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THE SPRING 2002 BONE SEMINAR SERIES
The Bone Seminar Series has as its focus the mechanosensory system in
bone. The seminar series has eight meetings a year beginning in
October and continuing until April or May. The seminar program will
be posted on www.bonenet.net, a website dedicated to research on the
mechanosensory system in bone.
The Spring 2002 Bone Seminar Program
The seminar series will be held in Room 9207 at the CUNY Graduate
Center on Wednesdays from 7 to 8:30 PM. The CUNY Graduate Center is
in the newly renovated Altman Building at the corner of 34th Street
and 5th Avenue, catty-corner from the Empire State Building. There
will be some socializing before the seminar in the GC snack bar on
the first floor, besides the usual snacks and drinks the 365 Express
also carries beer and some other alcoholic beverages.
There are several subway lines nearby and it is less than a
ten-minute walk to either Grand Central Station or Penn Station.
There is money to support parking for graduate students, apply to
Steve Cowin (contact information at the bottom).
JANUARY 31st, 2001 in room 9207 at the CUNY Graduate Center at 7 PM.
Speaker: Mitchell B. Schaffler, Ph.D., Professor of Orthopaedics,
Cell Biology and Anatomy & Director of Orthopaedic Research,
Department of Orthopaedics, The Mount Sinai School of Medicine and
Co-Director, New York Center for Biomedical Engineering, City College
of New York
Title: MECHANICAL FACTORS AND REMODELING OF COMPACT BONE
Abstract: Skeletal tissues maintain a balance between mechanical wear
and tear (i.e. fatigue) damage and intrinsic, matrix-level repair.
Imbalance in this damage-repair homeostasis, either because of
excessively rapid damage accumulation or because of ineffective,
inadequate or inappropriate biological responses to chronic injury,
leads to pathology and, ultimately, mechanical failure of skeletal
elements. These processes are implicated in a wide range of
conditions, including overuse injuries, tissue fragility in aging,
tendon and ligament failures and degenerative joint disease.
A major function of Haversian (osteonal) remodeling is to
remove and replace regions of compact bone that accumulate
microdamage due to fatigue. However, little is known about the
damage or remodeling responses that occur at the levels of fatigue
expected to result from normal wear and tear. In particular, how
bone-remodeling units "target" microscopically damaged areas of bone
is unknown. Our recent studies of remodeling-repair of microdamage
find that intracortical resorption effectively removes both
linear-type microcracks and diffuse matrix damage. Alterations of
osteocyte and canalicular integrity are observed in microdamaged
areas. Resorption spaces were also seen within areas of cortex in
which no bone matrix damage occurred, but alterations of osteocyte
and canalicular integrity were evident. Recent studies indicate that
these alterations of osteocyte integrity correspond to osteocyte
apoptosis, or programmed cell death. Thus, osteocyte death or damage
may provide a key stimulus for this signaling or targeting the
remodeling process in bone.
RESEARCH INTERESTS OF MITCH SCHAFFLER: Major research efforts in bone
biomechanics and tissue physiology, with emphasis on understanding
mechanical wear and tear (fatigue) processes in skeletal tissues, and
the cellular/molecular mechanisms used in the detection and repair of
connective tissue matrix injury. Related areas of interest extend to
aging and skeletal fragility, including osteoporosis, and the healing
and regeneration of bone.
February 21, 2002 in room 9207 at the CUNY Graduate Center at 7 PM.
Speaker: Yixian Qin, Ph.D., Assistant Professor of Biomedical
Engineering, SUNY Stony Brook
Title: FLUID FLOW STIMULATES THE FORMATION OF BONE AS DEPENDENT ON
TRANSCORTICAL FLUID PRESSURE GRADIENTS
Abstract: Considering the strong anabolic potential of mechanical
stimuli, and the devastating consequences of removing these
regulatory signals, it becomes critical to determine how the bone
cell population perceives subtle changes in their functional
environment. Indeed, improving our understanding of the manner in
which mechanical signals influence the temporal and spatial dynamics
of bone remodeling may help to devise a biomechanically based
intervention for treating osteoporosis, accelerating fracture healing
or promoting bony ingrowth into prostheses. The motion of
interstitial fluid within bone, which arises as a result of
functional load bearing, is hypothesized to be a critical mediator in
the perception and response of skeletal tissue to mechanical stimuli.
