Boneremodeling involves the removal of old or damaged bone by osteoclasts (bone resorption) and the subsequent replacement of new bone formed by osteoblasts (bone formation). Normal boneremodeling requires a tight coupling …
AbstractThe skeleton provides mechanical support for stature and
locomotion, protects vital organs, and controls mineral homeostasis. A
healthy skeleton must be maintained by constant bone modeling to carry
out these crucial functions throughout life. Bone remodeling involves
the removal of old or damaged bone by osteoclasts (bone resorption) and
the subsequent replacement of new bone formed by osteoblasts (bone
formation). Normal bone remodeling requires a tight coupling of bone
resorption to bone formation to guarantee no alteration in bone mass or
quality after each remodeling cycle. However, this important
physiological process can be derailed by a variety of factors, including
menopause-associated hormonal changes, age-related factors, changes in
physical activity, drugs, and secondary diseases, which lead to the
development of various bone disorders in both women and men. We review
the major diseases of bone remodeling, emphasizing our current
understanding of the underlying pathophysiological mechanisms.
Abstract: Osteocytes
are an ancient cell, appearing in fossilized skeletal remains of early
fish and dinosaurs. Despite its relative high abundance, even in the
context of nonskeletal cells, the osteocyte is perhaps among the least
studied cells in all of vertebrate biology. Osteocytes are cells
embedded in bone, able to modify their surrounding extracellular matrix
via specialized molecular remodeling mechanisms that are independent of
the bone forming osteoblasts and bone-resorbing osteoclasts. Osteocytes
communicate with osteoclasts and osteoblasts via distinct signaling
molecules that include the RankL/OPG axis and the Sost/Dkk1/Wnt axis,
among others. Osteocytes also extend their influence beyond the local
bone environment by functioning as an endocrine cellthat controlsphosphate reabsorption in the kidney,insulin secretion in the pancreas,
and skeletal muscle function. These cells are also finely tuned sensors
of mechanical stimulation to coordinate with effector cells to adjust
bone mass, size, and shape to conform to mechanical demands.
Abstract: Bone
remodeling is essential for the repair and replacement of damaged and
old bone. The major principle underlying this process is that
osteoclast-mediated resorption of a quantum of bone is followed by
osteoblast precursor recruitment; these cells differentiate to
matrix-producing osteoblasts,which form new bone to replace what was
resorbed. Evidence from osteopetrotic syndromes indicate that
osteoclasts not only resorb bone, but also provide signals to promote
bone formation. Osteoclasts act upon osteoblast lineage cells throughout
their differentiation by facilitating growth factor release from
resorbed matrix, producing secreted proteins and microvesicles, and
expressing membrane-bound factors. These multiple mechanisms mediate the
coupling of bone formation to resorption in remodeling. Additional
interactions of osteoclasts with osteoblast lineage cells, including
interactions with canopy and reversal cells, are required to achieve
coordination between bone formation and resorption during bone
remodeling. Keywords osteoclasts, osteoblasts, bone remodeling, coupling, reversal phase, exosomes
The
mechanical properties of bone are fundamental to the ability of our
skeletons to support movement and to provide protection to our vital
organs. As such, deterioration in mechanical behavior with aging and/or
diseases such as osteoporosis and diabetes can have profound
consequences for individuals’ quality of life. This article reviews
current knowledge of the basic mechanical behavior of bone at length
scales ranging from hundreds of nanometers to tens of centimeters. We
present the basic tenets of bone mechanics and connect them to some of
the arcs of research that have brought the field to recent advances. We
also discuss cortical bone, trabecular bone, and whole bones, as well as
multiple aspects of material behavior, including elasticity, yield,
fracture, fatigue, and damage. We describe the roles of bone quantity
(e.g., density, porosity) and bone quality (e.g., cross-linking, protein
composition), along with several avenues of future research.Keywords cortical bone, cancellous bone, trabecular bone, bone quality, multiaxial, multiscale
Wang Q, Xie Y, Du QS, Wu XJ, Feng X, Mei L, McDonald JM, Xiong WC.J Cell Biol. 2003 Feb 17;160(4):565-75. doi: 10.1083/jcb.200207036. Epub 2003 Feb 10.PMID: 12578912Free PMC article.
Osteoclast activation is important for boneremodeling and is altered in multiple bonedisorders.
This process requires cell adhesion and extensive actin cytoskeletal
reorganization. ...The interaction is mediated via the focal
adhesion-targeting domai …
DOI:
10.1083/jcb.200207036
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