Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Osteoporosis: HELP
Articles from New Jersey
Based on 107 articles published since 2008

These are the 107 published articles about Osteoporosis that originated from New Jersey during 2008-2019.
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5
1 Editorial No vitamin D threshold for calcium absorption: why does this matter? 2014

Shapses, Sue A. ·Department of Nutritional Sciences, Rutgers University, New Brunswick, NJ. ·Am J Clin Nutr · Pubmed #24477041.

ABSTRACT: -- No abstract --

2 Review Animal versus plant protein and adult bone health: A systematic review and meta-analysis from the National Osteoporosis Foundation. 2018

Shams-White, Marissa M / Chung, Mei / Fu, Zhuxuan / Insogna, Karl L / Karlsen, Micaela C / LeBoff, Meryl S / Shapses, Sue A / Sackey, Joachim / Shi, Jian / Wallace, Taylor C / Weaver, Connie M. ·Department of Public Health and Community Medicine, School of Medicine, Tufts University, Boston, MA United States of America. · Friedman School of Nutrition Science and Policy, Tufts University, Boston, MA United States of America. · Yale Bone Center at the Yale School of Medicine, Yale University, New Haven, CT United States of America. · Skeletal Health and Osteoporosis Center and Bone Density Unit; Harvard Medical School, Boston, MA United States of America. · Endocrine, Diabetes and Hypertension Division, Brigham and Women's Hospital, Boston, MA United States of America. · Department of Nutritional Sciences, Rutgers University, New Brunswick, NJ United States of America. · Department of Nutritional Sciences, Rutgers School of Health Professions, Newark, NJ United States of America. · Department of Nutrition and Food Studies, George Mason University, Fairfax, VA United States of America. · Think Healthy Group, Inc, Washington DC United States of America. · Department of Nutrition Science, Women's Global Health Institute, Purdue University, Nutrition Science, West Lafayette, IN United States of America. ·PLoS One · Pubmed #29474360.

ABSTRACT: BACKGROUND: Protein may have both beneficial and detrimental effects on bone health depending on a variety of factors, including protein source. OBJECTIVE: The aim was to conduct a systematic review and meta-analysis evaluating the effects of animal versus plant protein intake on bone mineral density (BMD), bone mineral content (BMC) and select bone biomarkers in healthy adults. METHODS: Searches across five databases were conducted through 10/31/16 for randomized controlled trials (RCTs) and prospective cohort studies in healthy adults that examined the effects of animal versus plant protein intake on 1) total body (TB), total hip (TH), lumbar spine (LS) or femoral neck (FN) BMD or TB BMC for at least one year, or 2) select bone formation and resorption biomarkers for at least six months. Strength of evidence (SOE) was assessed and random effect meta-analyses were performed. RESULTS: Seven RCTs examining animal vs. isoflavone-rich soy (Soy+) protein intake in 633 healthy peri-menopausal (n = 1) and post-menopausal (n = 6) women were included. Overall risk of bias was medium. Limited SOE suggests no significant difference between Soy+ vs. animal protein on LS, TH, FN and TB BMD, TB BMC, and bone turnover markers BSAP and NTX. Meta-analysis results showed on average, the differences between Soy+ and animal protein groups were close to zero and not significant for BMD outcomes (LS: n = 4, pooled net % change: 0.24%, 95% CI: -0.80%, 1.28%; TB: n = 3, -0.24%, 95% CI: -0.81%, 0.33%; FN: n = 3, 0.13%, 95% CI: -0.94%, 1.21%). All meta-analyses had no statistical heterogeneity. CONCLUSIONS: These results do not support soy protein consumption as more advantageous than animal protein, or vice versa. Future studies are needed examining the effects of different protein sources in different populations on BMD, BMC, and fracture.

3 Review Non-musculoskeletal benefits of vitamin D. 2018

Wimalawansa, Sunil J. ·Endocrinology & Nutrition, Cardio Metabolic Institute, 661 Darmody Avenue, North Brunswick, NJ, USA. Electronic address: suniljw@hotmail.com. ·J Steroid Biochem Mol Biol · Pubmed #27662817.

