Dr. Richard Bockman, MD, PhD, is the Chief of the Endocrine Service at Hospital for Special Surgery and Professor of Medicine in the Endocrine Division of the Joan and Sanford Weill Cornell Medical College. Dr. Bockman received his undergraduate training in biology at The Johns Hopkins University, graduate training in Medicine at Yale University Medical School, and then attended Rockefeller University, where he received his PhD in physical biochemistry. He completed a residency program at New York University Bellevue Hospital, and received postgraduate training in medicine and endocrinology at Cornell University Medical College. He is Board-certified in Internal Medicine.
Dr. Bockman directed basic and clinical research under NIH-sponsored grants and has published over 100 articles in many scientific and clinical journals, including Science, Journal of Clinical Investigation, Journal of Bone and Mineral Research, and Endocrinology. He is a member of the American Society for Bone and Mineral Research (where he has served on the professional practice committee), and The Endocrine Society (where he serves on the Clinical Endocrine Update steering committee) , and is a Fellow of the American College of Physicians. He currently serves on the Editorial Board of The Journal of Clinical Endocrinology and Metabolism.
One of the goals of Hospital for Special Surgery (HSS) is to advance the science of orthopedic surgery, rheumatology, and related disciplines for the benefit of patients. Physicians at HSS may collaborate with outside companies for education, research and medical advances. HSS supports this collaboration in order to foster medical breakthroughs; however HSS also believes that these collaborations must be disclosed.
As part of the disclosure process, this website lists physician collaborations with outside companies if payments were received during the prior year, or if the HSS physician currently receives payment. The disclosures are provided by information provided by the physician and other sources and are updated regularly. Further information may be available on individual company websites.
As of March 18, 2014, Dr. Bockman reported no financial interest relationships with healthcare industry.
By disclosing the collaborations of HSS physicians with industry on this website, HSS and its physicians make this information available to their patients and the public, thus creating a transparent environment for those who are interested in this information. Further, HSS’ Conflicts of Interest Policy does not permit physicians to collect royalties on products developed by him/her that are used on patients at HSS.
New York University Medical Center, Bellevue Program, New York
Weill Cornell Medical College, New York Hospital
Kurland J, Bockman RS, Broxmeyer H, Moore M. Limitation of excessive myelopoiesis by the extrinsic modulation of macrophage derived prostaglandin E. Science, 199:552-555. 1978.
Bockman RS. Stage-dependent reduction in T-colony formation in Hodgkin's disease: Coincidence with monocyte synthesis of prostaglandins. Journal of Clinical Investigation, 66:523-531. 1980.
Bockman RS, Repo MA, Warrell, Jr. RP, Pounds JG, Schidlovsky BM, Gordon BM, and Jones KW. Distribution of Trace Levels of Therapeutic Gallium in Bone as Mapped by Synchrotron X-Ray Microscopy. Proc. Nat'l Acad of Sci. 87:4149-4153. 1990.
Bockman, RS, Guidon, Jr. PT, Salvatori R, Kawaguchi A, Pan LC. Gallium nitrate increases type I collagen and fibronectin mRNA and collagen protein levels in bone and fibroblast cells. J. Cellular Biochem. 52:396-403. 1993.
Blank, RD, and Bockman, RS. A Review of Clinical Trials of Therapies for Osteoporosis Using Fracture as an Endpoint. J. Clin Densitometry. 2(4)379-396. 2000.
Yershov Y, Baldini TH, Villagomez S, Young T, Martin ML, Bockman RS, Peterson MGE, and Blank RD. Bone Strength and Related Traits in HcB/Dem Recombinant Congenic Mice. J Bone Min Research. 16: 992-1003. 2001.
Goncalves J, Wasif N, Esposito D, Coico JM, Schwartz B, Higgins PJ, Bockman RS, Staiano-Coico L. Gallium Nitrate Accelerates Partial Thickness Wound Repair and Alters Keratinocyte Integrin Expression to Favor a Motile Phenotype. J Surgical Research. 103: 134-140. 2002.
Siris E, Bilezikian J, Rubin DM, Black D, Bockman RS, Bone H, Hochberg M, McClung M, Schnitzer T. Pins and Plaster Aren’t Enough: A Call for the Evaluation and Treatment of Patients with Osteoporotic Fractures. J Clin Endocrinol Metab. Aug;88(8):3482-6. 2003.
