The Experts below are selected from a list of 68640 Experts worldwide ranked by ideXlab platform

Kanya Suphapeetiporn - One of the best experts on this subject based on the ideXlab platform.

  • Compromised alveolar Bone cells in a patient with dentinogenesis imperfecta caused by DSPP mutation
    Clinical Oral Investigations, 2019
    Co-Authors: Thantrira Porntaveetus, Nunthawan Nowwarote, Thanaphum Osathanon, Thanakorn Theerapanon, Prasit Pavasant, Lawan Boonprakong, Kittisak Sanon, Sirivimol Srisawasdi, Kanya Suphapeetiporn, Vorasuk Shotelersuk
    Abstract:

    Objectives Dentin sialophosphoprotein ( DSPP ) plays an important role in the mineralization of both dentin and Bones. The Dspp null mice developed periodontal diseases. Patients with DSPP mutations have dentinogenesis imperfecta (DGI), but very little is known about their Bone Characteristics. This study aims to characterize alveolar Bone cells of a DGI patient with DSPP mutation. Materials and methods Pathogenic variants were identified by whole exome and sanger sequencing. Cells isolated from the alveolar Bones of a DSPP patient were investigated for their Characteristics including cell morphology, attachment, spreading, proliferation, colony formation, mineralization, and osteogenic differentiation. Results We identified a Thai family with three members affected with autosomal dominant DGI harboring a heterozygous pathogenic missense mutation, c.50C > T, p.P17L, in exon 2 of the DSPP gene. The patients’ phenotypes presented deteriorated opalescent teeth with periapical lesions, thickening of lamina dura, furcation involvement, alveolar Bone loss, and Bone exostoses. The alveolar Bone cells isolated from DSPP patient exhibited compromised proliferation and colony formation. Scanning electron microscope revealed altered cellular morphology and spreading. The DSPP cells showed deviated mRNA levels of OCN , ALP , and COL1 but maintained in vitro mineralization ability compared to the control. Conclusions We demonstrate that the DSPP p.P17L mutant alveolar Bone cells had compromised cell spreading, proliferation, colony formation, and osteogenic induction, suggesting abnormal Bone Characteristics in the patient with DGI caused by DSPP mutation. Clinical relevance DSPP mutation can induce the behavior alterations of alveolar Bone cells.

  • compromised alveolar Bone cells in a patient with dentinogenesis imperfecta caused by dspp mutation
    Clinical Oral Investigations, 2019
    Co-Authors: Thantrira Porntaveetus, Nunthawan Nowwarote, Thanaphum Osathanon, Thanakorn Theerapanon, Prasit Pavasant, Lawan Boonprakong, Kittisak Sanon, Sirivimol Srisawasdi, Kanya Suphapeetiporn
    Abstract:

    Dentin sialophosphoprotein (DSPP) plays an important role in the mineralization of both dentin and Bones. The Dspp null mice developed periodontal diseases. Patients with DSPP mutations have dentinogenesis imperfecta (DGI), but very little is known about their Bone Characteristics. This study aims to characterize alveolar Bone cells of a DGI patient with DSPP mutation. Pathogenic variants were identified by whole exome and sanger sequencing. Cells isolated from the alveolar Bones of a DSPP patient were investigated for their Characteristics including cell morphology, attachment, spreading, proliferation, colony formation, mineralization, and osteogenic differentiation. We identified a Thai family with three members affected with autosomal dominant DGI harboring a heterozygous pathogenic missense mutation, c.50C > T, p.P17L, in exon 2 of the DSPP gene. The patients’ phenotypes presented deteriorated opalescent teeth with periapical lesions, thickening of lamina dura, furcation involvement, alveolar Bone loss, and Bone exostoses. The alveolar Bone cells isolated from DSPP patient exhibited compromised proliferation and colony formation. Scanning electron microscope revealed altered cellular morphology and spreading. The DSPP cells showed deviated mRNA levels of OCN, ALP, and COL1 but maintained in vitro mineralization ability compared to the control. We demonstrate that the DSPP p.P17L mutant alveolar Bone cells had compromised cell spreading, proliferation, colony formation, and osteogenic induction, suggesting abnormal Bone Characteristics in the patient with DGI caused by DSPP mutation. DSPP mutation can induce the behavior alterations of alveolar Bone cells.

Thantrira Porntaveetus - One of the best experts on this subject based on the ideXlab platform.

