Immune defense mechanisms of the dentin/pulp complex. An immunological and molecular biological analysis

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Immunohistochemical and molecular biological analyzes were conducted in order to investigate the roles of pulpal densritic cells (DCs) in the pathogenesis of pulpal diseases. Results obtained were as follows:1. In human teeth bearing pulp exposure-free dentinal caries, HLA-DR-expressing pulpal DCs exhibited a localized accumulation beneath the affected dentinal tubules. The accumulation was evident in teeth with a shallow carious lesion. The majority of'the pulpal DCs expressed CD14 and CD68. In teeth with a deep carious lesion, expression of CD83 and CD86 was detected on some DCs. T cells showed a marked increase in teeth with shallow dentinal caries. These T cells were mostly memory cells expressing CD45RO, and some of them co-expressed CD25, a marker for activated T cells. However, B cells showed an increase only in teeth with deep dentinal caries. These results suggest that DC-T cell interaction and subsequent activation of T cells are involved in the initial pathogenesis of pulpal diseases.2. Expression of inducible nitric oxide synthase (iNOS) mRNA in LPS-induced pulpitis of rat upper incisors peaked at 6 hrs, which was detected by means of reverse transcription polymerase chain reaction (RT-PCR). Immunohistochemical staining for rat iNOS revealed that most of the iNOS-positive cells were macrophages. The expression of mRNAs for cyclooxygenase-2 (COX-2) and pro-inflammatory cytokines peaked at 3 to 6 hrs, whereas IL-10 (anti-inflammatory cytokine) mRNA was first detected at 6 hrs. Administration of an iNOS inhibitor caused drastic decrease in the expression of mRNAs for COX-2 and inflammatory cytokines in the inflamed pulp. These results indicate that NO generated by macrophages may regulate the pulpal inflammatory reactions.