Kallikrein-related peptidase 4, matrix metalloproteinase 20, and the maturation of murine and porcine enamel

Authors

  • Yuanyuan Hu,

    1. Department of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI, USA
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  • Jan C-C. Hu,

    1. Department of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI, USA
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  • Charles E. Smith,

    1. Department of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI, USA
    2. Facility for Electron Microscopy Research, Department of Anatomy & Cell Biology, and Faculty of Dentistry, McGill University, Montreal, QC, Canada
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  • John D. Bartlett,

    1. Department of Cytokine Biology, Forsyth Institute and Department of Developmental Biology, Harvard School of Dental Medicine, Cambridge, MA, USA
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  • James P. Simmer

    1. Department of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI, USA
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James P. Simmer, Department of Biologic and Materials Sciences, University of Michigan Dental Research Lab, 1210 Eisenhower Place, Ann Arbor, MI 48108, USA

Telefax: +1–734–9759329
E-mail: jsimmer@umich.edu

Abstract

Hu Y, Hu JC-C, Smith CE, Bartlett JD, Simmer JP. Kallikrein-related peptidase 4, matrix metalloproteinase 20, and the maturation of murine and porcine enamel.
Eur J Oral Sci 2011; 119 (Suppl. 1): 217–225. © 2011 Eur J Oral Sci

The crowns of matrix metalloproteinase 20 (Mmp20) null mice fracture at the dentino–enamel junction (DEJ), whereas the crowns of kallikrein-related peptidase 4 (Klk4) null mice fracture in the deep enamel just above the DEJ. We used backscatter scanning electron microscopy to assess enamel mineralization in incisors from 9-wk-old wild-type, Klk4 null, and Mmp20 null mice, and in developing pig molars. We observed a line of hypermineralization along the DEJ in developing wild-type mouse and pig teeth. This line was discernible from the early secretory stage until the enamel in the maturation stage reached a similar density. The line was apparent in Klk4 null mice, but absent in Mmp20 null mice. Enamel in the Klk4 null mice matured normally at the surface, but was progressively less mineralized with depth. Enamel in the Mmp20 null mice formed as a mineral bilayer, with neither layer looking like true enamel. The most superficial mineral layer expanded during the maturation stage and formed irregular surface nodules. A surprising finding was the observation of electron backscatter from mid-maturation wild-type ameloblasts, which we attributed to the accumulation and release of iron. We conclude that enamel breaks in the deep enamel of Klk4 null mice because of decreasing enamel maturation with depth, and at the DEJ in Mmp20 null mice because of hypomineralization at the DEJ.

Ancillary