  • Compromised alveolar Bone cells in a patient with dentinogenesis imperfecta caused by DSPP mutation
    Clinical Oral Investigations, 2019
    Co-Authors: Thantrira Porntaveetus, Nunthawan Nowwarote, Thanaphum Osathanon, Thanakorn Theerapanon, Prasit Pavasant, Lawan Boonprakong, Kittisak Sanon, Sirivimol Srisawasdi, Kanya Suphapeetiporn, Vorasuk Shotelersuk
    Abstract:

    Objectives Dentin sialophosphoprotein ( DSPP ) plays an important role in the mineralization of both dentin and Bones. The Dspp null mice developed periodontal diseases. Patients with DSPP mutations have dentinogenesis imperfecta (DGI), but very little is known about their Bone Characteristics. This study aims to characterize alveolar Bone cells of a DGI patient with DSPP mutation. Materials and methods Pathogenic variants were identified by whole exome and sanger sequencing. Cells isolated from the alveolar Bones of a DSPP patient were investigated for their Characteristics including cell morphology, attachment, spreading, proliferation, colony formation, mineralization, and osteogenic differentiation. Results We identified a Thai family with three members affected with autosomal dominant DGI harboring a heterozygous pathogenic missense mutation, c.50C > T, p.P17L, in exon 2 of the DSPP gene. The patients’ phenotypes presented deteriorated opalescent teeth with periapical lesions, thickening of lamina dura, furcation involvement, alveolar Bone loss, and Bone exostoses. The alveolar Bone cells isolated from DSPP patient exhibited compromised proliferation and colony formation. Scanning electron microscope revealed altered cellular morphology and spreading. The DSPP cells showed deviated mRNA levels of OCN , ALP , and COL1 but maintained in vitro mineralization ability compared to the control. Conclusions We demonstrate that the DSPP p.P17L mutant alveolar Bone cells had compromised cell spreading, proliferation, colony formation, and osteogenic induction, suggesting abnormal Bone Characteristics in the patient with DGI caused by DSPP mutation. Clinical relevance DSPP mutation can induce the behavior alterations of alveolar Bone cells.

  • compromised alveolar Bone cells in a patient with dentinogenesis imperfecta caused by dspp mutation
    Clinical Oral Investigations, 2019
    Co-Authors: Thantrira Porntaveetus, Nunthawan Nowwarote, Thanaphum Osathanon, Thanakorn Theerapanon, Prasit Pavasant, Lawan Boonprakong, Kittisak Sanon, Sirivimol Srisawasdi, Kanya Suphapeetiporn
    Abstract:

    Dentin sialophosphoprotein (DSPP) plays an important role in the mineralization of both dentin and Bones. The Dspp null mice developed periodontal diseases. Patients with DSPP mutations have dentinogenesis imperfecta (DGI), but very little is known about their Bone Characteristics. This study aims to characterize alveolar Bone cells of a DGI patient with DSPP mutation. Pathogenic variants were identified by whole exome and sanger sequencing. Cells isolated from the alveolar Bones of a DSPP patient were investigated for their Characteristics including cell morphology, attachment, spreading, proliferation, colony formation, mineralization, and osteogenic differentiation. We identified a Thai family with three members affected with autosomal dominant DGI harboring a heterozygous pathogenic missense mutation, c.50C > T, p.P17L, in exon 2 of the DSPP gene. The patients’ phenotypes presented deteriorated opalescent teeth with periapical lesions, thickening of lamina dura, furcation involvement, alveolar Bone loss, and Bone exostoses. The alveolar Bone cells isolated from DSPP patient exhibited compromised proliferation and colony formation. Scanning electron microscope revealed altered cellular morphology and spreading. The DSPP cells showed deviated mRNA levels of OCN, ALP, and COL1 but maintained in vitro mineralization ability compared to the control. We demonstrate that the DSPP p.P17L mutant alveolar Bone cells had compromised cell spreading, proliferation, colony formation, and osteogenic induction, suggesting abnormal Bone Characteristics in the patient with DGI caused by DSPP mutation. DSPP mutation can induce the behavior alterations of alveolar Bone cells.

Vorasuk Shotelersuk - One of the best experts on this subject based on the ideXlab platform.

  • Compromised alveolar Bone cells in a patient with dentinogenesis imperfecta caused by DSPP mutation
    Clinical Oral Investigations, 2019
    Co-Authors: Thantrira Porntaveetus, Nunthawan Nowwarote, Thanaphum Osathanon, Thanakorn Theerapanon, Prasit Pavasant, Lawan Boonprakong, Kittisak Sanon, Sirivimol Srisawasdi, Kanya Suphapeetiporn, Vorasuk Shotelersuk
    Abstract:

