H D Rodd1, C R Morgan, P F Day, F M Boissonade. 1. Dept. Oral Health and Development, School of Clinical Dentistry, University of Sheffield, Sheffield; England. h.d.rodd@sheffield.ac.uk
Abstract
AIM: This was to compare the pulpal expression of the transient receptor potential ion channel (TRPV1), a noxious heat receptor, in sound and hypomineralised human first permanent molars. The rationale for the investigation was to gain further insight into pulpal changes in hypomineralised teeth and the possible biological mechanisms underlying thermal hypersensitivity. STUDY DESIGN: This was a laboratory study using a quantitative immuncocytochemical approach. METHODS: The experimental material comprised 17 sound and 18 hypomineralised molars (10 with intact enamel and 8 with enamel loss), obtained from children requiring dental extractions under general anaesthesia. Coronal pulps were removed and processed for indirect immunofluorescence using antibodies raised against TRPV1 and either the general neuronal marker, protein gene-product 9.5 or alpha smooth muscle actin in conjunction with Ulex europaeus agglutinin 1 lectin to fully label the pulp vasculature. Computerised image analysis was used to quantify the expression of TRPV1 in both pulpal nerves and blood vessels within different regions of the pulp including the pulp horn, subodontoblastic plexus and mid-coronal region. RESULTS: Mean neuronal and vascular TRPV1 expression was significantly greater in some pulpal regions of hypomineralised teeth (both with and without enamel loss) than for sound samples (p<0.05, ANOVA). CONCLUSIONS: Increased TRPV1 expression within the pulps of hypomineralised teeth may be indicative of an underlying pulpal inflammation and may help to explain the heat sensitivity experienced by some patients with this condition. However, future lines of enquiry should seek to correlate patient symptoms and responses to controlled hot and cold stimuli with pulpal expression of a variety of thermal receptors to gain further insight into dental pain mechanisms.
AIM: This was to compare the pulpal expression of the transient receptor potential ion channel (TRPV1), a noxious heat receptor, in sound and hypomineralised human first permanent molars. The rationale for the investigation was to gain further insight into pulpal changes in hypomineralised teeth and the possible biological mechanisms underlying thermal hypersensitivity. STUDY DESIGN: This was a laboratory study using a quantitative immuncocytochemical approach. METHODS: The experimental material comprised 17 sound and 18 hypomineralised molars (10 with intact enamel and 8 with enamel loss), obtained from children requiring dental extractions under general anaesthesia. Coronal pulps were removed and processed for indirect immunofluorescence using antibodies raised against TRPV1 and either the general neuronal marker, protein gene-product 9.5 or alpha smooth muscle actin in conjunction with Ulex europaeus agglutinin 1 lectin to fully label the pulp vasculature. Computerised image analysis was used to quantify the expression of TRPV1 in both pulpal nerves and blood vessels within different regions of the pulp including the pulp horn, subodontoblastic plexus and mid-coronal region. RESULTS: Mean neuronal and vascular TRPV1 expression was significantly greater in some pulpal regions of hypomineralised teeth (both with and without enamel loss) than for sound samples (p<0.05, ANOVA). CONCLUSIONS: Increased TRPV1 expression within the pulps of hypomineralised teeth may be indicative of an underlying pulpal inflammation and may help to explain the heat sensitivity experienced by some patients with this condition. However, future lines of enquiry should seek to correlate patient symptoms and responses to controlled hot and cold stimuli with pulpal expression of a variety of thermal receptors to gain further insight into dental pain mechanisms.
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