Tunnel defects in dentin bridges: their formation following direct pulp capping

Abstract

This study was conducted to observe the formation and nature of tunnel defects in dentin bridges, assess the nature of the associated soft tissue elements, and note the relationship of pulp inflammation and necrosis associated with these defects. A total of 235 teeth with class 5 cavity preparation exposures were randomly distributed throughout the dentitions of 14 adult rhesus monkeys. Each pulp was exposed and left open to the oral microflora at one of four time intervals, flushed with saline, debrided, capped with one of two hard-set calcium hydroxide medicaments [Ca(OH)2 (Dycal or Life)] and restored with a dispersed-phase amalgam alloy. Observation times were 14 days, 5 weeks, and 1 and 2 years. A total of 192 dentin bridges formed against the Ca(OH)2 medicaments Life or Dycal in 235 pulp-capped teeth. Considering all four capping periods, 89% of all dentin bridges contained tunnel defects (172 of 192). Forty-one percent (78) of the 192 dentin bridges were associated with recurring pulp inflammation or necrosis and were always associated with the presence of inflammatory cells and stained bacterial profiles. This study demonstrates that a statistically significant number of dentin bridges contain multiple tunnel defects, most of which appear to remain patent. These patent tunnels fail to provide a hermetic seal to the underlying pulp against recurring infection due to microleakage. Most Ca(OH)2 medicaments have been reported to disintegrate and wash out after 6 months, leaving a void underneath the restoration and thereby a pathway for bacterial infection. This study reemphasizes the need to employ biologically relevant measures that will provide a long-term clinical seal against microleakage following direct pulp capping with Ca(OH)2 medicaments alone.