The high prevalence of tooth agenesis outside the cleft area might be attributed to the different ethnic and/or genetic backgrounds of the groups examined. The term “patterns” of tooth agenesis in UCLP
patients is often used in the dental literature. These patterns mostly referred to maxillary laterals incisors and/or maxillary first and second premolars,32 and 33 and not to tooth agenesis patterns of the whole mouth. this website To our knowledge, the present study is the second one to analyse “symmetry and combinations of hypodontia in UCPL patients” in the whole mouth.15 It has been suggested previously that the high prevalence of tooth agenesis outside the cleft area might point to common developmental or interacting genetic pathways.29, 34, 35, 36 and 37 A precise description of dental subphenotypes in OFCs would be useful for identifying genes responsible for OFC and tooth agenesis.37 In addition, the genes that contribute to laterality of clefts, may result in alternate phenotypes for dental anomalies. 37 If the mechanism of these pathways could be unravelled, it may create opportunities to find targets for compounds that could prevent the disruption of these interacting pathways. There is no source of funding for selleck chemicals our research. There is no conflicts of interests. Not required Theodosia N.
Bartzela: data collection, data interpretation, manuscript preparation. Carine Carels: data interpretation related to genetics, manuscript preparation. Ewald M. Bronkhorst: statistical analysis and data interpretation. Anne Marie Kuijpers-Jagtman: data interpretation, manuscript preparation. “
“Dentinogenesis is the dentine formation process in which the
odontoblasts are responsible for the organic matrix synthesis, and posterior mineral crystal deposition in this matrix. This pattern of formation is similar to that of bone, another mineralized connective tissue. For both mineralized tissues, it is of fundamental importance understanding how the ions constituting the inorganic phase are transported from the circulation to the site of mineral formation and how this transport is regulated.1 Calcium is an essential ion for the composition of the mineral next crystals during dentinogenesis. Changes in the serum calcium levels lead to structural alterations of the forming dentine.2, 3, 4 and 5 Calcium metabolism is regulated mainly by parathyroid hormone (PTH), and studies have been performed to understand how PTH influences the mineralization process.6, 7 and 8 The overall function of endogenous PTH, an 84-amino acid peptide secreted by the parathyroid glands, is to maintain normal extracellular calcium levels by enhancing gastrointestinal calcium absorption, renal tubular calcium and phosphate resorption, and osteoclastic bone resorption, thereby releasing calcium from the skeleton.9 The PTH primary biological activity is similar to PTHrP (parathyroid hormone-related protein), and its activity resides mainly within the 1–34 N-terminal fragment.