Genetic regulation of bone mass: From bone density to bone strength

Craig Langman*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

6 Scopus citations

Abstract

Osteoporosis is a common disease characterized in adults by diminished bone density. Bone is an organ that evolves and grows throughout life, and establishing optimal bone density in childhood and adolescence serves to buffer bone loss later in life. Bone density, a measurable entity, is the clinical substitute for bone strength, or the ability to defend against fracture. Chronic diseases may adversely affect optimal peak bone density. Bone density is under genetic control, as revealed by three lines of investigations. These include (1) the finding of quantitative trait loci for bone density, (2) the finding that specific mutations in genes that are important in the development of osteoblast or osteoclast lineages alter bone density, and (3) the linkeage of known polymorphisms for genes involved in mineral homeostasis to bone density and/or fracture. Future therapeutics for improving peak bone density or delaying bone loss later in life may take advantage of the genetic nature of bone density development.

Original languageEnglish (US)
Pages (from-to)352-355
Number of pages4
JournalPediatric Nephrology
Volume20
Issue number3 SPEC. ISS.
DOIs
StatePublished - Mar 1 2005

Keywords

  • Estrogen receptor gene
  • Mineral metabolism
  • Osteoblast
  • Osteoclast
  • Osteoporosis
  • Polymorphisms
  • Quantitative trait loci
  • Vitamin D receptor gene

ASJC Scopus subject areas

  • Nephrology
  • Pediatrics, Perinatology, and Child Health

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