caa a22 4500 605520917 CHVBK 20210128100737.0 cr unu---uuuuu 210128e20151101xx s 000 0 eng 10.1007/s00223-015-0030-5 doi (NATIONALLICENCE)springer-10.1007/s00223-015-0030-5 Uremia Induces Dental Pulp Ossification but Reciprocally Inhibits Adjacent Alveolar Bone Osteogenesis [Elektronische Daten] [Chih-Yu Yang, Zee-Fen Chang, Yat-Pang Chau, Ann Chen, Oscar Lee, An-Hang Yang] Uremic patients are predisposed to atrophy of the alveolar bone and narrowing of the dental pulp chamber. Such pulp chamber changes have only been diagnosed radiologically; however, this has not been supported by any pathological evidence. We used a uremic rat model with secondary hyperparathyroidism induced by 5/6 nephrectomy surgery and high-phosphate diet to examine the dental pulp and adjacent alveolar bone pathology. In addition, we collected pulp tissues for real-time PCR. We found an opposite histopathological presentation of the ossified dental pulp and the osteomalacic adjacent alveolar bone. Furthermore, pulp cells with positive staining for Thy-1, a surrogate stem cell marker, were significantly reduced in the pulp of uremic rats compared to the controls, indicating a paucity of stem cells. This was further evidenced by the reduced pulp expression of dickkopf-1 (Dkk-1), a Wnt/β-catenin signaling inhibitor produced by mesenchymal stem cells. In contrast, expressions of receptor activator of nuclear factor κB ligand (RANKL) and RANK in uremic pulp were up-regulated, probably to counteract the ossifying process of uremic pulp. In conclusion, uremic pulp ossifications were associated with a paucity of stem cells and dysregulated Dkk-1 and RANKL signaling systems, further shifting the imbalance toward osteogenesis. Strategies to counteract such an imbalance may offer a potential therapeutic target to improve dental health in uremic patients, which warrants further interventional studies. Springer Science+Business Media New York, 2015 Uremia nationallicence Pulp ossification nationallicence Stem cells nationallicence Dickkopf-1 nationallicence RANKL nationallicence Osteomalacia nationallicence Yang Chih-Yu Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan aut Chang Zee-Fen Institute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan aut Chau Yat-Pang Department of Medicine, Mackay Medical College, New Taipei City, Taiwan aut Chen Ann Department of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan aut Lee Oscar Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan aut Yang An-Hang Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan aut Calcified Tissue International Springer US; http://www.springer-ny.com 97/5(2015-11-01), 466-475 0171-967X 97:5<466 2015 97 223 https://doi.org/10.1007/s00223-015-0030-5 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s00223-015-0030-5 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Yang Chih-Yu Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan aut NATIONALLICENCE 700 1- Chang Zee-Fen Institute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan aut NATIONALLICENCE 700 1- Chau Yat-Pang Department of Medicine, Mackay Medical College, New Taipei City, Taiwan aut NATIONALLICENCE 700 1- Chen Ann Department of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan aut NATIONALLICENCE 700 1- Lee Oscar Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan aut NATIONALLICENCE 700 1- Yang An-Hang Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan aut NATIONALLICENCE 773 0- Calcified Tissue International Springer US; http://www.springer-ny.com 97/5(2015-11-01), 466-475 0171-967X 97:5<466 2015 97 223