Spontaneous Development of Dental Dysplasia in Aged Parp-1 Knockout Mice.

Poly(ADP-ribose) polymerase (Parp)-1 catalyzes polyADP-ribosylation using NAD+ and is involved in the DNA damage response, genome stability, and transcription. In this study, we demonstrated that aged Parp-1-/- mouse incisors showed more frequent dental dysplasia in both ICR/129Sv mixed background and C57BL/6 strain compared to aged Parp-1+/+ incisors, suggesting that Parp-1 deficiency could be involved in development of dental dysplasia at an advanced age. Computed tomography images confirmed that dental dysplasia was observed at significantly higher incidences in Parp-1-/- mice. The relative calcification levels of Parp-1-/- incisors were higher in both enamel and dentin (p < 0.05). Immunohistochemical analysis revealed (1) Parp-1 positivity in ameloblasts and odontoblasts in Parp-1+/+ incisor, (2) weaker dentin sialoprotein positivity in dentin of Parp-1-/- incisor, and (3) bone sialoprotein positivity in dentin of Parp-1-/- incisor, suggesting ectopic osteogenic formation in dentin of Parp-1-/- incisor. These results indicate that Parp-1 deficiency promotes odontogenic failure in incisors at an advanced age. Parp-1 deficiency did not affect dentinogenesis during the development of mice, suggesting that Parp-1 is not essential in dentinogenesis during development but is possibly involved in the regulation of continuous dentinogenesis in the incisors at an advanced age.

Periapical Microsurgery: Do Root Canal-retreated Teeth Have More Dentinal Defects?

INTRODUCTION: This microsurgical clinical study evaluated if teeth that have undergone endodontic retreatment are associated with more dentinal defects than primary root canal-treated teeth. METHODS: One hundred fifty-five patients who underwent periapical microsurgery treatment in a private practice setting were evaluated. The root ends were resected, and the roots were inspected for the presence of dentinal defects through the surgical operating microscope with the help of a 0.8-mm-diameter light-emitting diode probe light and methylene blue dye. The root canal treatment history (primary vs retreatment) of the teeth was documented and related to the presence or absence of dentinal defects. Bivariate analysis was performed using the chi-square test, and a multivariate analysis was performed using logistic regression to evaluate possible confounding effects of patient age, sex, and tooth location on the association between treatment and the presence of dentinal defects. RESULTS: Of the 155 treated teeth, 33 were excluded (3 fractured and 30 missing treatment history). Of the remaining 122 included teeth, 73 (59.8%) had undergone primary root canal treatment and 49 (40.2%) retreatment. Sixteen teeth (22.5%) of the primary root canal group versus 33 (64.7%) of the retreatment group had dentinal defects. The proportion of retreated teeth with dentinal defects compared with primary treatment was statistically significant (P < .001) with a higher proportion of retreated teeth having dentinal defects. In the multivariate analysis, only the type of treatment was statistically significant (P < .001). CONCLUSIONS: This clinical study showed that root canal-retreated teeth are associated with more dentinal defects than primary root canal-treated teeth.

Root anomalies and dentin dysplasia in autosomal recessive hyperphosphatemic familial tumoral calcinosis (HFTC).

Hyperphosphatemic familial tumoral calcinosis (HFTC, OMIM #211900) is an autosomal recessive metabolic disorder characterized by hyperphosphatemia, tooth root defects, and the progressive deposition of calcium phosphate crystals in periarticular spaces, soft tissues, and sometimes bone.(1) In this HFTC case report, we document the dental phenotype associated with a homozygous missense mutation (g.29077 C>T; c.484 C>T; p.Arg162*) in GALNT3 (OMIM 6017563), a gene encoding UDP-GalNAc transferase 3 that catalyzes the first step of O-linked oligosaccharide biosynthesis in the Golgi. The medical and dental pathology is believed to be caused primarily by high serum phosphate levels (hyperphosphatemia), which, in turn, is caused by failure of GALNT3 to glycosylate the phosphate regulator protein FGF23, impairing its ability inhibit reabsorption of filtered phosphate in the kidneys.

The effect of lathyrism on dentin structure of the rat incisors: a morphometric and scanning electron microscopic investigation.

