Cementum: A Phosphate-sensitive Tissue

Nociti, Francisco Humberto; Berry, Janice E.; Foster, Brian L.; Gurley, Kyle A.; Kingsley, David M.; Takata, Takashi; Miyauchi, Mutsumi; Somerman, Martha J.

doi:10.1177/154405910208101204

Cited by 76 publications

(101 citation statements)

References 29 publications

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“…These individuals can have only mildly reduced serum ALP levels. This milder clinical form of HPP suggests that tooth development is the most sensitive developmental process dependent upon TNALP function, a notion supported by studies in mice on cementum indicating a particular sensitivity of this tissue to local phosphate and pyrophosphate levels (Nociti et al, 2002;Foster et al, 2006). In some cases, tooth roots may have an absence or aplasia of acellular cementum presumably responsible for early tooth exfoliation (Bruckner et al, 1962;el-Labban et al, 1991;Olsson et al, 1966;Hu et al, 2000), and enlarged pulp chambers associated with defective dentin mineralization (Beumer et al, 1973;Jedrychowski and Duperon, 1979;Olsson et al, 1996;Liu et al, 2010).…”

Section: Discussionmentioning

confidence: 82%

Enzyme Replacement Therapy Prevents Dental Defects in a Model of Hypophosphatasia

et al. 2011

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Section: Discussionmentioning

confidence: 82%

Enzyme Replacement Therapy Prevents Dental Defects in a Model of Hypophosphatasia

et al. 2011

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“…In addition to articular cartilage calcification, ankylosis, and increased cementum, these animals display vascular calcification. [61][62][63][64][65] A growing number of other putative calcification inhibitory molecules have been identified using mouse mutational analyses, including MGP, ␤-glucosidase, carbonic anhydrase II, fetuin, osteoprotegerin, desmin, and Smad 6. 34,66 -73 Mutant mice deficient in these molecules present with enhanced cardiovascular calcification as part of their phenotype and demonstrate that specific proteins and small molecules are normally important in suppressing ectopic calcification, including vascular calcification.…”

Section: Role Of Osteopontinmentioning

confidence: 99%

Regulation of Vascular Calcification

Giachelli

Speer

et al. 2005

Circulation Research

260

122

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Abstract-Vascular calcification is prevalent in aging as well as a number of pathological conditions, and it is nowrecognized as a strong predictor of cardiovascular events in the general population as well as diabetic and end-stage renal disease patients. Vascular calcification is a highly regulated process involving inductive and inhibitory mechanisms. In contrast, age and vascular disease-related vascular calcifications were previously considered benign. However, recent clinical studies have challenged this dogma. Calcification has been positively correlated with coronary atherosclerotic plaque burden, 11,12 increased risk of myocardial infarction, 13-15 and plaque instability. 2,16 Furthermore, in the Rotterdam Coronary Calcification Study, a large populationbased study, graded associations between coronary calcification score and stroke were identified. 17 Similarly, medial arterial calcification is strongly correlated with coronary artery disease and future cardiovascular events in type I diabetic subjects, 18,19 and is a strong prognostic marker of cardiovascular disease mortality in ESRD patients. 20 These findings may be explained by growing evidence that vascular medial calcification in large arteries leads to increased stiffness and therefore decreased compliance of these vessels. These mechanical changes are associated with increased arterial pulse wave velocity and pulse pressure, and lead to impaired arterial distensibility, increased afterload favoring left ventricular hypertrophy, and compromised coronary perfusion. 21 Thus, intimal and medial calcifications may contribute to the morbidity and mortality associated with cardiovascular disease.It is becoming increasingly clear that vascular calcification is an actively regulated process that may be initiated by a number of different, nonmutually exclusive mechanisms. These mechanisms have been extensively reviewed elsewhere 22 and include: (1) loss of mineral inhibiting factors; (2) induction of bone formation; (3) cell death; and (4) circulating nucleational complexes (ie, aggregates of calcium phosphate and proteins released from remodeling bone that may initiate ectopic mineralization). Abnormalities in mineral metabolism that enhance the calcium ϫ phosphate product (Ca ϫ P) may further exacerbate vascular calcification initiated by any of these mechanisms. This article focuses on recent evidence implicating elevated phosphate as a major inductive factor for vascular calcification and osteopontin as an inducible inhibitor of vascular calcification, and our current understanding of their mechanisms of action.

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“…The overall different behavior of root cementum when compared with other periodontal tissues was previously established in a study demonstrating the susceptibility of cementum to a lack of alkaline phosphatase [50] and changes in extracellular pyrophosphate levels [51]. Moreover, in comparison to AB osteoblasts, cementoblasts were characterized by a number of unique signature genes, including the chemoattractant Netrin 4, the intermediate filament keratin 18, the notch signaling mediator JAG1, and Dkk1.…”

mentioning

confidence: 94%

Differentiation of Neural-Crest-Derived Intermediate Pluripotent Progenitors into Committed Periodontal Populations Involves Unique Molecular Signature Changes, Cohort Shifts, and Epigenetic Modifications

Dangaria

Ito

Diekwisch

2011

Stem Cells and Development

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Intermediate progenitor populations play a crucial role in the regional specification and differentiation of the cranial neural crest. On the basis of global gene expression profiles, gene cohort expression levels, and epigenetic modifications, we have defined key factors involved in the differentiation of dental follicle (DF) intermediate progenitors into periodontal lineages, including alveolar bone (AB) osteoblasts, cementoblasts, and periodontal ligament (PDL) cells. When comparing differentially expressed genes, PDL cells most closely resembled DF progenitors, followed by AB osteoblasts and cementoblasts as the most distant population. According to gene ontology analyses, extracellular matrix-adhesion proteins were substantially increased in PDL cells, osteogenesis factors were elevated in AB osteoblasts, and gene expression levels were lower in cementoblasts, especially in the cytokine group. Unique signature proteins included interleukin 6, paired-like homeodomain transcription factor 2, thrombospondin 2, and glial cell line-derived neurotrophic factor for DF progenitors; asporin and prostaglandin-H2 D-isomerase for AB osteoblasts; and keratin 18, Netrin 4, Jagged 1, and Dickkopf1 for cementoblasts, as verified by western blot analysis. Secreted frizzled-related protein 1 was preferentially expressed in PDL cells, whereas matrix Gla-protein, bone sialoprotein, and insulin-like growth factor binding protein 5 were higher in AB osteoblasts than in cementoblasts. On an epigenetic level, DF progenitors featured high levels of the euchromatin marker H3K4me3, whereas PDL cells, AB osteoblasts, and cementoblasts contained high levels of the transcriptional repressor H3K9me3. Together, our data indicate that in addition to changes in signature gene expression, unique shifts in gene cohort expression levels, epigenetic modifications, and changes in cell morphology contribute to the individuation of tissue populations from a common neural-crest-derived ancestor.

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Cementum: A Phosphate-sensitive Tissue

Cited by 76 publications

References 29 publications

Enzyme Replacement Therapy Prevents Dental Defects in a Model of Hypophosphatasia

Enzyme Replacement Therapy Prevents Dental Defects in a Model of Hypophosphatasia

Regulation of Vascular Calcification

Differentiation of Neural-Crest-Derived Intermediate Pluripotent Progenitors into Committed Periodontal Populations Involves Unique Molecular Signature Changes, Cohort Shifts, and Epigenetic Modifications

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