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• Clinical Aspects of Diabetic Bone Disease (Ann Schwartz, University of California, San Francisco) 
• Bone Marrow Stem Cells Status and Bone Turnover in Diabetic Disease (Laura McCabe, Michigan State University) 
• Contributors of the Insulin/Insulin-Like Growth Factor- 1 Axis to Diabetic Osteopathy (John L. Fowlkes, Arkansas Children's Hospital Research Institute, Little Rock)
• Inducible Brown Adipose Tissue or "Beige" Fat Sensitizes to Insulin and Secretes Bone Anabolic Activities (Beata Lecka-Czernik, University of Toledo Health Sciences) 
• Skeletally Immature Mice are More Susceptible than Mature Mice to the Detrimental Effects of a High Fat Diet on Cancellous Bone in the Distal Femur (Jason Inzana, Alice L. Jee award winner, University of Rochester Medical Center) 

There is a growing interest within the research community regarding newly described relationships between energy balance and bone homeostasis. Recent progress in unraveling such cross-talk highlights diabetes as a pathologic condition from which to better illuminate these potential connections. There is now substantial evidence showing that diabetes can affect skeletal well-being. Furthermore, the skeleton has been implicating in regulating glucose metabolism and insulin secretion.

In this session, we will cover different aspects of these relationships. Ann Schwartz, Ph.D. (UCSF, San Francisco, CA), known for her pioneering work on epidemiology of diabetic bone disease, will discuss clinical aspects of diabetic bone disease and the effects of anti-diabetic drugs on the human skeleton. Laura McCabe, Ph.D. (Michigan State University, East Lansing, MI), who has extensive expertise in the effects of glucose and insulin on osteoblast differentiation, will discuss the effects of diabetes on bone marrow immune and stem cell status as well as bone remodeling. These discussions will be complemented by a discussion about the effects of insulin and IGF-1 on diabetic osteopathy presented by John Fowlkes, M.D. (University of Arkansas for Medical Sciences and Arkansas Children’s Hospital Research Institute, Little Rock, AR) The session will be concluded with a presentation by Beata Lecka-Czernik (University of Toledo Health Sciences Campus, Toledo, OH), whose work has contributed to the understanding the relationship between fat and bone. She will present findings of a newly discovered form of metabolically active “beige” fat which secretes bone anabolic activities - a new paradigm of ties between bone and energy metabolism system. 

Alice L. Jee Award Winners

Samir Abdelmagid, Northest Ohio Medical University
Mutation in OA/Gpnmb Decreases Osteogenesis Independent of ER-Stress

Qianqian Han, Tufts University School of Dental Medicine
Diabetes Inhibits Bone Formation via Regulation of Histone Acetylation by HDAC2

Kyu Sang Joeng, Baylor College of Medicine
Mutations in WNT1 Cause Early-onset Osteoporosis and Osteogenesis Imperfect

Julia Kuliwaba, University of Adelaide
The Pathophysiology of Subchondral Cancellous Bone in Postmenopausal Knee Osteoarthritis: Diffuse Microdamage Accumulation and Osteocyte Cell Network Deficiency

Tieshi Li, University of North Carolina at Chapel Hill
Identification of Specific Niches for Tgfbr2- Slow Proliferating Joint Progenitor Cells and Their Responses During Post-traumatic Osteoarthritis Development

Joshua Padovano, University of Illinois
Bone-Specific DMP1 Overexpression: Implications on Endochondral Ossification

 

Additional Alice L. Jee Award Winners presenting in other sessions

Jason Inzana, University of Rochester Medical Center
Skeletally Immature Mice are More Susceptible than Mature Mice to the Detrimental Effects of a High Fat Diet on Cancellous Bone in the Distal Femur

 

Christopher Newman, Indiana University
Cortical Bone Material Properties in an Animal Model of Chronic Kidney Disease

Kyle Nishiyama, Columbia University
Marked Increases in Cortical Porosity after Kidney Transplantation Especially near the Endocortical Surface: an HR-pQCT Study

Michaela Reagan, Harvard Medical School
Novel Target Identification: Multiple Myeloma Bone Marrow Derived Mesenchymal Stem Cells (MSCs) Show Decreased Osteogenesis in Part due to Decreased Expression of microRNA hsa-mir-199a-3p

Under-Represented Minority Travel Grant Winners

Jean de la croix Ndong, Vanderbilt University
A New Inducible Pre-clinical Model and a Novel Strategy to Understand and Treat NF1 Tibial Pseudoarthrosis

Nilsson Holguin, Washington University  
Reduced Bone Formation in Aged Mice by Tibial Compression May be Due to Reduced Retention of Wnt Activity in Osteocytes

Patricia Juarez-Camacho, Indiana University
Beneficial Effects of Combined Therapy of Halofuginone and Zoledronic Acid on Breast Cancer Bone Metastases and Normal Bone Remodeling

Alicia Ortega, University of Colorado at Boulder
Effects of Microgravity and Myostatin Inhibition on Bone Microarchitecture and Metabolism: Results from Mice Flown on Space Shuttle Mission STS-118