However, little is known about the remodeling responses that occur
during in vivo fluid flow stimuli in the absence of matrix
deformation. In particular, how bone-remodeling response to specific
mechanical fluid parameters is unknown. Our recent studies of bone
remodeling and formation demonstrate a strong correlation between the
fluid pressure gradient and the surface new bone formation. Fluid
flow applied at physiological level not only inhibits disuse induced
bone resorption, but also, dose-dependently, encourage bone formation
while applied in dynamic frequency. These results can also extend to
the trabecular region which low magnitude of fluid pressure and/or
surface fluid shear stress can initiate sufficient adaptive response
in trabeculae without matrix strain. The results suggest that the
fluid flow, which arises by functional loading, is an important
mediator in retaining bone quality and quantity, and that small
fluctuations in fluid flow, achieved via pressure differentials, has
potential for therapeutic applications against skeletal disorders
even in the absence of mechanical strain.
RESEARCH INTERESTS OF YIXIAN QIN: Major research efforts in tissue
remodeling and non-invasive assessment of bone physiology and
quality, with emphasis on understanding fluid flow mechanism in
skeletal tissues, and mechanotransduction of physical stimuli.
Related areas of interest extend to diagnostics of skeletal tissue
quality, including osteoporosis, space osteopenia and fracture
healing.
March 21, 2001 in room 9207 at the CUNY Graduate Center at 7 PM.
Speaker: Peter S. Walker
Title: TBA
April 18, 2002 in room 9207 at the CUNY Graduate Center at 7 PM.
Speaker: Professor Susannah P. Fritton, PhD, Associate Professor of
Mechanical Engineering, The City College
Title: DELINEATING THE PATHWAY OF INTERSTITIAL FLUID FLOW IN BONE
Abstract: Although it is well accepted that mechanical signals are
critical to maintain an adequate skeleton, the mechanism by which
bone cells sense their mechanical environment and initiate the
resorption and/or deposition of bone tissue is not known.
Load-induced interstitial fluid flow is believed to play a role in
bone's mechanosensory system via the shear stresses that it produces
on bone cells, stresses that have been shown to produce biochemical
responses in bone cells in vitro. Load-induced bone fluid flow has
also been proposed to enhance mass transport in bone to ensure the
metabolic function of bone cells that is crucial for bone growth,
maintenance, and adaptation.
Diffusion of molecules through the porous bone matrix has been
studied in animal models using injected tracers, and recently tracer
methods have been used to experimentally confirm the existence of
load-induced transport within bone tissue. However, because bone
tissue has three distinct porosities (vascular, lacunar-canalicular,
and collagen-hydroxyapatite), understanding bone fluid flow remains a
challenge. A fundamental question remains unanswered: What is the
size of the smallest bone pore that is available for interstitial
fluid flow? Conflicting reports exist in the literature as to whether
bone fluid can flow through the smallest pores in the mineralized
matrix (the collagen-hydroxyapatite microporosity) in addition to
flowing through the lacunar-canalicular porosity. In this seminar,
our recent work documenting where injected tracers of different sizes
travel in the bone microporosity will be presented and compared to
findings from the literature. Delineating the pathway of bone
interstitial fluid flow will help to further delineate bone's
microstructure and should contribute to the understanding of bone's
mechanosensory system.
RESEARCH INTERESTS OF SUSANNAH FRITTON: Understanding the adaptive
response of bone to mechanical forces; bone's mechanosensory system.
ORGANIZATION OF THE SEMINAR SERIES
The Interinstitutional Steering Committee (ISC) will make decisions
concerning the seminar series, including the selection of speakers.
Interesting, high quality seminar speakers are sought. Seminar
attendees are asked to help in the identification of investigators
with new results relative to the bone research questions of current
interest and distinguished bone researchers visiting New York City
who might be persuaded to present a seminar. Presentations by
advanced graduate students and are encouraged.
