Fall 2005 Bone Seminar Series
Click on any of the following links for details:
October 18 , 2005 Bone Seminar:
Johanna Warshaw PhD candidate on “Diversity in Primate Bone Microstructure”
November 15, 2005 Bone Seminar:
Lawrence G. Raisz MD
on “ Pathogenesis of Osteoporosis”
December 13 , 2005 Bone Seminar:
Adele Boskey PhD on “Insights into the Mechanism of Biologic
Mineralization: Roles of DMP1 and MEPE”
October 18 , 2005 Bone Seminar
Speaker: Johanna Warshaw, PhD candidate in Physical Anthropology, The City University of New York
Topic: Diversity in Primate Bone Microstructure
Ms. Warshaw’s Research Interests: Comparative primate and non-primate mammalian bone biology and microanatomy; bone micro-anatomical correlates of locomotor adaptation; life history and phylogeny in prosimians and South American monkeys; early primate paleobiology and evolution.
[Image: Propithecus (sifaka) midshaft femur; conventional transmitted light image and tissue type map.]
Abstract
The microscopic organization of bone constitutes an important source of information about the growth patterns and behaviors characterizing organismal life histories. Studies have shown that bone microstructure reflects ontogenetic variation in bone depositional rates, and mechanical influences on skeletal development and maintenance. As part of an ongoing effort to characterize variability in primates, this study examines several bone microstructural features from a broadly comparative perspective. I present results from analyses of primary bone tissue types, secondary intracortical remodeling and collagen fiber orientation at the mid-diaphysis of the femur, humerus, radius, ulna and tibia. These features were examined on 100-micron-thick cross-sections, imaged in conventional transmitted and circularly polarized light microscopy. The research demonstrates extensive variability in the organization of tissues among primates, which has not previously been systematically documented. Such diversity is suggested to reflect element-specific growth patterns, and taxon differences in life history and locomotor adaptations. This work forms a foundation for future investigations of bone microstructural variability, which may include paleontological taxa and implications for the reconstruction of fossil primate and mammalian biology.
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November 15, 2005 Bone Seminar
Speaker: Lawrence G. Raisz MD, Board of Trustees Distinguished Professor of Medicine and Director, Musculoskeletal Institute, University of Connecticut Health Center
Topic: Pathogenesis of Osteoporosis
Dr. Raisz’s Research Interests: Factors influencing bone metabolism; mechanisms of the effects of prostaglandins on bone, particularly with regard to the specific receptors that mediate these effects; clinical research on mechanisms of estrogen action and on the effects of calcium and vitamin D on bone metabolism.
Abstract
Osteoporosis is a disorder in which decreased bone strength leads to increased risk of fractures. Strength can be reduced because of failure to achieve optimal peak bone mass and architecture, excessive bone resorption or inadequate bone formation. Clinically all three mechanisms are likely to operate in patients with osteoporosis. There is substantial new information concerning the genetic determinants of optimal peak bone mass and strength as well as the influence of lifestyle and nutrition. Excessive bone resorption appears to have two major causes, estrogen deficiency and deficiency of calcium and vitamin D leading to secondary hyperparathyroidism. Inadequate bone formation can clearly be caused by glucocorticoid excess, but the mechanism of decreased bone formation in other forms of osteoporosis is not clear. Biochemical and morphologic data suggest that increased bone resorption with inadequate local bone formation responses during remodeling, despite an overall increase in bone formation rate, represent the most common pathogenetic picture in postmenopausal and age related osteoporosis.
While the specific pathways by which estrogen deficiency causes bone loss are not fully understood one concept is that there is an impaired response to mechanical loading. In addition estrogen may regulate the many cytokines and growth factors that have been implicated as mediators of excessive bone resorption and inadequate bone formation. Much of our current information is based on animal models and the relevance to human disease is not well documented. New molecular and biochemical approaches as well as more extensive epidemiologic studies will not only produce a better understanding of the pathogenesis of osteoporosis, but may also lead to ways to differentiate the specific pathogenetic mechanisms among individual patients and to targeted therapy.
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December 13, 2005 Bone Seminar
Speaker: Adele L. Boskey PhD, Starr Chair in Mineralized
Tissue Research and Director of the Mineralized Tissue Laboratory, Hospital
for Special Surgery; Professor of Biochemistry, Weill Medical College
of Cornell University; Adjunct Professor of Biomedical Engineering, The
City College of New York
Topic: Insights into the Mechanism of Biologic Mineralization:
Roles of DMP1 and MEPE
Dr. Boskey’s Research Interests: Factors regulating
mineral deposition, mineral growth, and remodeling in bones and teeth.
These questions have a bearing on treatment of diseases in which mineralization
is altered (osteoporosis, osteogenesis imperfecta, osteomalacia, osteopetrosis,
etc.), in the prevention of dystrophic calcification in arteries, prosthetic
valves, and other soft tissues, and in engineering bone replacement.
Abstract
Hydroxyapatite formation in bones and teeth is under the controlled
by physical chemistry, cells, and extracellular matrix molecules. The
goal of our studies is to elucidate the mechanism that allows the mineralization
of these tissues to occur in an oriented fashion. Our underlying hypothesis
is that post-translational modifications of extracellular matrix proteins
enable them to regulate the mineralization process in bones, teeth, and
other tissues. The post-translational modifications we are currently investigating
are: Fragmentation, Phosphorylation, and Dephosphorylation. In this seminar
we will review our approach (using in vitro, structural, and in vivo systems),
and demonstrate how we are probing this hypothesis using two related SIBLING
proteins, which have distinct effects on mineralization.
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