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Spring 2008 Bone Seminar Series
Tuesday February 19, 2008
Host: Karl Jepson, Mount Sinai School of Medicine Topic: Bone Remodeling and Skeletal Metastasis: Making Things Too Cozy? Abstract: Certain forms of cancer, including breast and prostate carcinoma, preferentially metastasize to the skeleton, and indeed appear to prefer certain sites within certain bones. Responsibility for this tissue- and site-selectivity is thought to lie largely with bone itself, following Paget’s century-old “seed-and-soil” hypothesis that metastasis depends on the ability of remote host tissues to provide a favorable environment for the survival and growth of tumor cells. Both experimental evidence and clinical experience have supported Paget’s hypothesis as it relates to skeletal metastasis, and have implicated bone remodeling, particularly bone resorption, as its underlying mechanistic basis. In this presentation, I will review evidence that bone resorption favors the development of metastatic lesions in bone by promoting the growth and survival of tumor cells present in bone or marrow, describe results from our laboratory indicating that resorption may also regulate even earlier steps in metastasis, i.e., initial arrest and extravasation of circulating tumor cells, and finally discuss the use and effectiveness of bone resorption inhibitors like bisphosphonates as antimetastatic agents. Tuesday March 18, 2008
Speaker: Van P. Thompson, DDS, PhD, Professor and Chair, Department of Biomaterials and Biomimetics, NYU College of Dentistry Host: Tim Bromage, NYU College of Dentistry Topic: Enamel: Nature’s Epithelially Derived, Damage-tolerant Ceramic Abstract: Recent studies have elucidated the damage and fatigue modes of ceramic layer structure analogs of enamel supported by dentin. Conventional static tests indicate that dental crown porcelains and structural ceramic cores are stronger than enamel, while fatigue testing indicates that enamel has evolved to accommodate damage modes that cause clinical failure in all-ceramic crowns. The lecture will compare the fatigue and failure modes of ceramics with enamel. Emphasis will be on how the enamel structure, including rod and rod decussation, limit damage. Evidence suggesting self-repair of enamel will be presented. Tuesday April 8, 2008 Host: Ericka Calton, City University of New York, Hospital for Special Surgery Topic: Role of Cell-Substrate Interactions: Pathology Teaches Physiology Abstract: Osteoclasts are derived from monocyte/macrophage lineage precursors that are recruited to the bone microenvironment where locally produced cytokines and growth factors, as well as endocrine hormones, induce their differentiation into actively resorbing osteoclasts. Of interest, in both physiologic and pathologic bone resorption, cells expressing the full morphological and functional properties of mature osteoclasts are almost invariably restricted to the immediate bone surface (Shen et al. Arthritis Res Ther, 2006). This observation suggests that interaction of osteoclast precursors with the bone substrate may provide signals that are essential for the terminal differentiation and activation of resorbing osteoclasts. We have used transcriptional profiling of osteoclasts differentiated on defined substrates to gain insights into the molecular pathways by which cell-matrix interactions regulate the genetic repertoire and functional properties of osteoclasts. Transcriptional analysis was performed using oligonucleotide array expression profiling on Affymetrix Mouse Genome 430 2.0 GeneChips. Results were validated using quantitative RT-PCR. Following microarray normalization and gene comparison, hierarchical clustering was performed and pathways regulated by bone matrix adherence identified using the Ingenuity Pathway Analysis program. In preliminary studies we have identified genes and molecular pathways that are uniquely regulated by interaction of osteoclast precursors with the mineralized bone substrate. The expression of these osteoclast-associated genes has been verified in vivo by examining their expression pattern in tissues from patients with specific forms of pathologic osteoclast-mediated bone resorption. These genes represent potential novel molecular targets for inhibiting osteoclast-mediated bone resorption in disorders associated with pathologic bone loss. Tuesday May 13, 2008
Host: Steve Cowin, City College of New York Topic: Can Knee Replacements be Improved? A Holistic View Abstract: Almost 40 years of evolution have resulted in artificial knee designs and surgical techniques, which provide the patient with restoration of function for over two decades in the majority of the patients. Further improvements in function could likely be achieved by the use of more conservative implants, and by earlier intervention than is the norm for total knees. Even at the stage of carrying out a TKR, recent research shows that a significant percentage could be treated with a unicompartmental replacement. However, the function of total knees themselves could possibly be improved using guided-motion designs which restored the normal neutral path of motion, and which provided the optimal laxity and stability during the flexion range. Finally, in order to obtain consistent alignment and soft tissue tensions at surgery, more quantitative techniques are required, with computer-assisted surgery being a promising approach. Research studies will be described which address the various facets noted above. |
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