Elevated TGF-β2 signaling in dentin results in sex related enamel defects

Saeki, Kuniko; Hilton, Joan F.; Alliston, Tamara; Habelitz, Stefan; Marshall, Sally J.; Marshall, Grayson W.; DenBesten, Pamela

doi:10.1016/j.archoralbio.2007.01.015

Cited by 13 publications

(8 citation statements)

References 32 publications

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“…Dental‐targeted over‐expression of TGF‐ β 1 (using a Dspp–Tgfβ1 transgene) results in a phenotype similar to dentin dysplasia , and over‐expression of TGF‐ β 2 in the dentin matrix results in the reduction of dentin hardness and elasticity in male mice . Our histological analysis shows no obvious changes in dentin or odontoblasts in Ltbp3‐/‐ mutants.…”

Section: Discussionmentioning

confidence: 65%

Enamel and dental anomalies in latent‐transforming growth factor beta‐binding protein 3 mutant mice

Morkmued

Hemmerlé

Mathieu

et al. 2017

European J Oral Sciences

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Latent‐transforming growth factor beta‐binding protein 3 (LTBP‐3) is important for craniofacial morphogenesis and hard tissue mineralization, as it is essential for activation of transforming growth factor‐β (TGF‐β). To investigate the role of LTBP‐3 in tooth formation we performed micro‐computed tomography (micro‐CT), histology, and scanning electron microscopy analyses of adult Ltbp3‐/‐ mice. The Ltbp3‐/‐ mutants presented with unique craniofacial malformations and reductions in enamel formation that began at the matrix formation stage. Organization of maturation‐stage ameloblasts was severely disrupted. The lateral side of the incisor was affected most. Reduced enamel mineralization, modification of the enamel prism pattern, and enamel nodules were observed throughout the incisors, as revealed by scanning electron microscopy. Molar roots had internal irregular bulbous‐like formations. The cementum thickness was reduced, and microscopic dentinal tubules showed minor nanostructural changes. Thus, LTBP‐3 is required for ameloblast differentiation and for the formation of decussating enamel prisms, to prevent enamel nodule formation, and for proper root morphogenesis. Also, and consistent with the role of TGF‐β signaling during mineralization, almost all craniofacial bone components were affected in Ltbp3‐/‐ mice, especially those involving the upper jaw and snout. This mouse model demonstrates phenotypic overlap with Verloes Bourguignon syndrome, also caused by mutation of LTBP3, which is hallmarked by craniofacial anomalies and amelogenesis imperfecta phenotypes.

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Section: Discussionmentioning

confidence: 65%

Enamel and dental anomalies in latent‐transforming growth factor beta‐binding protein 3 mutant mice

Morkmued

Hemmerlé

Mathieu

et al. 2017

European J Oral Sciences

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“…This has been reported for the other major hypomineralized condition of enamel, dental fluorosis, 34,35 and animal models also indicate a genetic risk component for non-fluorotic hypomineralized enamel. 36,37 The exact aetiological mechanism(s) of enamel hypomineralization and why there is markedly asymmetric presentation in individuals remain unknown. While most respondents believed medical conditions to be involved in the aetiology, which is supported by several studies reporting a higher incidence of developmental enamel defects in medically compromised populations, [16][17][18][19] just over half in the present study thought there was a genetic component.…”

Section: Discussionmentioning

confidence: 99%

Molar incisor hypomineralization: a survey of members of the Australian and New Zealand Society of Paediatric Dentistry

