“…Since the lesion was observed only after incisal fractures and long sustained high PTHrP concentration, the lesion is neither the cause of the fracture, nor the early response to the high PTHrP concentration of this model. Additionally, the lesion was identical to those occurring in response to the treatment with several cytotoxic agents, and considered to be the reparative response to the preceding cytotoxic effect of those agents, which restricted to certain susceptible populations of the odontoblasts (Adkins, 1972;Koppang, 1973;Adatia, 1975;Mikkelsen, 1978;Koppang, 1976, 1980;Stene, 1978Stene, , 1979Nogueira et al, 1981;Dahl, 1984Dahl, , 1985Karim and Eddy, 1984;Dahl and Koppang, 1985;Moule et al, 1993). According to the accumulating knowledge of PTHrP, it is not known as a cytotoxic agent but as one of the factors related to the reparative response in several tissues (Ferguson et al, 1998;Vortkamp et al, 1998;Blomme et al, 1999;Kudo et al, 2000;Nakase et al, 2001;Okazaki et al, 2003).…”