Targeted expression of csCSF-1 in op/op mice ameliorates tooth defects

Werner, S.; Gluhak-Heinrich, Jelica; Woodruff, Katie; Wittrant, Yohann; Cardenas, Lina; Roudier, Martine P.; MacDougall, Mary

doi:10.1016/j.archoralbio.2006.10.018

Cited by 13 publications

(14 citation statements)

References 47 publications

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“…RNA was extracted and quantitative real-time PCR was performed to examine mRNA expression levels of molecules that are known to regulate osteoclast number and behavior and the tooth eruption cycle including RANKL, OPG, CSF-1, and PTH1R (Garlet et al, 2006) (Heinrich et al, 2005; Rani and MacDougall, 2000; Werner et al, 2007). CSF-1 expression was below the level of detection in the samples tested.…”

Section: Resultsmentioning

confidence: 99%

Inactivation of Tgfbr2 in Osterix-Cre expressing dental mesenchyme disrupts molar root formation

Wang¹,

Cox²,

Coricor³

et al. 2013

Developmental Biology

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It has been difficult to examine the role of TGF-ß in post-natal tooth development due to perinatal lethality in many of the signaling deficient mouse models. To address the role of Tgfbr2 in postnatal tooth development, we generated a mouse in which Tgfbr2 was deleted in odontoblast-and bone-producing mesenchyme. Osx-Cre;Tgfbr2fl/fl mice were generated (Tgfbr2cko) and postnatal tooth development was compared in Tgfbr2cko and control littermates. X-ray and μCT analysis showed that in Tgfbr2cko mice radicular dentin matrix density was reduced in the molars. Molar shape was abnormal and molar eruption was delayed in the mutant mice. Most significantly, defects in root formation, including failure of the root to elongate, were observed by postnatal day 10. Immunostaining for Keratin-14 (K14) was used to delineate Hertwig's epithelial root sheath (HERS). The results showed a delay in elongation and disorganization of the HERS in Tgfbr2cko mice. In addition, the HERS was maintained and the break up into epithelial rests was attenuated suggesting that Tgfbr2 acts on dental mesenchyme to indirectly regulate the formation and maintenance of the HERS. Altered odontoblast organization and reduced Dspp expression indicated that odontoblast differentiation was disrupted in the mutant mice likely contributing to the defect in root formation. Nevertheless, expression of Nfic, a key mesenchymal regulator of root development, was similar in Tgfbr2cko mice and controls. The number of osteoclasts in the bone surrounding the tooth was reduced and osteoblast differentiation was disrupted likely contributing to both root and eruption defects. We conclude that Tgfbr2 in dental mesenchyme and bone is required for tooth development particularly root formation.

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Section: Resultsmentioning

confidence: 99%

Inactivation of Tgfbr2 in Osterix-Cre expressing dental mesenchyme disrupts molar root formation

Wang¹,

Cox²,

Coricor³

et al. 2013

Developmental Biology

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“…In all, 5- μ m thick sections were stained with H&E to evaluate morphology, Brown & Hopp’s stain to detect gram-positive/negative bacterial organisms and tartrate resistant acid phosphatase (TRAP) to identify osteoclasts as previously described. 21 Immunohistochemical staining was performed to assess amelogenin (Amel) and ameloblastin (Ambn) expression in ameloblasts using a rabbit polyclonal anti-human Amel (FL-191) and goat polyclonal anti-human Ambn (C-17); 1:100, Santa Cruz. Following incubation with each primary antibody, sections were incubated with a standard HRP-polymer detection kit (Biocare Medical) and 3,3′-diaminobenzidine substrate was used to visualize immunoreaction sites.…”

Section: Methodsmentioning

confidence: 99%

Hyperglycemia and xerostomia are key determinants of tooth decay in type 1 diabetic mice