    Objectives Dentin sialophosphoprotein ( DSPP ) plays an important role in the mineralization of both dentin and Bones. The Dspp null mice developed periodontal diseases. Patients with DSPP mutations have dentinogenesis imperfecta (DGI), but very little is known about their Bone Characteristics. This study aims to characterize alveolar Bone cells of a DGI patient with DSPP mutation. Materials and methods Pathogenic variants were identified by whole exome and sanger sequencing. Cells isolated from the alveolar Bones of a DSPP patient were investigated for their Characteristics including cell morphology, attachment, spreading, proliferation, colony formation, mineralization, and osteogenic differentiation. Results We identified a Thai family with three members affected with autosomal dominant DGI harboring a heterozygous pathogenic missense mutation, c.50C > T, p.P17L, in exon 2 of the DSPP gene. The patients’ phenotypes presented deteriorated opalescent teeth with periapical lesions, thickening of lamina dura, furcation involvement, alveolar Bone loss, and Bone exostoses. The alveolar Bone cells isolated from DSPP patient exhibited compromised proliferation and colony formation. Scanning electron microscope revealed altered cellular morphology and spreading. The DSPP cells showed deviated mRNA levels of OCN , ALP , and COL1 but maintained in vitro mineralization ability compared to the control. Conclusions We demonstrate that the DSPP p.P17L mutant alveolar Bone cells had compromised cell spreading, proliferation, colony formation, and osteogenic induction, suggesting abnormal Bone Characteristics in the patient with DGI caused by DSPP mutation. Clinical relevance DSPP mutation can induce the behavior alterations of alveolar Bone cells.

Thanakorn Theerapanon - One of the best experts on this subject based on the ideXlab platform.

  • Compromised alveolar Bone cells in a patient with dentinogenesis imperfecta caused by DSPP mutation
    Clinical Oral Investigations, 2019
    Co-Authors: Thantrira Porntaveetus, Nunthawan Nowwarote, Thanaphum Osathanon, Thanakorn Theerapanon, Prasit Pavasant, Lawan Boonprakong, Kittisak Sanon, Sirivimol Srisawasdi, Kanya Suphapeetiporn, Vorasuk Shotelersuk
    Abstract:

    Objectives Dentin sialophosphoprotein ( DSPP ) plays an important role in the mineralization of both dentin and Bones. The Dspp null mice developed periodontal diseases. Patients with DSPP mutations have dentinogenesis imperfecta (DGI), but very little is known about their Bone Characteristics. This study aims to characterize alveolar Bone cells of a DGI patient with DSPP mutation. Materials and methods Pathogenic variants were identified by whole exome and sanger sequencing. Cells isolated from the alveolar Bones of a DSPP patient were investigated for their Characteristics including cell morphology, attachment, spreading, proliferation, colony formation, mineralization, and osteogenic differentiation. Results We identified a Thai family with three members affected with autosomal dominant DGI harboring a heterozygous pathogenic missense mutation, c.50C > T, p.P17L, in exon 2 of the DSPP gene. The patients’ phenotypes presented deteriorated opalescent teeth with periapical lesions, thickening of lamina dura, furcation involvement, alveolar Bone loss, and Bone exostoses. The alveolar Bone cells isolated from DSPP patient exhibited compromised proliferation and colony formation. Scanning electron microscope revealed altered cellular morphology and spreading. The DSPP cells showed deviated mRNA levels of OCN , ALP , and COL1 but maintained in vitro mineralization ability compared to the control. Conclusions We demonstrate that the DSPP p.P17L mutant alveolar Bone cells had compromised cell spreading, proliferation, colony formation, and osteogenic induction, suggesting abnormal Bone Characteristics in the patient with DGI caused by DSPP mutation. Clinical relevance DSPP mutation can induce the behavior alterations of alveolar Bone cells.

  • compromised alveolar Bone cells in a patient with dentinogenesis imperfecta caused by dspp mutation
    Clinical Oral Investigations, 2019
    Co-Authors: Thantrira Porntaveetus, Nunthawan Nowwarote, Thanaphum Osathanon, Thanakorn Theerapanon, Prasit Pavasant, Lawan Boonprakong, Kittisak Sanon, Sirivimol Srisawasdi, Kanya Suphapeetiporn
    Abstract:

    Dentin sialophosphoprotein (DSPP) plays an important role in the mineralization of both dentin and Bones. The Dspp null mice developed periodontal diseases. Patients with DSPP mutations have dentinogenesis imperfecta (DGI), but very little is known about their Bone Characteristics. This study aims to characterize alveolar Bone cells of a DGI patient with DSPP mutation. Pathogenic variants were identified by whole exome and sanger sequencing. Cells isolated from the alveolar Bones of a DSPP patient were investigated for their Characteristics including cell morphology, attachment, spreading, proliferation, colony formation, mineralization, and osteogenic differentiation. We identified a Thai family with three members affected with autosomal dominant DGI harboring a heterozygous pathogenic missense mutation, c.50C > T, p.P17L, in exon 2 of the DSPP gene. The patients’ phenotypes presented deteriorated opalescent teeth with periapical lesions, thickening of lamina dura, furcation involvement, alveolar Bone loss, and Bone exostoses. The alveolar Bone cells isolated from DSPP patient exhibited compromised proliferation and colony formation. Scanning electron microscope revealed altered cellular morphology and spreading. The DSPP cells showed deviated mRNA levels of OCN, ALP, and COL1 but maintained in vitro mineralization ability compared to the control. We demonstrate that the DSPP p.P17L mutant alveolar Bone cells had compromised cell spreading, proliferation, colony formation, and osteogenic induction, suggesting abnormal Bone Characteristics in the patient with DGI caused by DSPP mutation. DSPP mutation can induce the behavior alterations of alveolar Bone cells.