The members of the Interinstitutional Steering Committee (ISC) are
Adele Boskey (Head of the Mineralized Tissue Section at the Hospital
for Special Surgery and Professor of Biochemistry at the Weill
Medical College of Cornell University), Timothy Bromage (Director of
the Hard Tissue Research Unit and Professor of Anthropology at Hunter
College of CUNY), Stephen C. Cowin (Director of the New York Center
for Biomedical Engineering (NYCBE) and Professor of Mechanical
Engineering at the City College of the City University of New York
(CUNY)), Susannah P. Fritton (Director of the Tissue Mechanics
Laboratory, New York Center for Biomedical Engineering and Associate
Professor of Mechanical Engineering at the City College of CUNY), X.
Edward Guo (Director of the Bone Bioengineering Laboratory and
Assistant Professor of Bioengineering at Columbia University),
Clinton T. Rubin (Director of the Musculo-Skeletal Research
Laboratory and Professor in the Departments of Orthopedics and
Mechanical Engineering at SUNY Stony Brook) and Mitchell B. Schaffler
(Director of Orthopaedic Research and Professor of Orthopedics, Cell
Biology and Anatomy at the Mount Sinai School of Medicine). Each of
these people represents a community consisting of senior bone
research people, graduate students and, in most cases, undergraduate
students.
--
************************************
For bone research information, visit .
************************************
PREFERRED MAILING ADDRESS
Stephen C. Cowin
2166 Broadway
Apartment 12D
New York, NY 10024
Phone (212) 799-7970 (Office at Home)
Fax (212) 799-7970 (Office at Home)
Phone (212) 650-5208 (Work)
Fax (212) 650-6727 (Work)
Email
WORK ADDRESS:
Stephen C. Cowin
Director, New York Center for Biomedical Engineering
School of Engineering
The City College
138th Street and Convent Avenue
New York, NY 10031-9198, U. S. A.
*************************************
For information about the New York Center for Biomedical
Engineering visit
*************************************
---------------------------------------------------------------
To unsubscribe send SIGNOFF BIOMCH-L to LISTSERV@nic.surfnet.nl
For information and archives: http://isb.ri.ccf.org/biomch-l
---------------------------------------------------------------
The Bone Seminar Series has as its focus the mechanosensory system in
bone. The seminar series has eight meetings a year beginning in
October and continuing until April or May. The seminar program will
be posted on www.bonenet.net, a website dedicated to research on the
mechanosensory system in bone.
The Spring 2002 Bone Seminar Program
The seminar series will be held in Room 9207 at the CUNY Graduate
Center on Wednesdays from 7 to 8:30 PM. The CUNY Graduate Center is
in the newly renovated Altman Building at the corner of 34th Street
and 5th Avenue, catty-corner from the Empire State Building. There
will be some socializing before the seminar in the GC snack bar on
the first floor, besides the usual snacks and drinks the 365 Express
also carries beer and some other alcoholic beverages.
There are several subway lines nearby and it is less than a
ten-minute walk to either Grand Central Station or Penn Station.
There is money to support parking for graduate students, apply to
Steve Cowin (contact information at the bottom).
JANUARY 31st, 2001 in room 9207 at the CUNY Graduate Center at 7 PM.
Speaker: Mitchell B. Schaffler, Ph.D., Professor of Orthopaedics,
Cell Biology and Anatomy & Director of Orthopaedic Research,
Department of Orthopaedics, The Mount Sinai School of Medicine and
Co-Director, New York Center for Biomedical Engineering, City College
of New York
Title: MECHANICAL FACTORS AND REMODELING OF COMPACT BONE
Abstract: Skeletal tissues maintain a balance between mechanical wear
and tear (i.e. fatigue) damage and intrinsic, matrix-level repair.
Imbalance in this damage-repair homeostasis, either because of
excessively rapid damage accumulation or because of ineffective,
inadequate or inappropriate biological responses to chronic injury,
leads to pathology and, ultimately, mechanical failure of skeletal
elements. These processes are implicated in a wide range of
conditions, including overuse injuries, tissue fragility in aging,
tendon and ligament failures and degenerative joint disease.