Yeh

Harris

Mohan

et al. 2012

Laboratory Investigation

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Insulin-dependent type 1 diabetes mellitus (DM) and oral diseases are closely interrelated. Poor metabolic control in diabetics is associated with a high risk of gingivitis, periodontitis and tooth loss. Salivary flow declines in diabetics and patients suffer from xerostomia. Reduced saliva predisposes to enamel hypomineralization and caries formation; however, the mechanisms that initiate and lead to progression of tooth decay and periodontitis in type 1 DM have not been explored. To address this issue, we analyzed tooth morphology in Akita −/− mice that harbor a point mutation in the Ins2 insulin gene, which leads to progressive hyperglycemia. Mandibles from Akita −/− and wild-type littermates were analyzed by microCT, scanning EM and histology; teeth were examined for amelogenin (Amel) and ameloblastin (Ambn) expression. Mice were injected with pilocarpine to assess saliva production. As hyperglycemia may alter pulp repair, the effect of high glucose levels on the proliferation/differentiation of cultured MD10-F2 pulp cells was also analyzed. Results showed that Akita −/− mice at 6 weeks of age showed chalky white incisors that correlated with marked hyperglycemia and impaired saliva production. MicroCT of Akita −/− teeth revealed excessive enamel wearing and hypomineralization; immunostaining for Amel and Ambn was decreased. A striking feature was invasion of dentinal tubules with Streptococcus mitis and microabcesses that originated in the coronal pulp and progressed to pulp necrosis and periapical periodontitis. High levels of glucose also inhibited MD10-F2 cell proliferation and differentiation. Our findings provide the first evidence that hyperglycemia in combination with reduced saliva in a model of type1 DM leads to decreased enamel mineralization/matrix proteins and predisposes to excessive wearing and decay. Importantly, hyperglycemia adversely affects enamel matrix proteins and pulp repair. Early detection and treatment of hyperglycemia and hyposalivation may provide a useful strategy for preventing the dental complications of diabetes and promoting oral health in this population.

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“…Oral physiological processes are unique and diverse owing to the specific embryological pattern of differentiation of cells and the unique functions of the oral cavity. LCM technology has been used to elucidate the molecular basis of taste sensation (Neira et al , ; Suzuki et al , ; Gao et al , ; Hevezi et al , ; Moyer et al , ), eruption (Wise et al , ; Yao et al , , ; Liu et al , ; Wise and Yao, ; Werner et al , ; Oikawa et al , ), and oral bone healing and osseointegration (Lin et al , ). LCM has been utilized to build the gene expression atlas of salivary glands, which has given valuable insights into the molecular mechanism of branching morphogenesis during normal salivary gland development (Musselmann et al , ).…”

Section: Lcm For Integrated Oral Biosciencesmentioning

confidence: 99%

Exploring the potential of laser capture microdissection technology in integrated oral biosciences

et al. 2016

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Laser capture microdissection (LCM) is a high‐end research and diagnostic technology that helps in obtaining pure cell populations for the purpose of cell‐ or lesion‐specific genomic and proteomic analysis. Literature search on the application of LCM in oral tissues was made through PubMed. There is ample evidence to substantiate the utility of LCM in understanding the underlying molecular mechanism involving an array of oral physiological and pathological processes, including odontogenesis, taste perception, eruptive tooth movement, oral microbes, and cancers of the mouth and jaw tumors. This review is aimed at exploring the potential application of LCM in oral tissues as a high‐throughput tool for integrated oral sciences. The indispensable application of LCM in the construction of lesion‐specific genomic libraries with emphasis on some of the novel molecular markers thus discovered is also highlighted.

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Targeted expression of csCSF-1 in op/op mice ameliorates tooth defects

Cited by 13 publications

References 47 publications

Inactivation of Tgfbr2 in Osterix-Cre expressing dental mesenchyme disrupts molar root formation

Inactivation of Tgfbr2 in Osterix-Cre expressing dental mesenchyme disrupts molar root formation

Hyperglycemia and xerostomia are key determinants of tooth decay in type 1 diabetic mice

Exploring the potential of laser capture microdissection technology in integrated oral biosciences

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