Format

Send to

Choose Destination
See comment in PubMed Commons below
J Dent Res. 1985 Apr;64 Spec No:541-8.

Effects of calcium hydroxide-containing pulp-capping agents on pulp cell migration, proliferation, and differentiation.

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.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID:
3857254
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Loading ...
    Support Center