The objective of these studies was to follow early healing at the dentin-connective tissue interface. Small dentin blocks were surgically implanted in bone cavities under mucoperiosteal flaps in the edentulous alveolar ridges of five beagle dogs at various times. In two separate experiments, wound maturation on native dentin surfaces and on citric acid or heparin conditioned dentin surfaces was observed. Block specimens including bone, dentin, and surrounding soft tissues were obtained at 10 minutes, 1 and 6 hours, and 1, 3, and 7 days after flap closure and prepared for light and transmission electron microscopic examination of the interface. The very initial attachment to native dentin was mediated by a granular precipitate. At 1 and 6 hours, the intercellular matrix was more organized with fibrin formation around red blood cell aggregates and at the dentin surface. Polymorphonuclear leukocytes were observed throughout the interface. Red blood cells were undergoing degradation at day 1 and polymorphonuclear cells were prevalent at the dentin surface. The 3-day observation interval was characterized by further maturation of the fibrin clot. Macrophages were observed near the dentin surface and fibroblasts could be identified. The 7-day specimens exhibited areas of cell rich connective tissue attachment without inflammatory cells as well as areas showing the fibrin clot in various stages of decomposition. These observations suggest that connective tissue attachment to dentin surfaces is mediated by adsorption of plasma proteins to the surface and subsequent development and maturation of a fibrin clot. The sequence of healing events at dentin surfaces conditioned with citric acid or heparin was largely similar to healing at native dentin surfaces. However, at day 1 and later time points, clot adhesion to heparin-conditioned dentin appeared compromised, whereas the fibrin clot seemed to adhere to citric acid-conditioned dentin at all observation periods. These observations indicate that in the absence of mechanical trauma, epithelial proliferation, and infection, wound maturation at the dentin-connective tissue interface may not necessarily be affected by treatments that either enhance or inhibit clot adhesion to the dentin surface.
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