ABSTRACT: The aim of this study is to determine and critically evaluate the plausible relationships of vitamin D with extra-skeletal tissues in humans. Severe vitamin D deficiency results in rickets in children and osteomalacia in adults; these beneficial effects in the musculoskeletal system and certain physiological functions are well understood. Nevertheless, mounting reports support additional beneficial effects of vitamin D, outside the musculoskeletal system. This review explores the recent advances in knowledge about the non-skeletal effects of vitamin D. Peer-reviewed papers were extracted from research databases using key words, to assess correlations between vitamin D and extra-skeletal diseases and conditions. As per the guidelines of the Preferred Reporting Items for Systematic Reviews (PRISMA); general interpretations of results are included; taking into consideration the broader evidence and implications. This review summarizes current knowledge of the effects of vitamin D status on extra-skeletal tissues with special attention given to relationships between vitamin D status and various diseases commonly affecting adults; the effects of intervention with vitamin D and exposure to sunlight. Evidence suggests that vitamin D facilitates the regulation of blood pressure; and cardiac; endothelial; and smooth muscle cell functions; playing an important role in cardiovascular protection. In addition; 1,25(OH)

4 Review Dietary protein and bone health: a systematic review and meta-analysis from the National Osteoporosis Foundation. 2017

Shams-White, Marissa M / Chung, Mei / Du, Mengxi / Fu, Zhuxuan / Insogna, Karl L / Karlsen, Micaela C / LeBoff, Meryl S / Shapses, Sue A / Sackey, Joachim / Wallace, Taylor C / Weaver, Connie M. ·Department of Public Health and Community Medicine, School of Medicine, and. · Friedman School of Nutrition Science and Policy, Tufts University, Boston, MA. · Yale Bone Center at the Yale School of Medicine, Yale University, New Haven, CT. · Skeletal Health and Osteoporosis Center and Bone Density Unit, Harvard Medical School, Boston, MA. · Endocrine, Diabetes and Hypertension Division, Brigham and Women's Hospital, Boston, MA. · Department of Nutritional Sciences, Rutgers University, New Brunswick, NJ. · National Osteoporosis Foundation, Arlington, VA; taylor.wallace@me.com. · Department of Nutrition and Food Studies, George Mason University, Fairfax, VA; and. · Department of Nutrition Science, Women's Global Health Institute, Purdue University, West Lafayette, IN. ·Am J Clin Nutr · Pubmed #28404575.


5 Review Bone loss at the distal femur and proximal tibia in persons with spinal cord injury: imaging approaches, risk of fracture, and potential treatment options. 2017

Cirnigliaro, C M / Myslinski, M J / La Fountaine, M F / Kirshblum, S C / Forrest, G F / Bauman, W A. ·Department of Veterans Affairs Rehabilitation Research & Development Service National Center for the Medical Consequences of Spinal Cord Injury, James J. Peters Veterans Affairs Medical Center, Bronx, NY, USA. · Department of Physical Therapy, School of Health Related Professions, Rutgers New Jersey Medical School, Newark, NJ, USA. · Department of Physical Therapy, School of Health and Medical Sciences, Seton Hall University, South Orange, NJ, USA. · The Institute for Advanced Study of Rehabilitation and Sports Science, School of Health and Medical Sciences, Seton Hall University, South Orange, NJ, USA. · Kessler Institute for Rehabilitation, West Orange, NJ, USA. · Department of Physical Medicine and Rehabilitation, Rutgers New Jersey Medical School, Newark, NJ, USA. · Kessler Foundation, West Orange, NJ, USA. · Department of Veterans Affairs Rehabilitation Research & Development Service National Center for the Medical Consequences of Spinal Cord Injury, James J. Peters Veterans Affairs Medical Center, Bronx, NY, USA. william.bauman@va.gov. · Departments of Medicine and Rehabilitation Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA. william.bauman@va.gov. ·Osteoporos Int · Pubmed #27921146.

ABSTRACT: Persons with spinal cord injury (SCI) undergo immediate unloading of the skeleton and, as a result, have severe bone loss below the level of lesion associated with increased risk of long-bone fractures. The pattern of bone loss in individuals with SCI differs from other forms of secondary osteoporosis because the skeleton above the level of lesion remains unaffected, while marked bone loss occurs in the regions of neurological impairment. Striking demineralization of the trabecular epiphyses of the distal femur (supracondylar) and proximal tibia occurs, with the knee region being highly vulnerable to fracture because many accidents occur while sitting in a wheelchair, making the knee region the first point of contact to any applied force. To quantify bone mineral density (BMD) at the knee, dual energy x-ray absorptiometry (DXA) and/or computed tomography (CT) bone densitometry are routinely employed in the clinical and research settings. A detailed review of imaging methods to acquire and quantify BMD at the distal femur and proximal tibia has not been performed to date but, if available, would serve as a reference for clinicians and researchers. This article will discuss the risk of fracture at the knee in persons with SCI, imaging methods to acquire and quantify BMD at the distal femur and proximal tibia, and treatment options available for prophylaxis against or reversal of osteoporosis in individuals with SCI.