BACKGROUND: The present study was designed to study the effect of beta-aminopropionitrile (beta-APN), present in Lathyrus sativus grass pea consumed in drought prone areas, on dentin of the continuously erupting rat incisors. METHODS: Eighteen adult male rats were used. In the experimental group (18 rats), lathyrism was induced by a once daily subcutaneous administration of beta-APN for 40 days. The maxillary and mandibular incisors were examined ultrastructurally and morphometrically. RESULTS: The mean number of patent tubules, the mean area, perimeter and the area percent of the tubules were analyzed. Ultrastructurally, the dentinal tubules of both coronal and radicular dentin in the lathyritic group were narrower or even obliterated compared with those in the control. The coronal and radicular dentin of the lathyritic group exhibited an irregular lattice of non-mineralized small branching collagen fibrils obliterating the dentinal tubules. The mean number of patent tubules in the control and lathyritic groups revealed an insignificant difference. The mean area of the tubules showed a statistically significant difference in lathyritic radicular dentin (P = 0.0353). The percentage of the total surface area of the dentinal tubules significantly decreased in the radicular dentin of the lathyritic group (P = 0.024). CONCLUSIONS: These findings indicated a deleterious effect of lathyrism on dentin, with a possible negative impact on developing teeth integrity.

Familial hypophosphatemic rickets.

Rickets is the failure of mineralization of osteoid and newly formed bones in a child skeleton. It is commonly associated with vitamin D deficiency; however, it can be because of a decrease in the serum phosphate levels leading to inadequate mineralization of cartilage and bone, consequent skeletal deformities, and growth retardation. The hypophosphatemic conditions that interfere in bone mineralization comprise many hereditary or acquired diseases. One of the hereditary types of hypophosphatemic rickets is the familial hypophosphatemic rickets. This rare variety was diagnosed in a 9-year-old patient who had come with a chief complaint of a missing tooth. In the present case, radiographic aspects of oral and systemic manifestations of familial hypophosphatemic rickets are highlighted.

Mutation of the signal peptide region of the bicistronic gene DSPP affects translocation to the endoplasmic reticulum and results in defective dentine biomineralization.

Dentine dysplasia type II is an autosomal dominant disorder in which mineralization of the dentine of the primary teeth is abnormal. On the basis of the phenotypic overlap between, and shared chromosomal location with, dentinogenesis imperfecta type II, a second disorder of dentine mineralization, it has been proposed that the two conditions are allelic. As recent studies have shown that dentinogenesis imperfecta type II results from mutation of the bicistronic dentine sialophosphoprotein gene (DSPP ), we have tested this hypothesis by sequencing DSPP in a family with a history of dentine dysplasia type II. Our results have shown that a missense change, which causes the substitution of a tyrosine for an aspartic acid in the hydrophobic signal peptide domain of the protein, underlies the phenotype in this family. Biochemical analysis has further demonstrated that this mutation causes a failure of translocation of the encoded proteins into the endoplasmic reticulum, and is therefore likely to lead to a loss of function of both dentine sialoprotein and dentine phosphoprotein.

Transforming growth factor-beta1 negatively regulates crystallin expression in teeth.

Previously, we have reported that targeted overexpression of transforming growth factor (TGF) beta1 in the teeth of the transgenic mice (dTGF-beta1) results in a novel tooth phenotype phenomimicking the most prevalent tooth disorders in human. This phenotype was associated with discoloration and attrition of teeth due to defective mineralization. Here, we report a novel expression of crystallin family members in developing mouse teeth and its regulation by TGF-beta1 in these transgenic mice. AlphaB- and beta-crystallins were found to be elevated in dTGF-beta1 mouse teeth, whereas gamma-crystallin (gammaB, gammaC, and gammaF), a marker of cell differentiation, was significantly reduced. Because crystallins are believed to be stress-related proteins, their expression in teeth implicates them in a similar role because teeth are constantly subjected to physical friction and temperature fluctuations.

Dysosteosclerosis: a case with unique dental findings and SEM evaluation of a hypoplastic tooth.

A ten-year-old boy, who had the typical dental findings of dysosteosclerosis such as yellowish, hypoplastic teeth, retarded eruption, which upon eruption, decayed rapidly, is presented. To date this is the first known case reported with a congenital absence of the first permanent molars. Furthermore, SEM evaluation of the enamel and dentin was performed on a tooth from a patient with dysosteosclerosis for the first time. These studies showed weak ultrastructural compositions due to irregular calcification.