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Printable Handouts
Navigable Slide Index
- Introduction
- Disclosures
- Use of oral glucocorticoids
- Corticosteroids: bone strength
- Effects of glucocorticoids on bone
- Corticosteroids: deleterious effects of low doses
- GIOP: asymptomatic vertebral fractures
- GIOP: dose - effect
- GIOP: BMD effect?
- GIOP: risk factors
- Corticosteroids: bone strength (explanation)
- Bone loss in early rheumatoid arthritis (RA)
- RA: clinical risk factor for osteoporotic fracture
- WHO fracture risk assessment tool
- Inflammation: a risk factor for fracture
- Spondyloarthropathies and vertebral fractures
- Early inflammatory back pain and BMD
- Bone remodeling
- Cytokines and bone loss
- Bone loss: role of T lymphocytes
- MCV-ACPAs induce bone loss in-vivo
- PTH and inflammation effects on bone formation
- Sclerostin inhibition in arthritis
- Anti-TNF and bone remodeling
- Anti-TNF and BMD
- Fracture and anti TNF
- Management of GIOP
- GIOP: Risedronate effects on lumbar spine BMD
- GIOP: comparison of ZOL, RIS: effects on BMD
- GIOP: comparison of TPT, ALN: effects on BMD
- Conclusions
Topics Covered
- Direct & indirect effects of glucocorticoids on bone
- Management of Glucocorticoid-Induced Osteoporosis (GIOP)
- Inflammation and bone loss in back pain & rheumatoid arthritis (RA)
- Cytokines, T lymphocytes & autoimmunity in bone loss
- Sclerostin inhibition, PTH and inflammation effects on bone formation
- Anti-TNF effects on bone remodeling, BMD and fractures
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Roux, C. (2015, July 30). Glucocorticoids, inflammation and bone loss [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved October 11, 2024, from https://doi.org/10.69645/THWZ7884.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Christian Roux has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Other Talks in the Series: Bone in Health and Disease
Transcript
Please wait while the transcript is being prepared...
0:00
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.
0:17
Here are my disclosures,
related to this talk.
0:22
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.
0:44
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.
1:33
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