6 Review Macronutrient Intake and Distribution in the Etiology, Prevention and Treatment of Osteosarcopenic Obesity. 2017

Kelly, Owen J / Gilman, Jennifer C / Kim, Youjin / Ilich, Jasminka Z. ·Abbott Nutrition, Columbus, Ohio, United States. · School of Environmental and Biological Sciences, Rutgers University, New Brunswick, New Jersey, United States. · Department of Nutrition, Food and Exercise Sciences, Florida State University, Tallahassee, Florida, United States. ·Curr Aging Sci · Pubmed #27156951.

ABSTRACT: BACKGROUND: Osteosarcopenic obesity, the combined deterioration of bone, muscle and fat tissues, could become the ultimate trajectory of aging. Aging stem cells are deregulated by low-grade chronic inflammation and possibly by diet. The metabolic shift of stem cells towards adipogenesis results in osteo obesity, sarco obesity and obesity. Macronutrients have numerous physiological functions but are regarded mainly for their energy contribution. Currently, no nutritional causes or treatment/prevention guidelines exist for osteosarcopenic obesity. OBJECTIVE: The aim of this review is to assemble the evidence to elucidate if the macronutrient composition of the Western diet has an effect on the development of osteosarcopenic obesity. In view of the role of brain in locomotion a section examining the macronutrients as possible modulators of brain functioning was included. METHOD: An extensive literature search of PubMed and Medline was conducted for human data using combinations and synonyms of osteoporosis, sarcopenia and obesity, and energy, carbohydrate, protein and lipid, and brain. US National Health and Nutrition Examination Survey (NHANES) food intake data from 2002-2012 were obtained and transposed to Microsoft Excel for analysis. RESULTS: NHANES data showed that energy imbalances in aging, excess high glycemic carbohydrate, lower protein intakes and low long chain polyunsaturated fat intakes may contribute to osteosarcopenic obesity. 135 articles were included in the review. CONCLUSION: Early humans probably consumed a diet closer to what the human body was designed for; however, we do not know the ideal energy and macronutrient proportions for optimal health or for preventing/treating aging and osteosarcopenic obesity.

7 Review Cathepsin K Inhibition: A New Mechanism for the Treatment of Osteoporosis. 2016

Duong, Le T / Leung, Albert T / Langdahl, Bente. ·Merck & Co. Inc., Kenilworth, NJ, USA. le_duong@merck.com. · Former Employee, Merck & Co. Inc., Kenilworth, NJ, USA. · Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark. ·Calcif Tissue Int · Pubmed #26335104.

ABSTRACT: Cathepsin K (CatK), a cysteine protease, is highly expressed by osteoclasts and very efficiently degrades type I collagen, the major component of the organic bone matrix. Robust genetic and pharmacological preclinical studies consistently demonstrate that CatK inhibition increases bone mass, improves bone microarchitecture and strength. Recent advances in the understanding of the molecular and cellular mechanisms involved in bone modeling and remodeling suggest that inhibition of CatK decreases bone resorption, but increases the number of cells of osteoclast lineage. This in turn maintains the signals for bone formation, and perhaps may even increase bone formation on some cortical surfaces. Several CatK inhibitors, including relacatib, balicatib, odanacatib and ONO-5334 had entered clinical development for metabolic bone disorders with increased bone resorption, such as postmenopausal osteoporosis. However, odanacatib (ODN) is the only candidate continuing in development. ODN is a highly selective oral CatK inhibitor dosed once-weekly in humans. In a Phase 2 clinical trial, postmenopausal women treated with ODN had sustained reductions of bone resorption markers, while bone formation markers returned to normal after an initial decline within the first 2 years on treatment. In turn areal bone mineral density increased continuously at both spine and hip for up to 5 years. ODN has also been demonstrated to improve bone mass in women with postmenopausal osteoporosis previously treated with alendronate and in men with osteoporosis. ODN is currently in a worldwide Phase 3 fracture outcome trial for the treatment of postmenopausal osteoporosis with interim results supporting its anti-fracture efficacy at the spine, hip and non-vertebral sites.

