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The human skeleton is a complex structure made up of 206 bones, which constitute a rigid, supportive framework for the body. It acts as a shield to protect internal organs and plays a crucial role in locomotion by anchoring the force arising from muscle contraction. In spite of its inert appearance, bone is an extremely dynamic tissue that is continuously being remodeled to adapt to changing mechanical demands. Such remodeling, which is carried out on a microscopic scale, consists in the removal of low-performing bone and its replacement by new, fully functional bone.
Which of the following is UNLIKELY to affect bone remodeling?
B. hormone low blood
C. Ca2+ concentration
D. mechanical stress
Answer: E. glucagon
The process of bone remodeling is controlled by the hormones and the mechanical stress the bone faces. The hormone which controls the process is the parathyroid hormone and the calcium which is required during the process of synthesis of bones. The factor which is not involved in the process is glucagon.
Thus, glucagon concentration does not affect bone remodeling.
The Cellular and Molecular Basis of Bone Remodelling
Remodelling occurs via basic multicellular units (BMUs). These are composed from discrete packets of osteoclasts and osteoblasts accompanied by a blood supply and supporting connective tissue. BMUs form and refill tunnels through cortical bone and in trabecular bone they create trenches on the surface. The osteoclasts are at the front, forming the cutting cone or hemi-cone in the case of trabecular BMUs, with osteoblasts behind forming the closing cone or hemi-cone. The BMU can move in all three axes in cortical BMUs and two axes in trabecular BMUs as they are on the surface.
Whilst osteoblasts and osteoclasts are directly involved in the bone remodelling process, they are not the only bone cells involved.
Osteoblast precursors present in the bone marrow,
often referred to as mesenchymal progenitors, mesenchymal stromal cells or mesenchymal stem cells (MSCs),
are required to differentiate into osteoblasts and support osteoclast formation.
Osteocytes are terminally differentiated osteoblasts that become embedded in the bone during formation in pits called lacunae.
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They are star shaped (stellate) with multiple cytoplasmic extensions
that occupy the canaliculi that connect the lacunae and make contact with other osteocytes, osteoblasts,
cells lining the bone surface, and vasculature via gap junctions.
This network of osteocytes forms a complex communication system that enables them to sense
and respond to stresses placed upon the bone by releasing paracrine factors that regulate bone remodelling.
Improving Skeletal Fragility by Bone Modeling
Normal bone growth is important not only for children but also for adults to prevent age-related fragility fracture .
Appropriate weight-bearing physical activities and calcium/vitamin D intakes support good bone acquisition during growth,
but the treatment of severe pediatric osteoporosis has been highly limited.
For instance, spontaneous fracture in children with physical disability, such as cerebral palsy,
is a long-standing problem that affects their quality of life;
the latest clinical practice guideline does not recommend regular use of bisphosphonates because
their long-term effects on the growing skeleton are unclear .
Although reduced mechanical loading is the major cause of skeletal fragility in individuals with physical disability, static weight-bearing physical activities as well as calcium/vitamin D supplementation are unlikely to prevent their fragility fractures . Fundamental rules of mechanical strain-related stimulus include strain rate as a key determinant of the stimulus and bones respond to dynamic, but not static, mechanical loading .
In the management of osteoporosis in children, it is important to note that their skeleton is different from the adult skeleton. Bone growth requires bone modeling that is predominantly influenced by mechanical environment and, therefore, cortical bone in lower limbs is very thin in children who cannot stand and walk. Consequently, an ideal method toward a cure for skeletal fragility during growth is pharmacologically stimulating mechanical strain-related bone modeling.
Furthermore, bone modeling would also be useful for adults. One unmet need in elderly patients at high risk for fracture is to improve their skeletal fragility more rapidly; in this regard, bone modeling is superior to bone remodeling as with building reinforcement rather than rebuilding generally performed against earthquakes in Japan.