The Crowning Achievement: Getting to the Root of the Problem

Fong, Hanson; Foster, Brian L.; Popowics, Tracy; Somerman, Martha J.

doi:10.1002/j.0022-0337.2005.69.5.tb03942.x

Cited by 22 publications

(12 citation statements)

References 89 publications

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“…Yet, it is widely believed that an extension of the inner and outer dental epithelia in the tooth cervical loop, namely the Hertwig’s epithelial root sheath, probably initiates differentiation of odontoblasts from the peripheral mesenchymal cells followed by tooth root formation. Interestingly, there is no report of successful attempts to induce tooth root formation either in vitro or in vivo , although significant progress has been achieved in regenerating the tooth crown (34). In the present study, we demonstrated that osteoclasts play an essential role in root formation.…”

Section: Discussionmentioning

confidence: 99%

A new osteopetrosis mutant mouse strain (ntl) with odontoma‐like proliferations and lack of tooth roots

Ríos

Jiang

et al. 2009

European J Oral Sciences

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A new spontaneous mouse mutant (ntl) with autosomal-recessive osteopetrosis was characterized. These mice formed tartrate-resistant acid phosphate (TRAP)-positive osteoclasts but their osteoclasts had no ruffled border and did not resorb bone. These mice displayed no tooth eruption or tooth root formation. Adult mutant mice developed odontoma-like proliferations near the proximal ends of the incisors. Intraperitoneal injection of progenitor cells from the liver of 16.5 days postcoitum wild-type embryos into newborn mutants rescued the osteopetrosis phenotype, indicating that the defects were intrinsic to the osteoclasts. Our findings not only provide further support for a critical role of osteoclasts in tooth eruption and tooth root development, but also suggest that the perturbation of the homeostasis of the odontogenic precursors of the incisors is primarily responsible for the development of the odontoma-like proliferations in this osteopetrosis mutant. Genetic mapping has narrowed down the location of the mutant allele to a genetic interval of 3.2 cM on mouse chromosome 17.

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Section: Discussionmentioning

confidence: 99%

A new osteopetrosis mutant mouse strain (ntl) with odontoma‐like proliferations and lack of tooth roots

Ríos

Jiang

et al. 2009

European J Oral Sciences

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“…The periodontium can be defined as ‘an intricate mosaic of cells and proteins that is primarily responsible for the attachment of teeth in the oral cavity’ (144). Several excellent reviews have been published describing the embryonic lineage of the principal periodontal tissues (cementum, periodontal ligament, gingiva and alveolar bone), as well as the cells and extracellular matrix components of the periodontium (10, 13, 14, 21, 19, 46, 45, 51, 71, 80, 82, 144, 158, 185, 186, 193, 212, 214, 243, 244, 245).…”

Section: Development Of the Periodontiummentioning

confidence: 99%

Regeneration of periodontal tissues: cementogenesis revisited

Zeichner‐David¹

2006

Periodontology 2000

117

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“…Epithelial–mesenchymal interactions between odontogenic epithelium and ectomesenchymal cells typically include the dental epithelium and ectomesenchymal cells during the initial stage of tooth development, ameloblasts and odontoblasts during the crown‐formation process, and HERS and cementoblasts during root formation (20). In the present study, dental follicle cells and cementoblasts induced the apoptosis of ameloblasts and HERS/ERM cells.…”

Section: Discussionmentioning

confidence: 99%

Dental follicle cells and cementoblasts induce apoptosis of ameloblast‐lineage and Hertwig’s epithelial root sheath/epithelial rests of Malassez cells through the Fas–Fas ligand pathway

Lee¹,

Lee²,

Nam

et al. 2011

European J Oral Sciences

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Hertwig's epithelial root sheath (HERS), epithelial rests of Malassez (ERM) cells, and reduced ameloblasts undergo apoptosis during tooth development. This study examined the effects of dental follicle cells and cementoblasts on the apoptosis of ameloblast-lineage and HERS/ERM cells derived from the enamel organ. We also elucidated the induction pathways and identified the apoptotic pathway involved in this process. Here, we showed terminal deoxynucleotidyl transferase-mediated biotin-dUTP nick-end labeling (TUNEL)-positive HERS cells and reduced ameloblasts near dental follicle cells during tooth development. Co-culturing ameloblast-lineage cell line (ALC) ameloblasts and HERS/ERM cells with either dental follicle cells or OCCM-30 cementoblasts markedly enhanced the apoptosis of ameloblasts and HERS/ERM cells compared with cells cultured alone. However, dental follicle cells and cementoblasts did not modulate the apoptotic responses of co-cultured non-odontogenic MCF10A or KB cells. When ameloblasts + HERS and cementoblasts + dental follicle cells were co-cultured, the expression of Fas ligand (FasL) increased in cementoblasts + dental follicle cells, while the expression of Fas increased in ameloblasts + HERS. Interestingly, recombinant FasL induced ameloblast apoptosis while the cementoblast-induced ameloblast apoptosis was suppressed by the Fas/FasL antagonist Kp7-6. These results suggest that during tooth development, dental follicle cells and cementoblasts induce apoptosis of ameloblast-lineage and HERS/ERM cells through the Fas-FasL pathway, but do not induce the apoptosis of non-odontogenic epithelial cells.

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The Crowning Achievement: Getting to the Root of the Problem

Cited by 22 publications

References 89 publications

A new osteopetrosis mutant mouse strain (ntl) with odontoma‐like proliferations and lack of tooth roots

A new osteopetrosis mutant mouse strain (ntl) with odontoma‐like proliferations and lack of tooth roots

Regeneration of periodontal tissues: cementogenesis revisited

Dental follicle cells and cementoblasts induce apoptosis of ameloblast‐lineage and Hertwig’s epithelial root sheath/epithelial rests of Malassez cells through the Fas–Fas ligand pathway

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