Molecular regulation of osteoclast activity

Angela Bruzzaniti, Roland Baron

Research output: Contribution to journalArticle

105 Citations (Scopus)

Abstract

Osteoclasts are multinucleated cells derived from hematopoietic precursors that are primarily responsible for the degradation of mineralized bone during bone development, homeostasis and repair. In various skeletal disorders such as osteoporosis, hypercalcemia of malignancy, tumor metastases and Paget's disease, bone resorption by osteoclasts exceeds bone formation by osteoblasts leading to decreased bone mass, skeletal fragility and bone fracture. The overall rate of osteoclastic bone resorption is regulated either at the level of differentiation of osteoclasts from their monocytic/macrophage precursor pool or through the regulation of key functional proteins whose specific activities in the mature osteoclast control its attachment, migration and resorption. Thus, reducing osteoclast numbers and/or decreasing the bone resorbing activity of osteoclasts are two common therapeutic approaches for the treatment of hyper-resorptive skeletal diseases. In this review, several of the key functional players involved in the regulation of osteoclast activity will be discussed.

Original languageEnglish (US)
Pages (from-to)123-139
Number of pages17
JournalReviews in Endocrine and Metabolic Disorders
Volume7
Issue number1-2
DOIs
StatePublished - Jun 2006
Externally publishedYes

Fingerprint

Osteoclasts
Bone Resorption
Osteitis Deformans
Bone and Bones
Bone Development
Bone Fractures
Hypercalcemia
Osteoblasts
Osteogenesis
Osteoporosis
Neoplasms
Homeostasis
Macrophages
Neoplasm Metastasis
Proteins

Keywords

  • Cytoskeleton
  • Integrins
  • Osteoclast
  • Podosome
  • Resorption
  • Signaling
  • Src

ASJC Scopus subject areas

  • Endocrinology
  • Internal Medicine

Cite this

Molecular regulation of osteoclast activity. / Bruzzaniti, Angela; Baron, Roland.

In: Reviews in Endocrine and Metabolic Disorders, Vol. 7, No. 1-2, 06.2006, p. 123-139.

Research output: Contribution to journalArticle

@article{322389f159114083828a695089529bb8,
title = "Molecular regulation of osteoclast activity",
abstract = "Osteoclasts are multinucleated cells derived from hematopoietic precursors that are primarily responsible for the degradation of mineralized bone during bone development, homeostasis and repair. In various skeletal disorders such as osteoporosis, hypercalcemia of malignancy, tumor metastases and Paget's disease, bone resorption by osteoclasts exceeds bone formation by osteoblasts leading to decreased bone mass, skeletal fragility and bone fracture. The overall rate of osteoclastic bone resorption is regulated either at the level of differentiation of osteoclasts from their monocytic/macrophage precursor pool or through the regulation of key functional proteins whose specific activities in the mature osteoclast control its attachment, migration and resorption. Thus, reducing osteoclast numbers and/or decreasing the bone resorbing activity of osteoclasts are two common therapeutic approaches for the treatment of hyper-resorptive skeletal diseases. In this review, several of the key functional players involved in the regulation of osteoclast activity will be discussed.",
keywords = "Cytoskeleton, Integrins, Osteoclast, Podosome, Resorption, Signaling, Src",
author = "Angela Bruzzaniti and Roland Baron",
year = "2006",
month = "6",
doi = "10.1007/s11154-006-9009-x",
language = "English (US)",
volume = "7",
pages = "123--139",
journal = "Reviews in Endocrine and Metabolic Disorders",
issn = "1389-9155",
publisher = "Springer Netherlands",
number = "1-2",

}

TY - JOUR

T1 - Molecular regulation of osteoclast activity

AU - Bruzzaniti, Angela

AU - Baron, Roland

PY - 2006/6

Y1 - 2006/6

N2 - Osteoclasts are multinucleated cells derived from hematopoietic precursors that are primarily responsible for the degradation of mineralized bone during bone development, homeostasis and repair. In various skeletal disorders such as osteoporosis, hypercalcemia of malignancy, tumor metastases and Paget's disease, bone resorption by osteoclasts exceeds bone formation by osteoblasts leading to decreased bone mass, skeletal fragility and bone fracture. The overall rate of osteoclastic bone resorption is regulated either at the level of differentiation of osteoclasts from their monocytic/macrophage precursor pool or through the regulation of key functional proteins whose specific activities in the mature osteoclast control its attachment, migration and resorption. Thus, reducing osteoclast numbers and/or decreasing the bone resorbing activity of osteoclasts are two common therapeutic approaches for the treatment of hyper-resorptive skeletal diseases. In this review, several of the key functional players involved in the regulation of osteoclast activity will be discussed.

AB - Osteoclasts are multinucleated cells derived from hematopoietic precursors that are primarily responsible for the degradation of mineralized bone during bone development, homeostasis and repair. In various skeletal disorders such as osteoporosis, hypercalcemia of malignancy, tumor metastases and Paget's disease, bone resorption by osteoclasts exceeds bone formation by osteoblasts leading to decreased bone mass, skeletal fragility and bone fracture. The overall rate of osteoclastic bone resorption is regulated either at the level of differentiation of osteoclasts from their monocytic/macrophage precursor pool or through the regulation of key functional proteins whose specific activities in the mature osteoclast control its attachment, migration and resorption. Thus, reducing osteoclast numbers and/or decreasing the bone resorbing activity of osteoclasts are two common therapeutic approaches for the treatment of hyper-resorptive skeletal diseases. In this review, several of the key functional players involved in the regulation of osteoclast activity will be discussed.

KW - Cytoskeleton

KW - Integrins

KW - Osteoclast

KW - Podosome

KW - Resorption

KW - Signaling

KW - Src

UR - http://www.scopus.com/inward/record.url?scp=33845984343&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33845984343&partnerID=8YFLogxK

U2 - 10.1007/s11154-006-9009-x

DO - 10.1007/s11154-006-9009-x

M3 - Article

C2 - 16951988

AN - SCOPUS:33845984343

VL - 7

SP - 123

EP - 139

JO - Reviews in Endocrine and Metabolic Disorders

JF - Reviews in Endocrine and Metabolic Disorders

SN - 1389-9155

IS - 1-2

ER -