Prasit Pavasant - One of the best experts on this subject based on the ideXlab platform.

  • Compromised alveolar Bone cells in a patient with dentinogenesis imperfecta caused by DSPP mutation
    Clinical Oral Investigations, 2019
    Co-Authors: Thantrira Porntaveetus, Nunthawan Nowwarote, Thanaphum Osathanon, Thanakorn Theerapanon, Prasit Pavasant, Lawan Boonprakong, Kittisak Sanon, Sirivimol Srisawasdi, Kanya Suphapeetiporn, Vorasuk Shotelersuk
    Abstract:

    Objectives Dentin sialophosphoprotein ( DSPP ) plays an important role in the mineralization of both dentin and Bones. The Dspp null mice developed periodontal diseases. Patients with DSPP mutations have dentinogenesis imperfecta (DGI), but very little is known about their Bone Characteristics. This study aims to characterize alveolar Bone cells of a DGI patient with DSPP mutation. Materials and methods Pathogenic variants were identified by whole exome and sanger sequencing. Cells isolated from the alveolar Bones of a DSPP patient were investigated for their Characteristics including cell morphology, attachment, spreading, proliferation, colony formation, mineralization, and osteogenic differentiation. Results We identified a Thai family with three members affected with autosomal dominant DGI harboring a heterozygous pathogenic missense mutation, c.50C > T, p.P17L, in exon 2 of the DSPP gene. The patients’ phenotypes presented deteriorated opalescent teeth with periapical lesions, thickening of lamina dura, furcation involvement, alveolar Bone loss, and Bone exostoses. The alveolar Bone cells isolated from DSPP patient exhibited compromised proliferation and colony formation. Scanning electron microscope revealed altered cellular morphology and spreading. The DSPP cells showed deviated mRNA levels of OCN , ALP , and COL1 but maintained in vitro mineralization ability compared to the control. Conclusions We demonstrate that the DSPP p.P17L mutant alveolar Bone cells had compromised cell spreading, proliferation, colony formation, and osteogenic induction, suggesting abnormal Bone Characteristics in the patient with DGI caused by DSPP mutation. Clinical relevance DSPP mutation can induce the behavior alterations of alveolar Bone cells.

  • compromised alveolar Bone cells in a patient with dentinogenesis imperfecta caused by dspp mutation
    Clinical Oral Investigations, 2019
    Co-Authors: Thantrira Porntaveetus, Nunthawan Nowwarote, Thanaphum Osathanon, Thanakorn Theerapanon, Prasit Pavasant, Lawan Boonprakong, Kittisak Sanon, Sirivimol Srisawasdi, Kanya Suphapeetiporn
    Abstract:

    Dentin sialophosphoprotein (DSPP) plays an important role in the mineralization of both dentin and Bones. The Dspp null mice developed periodontal diseases. Patients with DSPP mutations have dentinogenesis imperfecta (DGI), but very little is known about their Bone Characteristics. This study aims to characterize alveolar Bone cells of a DGI patient with DSPP mutation. Pathogenic variants were identified by whole exome and sanger sequencing. Cells isolated from the alveolar Bones of a DSPP patient were investigated for their Characteristics including cell morphology, attachment, spreading, proliferation, colony formation, mineralization, and osteogenic differentiation. We identified a Thai family with three members affected with autosomal dominant DGI harboring a heterozygous pathogenic missense mutation, c.50C > T, p.P17L, in exon 2 of the DSPP gene. The patients’ phenotypes presented deteriorated opalescent teeth with periapical lesions, thickening of lamina dura, furcation involvement, alveolar Bone loss, and Bone exostoses. The alveolar Bone cells isolated from DSPP patient exhibited compromised proliferation and colony formation. Scanning electron microscope revealed altered cellular morphology and spreading. The DSPP cells showed deviated mRNA levels of OCN, ALP, and COL1 but maintained in vitro mineralization ability compared to the control. We demonstrate that the DSPP p.P17L mutant alveolar Bone cells had compromised cell spreading, proliferation, colony formation, and osteogenic induction, suggesting abnormal Bone Characteristics in the patient with DGI caused by DSPP mutation. DSPP mutation can induce the behavior alterations of alveolar Bone cells.