Responses of Pulp-Dentinal Complex to Carious Lesions

Caries is the most common dental disease known to man. Following caries formation, dentine and pulp react simultaneously as a functional unit to initiate reactionary or reparative dentinogenesis. In primary dentinogensis, the organic matrix is principally composed of type I collagen and noncollagen proteins. Two major noncollagenous proteins, phosphophoryn(PP) and dentin sialoprotein(DSP), are associated with mineralization of dentin. However, the nature of the pulp-dentinal complex reactions in different stages of carious lesion progression is still unclear. Objective: To understand the molecular events underlying carious progression, we analyzed the distribution of major dentin matrix proteins, collagen type I, DPP and DSP in non-carious, shallow and moderate carious teeth. Methods: Non-caries and caries affected human 3rd molar teeth were freshly collected. The ABC-peroxidase method was used for immunohistochemical staining of collagen type I, PP and DSP with individual antibodies. In situ hybridization studies were performed to examine the DSP-PP transcript expression. Results: Beneath the caries, cell proliferation was observed in the cell-free zone and reduced cell numbers in the odontoblast layer were noted. Collagen type I was present in the dentin and the predentin. PP and DSP were observed in newly mineralized dentin, odontoblasts and dental pulp. A progressive increase in the staining intensity for collagen type I, PP and DSP in pulp-dentinal complex was noted from the non-carious teeth to shallow and moderate carious teeth. Furthermore, the staining intensity for these antibodies was weaker directly underneath the caries as compared with the nearby area. In situ hybridization studies confirmed the immunohistochemical results. Conclusions: Caries stimulated the pulp-dentinal complex to actively synthesize collagen type I, PP and DSP. However, carious lesions may damage odontoblasts directly under the caries resulting in lower collagen type I, DPP and DSP staining in these areas. This work is supported by NIH DE11442.