Prenatal Influences on Tooth Development

Kreshover, Seymour J.; Clough, O. Wendell

doi:10.1177/00220345530320041801

Cited by 83 publications

(8 citation statements)

References 12 publications

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“…However, the changes seen in the enamel organ 1 month after the onset of diabetes were different from those reported in other studies (Kreshover et al, 1953). Extensive dental changes were observed both in pregnant rats made diabetic with alloxan and in the offspring of these diabetic rats.…”

Section: Long-term Effects Of Alloxancontrasting

confidence: 90%

“…These changes included degeneration of the ameloblasts and the presence of enamel droplets within the ameloblast layer. In some animals hyperemia and hemorrhage were observed in the pulp (Kreshover et al, 1953). One reason for these differences may be the fact that a multiple dose of alloxan (as many as 3 injections of 155 mg/kg) was used by Kreshover et al to render the animals diabetic.…”

Section: Long-term Effects Of Alloxanmentioning

confidence: 99%

“…This drug destroys the beta cells in the pancreas and produces an insulin-deficient state, comparable to juvenile-onset diabetes. Despite clinical evidence (GrahnBn and Edlund, 1967;Adler et al, 1973;Bohhtka et al, 1973) that there is a higher incidence of enamel hypoplasia in diabetic children and children of diabetic mothers, very limited attempts have been made to study the mechanism of formation of dental hard tissues during diabetes mellitus (Kreshover et al, 1953;Fleming, 1959;Betzler and Riedel, 1960). These studies have shown that, with few exceptions, the teeth of alloxan diabetic rats showed marked changes in the ameloblasts, organic enamel matrix, odontoblasts, and pulp.…”

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An ultrastructural study of the effect of a diabetogenic dose of alloxan on the secretory ameloblasts of the rat incisor

Karim

1983

Am. J. Anat.

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The effect of a single diabetogenic dose of alloxan on the ameloblasts of enamel secretion was investigated in rat incisor teeth prior to the onset of diabetes mellitus. This was compared with tissue from animals that were sacrificed a t the onset of diabetes, and with tissue from animals that had been diabetic for 1 month. Male Sprague-Dawley rats were given a single subcutaneous injection of alloxan at a dose of 150 mg/kg body weight; and the animals were sacrificed at 45 minutes, 2 hours, 24 hours, 48 hours and 29 days after injection. At the electron microscope level the following changes were observed. There was an early accumulation of secretion granules in the vicinity of the Golgi apparatus and within the proximal portion of Tomes' process. These accumulations were present at the onset of diabetes, 24 hours later. At 2 hours after injection a space appeared between the plasma membrane around Tomes' process and the interrod material. This space widened with time, and at 24 hours after injection it became continuous with enlarged intercellular spaces between the proximal portions of Tomes' processes. The widening of the intercellular space was restricted to the area above the distal cell web. At the onset of diabetes this compartment of the cells was similar to that of the control samples. Extracellular material which appeared to be the secretory product of the ameloblast was observed at two sites. On one occasion this material was seen in the wide intercellular spaces between the proximal portions of Tomes' processes 24 hours after injection. It was also seen at the onset of diabetes in the intercellular space at the level of the Golgi apparatus. The changes in the animals that had been diabetic for 1 month were a scarcity of secretion granules within Tomes' processes and an abnormal accumulation of secretion granules within the supranuclear and infranuclear compartents.This study has shown that the toxic effect of alloxan persists up to the time of onset of diabetes mellitus. However, since different morphological changes were observed during diabetes mellitus, it is suggested that the changes caused by diabetes are a separate entity, initially superimposed on and later replacing the acute, toxic effect of the drug.Alloxan has been used as early as 1948 (Lukens to induce diabetes in animals. This drug destroys the beta cells in the pancreas and produces an insulin-deficient state, comparable to juvenile-onset diabetes. Despite clinical evidence (GrahnBn and Edlund, 1967; Adler et al., 1973; Bohhtka et al., 1973) that there is a higher incidence of enamel hypoplasia in diabetic children and children of diabetic mothers, very limited attempts have been made to study the mechanism of formation of dental hard tissues during diabetes mellitus (Kreshover et al., 1953; Fleming, 1959; Betzler and Riedel, 1960). These studies have shown that, with few exceptions, the teeth of alloxan diabetic rats showed marked changes in the ameloblasts, organic enamel matrix, odontoblasts, and pulp. Since most of th...

