The Experts below are selected from a list of 228 Experts worldwide ranked by ideXlab platform
Kanya Suphapeetiporn - One of the best experts on this subject based on the ideXlab platform.
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Compromised alveolar bone cells in a patient with dentinogenesis imperfecta caused by DSPP mutation
Clinical Oral Investigations, 2019Co-Authors: Thantrira Porntaveetus, Nunthawan Nowwarote, Thanaphum Osathanon, Thanakorn Theerapanon, Prasit Pavasant, Lawan Boonprakong, Kittisak Sanon, Sirivimol Srisawasdi, Kanya Suphapeetiporn, Vorasuk ShotelersukAbstract: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.
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compromised alveolar bone cells in a patient with dentinogenesis imperfecta caused by dspp mutation
Clinical Oral Investigations, 2019Co-Authors: Thantrira Porntaveetus, Nunthawan Nowwarote, Thanaphum Osathanon, Thanakorn Theerapanon, Prasit Pavasant, Lawan Boonprakong, Kittisak Sanon, Sirivimol Srisawasdi, Kanya SuphapeetipornAbstract: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.
Jorgen Slots - One of the best experts on this subject based on the ideXlab platform.
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radiographic alveolar bone morphology and progressive periodontitis
Journal of Periodontology, 2018Co-Authors: Thomas E Rams, M A Listgarten, Jorgen SlotsAbstract:Background This study evaluated the relationship between radiographic crestal alveolar bone morphology and progressive periodontitis. Methods A total of 1,356 posterior interproximal sites in 56 adults treated for chronic periodontitis and receiving systematic 3-month maintenance care were scored for angular or horizontal marginal bone morphology, as well as for alveolar crestal Lamina Dura, on radiographs obtained at baseline of a 30-month post-treatment period. Semi-annually, the study patients were clinically evaluated for progressive periodontitis. Logistic regression analysis assessed baseline parameters to progressive periodontitis over the 30-month post-treatment period. Results Progressive periodontitis was detected at 33 (2.4%) posterior interproximal sites in 20 (35.7%) patients. Sites with post-treatment angular bony defects developed progressive periodontitis more frequently (14.7%) than sites with a horizontal bone topography (1.8%). Angular bony defects (odds ratio = 10.6) and periodontal probing depths ≥5 mm (odds ratio = 4.2) were identified as statistically significant independent predictors of progressive periodontitis at posterior interproximal sites. Angular bony and horizontal lesions with intact radiographic Lamina Dura revealed an absence of progressive periodontitis through 24 months. Conclusions Post-treatment presence of angular bone morphology and periodontal probing depths ≥5 mm significantly increased risk of progressive periodontitis at posterior interproximal sites. Sites of all morphology and probing depth that displayed radiographic crestal Lamina Dura at post-treatment baseline exhibited clinical stability for ≥24 months.
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utility of radiographic crestal Lamina Dura for predicting periodontitis disease activity
Journal of Clinical Periodontology, 1994Co-Authors: Thomas E Rams, M A Listgarten, Jorgen SlotsAbstract:The relationship between radiographic crestal Lamina Dura and periodontitis disease-activity was studied longitudinally in 51 treated adult patients on a systematic 3-month maintenance program. The presence or absence of crestal Lamina Dura at 1809 interproximal sites was scored from periapical and bitewing radiographs taken at baseline of a 36-month maintenance care period. Semi-annual clinical evaluations by 2 independent examiners were carried out on each patient, with disease recurrence defined as sites revealing a > or = 3 mm increase in probing depth from baseline, or a > or = 2 mm increase in probing depth together with a > or = 2 mm loss of relative attachment level from an occlusal reference stent. Over the 36-month study period, 23 (45%) patients exhibited disease recurrence at 55 (3%) interproximal tooth sites scored for baseline crestal Lamina Dura. Absence of detectable baseline crestal Lamina Dura yielded high sensitivity (87-100%), but low specificity (17%) and low positive predictive values (0.8-3.2%), for localized periodontitis recurrence. In contrast, no sites exhibiting an intact baseline crestal Lamina Dura demonstrated periodontitis recurrence up to 24 months from baseline (100% positive predictive values). Presence of radiographic crestal Lamina Dura was positively associated with clinical periodontal stability (summary odds ratio for sites = 2.6, P = 0.0004), and negatively associated with periodontitis recurrence (summary odds ratio for sites = 0.4, P = 0.0004), for the 36-month study period. Evaluation of radiographic crestal Lamina Dura status appears valuable for assessing the risk of periodontitis disease-activity at inter-proximal tooth sites in patients on maintenance care programs.
Thantrira Porntaveetus - One of the best experts on this subject based on the ideXlab platform.
