periostin null mice exhibit dwarfism, incisor enamel defects, and an early-onset periodontal disease-like phenotype

Hector Rios, Shrinagesh V. Koushik, Haiyan Wang, Jian Wang, Hong Ming Zhou, Andrew Lindsley, Rhonda Rogers, Zhi Chen, Manabu Maeda, Agnieszka Kruzynska-Frejtag, Jian Q. Feng, Simon Conway

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Abstract

Periostin was originally identified as an osteoblast-specific factor and is highly expressed in the embryonic periosteum, cardiac valves, placenta, and periodontal ligament as well as in many adult cancerous tissues. To investigate its role during development, we generated mice that lack the periostin gene and replaced the translation start site and first exon with a lacZ reporter gene. Surprisingly, although periostin is widely expressed in many developing organs, periostin-deficient (perilacZ) embryos are grossly normal. Postnatally, however, ∼14% of the nulls die before weaning and all of the remaining perilacZ nulls are severely growth retarded. Skeletal analysis revealed that trabecular bone in adult homozygous skeletons was sparse, but overall bone growth was unaffected. Furthermore, by 3 months, the nulls develop an early-onset periodontal disease-like phenotype. Unexpectedly, these mice also show a severe incisor enamel defect, although there is no apparent change in ameloblast differentiation. Significantly, placing the peri lacz nulls on a soft diet that alleviated mechanical strain on the periodontal ligament resulted in a partial rescue of both the enamel and periodontal disease-like phenotypes. Combined, these data suggest that a healthy periodontal ligament is required for normal amelogenesis and that periostin is critically required for maintenance of the integrity of the periodontal ligament in response to mechanical stresses.

Original languageEnglish
Pages (from-to)11131-11144
Number of pages14
JournalMolecular and Cellular Biology
Volume25
Issue number24
DOIs
StatePublished - Dec 2005

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Dwarfism
Periodontal Ligament
Periodontal Diseases
Incisor
Dental Enamel
Phenotype
Amelogenesis
Ameloblasts
Periosteum
Mechanical Stress
Lac Operon
Bone Development
Heart Valves
Weaning
Osteoblasts
Reporter Genes
Skeleton
Placenta
Exons
Embryonic Structures

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cell Biology

Cite this

periostin null mice exhibit dwarfism, incisor enamel defects, and an early-onset periodontal disease-like phenotype. / Rios, Hector; Koushik, Shrinagesh V.; Wang, Haiyan; Wang, Jian; Zhou, Hong Ming; Lindsley, Andrew; Rogers, Rhonda; Chen, Zhi; Maeda, Manabu; Kruzynska-Frejtag, Agnieszka; Feng, Jian Q.; Conway, Simon.

In: Molecular and Cellular Biology, Vol. 25, No. 24, 12.2005, p. 11131-11144.

Research output: Contribution to journalArticle

Rios, H, Koushik, SV, Wang, H, Wang, J, Zhou, HM, Lindsley, A, Rogers, R, Chen, Z, Maeda, M, Kruzynska-Frejtag, A, Feng, JQ & Conway, S 2005, 'periostin null mice exhibit dwarfism, incisor enamel defects, and an early-onset periodontal disease-like phenotype', Molecular and Cellular Biology, vol. 25, no. 24, pp. 11131-11144. https://doi.org/10.1128/MCB.25.24.11131-11144.2005
Rios, Hector ; Koushik, Shrinagesh V. ; Wang, Haiyan ; Wang, Jian ; Zhou, Hong Ming ; Lindsley, Andrew ; Rogers, Rhonda ; Chen, Zhi ; Maeda, Manabu ; Kruzynska-Frejtag, Agnieszka ; Feng, Jian Q. ; Conway, Simon. / periostin null mice exhibit dwarfism, incisor enamel defects, and an early-onset periodontal disease-like phenotype. In: Molecular and Cellular Biology. 2005 ; Vol. 25, No. 24. pp. 11131-11144.
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