Influence of estrogen and progesterone on matrix-induced endochondral bone formation

Cornell C. Burnett, A Hari Reddi

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

The influence of estradiol and progesterone, alone or in combination, on the discrete phases of matrix-induced endochondral bone formation was investigated. Administration of estradiol and progesterone in combination increased mesenchymal cell proliferation, as indicated by [3H] thymidine incorporaton into acid precipitable material. However, ornithine decarboxylase (ODC) activity was significantly suppressed by the combination of estradiol and progesterone. Also, this treatment did not influence the35SO4 incorporation into proteoglycans on day 7. Mineralization of newly induced bone was quantitated by alkaline phosphatase,45Ca incorporation into bone mineral and calcium content, and was found to be significantly increased by progesterone alone and in combination with estradiol in both matrix-induced plaques and tibial metaphysis. These results demonstrated the stimulatory role of progesterone in combination with estradiol in bone formation and mineralization.

Original languageEnglish (US)
Pages (from-to)609-614
Number of pages6
JournalCalcified Tissue International
Volume35
Issue number1
DOIs
StatePublished - Dec 1983
Externally publishedYes

Fingerprint

Osteogenesis
Progesterone
Estradiol
Estrogens
Physiologic Calcification
Ornithine Decarboxylase
Proteoglycans
Bone Density
Thymidine
Alkaline Phosphatase
Cell Proliferation
Calcium
Bone and Bones
Acids

Keywords

  • Estradiol and progesterone
  • Matrix-induced endochondral bone formation
  • Mesenchymal cell
  • Ornithine decarboxylase

ASJC Scopus subject areas

  • Endocrinology
  • Orthopedics and Sports Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

Influence of estrogen and progesterone on matrix-induced endochondral bone formation. / Burnett, Cornell C.; Reddi, A Hari.

In: Calcified Tissue International, Vol. 35, No. 1, 12.1983, p. 609-614.

Research output: Contribution to journalArticle

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