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My name is Christian Roux.
I am a professor of Rheumatology
in the Paris Descartes
University in Paris, France.
And the topic today is about
bone loss and osteoporosis
in patients with
inflammatory diseases,
receiving glucocorticoids.
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Here are my disclosures,
related to this talk.
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Glucocorticoids are very
effective in a number of diseases
with acute or chronic inflammation.
At any time, roughly 1%
of the world population
is receiving oral glucocorticoids,
and the highest prevalence of use
is in patients at the age of 70.
That is to say, we are underlying
quite high risk of osteoporosis.
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Glucocorticoids therapy is
the most common
cause of secondary osteoporosis.
This is a theoretical curve of
change in bone strength in patients
receiving such a treatment.
As you can appreciate, the
decrease is rapid and dramatic
within the first year, and
maybe during the first month
after initiating the treatment.
And then, this decrease occurs
more slowly, there after.
This rapid effect is
parallel with the risk
of fractures, which
increases rapidly
after the initiation of therapy.
And there is a strong rationale
for this effect, related
to both the underlying
effect of inflammation,
that we will see on one the slides,
but also the effect of steroids on bone
through direct or
indirect mechanisms.
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Here's a summary of these effects
of glucocorticoids on bone.
And first of all, the
first mechanism is direct.
Through a direct effect on
osteoblasts, and osteocytes,
with a decrease of a function
of this, as an increase
in the apoptosis of these cells.
That is to say a direct effect on
the capacity of bone formation.
There is also an
effect on osteoclasts,
with and increase of
osteoclast activity
through the wrong ligand system.
And of course, you have, then,
increase in bone formation
and increase in bone resorption,
which is a deleterious
and coupling phenomenon
on bone remodeling,
with an increase in risk of fracture.
Here is also an illustration
of indirect effect,
through the neuroendocrine systems,
mainly the GH/IGF-1 axis,
and also the decrease
in sex steroids,
which is well known in the clinical
aspect and of these patients.
The next point is the effect
on calcium metabolism,
with a decrease in the
intestinal absorption of calcium.
There is a debate about the role
of secondary hypothyroidism,
but it doesn't look to be an
important mechanism in the bone
fragility in these patients.
A very important one, in
contrast, is the effect on muscle.
It has been shown proteolysis of myofibrils,
and the myopathy is in
the elderly patients,
or in patients receiving
massive dose of glucocorticoids,
a huge determinant of muscle
weakness, risk of falls,
and then increase risk of fracture.
So certainly, we should
not neglect this point
on muscle, when we are considering
general musculo-skeletal fragility.
But again, the main effect
is the direct effect
of glucocorticoids on bone cells,
and mainly upper bone formation.
And to demonstrate that, we have
this very elegant study conducted
