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Osteoporosis

B. Pathology and Pathophysiology
  • Philip Sambrook

Abstract

  • The pathophysiology of osteoporosis includes many genetic, hormonal, nutritional, and environmental influences. Some risk factors for this condition are well defined.

  • Although genetic factors contribute strongly to determining peak bone mass, hormonal, nutritional, and environmental influences during intrauterine life, childhood, and adolescence modulate the genetically determined pattern of skeletal growth.

  • The bone mass of an individual in later life is a consequence of the peak bone mass accrued in utero and during childhood and puberty, as well as the subsequent rate of bone loss.

  • The high rate of hip fracture in older people is not only due to their lower bone strength but also their increased risk of falling. Established risk factors for falls and, hence, hip fracture include impaired balance, muscle weakness, cognitive impairment, and psychotropic medication.

  • Bone is continually undergoing a process of renewal called remodeling. In the normal adult skeleton, new bone laid down by osteoblasts exactly matches osteoclastic bone resorption; that is, bone formation and bone resorption are closely coupled.

  • The principal cell types within bone are the osteoclasts, osteoblasts, and osteocytes. Osteoclasts are responsible for resorption of bone; osteoblasts are responsible directly for bone formation; osteocytes, derived from osteoblasts, appear to play a role in response to mechanical loading.

  • ■ Key regulators of osteoclastic bone resorption include RANK ligand and its two known receptors, RANK and osteoprotegerin (OPG). RANK and OPG have opposing effects on bone resorption.

Keywords

Bone Mineral Density Bone Loss Bone Resorption Bone Turnover Trabecular Bone 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media, LLC. 2008

Authors and Affiliations

  • Philip Sambrook
    • 1
  1. 1.Department of RheumatologyUniversity of SydneySydneyAustralia

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