LETTER TO JMG

MMP-20 mutation in autosomal recessive pigmented hypomaturation amelogenesis imperfecta

J-W Kim¹, J P Simmer², T C Hart³, P S Hart⁴, M D Ramaswami⁵, J D Bartlett⁶, J C-C Hu⁷

¹ Department of Pediatric Dentistry, College of Dentistry & Dental Research Institute, Seoul National University, Seoul, Korea; and University of Michigan, School of Dentistry, Ann Arbor, MI, USA
² Department of Biological and Material Sciences, University of Michigan School of Dentistry, Ann Arbor, MI, USA
³ National Institutes of Health, NIDCR
⁴ National Institutes of Health, NHGRI
⁵ National Institutes of Health, NIDCR
⁶ Harvard-Forsyth Department of Cytokine Biology, The Forsyth Institute
⁷ Department of Pediatric Dentistry, University of Michigan School of Dentistry, Ann Arbor, MI, USA

Correspondence to:
Correspondence to:
Dr J C-C Hu
Department of Orthodontics and Pediatric Dentistry, University of Michigan Dental Research Laboratory, 1210 Eisenhower Place, Ann Arbor, MI 48108, USA; janhu@umich.edu

Keywords: amelogenesis imperfecta; enamel; enamelysin; hypomaturation AI; MMP-20

The first 150 words of the full text of this article appear below.

During mammalian tooth formation, two proteinases are secreted by ameloblasts: enamelysin (MMP-20) and kallikrein-4 (KLK4). Enamelysin is the early protease. It is expressed by ameloblasts throughout the secretory stage and part of the maturation stage.^1–3 KLK4 is the late protease; its expression by ameloblasts begins in the transition stage and continues throughout enamel maturation.^4,5 Expression of these two proteases overlaps during the transition and early maturation stages, when the bulk of the organic matrix component is removed from the enamel layer. Because of its early pattern of expression, its ability to generate the same pattern of amelogenin cleavages in vitro as those observed in vivo,⁶ and the nature of the dental phenotype in enamelysin knockout mice,⁷ MMP-20 cleavages are thought to play important roles in crystal elongation, proper formation of the dentino–enamel junction (DEJ), and in the maintenance of enamel rod organisation. The extracellular protein KLK4 is believed to be . . . [Full text of this article]

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