Odontoblast differentiation of human dental pulp cells in explant cultures.
Therefore, purpose of this prospective study was to examine the expression levels of VEGF and CD68 in the rat dental pulp to elucidate their role on vascular angiogenesis, inflammation and
odontoblast differentiation in pulp tissue depending on the possible damage of diabetes.
However, the genotype, phenotype, or cell responses in these in vitro models could differ from actual
odontoblast cell responses due to genetic changes [8] or environmental adaptations of the cell lines, which complicates the interpretation of cytotoxicity results.
The dental pulp is isolated from the lesion by the defensive response of a mature
odontoblast, which produces secondary and reparative dentin in response to external physiological and pathological stimuli.
Bracnhes of this vascular network connects its arterioles and venules under the
odontoblast layer and venules leave pulp using the same apical foramen (33,34).
A detailed screening on PRP components demonstrates that platelet-derived growth factor and insulin-like growth factor-1 promote cell proliferation; acidic fibroblast growth factor, insulin-like growth factor 1 and insulin-like growth factor 2 promote extracellular matrix synthesis; TGF-[beta], platelet-derived growth factor, acidic fibroblast growth factor and basic fibroblast growth factor are involved in DPSCs
odontoblast differentiation (9,14,24).
Calcium hydroxide - once considered the standard for pulp-capping material - provides an option for reparative dentin formation, but long term studies have shown results were variable and somewhat unpredictable.4 The material does not provide close adaptation to dentin, does not promote consistent
odontoblast differentiation and has been shown to be cytotoxic in cell cultures; the resultant reparative dentin formation can be characterized by tunnel defects.6,7 Tunnel defects within dentin bridges may provide a pathway for the penetration of microorganisms to activate circulating immune cells, induce pulpal irritation and produce subsequent dystrophic calcification.6