Previous in vi tro studies demonstrated that H202 or carbamide peroxide cou ld penetrate i nto pul p chambers through enamel and dentin (Benetti et a l., 2004; G okay et a l. , 2004‘ Suli eman et al .. 2005) ‘ Recently. Lee et al.(2006) demonstrated that H20Z enhanced the diffe rentiation of odontoblast like cell line, whereas it inhibited osteogenic diffe rentiation in pre 。steobl astic cell line, as seen by its efl"ecLs on an early difï"erentiation marker. ALP activity. I-lowever. the effects of HZ02 have not been well elucidated in primary cultured human pulp cells ln th is study‘ we investigated whether HO- 1 is involved in H20 2-induced cytotoxicity and examined the production 0 1" dent in sia lophosphoprotein (DSPP) and other minera li zation markers, in human pulp cells H20Z dec1'eased cell viabili ty. but increased HO-l and DSPP expression in a concentra t ion and time dependent manner. Inhibitors of guanylate cyclase, PI3K. ERK, and p38 MAP kinase blocked J-!?,0 2- induced cytot oxicity and the expression of HO-1 and DSPP mRNAs in pulp cells. These data suggest that t he induction of HO-l by H202 in pu lp cells plays a protective role against the cytotoxic effects of H202 and stimulates DSPP expression. resulting in prematu re oclontoblast differentiation th rough pathways t hat involve cGMP. p38. ancl ERK

Al though the changes in tooth morphology and hardness by hydrogen peroxide(H20 z) have been r‘epor‘.ted .‘ the pαr。o야t뻐ec야tive role of heme oxygenase-l(HO-l) against the cytotoxic effects of H202 has not been clarifïed i n human pulp cells ln this st udy. we investigated whether HO-l is involved in Hz0 2-induced cytoLox icity a nd examined the production 0 1' dentin sia lophosphoprotein(DSPP) and other mineralization markers‘ in hllman pu lp cells H202 decreased cell viabi lity, but increased HO-l and DSPP expression in a concentra tion and time dependent manner . Inhibitors of gllanylate cyclase. PI3K, ERK. and p38 MAP kinase blocked H202-indllced cytotoxicity and the expression of HO-l and DSPP mRNAs in pulp cells. These data suggest that the induction of HO-l by H202 in plllp cells plays a protective role against the cytotoxic effects 0 1' HzOz and stimulates DSPP expression‘ reslllting in prematllre odontoblast dilTerentiation throllgh pathways that involve cGMP‘ p38. and ERK.

Hereditary dentin defects consist of dentin dysplasia(DD) and dentinogenesis imperfecta(DI). The DI associated with osteogenesis imperfecta has been classified as DI type I, whereas isolated inherited defects have been categorized as DI types II and III. However, whether DI type III should be considered a distinct phenotype or a variation of DI type II is debatable. Recent genetic findings have focused attention on the role of the dentin sialophosphoprotein(DSPP) gene in the etiology of inherited defects of tooth dentin. We have identified a novel mutation(c.727G → A, p.D243N) at the 243th codon of exon 4 of the DSPP gene in a Korean patient with DI type III. The radiographic and histologic features of the patient revealed the classic phenotype of shell teeth. These findings suggest that DI type II and III are not separate diseases but rather the phenotypic variation of a single disease.

Hereditary dentin defects consists of dentin dysplasia(DD) and denti nogenesis imperfecta(Dr) ‘ The Dl associated with osteogenesis imperfecta has been classified as DI type 1. whereas isolated inherited defects have been categori zed as DI types II and III , However‘ whether DI type III should be considered a distinct phenotype 01' a variation of DI type 1I is debatable , Recent genetic findings have focused attention on the role of the dentin sialo phosphoprotein(DSPP) gene in the etiology of inherited defects of tooth dentin, We have identified novel mlltation( c,727G - > A, p,D243N) at the 243th codon of exon 4 of the DSPP gene in a Korean patient with DI type III The radiographic and histologic features of the patient revealed the classic phenotype of shell teeth These findings sllggest that DI type II and III are not separate diseases bllt rather the phenotypic variation 01' a s ingle disease