Morphological study of amelogenesis in the rat lower incisor after thyro-parathyroidectomy, parathyroidectomy and thyroidectomy

Acevedo, Ana Carolina; Chardin, Hélène; Staub, J. F.; Septier, D.; Goldberg, Michel

doi:10.1007/s004410050523

Cited by 11 publications

(6 citation statements)

References 24 publications

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“…This report shows that diet-induced hypocalcemia directly or indirectly results in major alterations of both the enamel organ and the enamel. The results are consistent with previous studies on experimentally induced chronic hypocalcemia suggesting that low calcium levels, rather than phosphate levels, cause enamel hypoplasia (Nikiforuk and Fraser 1979;Limeback et al 1992;Acevedo et al 1996). In the same experimental model as in the present study, it was previously found that diet-induced hypocalcemia results in hypocalcified enamel (Bonucci et al 1994).…”

Section: Discussionsupporting

confidence: 93%

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Morphological and Immunocytochemical Analyses on the Effects of Diet-induced Hypocalcemia on Enamel Maturation in the Rat Incisor

Nanci

Mocetti

Sakamoto

et al. 2000

J Histochem Cytochem.

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S U M M A R YDuring the maturation stage of amelogenesis, the loss of matrix proteins combined with an accentuated but regulated influx of calcium and phosphate ions into the enamel layer results in the "hardest" tissue of the body. The aim of the present investigation was to examine the effects of chronic hypocalcemia on the maturation of enamel. Twenty-one-day old male Wistar rats were given a calcium-free diet and deionized water for 28 days, while control animals received a normal chow. The rats were perfused with aldehyde and the mandibular incisors were processed for histochemical and ultrastructural analyses and for postembedding colloidal gold immunolabeling with antibodies to amelogenin, ameloblastin, and albumin. The maturation stage enamel organ in hypocalcemic rats exhibited areas with an apparent increase in cell number and the presence of cyst-like structures. In both cases the cells expressed signals for ameloblastin and amelogenin. The content of the cysts was periodic acid-Schiff-and periodic acid-silver nitrate-methanamine-positive and immunolabeled for amelogenin, ameloblastin, and albumin. Masses of a similar material were also found at the enamel surface in depressions of the ameloblast layer. In addition, there were accumulations of glycoproteinaceous matrix at the interface between ameloblasts and enamel. In decalcified specimens, the superficial portion of the enamel matrix sometimes exhibited the presence of tubular crystal "ghosts." The basal lamina, normally separating ameloblasts and enamel during the maturation stage, was missing in some areas. Enamel crystals extended within membrane invaginations at the apical surface of ameloblasts in these areas. Immunolabeling for amelogenin, ameloblastin, and albumin over enamel was variable and showed a heterogeneous distribution. In contrast, enamel in control rats exhibited a homogeneous labeling for amelogenin, a concentration of ameloblastin at the surface, and weak reactivity for albumin. These results suggest that diet-induced chronic hypocalcemia interferes with both cellular and extracellular events during enamel maturation.

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Section: Discussionsupporting

confidence: 93%

“…Complete absence of calcium in the diet results in the formation of hypomineralized enamel (Bonucci et al 1994). Furthermore, thyro-parathyroidectomy, which produces severe hypocalcemia, affects the morphology of ameloblasts as well as the organization and degree of mineralization of enamel (Acevedo et al 1996).…”

mentioning

confidence: 99%

Morphological and Immunocytochemical Analyses on the Effects of Diet-induced Hypocalcemia on Enamel Maturation in the Rat Incisor

Nanci

Mocetti

Sakamoto

et al. 2000

J Histochem Cytochem.

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“…(2) The cellular mechanisms that regulate the enamel maturation process are complex and poorly understood. Recent studies have shown that hypocalcemia either dietaryinduced (23,24) or experimentally induced (25) can cause enamel hypoplasia. Similarly, in vitro studies by Kukita and coworkers found that primary cultured rat ameloblasts responded to high concentrations of Ca 2ϩ in the medium by changing their morphology.…”

Section: Discussionmentioning

confidence: 99%

Identification of the Calcium-Sensing Receptor in the Developing Tooth Organ

Mathias

Mathews

Gao

et al. 2001

Journal of Bone and Mineral Research

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Calcium (Ca 2؉) is a critical component of tooth enamel, dentin, and the surrounding extracellular matrix. Ca 2؉ also may regulate tooth formation, although the mechanisms for such action are poorly understood. The Ca 2؉ -sensing receptor (CaR) that is expressed in the parathyroid gland, kidney, bone, and cartilage has provided a mechanism by which extracellular Ca 2؉ can regulate cell function. Because these tissues play an important role in maintaining mineral homeostasis and because Ca 2؉ is hypothesized to play a crucial role in tooth formation, we determined whether the CaR was present in teeth. In this study, using immunohistochemistry, CaR protein was detected in developing porcine molars localized in the predentin (

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“…The knowledge about PTH is even more limited. Evidence from animal studies suggests that reduced levels of PTH induce hypocalcemia and consequently enamel alterations 17 .…”

Section: Introductionmentioning

confidence: 99%

Association of defects of enamel with polymorphisms in the vitamin D receptor and parathyroid hormone genes

Renostro-Souza,

Fonseca-Souza,

Küchler

et al. 2024

Braz. Dent. J.

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This cross-sectional study aimed to investigate the association between developmental defects of enamel (DDE) and single nucleotide polymorphisms (SNPs) in the genes encoding the vitamin D receptor (VDR) and parathyroid hormone (PTH). Orthodontic patients receiving treatment at a dental school were selected through convenience sampling. Intra-oral photographs were used to assess DDE, which were classified according to the criteria proposed by Ghanim et al. (2015) by a single calibrated examiner (Kappa>0.80). Enamel hypoplasia, molar-incisor hypomineralization (MIH), hypomimineralized second primary molar (HSPM), and non-MIH/HSPM demarcated opacities were considered for the analysis. Genomic DNA was extracted from buccal cells. The SNPs in VDR (rs7975232) and PHT (rs694, rs6256, and rs307247) were genotyped using real-time polymerase chain reactions (PCR). Statistical analyses were performed using the PLINK software (version 1.03, designed by Shaun Purcell, EUA). Chi-square or Fisher's exact tests were performed at a significance level of 5%. Ninety-one (n=91) patients (49 females and 42 males) (mean age of 14.1±5.8 years) were included. The frequency of DDE was 38.5% (35 patients). Genotype distributions were in Hardy-Weinberg equilibrium. No significant statistical association was found between DDE and the SNPs evaluated. A borderline association (p=0.09) was observed between DDE and the CC haplotype for SNP rs7975232 in VDR. In conclusion, the selected SNPs in VDR and PTH genes were not associated with DDE in the studied samples.

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Morphological study of amelogenesis in the rat lower incisor after thyro-parathyroidectomy, parathyroidectomy and thyroidectomy

Cited by 11 publications

References 24 publications

Morphological and Immunocytochemical Analyses on the Effects of Diet-induced Hypocalcemia on Enamel Maturation in the Rat Incisor

Morphological and Immunocytochemical Analyses on the Effects of Diet-induced Hypocalcemia on Enamel Maturation in the Rat Incisor

Identification of the Calcium-Sensing Receptor in the Developing Tooth Organ

Association of defects of enamel with polymorphisms in the vitamin D receptor and parathyroid hormone genes

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