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Effects of insulin-like growth factor I on alveolar bone remodeling in diabetic rats.

Identifieur interne : 000258 ( Main/Exploration ); précédent : 000257; suivant : 000259

Effects of insulin-like growth factor I on alveolar bone remodeling in diabetic rats.

Auteurs : Y. Fang [République populaire de Chine] ; L-P Wang ; F-L Du ; W-J Liu ; G-L Ren

Source :

RBID : pubmed:22834984

Descripteurs français

English descriptors

Abstract

BACKGROUND AND OBJECTIVE

Diabetes is a chronic hyperglycemic disorder and results in a tendency to develop osteoporosis. Furthermore, the delayed healing of tooth-extraction wounds, the activation of alveolar resorption and the suppressed formation of bone around implants are difficult for dentists to resolve. In diabetes, insulin-like growth factor I (IGF-I) appears to enhance the differentiation of osteoblasts and to activate the mineralization of bone. Hence, the aim of this study was to investigate the effects of insulin-like growth factor I on the remodeling of alveolar bone in diabetic rats.

MATERIAL AND METHODS

Diabetes was induced in 40 male Sprague-Dawley rats by intravenous administration of alloxan. The teeth of the rats were extracted to investigate remodeling of alveolar bone. Insulin-like growth factor I was administered, via intraperitoneal injection, to diabetic rats following tooth extraction. The remodeling of alveolar bone was determined using radiographic data, histological analyses and tetracycline fluorescence labeling.

RESULTS

Compared with the control group, diabetes decreased alveolar bone formation. The height of alveolar bone and the bone-formation rate was significantly lower in the untreated diabetic group than in the control group or in the treated rats. Treatment with insulin-like growth factor I not only regulated abnormal blood glucose levels but also increased the height of the alveolar bone and increased the bone-formation rate relative to the results in diabetic animals. Furthermore, the expression of glucose transporter-1, the main transporter of glucose, was changed by hyperglycemia.

CONCLUSION

The results suggest that insulin-like growth factor I treatment increases the volume of newly formed bone following tooth extraction and normalizes the expression of glucose transporter-1 in diabetic rats, which may play an important role in bone formation and mineralization.


DOI: 10.1111/j.1600-0765.2012.01512.x
PubMed: 22834984


Affiliations:


