Registration for a live webinar on 'Neuroleptic malignant syndrome' is now open.
See webinar detailsWe noted you are experiencing viewing problems
-
Check with your IT department that JWPlatform, JWPlayer and Amazon AWS & CloudFront are not being blocked by your network. The relevant domains are *.jwplatform.com, *.jwpsrv.com, *.jwpcdn.com, jwpltx.com, jwpsrv.a.ssl.fastly.net, *.amazonaws.com and *.cloudfront.net. The relevant ports are 80 and 443.
-
Check the following talk links to see which ones work correctly:
Auto Mode
HTTP Progressive Download Send us your results from the above test links at access@hstalks.com and we will contact you with further advice on troubleshooting your viewing problems. -
No luck yet? More tips for troubleshooting viewing issues
-
Contact HST Support access@hstalks.com
-
Please review our troubleshooting guide for tips and advice on resolving your viewing problems.
-
For additional help, please don't hesitate to contact HST support access@hstalks.com
We hope you have enjoyed this limited-length demo
This is a limited length demo talk; you may
login or
review methods of
obtaining more access.
Printable Handouts
Navigable Slide Index
- Introduction
- Basic multicellular unit (BMU)
- Vital statistics of adult remodeling
- Birth and fate of osteoblasts and osteoclasts
- Mechanical loading and skeletal homeostasis
- Osteocyte-canalicular network
- Signal transduction followed by mechanical load
- Effect of mechanical load reduction in vivo
- A role of osteocytes in mineralization
- Van Buchem disease
- Paracrine activity of osteocyte-derived sclerostin
- Regulatory activities of osteocytes via sclerostin
- Elevated PTH decreases sclerostin expression
- The cell number concept
- Definition of osteoporosis
- Micrograph of abnormal human trabecular
- Normal vs. osteoporotic bone architecture
- Anti-osteoporotic effects of sex steroids (1)
- Anti-osteoporotic effects of sex steroids (2)
- Transcriptional regulation by estrogens
- Glucocorticoid-induced bone disease
- Glucocorticoids induce osteocyte apoptosis
- Remodeling balance in GC excess
- GC-induced osteonecrosis is apoptosis
- Location of osteocyte apoptosis centers
- Effect of GC excess on bone strength and BMD
- Bones of mice overexpressing 11beta-HSD2
- Effects of thyroid hormones on the skeleton
- Multi-factorial pathogenesis of osteoporosis
- Pattern of involutional bone loss (1)
- Pattern of involutional bone loss (2)
- Trabecular bone loss in young women and men
- Estrogen-deficiency-centric paradigm limitations
- Age is a critical determinant of fracture risk
- Decrease in bone strength vs. mass in mice
- Increased oxidative stress and skeletal changes
- ROS and sex steroid loss cause bone changes
- Oxidative stress antagonizes Wnt signaling
- Consequences of LRP6 mutation
- Wnt signaling antagonism and other diseases
- Hypothalamic-pituitary-adrenal system
- Aging in humans
- Aging and glucocorticoids in mice (1)
- Demonstrating osteocyte-canalicular network
- Aging and glucocorticoids in mice (2)
- Other contributors to osteoporosis
- Pathogenesis of osteoporosis - summary
- Future implications
Topics Covered
- Birth and fate of osteoblasts and osteoclasts
- Mechanical loading
- Role of osteocytes in mineralization
- Sclerostin
- The cell number concept
- Osteoporosis
- Anti-osteoporotic effects of sex steroids and their cellular mechanisms
- Transcriptional regulation by estrogens
- Glucocorticoid-induced bone disease
- Glucocorticoids induce osteocyte apoptosis
- Effects of thyroid hormones on the skeleton
- Involutional osteoporosis
- Age-dependent skeletal deterioration
- Age-associated oxidative stress
- Future implications
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Manolagas, S. (2020, May 21). Hormonal influence on bone remodeling and its implications for the pathophysiology of osteoporosis [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved October 8, 2024, from https://doi.org/10.69645/RHQI3625.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Stavros Manolagas has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Update Available
The speaker addresses developments since the publication of the original talk. We recommend listening to the associated update as well as the lecture.
- Full lecture Duration: 51:14 min
- Update interview Duration: 13:01 min
Hormonal influence on bone remodeling and its implications for the pathophysiology of osteoporosis
A selection of talks on Physiology & Anatomy
Transcript
Please wait while the transcript is being prepared...
0:00
I'm Stavros Manolagas,
Professor of Medicine and
the Director of the Division of
Endocrinology and Metabolism and
the Center for Osteoporosis and
Metabolic Bone Diseases at the University
of Arkansas for
Medical Sciences in Little Rock, AR.
The goal of the lecture is to
review current understanding of
the hormonal influences on bone
remodeling and their implications for
the pathophysiology and
treatment of osteoporosis.
0:30
During development and growth,
the skeleton is sculpted to
achieve its shape and size by
the removal of bone from one site and
deposition at a different one,
this process is called modeling.
Once the skeleton has reached maturity,
however,
regeneration continues in the form of
a periodic replacement of all bone
with new at the same location,
this process is called remodeling.
Removal of bone,
otherwise known as bone resorption,
is the task of osteoclasts, formation
of new bone is the task of osteoblasts.
Bone resorption and
bone formation, however,
are not separate independent processes.
In the adult skeleton, all osteoclasts and
osteoblasts belong to a unique
temporary structure known as a basic
multicellular unit or BMU,
which is depicted in this cartoon.
The BMU is approximately 1 to 2
mm long and 0.2 to 0.4 mm wide,
it comprises a team of osteoclasts in the
front, a team of osteoblasts in the rear,
depicted here with a yellow monolayer of
cells, and a central vascular capillary.
Osteoclasts adhere to bone and
subsequently remove it by acidification
and proteolytic digestion.
As the BMU advances, in this cartoon
from the top of the image to the bottom,
osteoclasts leave the resorption site and
osteoblasts move in to
cover the excavated area and
begin the process of new bone formation
by secreting osteoid which is
eventually mineralized into new bone.
Importantly, some osteoblasts,
after they have finished their
bone-forming function are buried within
the mineralized matrix that they have
created and these are termed osteocytes.
Osteocytes are depicted as individual
cells in this cartoon with multiple
processes connected with each other
in the matrix surrounding the BMU.
A microscopic image of
an actual BMU in a section of
murine trabecular bone is shown here.
In this instance, the BMU travels from
the left to the right of the section.
Please note the group of
red osteoclasts stained for
tartrate-resistant acid phosphatase.
Trailing behind
the osteoclasts are teams of
teal-colored osteoblasts
bringing up the rear of the BMU.
Pale-yellow erythrocytes
are seen here in the vessel
that brought the osteoclast
precursors to the erosion cavity.
Hide