at the time of treatment and/or is induced by improper wound treatment, such as leaving a blood clot between the wound surface and the calcium hydroxide.
Concerning the addition of corticosteroids to calcium hydroxide-containing pulp-capping agents, no biologically acceptable histological results have been reported so far.
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