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Le document en format XML

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<term>Alloxan (MeSH)</term>
<term>Alveolar Process (drug effects)</term>
<term>Alveolar Process (pathology)</term>
<term>Animals (MeSH)</term>
<term>Blood Glucose (analysis)</term>
<term>Bone Density (drug effects)</term>
<term>Bone Remodeling (drug effects)</term>
<term>Calcification, Physiologic (drug effects)</term>
<term>Diabetes Mellitus, Experimental (drug therapy)</term>
<term>Diabetes Mellitus, Experimental (metabolism)</term>
<term>Diabetes Mellitus, Experimental (physiopathology)</term>
<term>Fluorescent Dyes (MeSH)</term>
<term>Glucose Transporter Type 1 (analysis)</term>
<term>Hyperglycemia (drug therapy)</term>
<term>Hyperglycemia (metabolism)</term>
<term>Hyperglycemia (physiopathology)</term>
<term>Hypoglycemic Agents (therapeutic use)</term>
<term>Injections, Intraperitoneal (MeSH)</term>
<term>Insulin (therapeutic use)</term>
<term>Insulin-Like Growth Factor I (administration & dosage)</term>
<term>Insulin-Like Growth Factor I (therapeutic use)</term>
<term>Male (MeSH)</term>
<term>Osteoblasts (drug effects)</term>
<term>Osteoblasts (pathology)</term>
<term>Osteogenesis (drug effects)</term>
<term>Rats (MeSH)</term>
<term>Rats, Sprague-Dawley (MeSH)</term>
<term>Tetracycline (MeSH)</term>
<term>Tooth Extraction (MeSH)</term>
<term>Tooth Socket (drug effects)</term>
<term>Tooth Socket (pathology)</term>
</keywords>
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<term>Alloxane (MeSH)</term>
<term>Alvéole dentaire (anatomopathologie)</term>
<term>Alvéole dentaire (effets des médicaments et des substances chimiques)</term>
<term>Animaux (MeSH)</term>
<term>Calcification physiologique (effets des médicaments et des substances chimiques)</term>
<term>Colorants fluorescents (MeSH)</term>
<term>Densité osseuse (effets des médicaments et des substances chimiques)</term>
<term>Diabète expérimental (métabolisme)</term>
<term>Diabète expérimental (physiopathologie)</term>
<term>Diabète expérimental (traitement médicamenteux)</term>
<term>Extraction dentaire (MeSH)</term>
<term>Facteur de croissance IGF-I (administration et posologie)</term>
<term>Facteur de croissance IGF-I (usage thérapeutique)</term>
<term>Glycémie (analyse)</term>
<term>Hyperglycémie (métabolisme)</term>
<term>Hyperglycémie (physiopathologie)</term>
<term>Hyperglycémie (traitement médicamenteux)</term>
<term>Hypoglycémiants (usage thérapeutique)</term>
<term>Injections péritoneales (MeSH)</term>
<term>Insuline (usage thérapeutique)</term>
<term>Mâle (MeSH)</term>
<term>Ostéoblastes (anatomopathologie)</term>
<term>Ostéoblastes (effets des médicaments et des substances chimiques)</term>
<term>Ostéogenèse (effets des médicaments et des substances chimiques)</term>
<term>Processus alvéolaire (anatomopathologie)</term>
<term>Processus alvéolaire (effets des médicaments et des substances chimiques)</term>
<term>Rat Sprague-Dawley (MeSH)</term>
<term>Rats (MeSH)</term>
<term>Remodelage osseux (effets des médicaments et des substances chimiques)</term>
<term>Transporteur de glucose de type 1 (analyse)</term>
<term>Tétracycline (MeSH)</term>
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<term>Insulin-Like Growth Factor I</term>
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<term>Blood Glucose</term>
<term>Glucose Transporter Type 1</term>
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<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en">
<term>Hypoglycemic Agents</term>
<term>Insulin</term>
<term>Insulin-Like Growth Factor I</term>
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<term>Alloxan</term>
<term>Fluorescent Dyes</term>
<term>Tetracycline</term>
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<keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr">
<term>Facteur de croissance IGF-I</term>
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<term>Glycémie</term>
<term>Transporteur de glucose de type 1</term>
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<term>Alvéole dentaire</term>
<term>Ostéoblastes</term>
<term>Processus alvéolaire</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en">
<term>Alveolar Process</term>
<term>Bone Density</term>
<term>Bone Remodeling</term>
<term>Calcification, Physiologic</term>
<term>Osteoblasts</term>
<term>Osteogenesis</term>
<term>Tooth Socket</term>
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<term>Diabetes Mellitus, Experimental</term>
<term>Hyperglycemia</term>
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<term>Alvéole dentaire</term>
<term>Calcification physiologique</term>
<term>Densité osseuse</term>
<term>Ostéoblastes</term>
<term>Ostéogenèse</term>
<term>Processus alvéolaire</term>
<term>Remodelage osseux</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en">
<term>Diabetes Mellitus, Experimental</term>
<term>Hyperglycemia</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr">
<term>Diabète expérimental</term>
<term>Hyperglycémie</term>
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<term>Alveolar Process</term>
<term>Osteoblasts</term>
<term>Tooth Socket</term>
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<term>Diabète expérimental</term>
<term>Hyperglycémie</term>
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<term>Hyperglycemia</term>
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<term>Diabète expérimental</term>
<term>Hyperglycémie</term>
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<term>Insuline</term>
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<term>Injections, Intraperitoneal</term>
<term>Male</term>
<term>Rats</term>
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<term>Extraction dentaire</term>
<term>Injections péritoneales</term>
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<b>BACKGROUND AND OBJECTIVE</b>
</p>
<p>Diabetes is a chronic hyperglycemic disorder and results in a tendency to develop osteoporosis. Furthermore, the delayed healing of tooth-extraction wounds, the activation of alveolar resorption and the suppressed formation of bone around implants are difficult for dentists to resolve. In diabetes, insulin-like growth factor I (IGF-I) appears to enhance the differentiation of osteoblasts and to activate the mineralization of bone. Hence, the aim of this study was to investigate the effects of insulin-like growth factor I on the remodeling of alveolar bone in diabetic rats.</p>
</div>
<div type="abstract" xml:lang="en">
<p>
<b>MATERIAL AND METHODS</b>
</p>
<p>Diabetes was induced in 40 male Sprague-Dawley rats by intravenous administration of alloxan. The teeth of the rats were extracted to investigate remodeling of alveolar bone. Insulin-like growth factor I was administered, via intraperitoneal injection, to diabetic rats following tooth extraction. The remodeling of alveolar bone was determined using radiographic data, histological analyses and tetracycline fluorescence labeling.</p>
</div>
<div type="abstract" xml:lang="en">
<p>
<b>RESULTS</b>
</p>
<p>Compared with the control group, diabetes decreased alveolar bone formation. The height of alveolar bone and the bone-formation rate was significantly lower in the untreated diabetic group than in the control group or in the treated rats. Treatment with insulin-like growth factor I not only regulated abnormal blood glucose levels but also increased the height of the alveolar bone and increased the bone-formation rate relative to the results in diabetic animals. Furthermore, the expression of glucose transporter-1, the main transporter of glucose, was changed by hyperglycemia.</p>
</div>
<div type="abstract" xml:lang="en">
<p>
<b>CONCLUSION</b>
</p>
<p>The results suggest that insulin-like growth factor I treatment increases the volume of newly formed bone following tooth extraction and normalizes the expression of glucose transporter-1 in diabetic rats, which may play an important role in bone formation and mineralization.</p>
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<AbstractText Label="MATERIAL AND METHODS" NlmCategory="METHODS">Diabetes was induced in 40 male Sprague-Dawley rats by intravenous administration of alloxan. The teeth of the rats were extracted to investigate remodeling of alveolar bone. Insulin-like growth factor I was administered, via intraperitoneal injection, to diabetic rats following tooth extraction. The remodeling of alveolar bone was determined using radiographic data, histological analyses and tetracycline fluorescence labeling.</AbstractText>
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<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">The results suggest that insulin-like growth factor I treatment increases the volume of newly formed bone following tooth extraction and normalizes the expression of glucose transporter-1 in diabetic rats, which may play an important role in bone formation and mineralization.</AbstractText>
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