Thomas Siosi Mbimba Jr., Kent State University
TRAPPC9 Modulates Osteoblast Proliferation and Differentiation Through NIK – IKK Signaling

 

Osteoarthritis Award Winner

Zhechao Ruan, Baylor College of Medicine
Prevention of Osteoarthritis by Proteoglycan 4 Expression

Poster Session

Xiaohan Lai, University of Delaware
Imaging and Quantifying Muscle-Bone Crosstalk through Intact Periosteum

Russell Main, Purdue University
Load-induced Changes in Corticocancellous Gene Expression and Bone Mass are Regulated by a Load Threshold

Meghan Moran, Rush Medical College
Bone Regeneration Varies in Four Different Mouse Strains after Marrow Ablation

Carrie Nielson, Oregon Health & Science University
Gene by Gene Interactions on Femoral Neck BMD in MrOS and SOF: a Synergistic Effect of ALPL and LRAT

Jason Organ, Indiana University School of Medicine
In Vivo Assessment of Skeletal Biomechanical Properties Reveals Beneficial Effects of Combination Anti-remodeling Drug Treatment

Christopher Price, University of Delaware
Development of an Innovative Fluctuation-Based Imaging Method for Characterizing and Mapping Interstitial Fluid Movement in Cartilage

Joseph Wallace, Indiana University-Purdue University Indianapolis
Multiscale Phenotypic Analysis of Osteogenesis Imperfecta in Murine Bone

• Heterogeneity of the HSC Niche (Laura Calvi, University of Rochester) 
• MSC Homing in Relation to the Endosteal Niche (Anne Spagnoli, University of North Carolina at Chapel Hill)
• The HSC Niche Regulates Metastasis and Tumor Dormancy of Solid Tumors (Russell Taichman, University of Michigan) 
• Spatial Localization and Regulation of the Hematopoietic Stem Cell Niche(Gregor Adams, University of Southern California) 
• Novel Target Identification: Multiple Myeloma Bone Marrow Derived Mensenchymal Stem Cells (MSCs) Show Decreased Osteogenesis in part due to Decreased Expression of microRNA hsa-mir-199a-3p (Michaela Reagan, Alice L. Jee award winner, Harvard Medical School) 
• Primary Cilia in Bone Marrow Stromal Cells Mediate Mechanically Induced Osteogenesis (Julia Chen, Harold M. Frost award winner, Columbia University)  

The skeleton serves as the principal site for hematopoiesis all vertebrates except fish. The function of the hematopoietic system is to maintain homeostatic levels of all circulating blood cells, including myeloid cells, lymphoid cells, red blood cells, and platelets. These cells are synthesized in the bone marrow, where they derive from a limited number of hematopoietic stem cells (HSCs) that are multipotent and capable of extensive self-renewal. While HSC fate choices are in part determined by stochastic cell autonomous processes, according to the niche hypothesis, signals from the complex marrow microenvironment are also likely to determine stem cell fate. While it had long been postulated that signals within the bone marrow could provide regulation of hematopoietic cells, it is only in the past decade that advances in flow cytometry and genetic models have allowed for a deeper understanding of microenvironmental regulation of HSCs.  In this session, we will highlight the cellular regulatory components of the HSC niche and specifically focus on recent advances that have opened novel therapeutic opportunities. Dr. Adams will review spatial localization and regulation of the HSC niche. Dr. Calvi will highlight hormonal regulation of the heterogeneous HSC niche and opportunities for therapeutic manipulations. Dr. Spagnoli will address Mesenchymal Stem Cell homing in relation to the endosteal niche. Finally, Dr. Taichman will define how the HSC niche regulates metastasis and tumor dormancy of solid tumors.

• Grant writing, understanding NIH(Gayle Lester with a panel of experts) 
• Panel Discussion on Tenure and the Tenure dossier (Chairs: M. van der Meulen and D. Burr) Panelist: Rebecca Wagenaar-Miller, NIH
• Interactive activities: identifying Tenure letter writers, discussion of CV content 

There is no registration fee for this afternoon workshop, but pre-registration is required. It is required that you bring a printout of your CV if you participate in this afternoon session. 

• Vascular Calcification and Cardiovascular Risk in the CKD-MBD (Keith Hruska, Washington Univeristy) 
• Skeletal Imaging of Frailty in Renal Osteodystrophy (Mary Leonard, University of Pennsylvania) 
• Immunologic and Histochemical Assessment of Osteocyte Function in the CKD-MBD (Renata Pereira, University of California, Los Angeles) 
• The Function of c-klotho in the CKD-MBD (Ken White, Indiana University) 
• FGF23 and α-klotho in the CKD-MBD (Orson Moe, Univeristy of Texas) 
• Cortical Bone Material Properties in an Animal Mode of Chronic Kidney Disease (Christopher Newman, Alice L. Jee award winner, Indiana University School of Medicine) 
• Marked Increases in Cortical Porosity after Kidney Transplantation Especially near the Endocortical Surface: an HR-pQCT Study (Kyle Nishiyama, Alice L. Jee award winner, Columbia University) 

 

Harold M. Frost Award Winners 

Yohann Bala, University of Melbourne
Void-Bone Matrix (VBM) Frequency Distribution Curve Analysis Improves the Detection of Women with fragility fracture