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Compromised alveolar bone cells in a patient with dentinogenesis imperfecta caused by DSPP mutation
Clinical Oral Investigations, 2019Co-Authors: Thantrira Porntaveetus, Nunthawan Nowwarote, Thanaphum Osathanon, Thanakorn Theerapanon, Prasit Pavasant, Lawan Boonprakong, Kittisak Sanon, Sirivimol Srisawasdi, Kanya Suphapeetiporn, Vorasuk ShotelersukAbstract: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.
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compromised alveolar bone cells in a patient with dentinogenesis imperfecta caused by dspp mutation
Clinical Oral Investigations, 2019Co-Authors: Thantrira Porntaveetus, Nunthawan Nowwarote, Thanaphum Osathanon, Thanakorn Theerapanon, Prasit Pavasant, Lawan Boonprakong, Kittisak Sanon, Sirivimol Srisawasdi, Kanya SuphapeetipornAbstract: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.
Minoru Yamaoka - One of the best experts on this subject based on the ideXlab platform.
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bone formation without Lamina Dura in the middle aged and elderly possible dependence on enamel
Clinical Interventions in Aging, 2010Co-Authors: Minoru Yamaoka, Masahide Ishizuka, Kohji Ishihama, Masahiro Takahashi, Miho Takahashi, Hidefumi Yamada, Yuji Teramoto, Kouichi Yasuda, Toshikazu Shiba, Takashi UematsuAbstract:Bone formation below the crown of mandibular horizontal incompletely impacted third molar is frequently seen in the middle-aged and elderly. The phenomenon shows Lamina Dura loss without radiolucency and we hypothesized the participation of mature enamel without any influence on the environmental oral status. In order to investigate the characteristics of the phenomenon based on the presence/absence of the Lamina Dura and radiolucency below the crown, we studied the relationship between 58 men and 43 women with a Lamina Dura without radiolucency, 12 men and 8 women without a Lamina Dura with radiolucency, 34 men and 16 women without a Lamina Dura without radiolucency, and the status of teeth in the ipsilateral mandible. Subjects without a Lamina Dura without radiolucency were significantly older than those with a Lamina Dura without radiolucency in both men (P < 0.0001) and women (P <0.01), indicating different chronological causes. Men without Lamina Dura with radiolucency showed significantly more tooth loss than those with a Lamina Dura without radiolucency (P < 0.00001) and those without a Lamina Dura without radiolucency (P < 0.0001), indicating the influence of poor oral health. Thus, the phenomenon without a Lamina Dura without radiolucency may show the clinical importance of bone formation in the elderly.
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bone formation with disruption of the Lamina Dura in the mandibular third molar
Clinical Cosmetic and Investigational Dentistry, 2010Co-Authors: Minoru Yamaoka, Masahide Ishizuka, Masahiro Takahashi, Takashi Uematsu, Kiyofumi FurusawaAbstract:The Lamina Dura is a healthy structural component in teeth. This study highlights the association of bone formation with disruption of Lamina Dura below the crown of the mandibular horizontal incompletely impacted third molar.
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age related disruption of the Lamina Dura evidence in the mandibular horizontal incompletely impacted third molar
Clinical Interventions in Aging, 2009Co-Authors: Minoru Yamaoka, Kohji Ishihama, Masahiro Takahashi, Takashi Uematsu, Kiyofumi FurusawaAbstract:Changes in the Lamina Dura are associated with dental diseases around the root of the tooth and with systemic diseases; however, the Lamina Dura below the crown of horizontal, incompletely impacted third molars has not been studied. Using orthopantomography, we studied the age of subjects with and without the Lamina Dura in 419 subjects. The participants were between the ages of 21 and 89 years. Mean age in men with the Lamina Dura was 30.29 +/- 9.92 and without the Lamina Dura was 47.64 +/- 16.32 (P < 0.0001), and in women with a Lamina Dura it was 29.65 +/- 8.19 and without a Lamina Dura 41.97 +/- 11.07 (P < 0.0001). To study the effect of aging, the relationship between the Lamina Dura and dental status was assessed in subjects over the age of 31 years. Alveolar bone resorption in the canine and the first molar of the ipsilateral mandible in subjects without the Lamina Dura was not significantly higher than in those with the Lamina Dura. There were no significant differences in the number of teeth lost, except in men, the number of treated teeth and the number of decayed teeth differed between groups. Disruption of the Lamina Dura was related to age, but with no alveolar bone resorption in the mandible.
Vorasuk Shotelersuk - One of the best experts on this subject based on the ideXlab platform.
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Compromised alveolar bone cells in a patient with dentinogenesis imperfecta caused by DSPP mutation
Clinical Oral Investigations, 2019Co-Authors: Thantrira Porntaveetus, Nunthawan Nowwarote, Thanaphum Osathanon, Thanakorn Theerapanon, Prasit Pavasant, Lawan Boonprakong, Kittisak Sanon, Sirivimol Srisawasdi, Kanya Suphapeetiporn, Vorasuk ShotelersukAbstract: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.
