Christopher D Lynch1, Jessica L Roberts2, Ali Al-Shehri3, Paul J Milward4, Alastair J Sloan4. 1. University Dental School & Hospital, University College Cork, Wilton, Cork, Ireland. Electronic address: chris.lynch@ucc.ie. 2. North Wales Centre for Primary Care Research, Bangor University, Bangor, UK. 3. School of Dentistry, Cardiff University, UK. 4. Oral and Biomedical Sciences, School of Dentistry, Cardiff University, UK.
Abstract
AIM: Based on histological studies from the 1960s, it is recommended that dental pulp temperature increases should not exceed 5.5 °C. However, no contemporary reliable models exist to explore the effects of heat on living dental pulp. The aim of this project was to develop a clinically valid model for studying temperature increases caused by three commonly-used light curing units (LCUs). METHODS: Temperature increases caused by LCUs at varying exposure times and via various thicknesses of dentine were recorded using traditional approaches (i.e. thermocouple device on a laboratory bench) and an ex-vivo tooth slice model. Histomorphometric and immunohistochemical (IL-1β, HSP70, caspase-3) analysis was performed of the tooth slice model following varying exposure and culture times. RESULTS: Reduced dentine thickness and increased exposure time led to increases in temperature. Whilst the majority of temperature increases recorded using the traditional approach (53 of 60) were greater than the recommended 5.5 °C, 52 of the 60 reference points recorded using the ex-vivo tooth slice model resulted in temperature increases of less than 5.5 °C. Temperature increases of 5.5 °C or more that are prolonged for 40 s caused an immediate decrease in cell number. IL-1β was not detected in any samples, while HSP70 was detectable immediately after exposure to a temperature increase of 6 °C or more. Higher levels of HSP70 were detected after 24 h culture in tooth slices that experienced a temperature increase of 7.5 °C or more. Low levels of caspase-3 were detected in tooth slices exposed to temperature increase of 7.5 °C or more. CONCLUSION: Experimental arrangements for assessing LCU performance that measure temperature increases using a thermocouple device on a laboratory bench should no longer be used. Future studies in this area should include replication of the clinical environment using greater sophistication, such as the use of an ex-vivo tooth slice model as described here. Temperature increases of 5.5 °C or more for 40 s caused an immediate decrease in cell number, which supports previous findings. However, complex interactions at an immunohistochemical level suggest that while temperature increases of 5 °C or less are ideal, there may be some cell damage between 5-7 °C which might not result in pulpal death. Further investigations are indicated.
AIM: Based on histological studies from the 1960s, it is recommended that dental pulp temperature increases should not exceed 5.5 °C. However, no contemporary reliable models exist to explore the effects of heat on living dental pulp. The aim of this project was to develop a clinically valid model for studying temperature increases caused by three commonly-used light curing units (LCUs). METHODS: Temperature increases caused by LCUs at varying exposure times and via various thicknesses of dentine were recorded using traditional approaches (i.e. thermocouple device on a laboratory bench) and an ex-vivo tooth slice model. Histomorphometric and immunohistochemical (IL-1β, HSP70, caspase-3) analysis was performed of the tooth slice model following varying exposure and culture times. RESULTS: Reduced dentine thickness and increased exposure time led to increases in temperature. Whilst the majority of temperature increases recorded using the traditional approach (53 of 60) were greater than the recommended 5.5 °C, 52 of the 60 reference points recorded using the ex-vivo tooth slice model resulted in temperature increases of less than 5.5 °C. Temperature increases of 5.5 °C or more that are prolonged for 40 s caused an immediate decrease in cell number. IL-1β was not detected in any samples, while HSP70 was detectable immediately after exposure to a temperature increase of 6 °C or more. Higher levels of HSP70 were detected after 24 h culture in tooth slices that experienced a temperature increase of 7.5 °C or more. Low levels of caspase-3 were detected in tooth slices exposed to temperature increase of 7.5 °C or more. CONCLUSION: Experimental arrangements for assessing LCU performance that measure temperature increases using a thermocouple device on a laboratory bench should no longer be used. Future studies in this area should include replication of the clinical environment using greater sophistication, such as the use of an ex-vivo tooth slice model as described here. Temperature increases of 5.5 °C or more for 40 s caused an immediate decrease in cell number, which supports previous findings. However, complex interactions at an immunohistochemical level suggest that while temperature increases of 5 °C or less are ideal, there may be some cell damage between 5-7 °C which might not result in pulpal death. Further investigations are indicated.