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Osteoporosis – causes, symptoms, diagnosis, treatment, pathology

Learning medicine is hard work!
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Try it free today! Osteo- refers to bones and -porosis means
pores. So, osteoporosis is when there’s a higher breakdown of bone in comparison to
the formation of new bone which results in porous bones, meaning a decrease in bone density
to the point of potential fracture. Looking at a cross-section of a bone, there’s
a hard-external layer known as the cortical bone and a softer internal layer of spongy
bone or trabecular bone that is composed of trabeculae. The trabeculae are like a framework
of beams that give structural support to the spongy bone. The cortical bone, in turn, is
made up of many functional, pipe-like units called osteons, which run through the length
of the bone. In the center of these osteons, there are hollow spaces called Haversian canals,
which contain the blood supply and innervation for the bone cells. Around the Haversian canals,
there are concentric lamellae, which look a bit like tree rings. The lamellae have an
organic part, which is mostly collagen, and an inorganic part called hydroxyapatite, which
is mostly calcium phosphate. In between neighboring lamellae, there are spaces called lacunae,
which contain bone cells called osteocytes. At first glance, bone may appear inert and
unchanging, but it’s actually a very dynamic tissue. In fact, spongy bone is replaced every
3 to 4 years and compact bone is replaced every 10 years, in a process called bone remodeling,
which has two steps: bone resorption, when specialized cells called osteoclasts break
down bone, and bone formation, which is when another type of cells called osteoblasts form
new bone. Bone remodelling as a whole is highly dependent
on serum calcium levels, which, in turn, are kept in the normal range by a balance between
parathyroid hormone, or PTH, calcitonin and vitamin D. Parathyroid hormone is produced
by the parathyroid glands in response to low serum calcium, and it increases bone resorption
to release calcium into the bloodstream. On the other hand, calcitonin is produced by
the thyroid gland in response to high serum calcium, so it opposes the action of PTH – therefore
promoting bone formation and decreasing bone resorption. Finally, vitamin D promotes calcium
absorption in the gut, so it increases serum calcium, promoting bone formation and decreasing
bone resorption. The balance between these regulatory factors
results in a peak bone mass, usually by age 20 to 29 – and this usually occurs earlier
in females than in males. Factors that determine the peak bone mass are genetics (for example,
people of African descent tend to have greater bone mass), and nutrition (meaning adequate
vitamin D intake increases bone peak mass). Finally, strength training increases peak
bone mass, as well as hormones like estrogens and androgens that inhibit bone resorption. Ok, now, when osteoclasts break down bone
faster than the osteoblasts can rebuild, it results in the lowering of the bone mass and
eventually in osteoporosis. If we zoom into a cross-section of an osteoporotic bone, it
will show normal cells with normal mineralization, which differentiates it from osteomalacia
where there’s lack of mineralization. So with osteoporosis, abnormal findings include fewer
trabeculae in the spongy bone and thinning of the cortical bone, as well as the widening
of the Haversian canals. These bone changes increase the risk of fracture, and they are
known as fragility or pathologic fractures. Some bones like the vertebrae, shoulder blades,
and ribs consist mainly of spongy bone, so they are in great risk of fragility fractures. Factors that accelerate bone mass loss and
increase the risk of osteoporosis are low estrogen levels, like after menopause, and
low serum calcium. Additional factors include alcohol consumption, smoking, drugs like glucocorticoids,
which decrease calcium absorption from the gut through antagonism of vitamin D, and drugs
like heparin and L-thyroxine. Another factor is physical inactivity, as seen in astronauts
in a zero-gravity environment where they just don’t use their musculoskeletal system as
hard as when they’re on earth. As a result, bone deposition decreases due to a lack of
stress, while resorption increases. There are also diseases that can cause osteoporosis
like Turner syndrome, hyperprolactinemia, Klinefelter syndrome, Cushing syndrome, and
diabetes mellitus. Now, the two most common types of osteoporosis
are postmenopausal osteoporosis and senile osteoporosis. In postmenopausal osteoporosis,
decreased estrogen levels lead to increased bone resorption. With senile osteoporosis,
on the other hand, it’s believed that osteoblasts just gradually lose the ability to form bone,
while the osteoclasts keep doing their thing unabated. So, bone resorption usually overtakes
bone formation around the 8th decade of life. People with osteoporosis don’t usually have
symptoms until a fracture occurs. The most common type of fractures are vertebral fractures,
also known as compression fractures, and it occurs when one or more bones in the spine
weaken and shatter. Vertebral fracture cause back pain, height loss, and a hunched posture.
Femoral neck fractures and distal radius fractures can also occur, and they’re often associated
with postmenopausal osteoporosis. Osteoporosis is usually diagnosed with a dual-energy
X-ray absorptiometry or DEXA scan which tests for bone density. The test compares an individual’s
bone density to that of a normal adult which yields the result or the T score. A T score
less than or equal to -2.5 is diagnostic of osteoporosis. Treatment for osteoporosis usually relies
on bisphosphonate drugs like alendronate and risedronate. If osteoporosis is really advanced,
teriparatide, a recombinant parathyroid hormone can be used. Now, even though parathyroid
hormone stimulates bone resorption, it’s been found that intermittent injections with
teriparatide activates osteoblasts more than osteoclasts, therefore increasing bone formation.
Interestingly, a thiazide diuretic like Hydrochlorothiazide can be used to treat osteoporosis as well.
Hydrochlorothiazide boosts calcium retention in the kidney and directly stimulates osteoblast
differentiation, therefore decreasing mineral bone loss. Finally, medications like denosumab,
which is a monoclonal antibody that inhibits osteoclasts, and raloxifene, which is a selective
estrogen receptor modulator, can be used for postmenopausal osteoporosis. Alright, as a quick recap, osteoporosis refers
to decreased bone density, on account of increased bone resorption compared to bone formation.
In osteoporosis, there’s thinning of the cortical bone, widening of the Haversian canals
and a decrease in the number of trabeculae in the spongy bone. There are two common types
of osteoporosis, these are senile osteoporosis and postmenopausal osteoporosis. The most
common type of fracture in osteoporosis is a vertebral compression fracture. Diagnosis
is done with a dual-energy X-ray absorptiometry or DEXA scan, where a T score equal to or
less than -2.5 equals osteoporosis. First-line treatment relies on bisphosphonate drugs like
alendronate and risedronate.

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