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Skeletal overexpression of noggin results in osteopenia and reduced bone formation

R D Devlin1, Z Du, R C Pereira

  • 1Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105-1299, USA.

Endocrinology
|April 17, 2003
PubMed

Insights

Overexpressing noggin in bone cells impairs osteoblastic function, leading to reduced bone density, osteopenia, and fractures in mice. This study reveals noggin

Area of Science:

  • Bone biology
  • Skeletal cell function
  • Bone morphogenetic proteins (BMPs) antagonism

Background:

  • Skeletal cells produce bone morphogenetic proteins (BMPs) and their antagonists, like noggin.
  • Noggin, a glycoprotein, selectively binds BMPs, inhibiting their actions.
  • While noggin's in vitro effects on osteoblasts are known, its in vivo role in bone remodeling remains unclear.

Purpose of the Study:

  • To investigate the direct in vivo effects of noggin on bone remodeling.
  • To analyze bone structure and function in transgenic mice overexpressing noggin.

Main Methods:

  • Generation of transgenic mice overexpressing noggin under the osteocalcin promoter.
  • Assessment of bone mineral density (total, vertebral, femoral).
  • Histomorphometry and microcomputed tomography (micro-CT) of bone tissue.

Main Results:

  • Transgenic mice exhibited reduced bone mineral density (23-29%) and increased long bone fractures.
  • Histomorphometry showed decreased trabecular bone volume, reduced trabecular number, and lower bone formation rates.
  • Osteoblastic function appeared impaired, with normal/decreased osteoclast numbers and no increased bone resorption.

Conclusions:

  • Overexpression of noggin in the bone microenvironment leads to osteopenia and fractures.
  • Impaired osteoblastic function and decreased bone volume are key consequences of excessive noggin.
  • This study highlights noggin's critical role in maintaining bone health in vivo.

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