A major function of Haversian (osteonal) remodeling is to
remove and replace regions of compact bone that accumulate
microdamage due to fatigue. However, little is known about the
damage or remodeling responses that occur at the levels of fatigue
expected to result from normal wear and tear. In particular, how
bone-remodeling units "target" microscopically damaged areas of bone
is unknown. Our recent studies of remodeling-repair of microdamage
find that intracortical resorption effectively removes both
linear-type microcracks and diffuse matrix damage. Alterations of
osteocyte and canalicular integrity are observed in microdamaged
areas. Resorption spaces were also seen within areas of cortex in
which no bone matrix damage occurred, but alterations of osteocyte
and canalicular integrity were evident. Recent studies indicate that
these alterations of osteocyte integrity correspond to osteocyte
apoptosis, or programmed cell death. Thus, osteocyte death or damage
may provide a key stimulus for this signaling or targeting the
remodeling process in bone.
RESEARCH INTERESTS OF MITCH SCHAFFLER: Major research efforts in bone
biomechanics and tissue physiology, with emphasis on understanding
mechanical wear and tear (fatigue) processes in skeletal tissues, and
the cellular/molecular mechanisms used in the detection and repair of
connective tissue matrix injury. Related areas of interest extend to
aging and skeletal fragility, including osteoporosis, and the healing
and regeneration of bone.
February 21, 2002 in room 9207 at the CUNY Graduate Center at 7 PM.
Speaker: Yixian Qin, Ph.D., Assistant Professor of Biomedical
Engineering, SUNY Stony Brook
Title: FLUID FLOW STIMULATES THE FORMATION OF BONE AS DEPENDENT ON
TRANSCORTICAL FLUID PRESSURE GRADIENTS
Abstract: Considering the strong anabolic potential of mechanical
stimuli, and the devastating consequences of removing these
regulatory signals, it becomes critical to determine how the bone
cell population perceives subtle changes in their functional
environment. Indeed, improving our understanding of the manner in
which mechanical signals influence the temporal and spatial dynamics
of bone remodeling may help to devise a biomechanically based
intervention for treating osteoporosis, accelerating fracture healing
or promoting bony ingrowth into prostheses. The motion of
interstitial fluid within bone, which arises as a result of
functional load bearing, is hypothesized to be a critical mediator in
the perception and response of skeletal tissue to mechanical stimuli.
However, little is known about the remodeling responses that occur
during in vivo fluid flow stimuli in the absence of matrix
deformation. In particular, how bone-remodeling response to specific
mechanical fluid parameters is unknown. Our recent studies of bone
remodeling and formation demonstrate a strong correlation between the
fluid pressure gradient and the surface new bone formation. Fluid
flow applied at physiological level not only inhibits disuse induced
bone resorption, but also, dose-dependently, encourage bone formation
while applied in dynamic frequency. These results can also extend to
the trabecular region which low magnitude of fluid pressure and/or
surface fluid shear stress can initiate sufficient adaptive response
in trabeculae without matrix strain. The results suggest that the
fluid flow, which arises by functional loading, is an important
mediator in retaining bone quality and quantity, and that small
fluctuations in fluid flow, achieved via pressure differentials, has
potential for therapeutic applications against skeletal disorders
even in the absence of mechanical strain.
RESEARCH INTERESTS OF YIXIAN QIN: Major research efforts in tissue
remodeling and non-invasive assessment of bone physiology and
quality, with emphasis on understanding fluid flow mechanism in
skeletal tissues, and mechanotransduction of physical stimuli.
Related areas of interest extend to diagnostics of skeletal tissue
quality, including osteoporosis, space osteopenia and fracture
healing.
March 21, 2001 in room 9207 at the CUNY Graduate Center at 7 PM.
Speaker: Peter S. Walker
Title: TBA
April 18, 2002 in room 9207 at the CUNY Graduate Center at 7 PM.
Speaker: Professor Susannah P. Fritton, PhD, Associate Professor of
Mechanical Engineering, The City College
Title: DELINEATING THE PATHWAY OF INTERSTITIAL FLUID FLOW IN BONE
Abstract: Although it is well accepted that mechanical signals are
critical to maintain an adequate skeleton, the mechanism by which
bone cells sense their mechanical environment and initiate the
resorption and/or deposition of bone tissue is not known.
