Bone Remodeling

  title={Bone Remodeling},
  author={Dimitrios J Hadjidakis and Ioannis I. Androulakis},
  journal={Annals of the New York Academy of Sciences},
Abstract:  The skeleton is a metabolically active organ that undergoes continuous remodeling throughout life. Bone remodeling involves the removal of mineralized bone by osteoclasts followed by the formation of bone matrix through the osteoblasts that subsequently become mineralized. The remodeling cycle consists of three consecutive phases: resorption, during which osteoclasts digest old bone; reversal, when mononuclear cells appear on the bone surface; and formation, when osteoblasts lay down… 

The Role Of BMPs in the Regulation of Osteoclasts Resorption and Bone Remodeling: From Experimental Models to Clinical Applications

Current knowledge of BMP signaling in osteoclasts, its role in osteoclast resorption, bone remodeling, and osteoblast–osteoclast coupling is summarized and discussion of clinical application of recombinant BMP therapy is based on recent preclinical and clinical studies.

Pathophysiology of Osteoporosis

  • S. Ferrari
  • Biology, Engineering
    Pocket Reference to Osteoporosis
  • 2018
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Osteoblastogenesis regulation signals in bone remodeling

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RANKL regulates RAW 264 . 7 cell osteoclastogenesis in a manner

The osteoclastic differentiation and activation are triggered mainly by osteoblast cells and vice versa, and the major biological regulators of bone remodeling include parathyroid hormone and calcitriol as well as other hormones.

Bone Remodeling and the Role of TRAF3 in Osteoclastic Bone Resorption

Development of drugs to prevent TRAF3 degradation in immune and bone cells could be a novel therapeutic approach to prevent or reduce bone loss and the incidence of several common diseases associated with aging.

Is There a Governing Role of Osteocytes in Bone Tissue Regeneration?

It is postulate that osteocytes may have a pivotal role in bone regeneration as well, and consequently that the bone regeneration process may be improved effectively and rapidly if osteocytes are optimally used and stimulated.

Osteoimmunological Aspects on Inflammation and Bone Metabolism

The RANK/RANKL/OPG-system is actively involved in the differentiation and function of osteoclasts and is known to play a central role in the majority of pathophysiological mechanisms.

Osteocyte-Related Cytokines Regulate Osteoclast Formation and Bone Resorption

Findings suggest that osteocyte-related cytokines act directly to enhance osteoclast formation and bone resorption, and discuss the osteocyte as the master regulator of bone Resorption and effector in osteoc last formation.

Roles of fibrinolytic factors in the alterations in bone marrow hematopoietic stem/progenitor cells during bone repair

Establishment of a fibrinolytic factor-targeting method efficiently promoting bone repair/regeneration and fracture healing, and development of a new osteoporosis treatment method and diagnostic marker are awaited.



Increased bone formation in osteocalcin-deficient mice

This study provides the first evidence that osteocalcin is a determinant of bone formation, and generates osteocalin-deficient mice that develop a phenotype marked by higher bone mass and bones of improved functional quality.

Osteonal and hemi‐osteonal remodeling: The spatial and temporal framework for signal traffic in adult human bone

  • A. Parfitt
  • Biology, Engineering
    Journal of cellular biochemistry
  • 1994
The bone replacement process in the adult skeleton is known as remodeling. When bone is removed by osteoclasts, new bone is laid down by osteoblasts in the same place, because the load bearing

Bone resorption by osteoclasts.

Osteopetrotic mutants have provided a wealth of information about the genes that regulate the differentiation of osteoclasts and their capacity to resorb bone.

Osteocytes, strain detection, bone modeling and remodeling

  • L. Lanyon
  • Biology, Engineering
    Calcified Tissue International
  • 2005
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Evidence is provided that glucocorticoid-induced bone disease arises from changes in the numbers of bone cells, whereas decreased production and apoptosis of osteoblasts would account for the decline in bone formation and trabecular width.

Osteoblasts mediate thyroid hormone stimulation of osteoclastic bone resorption.

It is indicated that thyroid hormone can act on osteoblasts to indirectly stimulate osteoclastic bone resorption.

Osteoblasts are a new target for prolactin: analysis of bone formation in prolactin receptor knockout mice.

The PRL receptor knockout mouse model provides a new tool to investigate the involvement ofPRL in bone metabolism and suggests that an effect of PRL on osteoblasts could be required for normal bone formation and maintenance of bone mass.

Osteopontin--a possible anchor of osteoclasts to bone.

The results thus support the hypothesis that osteoclasts when resorbing bone are anchored by osteopontin bound both to the mineral of bone matrix and to a vitronectin receptor on the osteoclast plasma membrane.

Osteoblast-derived PTHrP is a potent endogenous bone anabolic agent that modifies the therapeutic efficacy of administered PTH 1-34.

A pivotal role is established for osteoblast-derived PTH-related protein (PTHrP) as a potent endogenous bone anabolic factor that potentiates bone formation by altering osteobine recruitment and survival and whose level of expression in the bone microenvironment influences the therapeutic efficacy of exogenous PTH 1-34.

Clinical implications of the osteoprotegerin/RANKL/RANK system for bone and vascular diseases.

RANKL blockade has prevented bone loss caused by osteoporosis, chronic inflammatory disorders, and malignant tumors in animal models and may emerge as a therapy in humans based on studies in postmenopausal osteop orosis, myeloma bone disease, and osteolytic metastases.