Yurong Fei, New York University
Role of Sirtuin 1 in the Function of PTH in Osteoblasts

Ronald Kwon, University of Washington
Mapping the Skeletal Connectome: Emergent Bone Signatures Following Neuronal Dysfunction in Zebrafish

Elizabeth Salisbury, Baylor College of Medicine
Astrocyte-like Cells from the Peripheral Nerve Generate Brown Adipocytes and Contribute to Endochondral Bone Formation

Jae Shim, Weill Cornell Medical College
A Novel Mouse Model of Paget’s Disease of Bone by CHMP5 Deletion

Xiaofang Wang, Baylor College of Dentistry
FAM20C is Essential to the Biomineralization of Bone and Tooth

Harold M. Frost Award Winners presenting in another session 

Julia Chen, Columbia University
Primary Cilia in Bone Marrow Stromal Cells Mediate Mechanically Induced Osteogenesis

Eve Donnelly, Cornell University
Reduced Cortical Tissue Heterogeneity with Bisphosphonate Treatment in Postmenopausal Women with Typical and Atypical Femoral Fractures

Sarah McBride, Washington University
Osteogenic-derived BMP2, but not Vascular-derived BMP2, Affects Non-endochondral Stress Fracture Healing

• Biomechanics of Fatigue (Jeffery Nyman, Vanderbilt University)
• How Does it Relate to a Stress Fracture? (Chris Hernandez, Cornell University) 
• Osteocyte Signaling/Targeted Remodeling (Repair) (Mitch Schaffler, The City University of New York) 
• Atypical Femoral Fractures (Elizabeth Shane, Columbia University) 
• Osteogenic-derived BMP2, but not Vascular-derived BMP2, Affects Non-endochondral Stress Fracture Healing (Sarah McBride, Harold M. Frost award winner, Washington University)
• Reduced Cortical Tissue Heterogeneity with Bisphosphonate Treatment in Postmenopausal Women with Typical and Atypical Femoral Fractures (Eve Donnelly, Harold M. Frost award winner, Cornell University) 

Stress fractures caused by excessive repetitive loading are a common injury in athletes and military recruits. Recent work has suggested that atypical femoral fractures associated with long-term anti-resorptive treatment are generated through the same processes as stress fractures, demonstrating that stress fractures occur not only in high performance athletes but also to older individuals with more normal loading.  Although stress fractures are not uncommon, the mechanisms leading to stress fracture remain poorly understood. 

Stress fractures are unusual in that they develop over time and are influenced by the accumulation of tissue damage during cyclic loading as well as local bone remodeling/modeling. The goal of the current workshop is to review the known interactions between cyclic loading in bone, damage accumulation and bone modeling/remodeling and identify current challenges in understanding the pathophysiology of stress fractures.  Dr. Jeffery Nyman, an expert in bone biomechanics will discuss the mechanical performance of bone under cyclic loading and how bone microstructure influences failure under cyclic loading. Dr. Christopher Hernandez will discuss recent studies examining bone remodeling as a stimulus for the formation of microscopic tissue damage.  Dr. Mitchell Schaffler has done pioneering work in teasing out the signaling mechanism for damage-induced remodeling, and will discuss how local bone cell populations respond to the appearance of microscopic tissue damage caused by cyclic loading.  Dr. Elizabeth Shane who recently served a co-chair of the ASBMR Task Force on Atypical Femoral Fractures will review clinical understanding of atypical femoral fractures and their similarities to stress fractures. 

• Bone and cartilage crosstalk (David Findlay, University of Adelaide) 
• Transmission of molecules between subchondral bone and cartilage in OA (Liyun Wang, University of Delaware) 
• Wnt signaling in OA (Daniel LaJeunesse, University of Montreal) 
• CITED2: A novel cartilage homeostasis regulator and therapeutic target for osteoarthritis (Hui Sun, Albert Einstein College of Medicine)
• Prevention of Osteoarthritis by Proteoglycan 4 Expression (Zhechao Ruan, Osteoarthritis award winner, Baylor College of Medicine) 

It is quite clear now that the progression of osteoarthritis requires active participation of both bone and cartilage, and that there is some temporal connection between  the processes that occur in the subchondral bone during development of joint disease, and the deterioration of the overlying cartilage. This requires some cross-talk between the two tissues, but exactly how this occurs, or what agents are responsible for the dialogue is unclear. Understanding this interaction and the molecules that signal between the tissues is critical to understanding and eventually controlling the process of joint degeneration.

This session convenes a panel of experts who will address different areas of this topic. David Findlay has worked in bone and joint research for over 30 years, focusing on the mechanisms of systemic and focal bone loss, and has recently turned his attention to the interaction of bone and cartilage in joint disease.  Liyun Wang has used novel fluorescent techniques to study fluid and solute transport in bone and cartilage, and is these novel imaging technologies in animal models to quantify interstitial fluid flow in bone and cartilage. Daniel LaJeunesse has been studying the basis for bone-cartilage crosstalk for many years, and has done pioneering work looking at the role of Wnt signaling in both of these tissues.