Stein, EM, Sinha, N, Ortiz, D, Strain, G, Pomp, A, Dakin, G, McMahon, D, Bockman, RS, and Silverberg, SJ. Vitamin D Insufficiency Prior to Bariatric Surgery: Risk Factors and a Pilot Treatment Study. Clinical Endocrinology. September, 2008.
Hobin JA, Deschamps AM, Bockman R, Cohen S, Dechow P, Eng C, Galey W, Morris M, Prabhakar S, Raj U, Rubenstein P, Smith JA, Stover P, Sung N, Talman W, Galbraith R. Engaging basic scientists in translational research: identifying opportunities, overcoming obstacles, Journal of Translational Medicine 2012, 10:72 (doi:10.1186/1479-5876-10-72)
Carmel AS, Shieh A, Bang H, Bockman RS. The 25(OH)D level needed to maintain a favorable bisphosphonate response is =33 ng/ml. Osteoporos Int.2012, 23, (DOI 10.1007/s00198-011-1868-7)
For more publications, please see the PubMed listing.
The major objective of the Dr. Bockman’s research is to elucidate the pathogenesis and genetic basis of metabolic bone diseases, including osteoporosis, and to develop new therapies for treating these diseases.
Current clinical research is being conducted through four active protocols at the Weill-Cornell Clinical Translational Science Center (CTSC) with former HSS - Endocrine Fellow, Dr. Naina Sinha (now Assistant Attending Physician at NYPH), and with former WMC-Fellow, Dr. Emily Stein. Please note that Dr. Bockman served as the mentor for Dr. Stein, who was awarded an NIH-sponsored CREFF award to carry out her research, and was the first to receive a Cornell “Masters Degree in Clinical Research” awarded through the WMC-CTSC.
In one on-going prospective CTSC-study, alterations in bone metabolism are studied in morbidly and super obese patients being evaluated for Roux-en-Y gastric bypass or biliopancreatic diversion with duodenal switch. At baseline and at various time points over 18 months post-operatively markers of bone turnover, calcitropic hormones and changes in bone density are followed. We specifically obtain anthropomorphic measurements, calcium, vit D and total caloric intake, serum calcium, 25-hydroxy vit D (25-OH VitD), intact PTH and urinary calcium, markers of bone formation, osteocalcin (OC) and bone-specific alkaline phosphatase (BSAP), and bone resorption, urine N-telopeptide (u-NTx) along with bone mineral density assessed by heel ultrasound, since the weight limit for standard densitometry is 300 pounds.
In the second CTSC study, we have initiated a clinical trial examining the efficacy of two regimens to replace vitamin D in D-deficient bariatric subjects.
The third CTSC study examines the role of potassium citrate in preserving bone mass in osteopenic, post-menopausal women.
A fourth CTSC study studies vitamin D status in the W-CIMA patient population with regards to their response to bisphosphonate therapies.
Basic research has examined the following topics:
Gallium Nitrate: Transient and stably transfected osteoblasts have been used to study the effects of gallium, a unique transitional element on the expression of specific matrix genes. Various aspects of cell-signaling that can lead to alterations in bone-matrix gene expression have been studied. Such studies can provide the scientific rationale for the development of clinical protocols measuring the ability of gallium to prevent and treat osteoporosis.
Cell and Molecular Regulation of Collagenase Gene Expression: Cell mediated damage to the major matrix components of connective tissues is an early and critical step in the pathogenesis of destructive arthritic diseases. Type I collagen is the major organic component of bone. In order to develop new therapeutic strategies for preserving and protecting connective tissue, a better understanding of the cellular controls on the degradation and synthesis of the key matrix components is required.
Genetics of Osteoporosis and Fragility fractures: While it is generally acknowledged that many of the factors that determine bone strength are genetically determined, little is known about which genes determine bone strength or how those genes might be affected by epistatic interactions. Recent studies with Dr. R. Blank in a recombinant-congenic mouse model (HcB/Dem) have demonstrated quantitative trait loci (QTLs) for failure load, a measure of a bone's overall strength. Moreover, by mapping QTLs for a variety of bone phenotypes in this system, we have shown that the relevant QTLs are often pleiotropic, each affecting distinct subsets of independently measured phenotypes: diaphyseal diameter, structural stiffness, ash percentage, and body mass. The mapping data, therefore, allow prediction of the general mechanisms as well as the locations by which the identified QTLs affect bone strength.