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Bone remodeling is when old, brittle bone
tissue is removed or resorbed and gets replaced
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by new bone tissue.
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Remodeling also occurs when reshaping your
bones after a fracture or when repairing micro-cracks
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which form during ordinary activities, especially
when your bones are under stress, like after
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lifting heavy weights.
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Now the bones’ surface is covered by a layer
called the periosteum except at the articular
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cartilages - the parts involved in the joints.
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The periosteum consists of an outer fibrous
layer which protects the bones and provides
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attachment for the tendons and the ligaments,
and it also has an inner cellular layer which
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houses progenitor stem cells.
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These progenitor stem cells develop into both
osteoblasts which secrete the bone matrix,
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and chondroblasts - which produce cartilage.
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Now let’s look at the femur - the longest
bone in the body.
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The two ends of the bone that forms the joints
are called epiphysis, while the shaft of the
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bone is called the diaphysis.
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Looking at the diaphysis; or the bone shaft,
it has an external part; the cortical bone,
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which consists of many tiny cylinders known
as osteons.
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Each osteon is made of many lamellae, which
are these concentric layers made of an organic
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part - mostly collagen, and an inorganic part
called hydroxyapatite, which is mostly calcium
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phosphate.
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In the center of every osteon is a Haversian
canal, which contains the blood supply and
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innervation for the bone cells.
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In the center of the bone, is the medullary
canal - a hollow space lined by a honeycomb-looking
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structure called the spongy or cancellous
bone.
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The medullary canal contains the bone marrow,
which is the site of blood cell production.
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Now the epiphysis is made of a lot of spongy
bone.
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And when you look closer at the spongy bone,
it’s made of crosslinking tiny roads called
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trabeculae, which make your bones resistant
to mechanical stress, so that they can bear
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weights without caving in.
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And just like the medullary cavity, the spaces
in the spongy bone of the epiphysis are occupied
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by bone marrow.
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Now, let’s jump into the bone marrow.
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That’s where we find the hematopoietic stem
cells, the blood-making cells of the bone
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marrow, which give rise to the lymphoid progenitor
cells - which mature and differentiate into
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lymphocytes like T and B cells, the main cells
involved in your adaptive immunity, and the
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myeloid progenitor cells, which differentiate
into red blood cells, platelets, and myeloblasts
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– the progenitors of basophils, neutrophils,
eosinophils and monocytes.
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There are a number of growth factors that
help these cells develop.
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For example, osteoblasts release a substance
called M-CSF - Macrophage colony-stimulating
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factor, which helps stimulate myeloid cells
like monocytes.
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Now in bone remodeling, the process begins
when osteoblasts sense micro cracks at their
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location, like when your bones are bearing
much weight.
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The osteoblasts produce a substance called
RANKL - receptor activator of nuclear factor
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κβ ligand, which binds to RANK receptors
on the surface of nearby monocytes.
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RANKL induces those monocytes to fuse together
to form a multinucleated osteoclast cell.
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RANKL also helps the osteoclast mature and
activate so that they can start resorbing
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bones.
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The osteoclast starts secreting lysosomal
enzymes – mostly collagenase, which digests
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the collagen protein in the organic matrix.
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This drills pits on the bone surface known
as the Howship’s lacunae.
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Osteoclasts also start producing hydrochloric
acid - HCl, which dissolves hydroxyapatite
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into soluble calcium – Ca2+ and phosphate
– PO42- ions, and these ions get released
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into the bloodstream.
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There are also a scattering of osteocytes
which are trapped within the bony matrix.
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When these get freed up by the dissolving
of bone, they get eaten up or phagocytosed
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by the osteoclasts.
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What a way to go!
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Now to keep bone resorption under control,
the osteoblasts also secrete Osteoprotegerin,
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which binds to RANKL and prevents it from
activating RANK receptors.
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This slows down the activation of osteoclasts.
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Finally, once osteoclasts complete their job,
they commit suicide by means of apoptosis.
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Following bone resorption, osteoblasts start
secreting osteoid seam, a substance mainly
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made of collagen, to fill in the lacunae created
by the osteoclasts.
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Calcium and phosphate begin to deposit on
the seam, forming hydroxyapatite.
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Also, as osteoblasts keep producing new bony
material, many get trapped within tiny lacunae
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within the bony matrix, and turn into osteocytes.
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Bone remodeling is affected by various hormones.
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The parathyroid glands, the four small pea-like
structures located on the thyroid gland in
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the neck, release parathyroid hormone in response
to a drop in blood calcium levels.
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The parathyroid hormone travels to the bones
and stimulates the osteoblasts to release
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RANKL, which triggers bone resorption.
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This allows calcium ions-Ca2+ to be released
into the bloodstream, and that corrects the
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deficiency.
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Now, when the blood calcium level is higher
than normal, the parathyroid gland releases
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less parathyroid hormone to have less bone
resorption.
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Now, in addition, parafollicular cells in
the thyroid gland produces a hormone called
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calcitonin.
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High calcitonin levels inhibit bone resorption
which results in lower blood calcium levels.
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Another factor on bone remodeling is mechanical
stress.
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That’s why bones that bear a lot of weight
remodel at such a high rate - a phenomenon
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called Wolff’s law.
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Next there’s Vitamin D which stimulates
intestinal absorption of calcium, which then
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causes calcitonin levels to increase and that
inhibits bone resorption.
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Alright, as a quick recap, we have seen that
bone remodeling is a continuous process by
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which bones are resorbed by osteoclasts, and
remade by osteoblasts.
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Osteoblasts release RANKL to initiate remodeling,
and osteoprotegerin to help turn it off.
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Bone remodeling is involved in repairing those
tiny cracks in your bones due to normal activities,
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and in helping bones heal after a fracture.