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Section: Long-term Effects Of Alloxancontrasting

confidence: 90%

Section: Long-term Effects Of Alloxanmentioning

confidence: 99%

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confidence: 99%

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An ultrastructural study of the effect of a diabetogenic dose of alloxan on the secretory ameloblasts of the rat incisor

Karim

1983

Am. J. Anat.

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“…The cellular changes observed in the present experiment may either be due to a specific sensitivity of the ameloblasts to fluoride, or may represent a local effect of a general intoxication. The latter explanation may be supported by the fact that the animals were strongly intoxicated and that similar changes in the enamel organ are also induced by a number of different substances and experimental conditions, such as alloxaninduced diabetes (KRESHOVER &: CLOUGH 1953a), artificially induced fever (KRESHOVER & CLOUGH 1953b), carbon tetrachloride intoxication (HALS, BJORLIN & JACOBSEN 1973) and administration of tetracycline (WESTERGAARD &: NYLEN 1975). However, it is interesting to note that several of the findings in the present study are similar to those observed in long-term experiments where fluoride has been added to the diet or to the drinking water, and in multiple injection experiments, where the rats did not show signs of general intoxication.…”

Section: Discussionmentioning

confidence: 99%

Morphologic changes in the rat enamel organ following a single intraperitoneal injection of sodium fluoride

Mörnstad

Hammarström

1978

European J Oral Sciences

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abstract— Enamel organs in developing teeth of young rats were studied after single intra peritoneal injections of a high dose of sodium fluoride (60 mg NaF/kg body wt.). The study employed primarily light microscopy, but electron microscopy was used to clarify some of the light microscopic findings. The pathogenesis of the fluoride‐induced changes was followed during 72 h. Cellular changes were consistently found in the molars, but were never seen in the incisors. In the maxillary molars, ameloblastic injury was most commonly seen on the mesial surfaces of the cusps. One hour after injection, the most prominent findings were swollen mitochondria in the secretory ameloblasts and cleft formations between the ameloblasts and the enamel matrix. The clefts were filled with a stippled material. Some of the clefts gradually expanded to cystic cavities. The stippled material began to calcify after 24 h and formed small, darkly stained globules. After 72 h dearranged ameloblasts were found as islands intermingled with calcified rounded structures in the stellate reticulum. In stratum intermedium numerous atypic autophagic vacuoles appeared 2 h after injection. No light microscopic changes were observed in the postsecretory ameloblasts.

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“…Maternal pyrexia has been shown experimentally to have a detrimental influence on amelogenesis, ranging from ameloblastic dysfunction to complete cellular degeneration. 11 In case of maternal diabetes hypocalcemia in the mother and oxygen shortage problems to the infant may result in enamel hypomineralization. 12 Prenatal conditions such as prolonged maternal nausea and vomiting jeopardize fluids and electrolytes, as well as nutritional status leading occasionally to fetal biochemical disturbance.…”

Section: Putative Etiological Factorsmentioning

confidence: 99%

Essentiality of Early Diagnosis of Molar Incisor Hypomineralization in Children and Review of its Clinical Presentation, Etiology and Management

Garg

Jain

Saha

et al. 2012

International Journal of Clinical Pediatric Dentistry

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Molar incisor hypomineralization (MIH) is a common developmental condition resulting in enamel defects in first permanent molars and permanent incisors. It presents at eruption of these teeth. One to four molars, and often also the incisors, could be affected. Since first recognized, the condition has been puzzling and interpreted as a distinct phenomenon unlike other enamel disturbances. Early diagnosis is essential since, rapid breakdown of tooth structure may occur, giving rise to acute symptoms and complicated treatment. The purpose of this article is to review MIH and illustrate its diagnosis and clinical management in young children.How to cite this article: Garg N, Jain AK, Saha S, Singh J. Essentiality of Early Diagnosis of Molar Incisor Hypomineralization in Children and Review of its Clinical Presentation, Etiology and Management. Int J Clin Pediatr Dent 2012;5(3):190-196.

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Prenatal Influences on Tooth Development

Cited by 83 publications

References 12 publications

An ultrastructural study of the effect of a diabetogenic dose of alloxan on the secretory ameloblasts of the rat incisor

An ultrastructural study of the effect of a diabetogenic dose of alloxan on the secretory ameloblasts of the rat incisor

Morphologic changes in the rat enamel organ following a single intraperitoneal injection of sodium fluoride

Essentiality of Early Diagnosis of Molar Incisor Hypomineralization in Children and Review of its Clinical Presentation, Etiology and Management

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