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Summary-Cellmigration and replication associated with odontoblast replacement occurring soon after pulp exposure in primate teeth were studied. Class 5 cavity preparations resulting in pulp exposures were restored with a calcium hydroxide-containing capping agent and amalgam. Eighty-four and 96 h after this the animals were injected with 0.5 pCi/g body wt tritiated thymidine (sp. act. 6.7 Ci/mM). Teeth were extracted 6, 8, 10 and 12 days after treatment. The number of labelled cells as well as the number of grains per labelled cell were counted for odontoblast-like, fibroblast-like and perivascular cells in three 60 x 260 pm zones. These zones represented the odontoblast and cell-free (zone l), cell-rich (zone 2) and deep pulp (zone 3) areas of normal pulp tissue. Ten sections centred around the mid-point of the exposure were counted for each tooth. Matrix formation and labelled odontoblast-like cells were observed at the interface between the capping agent and the pulp as early as day 8. Other significant findings were: (1) an increase In labelled odontoblast-like cells in zone 1 over time, suggesting a continual influx of differentiating cells; (2) an increase in labelled cells in zone 1 over time with a concurrent decrease in zone 3, suggesting that the influx of cells in zone 1 was from the deeper pulp; and (3) differences in grain counts between zones, treatment times and cell types, indicating that at least two DNA replications had occurred between initial treatment and final odontoblast-like cell differentiation.

Four adult Rhesus monkeys provided 120 teeth for buccal Class V cavities. Twenty‐nine were non‐exposed controls and 91 were exposed for 3 intervals. All 120 teeth were capped with a hard set Ca(OH)2, medicament, restored with amalgam, 57 evaluated after 1 year and 63 after 2 years. Of the 91 exposed pulps, 45 showed complete healing, 25 showed pulpal inflammation varying from acute to chronic, 12 showed severe pulpal breakdown and abscess formation and 9 were necrotic. No difference was observed in the healing response between the 3 exposure times. New hard tissue formed at, or subjacent to, the medicament in 77 of 91 exposed pulps with a tunnel defect frequently present, running from the medicament interlace to the pulp. This study demonstrates that recurring pulp inflammation observed after 1 & 2 year direct pulp capping, is associated with bacterial contamination.

The healing capacity of mechanically exposed and bacterially contaminated dental pulps was assessed in monkeys after capping with 2 commercial Ca(OH)2 containing compounds. One hundred eighty teeth in 7 monkeys were employed, 45 as untreated controls and 135 as treated exposures. Class V buccal cavity preparations resulting in pulpal exposure were prepared, left open to the oral cavity for 0, 1, 24 h or 7 days and employed as controls, or debrided, capped, restored with amalgam and left undisturbed for 5 weeks as treated exposures. Zero and 1 h untreated exposures presented damage from the mechanical trauma only, whereas 24 h and 7 day pulp wounds exhibited pronounced infiltrations of polymorphonuclear and mononuclear leukocytes. In addition, the 7 day exposures demonstrated several teeth with partial and total necrosis. Treated 0, 1 and 24 h exposures demonstrated wound healing, minimal pulp tissue inflammation, reorganization of soft tissue and formation of new hard tissue at the exposure site in 86 of 99 teeth. Treated 7 day exposures healed less frequently, showing signs of dentin bridging in 15 of 27 teeth. This study indicated that mechanically exposed and orally contaminated dental pulps in monkeys have a high capacity to resolve inflammation and initiate healing with new dentin formation at the exposure site when treated as described.

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