Crombie

Manton

Weerheijm³

et al. 2008

Australian Dental Journal

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Background: Worldwide, molar incisor hypomineralization (MIH) affects a substantial number of children and impacts greatly on treatment need and dental anxiety, yet there is little information regarding its prevalence, aetiology, presentation and management. The aims of this survey were to assess awareness and perceptions of the Australian paediatric dental community concerning MIH, and to describe current treatment strategies. Methods: A questionnaire, based upon a previous European study, was sent to all Australian members of the Australian and New Zealand Society of Paediatric Dentistry. The questionnaire sought information on clinical experience of MIH, knowledge of prevalence, aetiology and contemporary management strategies for MIH. Results: One hundred and thirty useable responses were received (58.8 per cent response rate) of which 36 were paediatric dentists, 6 paediatric dentistry postgraduate students, 59 general dentists, 14 dental therapists and 14 specialists in other fields. Most (98.5 per cent) respondents were familiar with MIH and encountered it in their practice. The majority (73.1 per cent) estimated that MIH occurred in between 5 to 25 per cent of their clinical practice and almost all (96.9 per cent) considered it to be a clinical problem. Only 16.9 per cent of respondents were aware of existing prevalence data and 96.9 per cent valued investigating the prevalence of MIH. No consensus existed regarding the aetiology of MIH or its restorative management. Paediatric dentists used preformed crowns significantly more than non-specialists, however glass ionomer cements were popular with all groups. Conclusions: MIH is a well recognized and widely encountered clinical condition. MIH presents several clinical problems and is worthy of further investigation. Currently, no consistent clinical management strategies are utilized.

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“…(13,14) TGF-b is one of the few factors known to regulate tissue-level properties. (15)(16)(17) When TGF-b signaling was decreased or increased in transgenic mouse models, the modulus and hardness of the tissue increased or decreased, respectively, as determined by nanoindentation. (15) Therefore, modulation of MMP activity also may influence mechanical properties via indirect effects on TGF-b activity in addition to direct effects on matrix processing.…”

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confidence: 99%

Differential effects between the loss of MMP-2 and MMP-9 on structural and tissue-level properties of bone

Nyman

Lynch

Perrien

et al. 2010

Journal of Bone and Mineral Research

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Matrix metalloproteinases (MMPs) are capable of processing certain components of bone tissue, including type 1 collagen, a determinant of the biomechanical properties of bone tissue, and they are expressed by osteoclasts and osteoblasts. Therefore, we posit that MMP activity can affect the ability of bone to resist fracture. To explore this possibility, we determined the architectural, compositional, and biomechanical properties of bones from wild-type (WT), Mmp2 À/À , and Mmp9 À/À female mice at 16 weeks of age. MMP-2 and MMP-9have similar substrates but are expressed primarily by osteoblasts and osteoclasts, respectively. Analysis of the trabecular compartment of the tibia metaphysis by micro-computed tomography (mCT) revealed that these MMPs influence trabecular architecture, not volume. Interestingly, the loss of MMP-9 improved the connectivity density of the trabeculae, whereas the loss of MMP-2 reduced this parameter. Similar differential effects in architecture were observed in the L 5 vertebra, but bone volume fraction was lower for both Mmp2 À/À and Mmp9 À/À mice than for WT mice. The mineralization density and mineral-to-collagen ratio, as determined by mCT and Raman microspectroscopy, were lower in the Mmp2 À/À bones than in WT control bones. Whole-bone strength, as determined by three-point bending or compression testing, and tissue-level modulus and hardness, as determined by nanoindentation, were less for Mmp2 À/À than for WT bones. In contrast, the Mmp9 À/À femurs were less tough with lower postyield deflection (more brittle) than the WT femurs. Taken together, this information reveals that MMPs play a complex role in maintaining bone integrity, with the cell type that expresses the MMP likely being a contributing factor to how the enzyme affects bone quality. ß

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Elevated TGF-β2 signaling in dentin results in sex related enamel defects

Cited by 13 publications

References 32 publications

Enamel and dental anomalies in latent‐transforming growth factor beta‐binding protein 3 mutant mice

Enamel and dental anomalies in latent‐transforming growth factor beta‐binding protein 3 mutant mice

Molar incisor hypomineralization: a survey of members of the Australian and New Zealand Society of Paediatric Dentistry

Differential effects between the loss of MMP-2 and MMP-9 on structural and tissue-level properties of bone

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