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We examined the effects of basic fibroblast growth factor (FGF-2) on cultured lower molar tooth germ at the differentiative (bell) stage. Although FGF-2 has been detected in odontogenesis, its roles in biological activities, such as cell proliferation, differentiation and extracellular matrix mineralization are unclear. We assayed mRNA levels of the differentiation markers, dentine sialophosphoprotein (DSPP), amelogenin and alkaline phosphatase (ALP) using reverse transcription-polymerase chain reaction (RT-PCR), and histological methods. Tooth germs dissected from 17-day-old embryonic mice were cultured for 4 days with either recombinant human FGF-2 or specific antisense phosphorothioate oligodeoxynucleotide (antisense ODN) for FGF-2. Exogenous FGF-2 decreased the gene expression of differentiation markers in molars at the bell stage. Abrogation of endogenous FGF-2 by antisense ODN increased the gene expression of differentiation markers, and also significantly enhanced enamel and dentine formation. This histological change was recovered by adding exogeneous FGF-2. These findings suggest that FGF-2 at the bell stage regulates cell differentiation and matrix secretion.

Emdogain showing both stimulation of cell proliferation and inhibition of cell differentiation has been shown to increase FGF-2 expression in the mediation of prostaglandin E2 and to decrease MMP-1 mRNA expression through the activation of FGF-2. FGF-2 may underlie in the action of EMD on osteoblasts during periodontal regeneration.

The application of photodynamic therapy (PDT) to hepatocellular carcinoma (HCC) has been difficult because hematoporphyrin derivatives (HpD) accumulate not only in cancer cells but also in normal hepatocytes and, hence, laser irradiation causes injuries in both tissues. Protection of the normal liver tissue from laser phototoxicity was demonstrated using indocyanine green (ICG) as a protective agent. In vitro, argon laser irradiation decolored the green tint of ICG much faster in solutions containing HpD than those without, suggesting that ICG captured singlet oxygen from HpD. Degeneration of Change hepatocytes induced by HpD and laser irradiation was prevented by an addition of ICG into the medium. In vivo, laser irradiation of the rat liver surface caused hyperemia when HpD was injected two days before, while the hyperemia was much milder in rats additionally receiving ICG injection 10 minutes before the irradiation. ICG injected into rat HCC accumulated only in the normal liver tissue. Laser irradiation of rat HCC preinjected with both HpD and ICG destroyed only the cancer tissue, while the surrounding liver tissue was preserved. Both in vitro and in vivo results suggest that ICG has a scavenger effect against excited oxygen and it might be used as a protective agent in PDT of HCC.

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