Effect of high phosphorus diet on tooth microstructure of rodent incisors Vladimir Jekl a, ⁎, Lenka Krejcirova b , Marcela Buchtova c , Zdenek Knotek a, d a Avian and Exotic Animal Clinic, Faculty of Veterinary Medicine, University of Veterinary and Pharmaceutical Sciences, Brno, Czech Republic b Department of Histology and Embryology, Faculty of Medicine, Masaryk University, Brno, Czech Republic c Department of Anatomy, Histology and Embryology, Faculty of Veterinary Medicine, University of Veterinary and Pharmaceutical Sciences, Brno, Czech Republic d Clinic for Avian, Reptile and Fish Medicine, University of Veterinary Medicine, Vienna, Austria abstract article info Article history: Received 16 January 2011 Revised 5 April 2011 Accepted 26 April 2011 Available online 5 May 2011 Edited by: Rene Rizzoli Keywords: Enamel Hypoplasia Dentin Phosphorus Calcium Scanning electron microscopy Enamel hypoplasia and disruption of dentinogenesis are the most common abnormalities of development and mineralization of human teeth. Several reports are available in the literature on the inﬂuence of dietary calcium on the formation of human and rodent tooth; however, the information about the inﬂuence of dietary phosphorus on the tooth formation is scarce. The aim of the present investigation was to examine the chronic effect of high phosphorus diet and improper dietary calcium to phosphorus ratio on the mandibular incisor microstructure in a hystricomorph rodent – Octodon degu – using macroscopic observation, histopathological examination, transmission and scanning electron microscopy. The present study shows that enamel and dentin development is disturbed under high phosphorus diet and improper calcium to phosphorus ratio. Disturbed mineral metabolism resulted in enamel depigmentation, enamel hypoplasia, enamel pitting and altered dentin morphology. The results suggest that more attention should be focused on dietary phosphorus content when facing altered tooth structure in young patients with deciduous or permanent dentition. Furthermore, we showed that degus can be used as an experimental animal model for the study of the developmental teeth disturbances. © 2011 Elsevier Inc. All rights reserved. Introduction Enamel is a hierarchically ordered bioceramic tissue, and its development involves typical bio-mineralization, in which a synthe- sized extracellular organic matrix induces and governs the subse- quent mineral deposition and organization under genetic control [1]. Matrix mineralization takes place almost immediately involving: (a) formation, nucleation, and elongation of apatite crystals and (b) removal of the organic matrix and crystal maturation [2]. Developmental defects of enamel and dentin are the results of alterations during amelogenesis and dentinogenesis due to hered- itary, systemic or environmental factors [3]. The extended tooth formative period during development of deciduous or permanent human dentition offers extremely large possibilities for various etiological factors to act. Higher prevalence of dental enamel defects in children with deciduous dentition is commonly associated with low birth weight, malnutrition, malabsorption, infant feeding, systemic diseases and socio-economic factors [4–7]. The shape and size of growing teeth are also inﬂuenced by functional occlusal forces [8,9]. Several reports are available in the literature on the inﬂuence of dietary calcium on the formation of human and rodent enamel [10–15]. Enamel hypoplasia, which is deﬁned as a deﬁciency of enamel formation, is the most common abnormality of development and mineralization of human teeth [10]. Enamel hypoplasia is important for clinicians because it can result in increased caries susceptibility, increased wear, tooth sensitivity and poor esthetics [16]. Dentin acquired pathology associated with disrupted calcium metabolism is in children mostly linked to hypovitaminosis D [15,17]. Despite the importance of calcium homeostasis, which is greatly inﬂuenced by dietary phosphorus, the information about the effect of high phosphorus diet on rodent or human enamel and dentin formation are scarce [18,19]. In human nutrition, phosphate is widely distributed in many foods and the amount of phosphorus intake is gradually increasing [20]. Phosphorus intake could be also abundant, whereas calcium ingestion fails to meet recommendations. In such cases, dietary calcium to phosphorus ratio (Ca:P) is therefore lower [21]. It is thought that excessive phosphorus intake for long periods is a strong factor in bone impairment and ageing [20]. Findings of Kemi et al. [21] suggest that in habitual diets low Ca:P ratios with adequate calcium intake may interfere with homoeostasis of calcium metabolism and increase bone resorption. A high phosphorus diet produces a higher level of plasma phosphate, which reduces urine calcium loss, reduces renal synthesis of 1.25-dihydroxycholekalciferol, reduces serum ionized calcium, and leads to increases in parathormone (PTH) release with subsequent Bone 49 (2011) 479–484 ⁎ Corresponding author at: Avian and Exotic Animal Clinic, Faculty of Veterinary Medicine, University of Veterinary and Pharmaceutical Sciences Brno, 1–3 Palackeho St., 612 42 Brno, Czech Republic. E-mail address: jeklv@vfu.cz (V. Jekl). 8756-3282/$ – see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.bone.2011.04.021 Contents lists available at ScienceDirect Bone journal homepage: www.elsevier.com/locate/bone