Load-induced interstitial fluid flow is believed to play a role in
bone's mechanosensory system via the shear stresses that it produces
on bone cells, stresses that have been shown to produce biochemical
responses in bone cells in vitro. Load-induced bone fluid flow has
also been proposed to enhance mass transport in bone to ensure the
metabolic function of bone cells that is crucial for bone growth,
maintenance, and adaptation.
Diffusion of molecules through the porous bone matrix has been
studied in animal models using injected tracers, and recently tracer
methods have been used to experimentally confirm the existence of
load-induced transport within bone tissue. However, because bone
tissue has three distinct porosities (vascular, lacunar-canalicular,
and collagen-hydroxyapatite), understanding bone fluid flow remains a
challenge. A fundamental question remains unanswered: What is the
size of the smallest bone pore that is available for interstitial
fluid flow? Conflicting reports exist in the literature as to whether
bone fluid can flow through the smallest pores in the mineralized
matrix (the collagen-hydroxyapatite microporosity) in addition to
flowing through the lacunar-canalicular porosity. In this seminar,
our recent work documenting where injected tracers of different sizes
travel in the bone microporosity will be presented and compared to
findings from the literature. Delineating the pathway of bone
interstitial fluid flow will help to further delineate bone's
microstructure and should contribute to the understanding of bone's
mechanosensory system.
RESEARCH INTERESTS OF SUSANNAH FRITTON: Understanding the adaptive
response of bone to mechanical forces; bone's mechanosensory system.
ORGANIZATION OF THE SEMINAR SERIES
The Interinstitutional Steering Committee (ISC) will make decisions
concerning the seminar series, including the selection of speakers.
Interesting, high quality seminar speakers are sought. Seminar
attendees are asked to help in the identification of investigators
with new results relative to the bone research questions of current
interest and distinguished bone researchers visiting New York City
who might be persuaded to present a seminar. Presentations by
advanced graduate students and are encouraged.
The members of the Interinstitutional Steering Committee (ISC) are
Adele Boskey (Head of the Mineralized Tissue Section at the Hospital
for Special Surgery and Professor of Biochemistry at the Weill
Medical College of Cornell University), Timothy Bromage (Director of
the Hard Tissue Research Unit and Professor of Anthropology at Hunter
College of CUNY), Stephen C. Cowin (Director of the New York Center
for Biomedical Engineering (NYCBE) and Professor of Mechanical
Engineering at the City College of the City University of New York
(CUNY)), Susannah P. Fritton (Director of the Tissue Mechanics
Laboratory, New York Center for Biomedical Engineering and Associate
Professor of Mechanical Engineering at the City College of CUNY), X.
Edward Guo (Director of the Bone Bioengineering Laboratory and
Assistant Professor of Bioengineering at Columbia University),
Clinton T. Rubin (Director of the Musculo-Skeletal Research
Laboratory and Professor in the Departments of Orthopedics and
Mechanical Engineering at SUNY Stony Brook) and Mitchell B. Schaffler
(Director of Orthopaedic Research and Professor of Orthopedics, Cell
Biology and Anatomy at the Mount Sinai School of Medicine). Each of
these people represents a community consisting of senior bone
research people, graduate students and, in most cases, undergraduate
students.
--
************************************
For bone research information, visit .
************************************
PREFERRED MAILING ADDRESS
Stephen C. Cowin
2166 Broadway
Apartment 12D
New York, NY 10024
Phone (212) 799-7970 (Office at Home)
Fax (212) 799-7970 (Office at Home)
Phone (212) 650-5208 (Work)
Fax (212) 650-6727 (Work)
WORK ADDRESS:
Stephen C. Cowin
Director, New York Center for Biomedical Engineering
School of Engineering
The City College
138th Street and Convent Avenue
New York, NY 10031-9198, U. S. A.
*************************************
For information about the New York Center for Biomedical
Engineering visit
*************************************
---------------------------------------------------------------
To unsubscribe send SIGNOFF BIOMCH-L to LISTSERV@nic.surfnet.nl
For information and archives: http://isb.ri.ccf.org/biomch-l
---------------------------------------------------------------