8 Review Systematic Literature Review and Meta-analysis of Medication Adherence With Once-weekly Versus Once-daily Therapy. 2015

Iglay, Kristy / Cao, Xiting / Mavros, Panagiotis / Joshi, Kruti / Yu, Shengsheng / Tunceli, Kaan. ·Merck & Co, Inc, Kenilworth, New Jersey. Electronic address: kristy.iglay@merck.com. · Merck & Co, Inc, Kenilworth, New Jersey. ·Clin Ther · Pubmed #26117406.

ABSTRACT: PURPOSE: To compare medication adherence rates for once-weekly (QW) versus once-daily (QD) dosing regimens in patients with chronic disease. METHODS: A systematic literature review was conducted to identify articles published in English-language journals examining the rate of adherence to medications in patients with chronic disease. Relevant studies were identified from January 2002 through August 2013 using PubMed, EMBASE, and the Cochrane Library databases. Twenty-two published observational studies reporting adherence were identified by 2 independent reviewers, and 7 articles reported relevant measures for analysis. All studies were conducted in patients with osteoporosis. Meta-analyses estimated (1) mean difference (MD) in adherence (defined using the mean medication possession ratio [MPR]) between QW and QD dosing groups and (2) odds ratio (OR) for adherence (defined using an MPR cutoff of ≥80%) for QW versus QD dosing. Heterogeneity was assessed using Cochran's Q and I(2) values, and meta-analyses used both fixed- and random-effects models. FINDINGS: The random-effects meta-analysis revealed a significantly greater MPR with QW compared with QD dosing (pooled MD = 12.29%; 95% CI, 10.76%-13.82%; n = 9 [data reported in 7 publications]). Because of the high level of heterogeneity (I(2) = 83.4%), the fixed-effects model results were not appropriate to report for the pooled MD. When examining the OR for adherence, both fixed- and random-effects models provided similar results due to the low level of heterogeneity (I(2) = 7.9%; n = 5 [data reported in 3 publications]). Using either model, the pooled odds of being adherent (MPR ≥80%) in the QW dosing group was approximately 1.9 times the odds in the QD dosing group (random-effects OR = 1.90; 95% CI, 1.81-2.00; fixed-effects OR = 1.92; 95% CI, 1.84-1.99). IMPLICATIONS: In our meta-analysis, QW dosing was associated with better adherence levels and greater odds of being adherent compared with QD dosing in patients with osteoporosis.

9 Review Turning Bone Morphogenetic Protein 2 (BMP2) on and off in Mesenchymal Cells. 2015

Rogers, Melissa B / Shah, Tapan A / Shaikh, Nadia N. ·Department of Microbiology, Biochemistry and Molecular Genetics, Rutgers New Jersey Medical School, Newark, NJ. ·J Cell Biochem · Pubmed #25776852.

ABSTRACT: The concentration, location, and timing of bone morphogenetic protein 2 (BMP2, HGNC:1069, GeneID: 650) gene expression must be precisely regulated. Abnormal BMP2 levels cause congenital anomalies and diseases involving the mesenchymal cells that differentiate into muscle, fat, cartilage, and bone. The molecules and conditions that influence BMP2 synthesis are diverse. Understandably, complex mechanisms control Bmp2 gene expression. This review includes a compilation of agents and conditions that can induce Bmp2. The currently known trans-regulatory factors and cis-regulatory elements that modulate Bmp2 expression are summarized and discussed. Bone morphogenetic protein 2 (BMP2, HGNC:1069, GeneID: 650) is a classical morphogen; a molecule that acts at a distance and whose concentration influences cell behavior. In mesenchymal cells, the concentration of BMP2 influences myogenesis, adipogenesis, chondrogenesis, and osteogenesis. Because the amount, timing, and location of BMP2 synthesis influence the allocation of cells to muscle, fat, cartilage, and bone, the mechanisms that regulate the Bmp2 gene are crucial. Key early mesodermal events that require precise Bmp2 regulation include heart specification and morphogenesis. Originally named for its osteoinductive properties, healing fractures requires BMP2. The human Bmp2 gene also has been linked to osteoporosis and osteoarthritis. In addition, all forms of pathological calcification in the vasculature and in cardiac valves involve the pro-osteogenic BMP2. The diverse tissues, mechanisms, and diseases influenced by BMP2 are too numerous to list here (see OMIM: 112261). However, in all BMP2-influenced pathologies, changes in the behavior and differentiation of pluripotent mesenchymal cells are a recurring theme. Consequently, much effort has been devoted to identifying the molecules and conditions that influence BMP2 synthesis and the complex mechanisms that control Bmp2 gene expression. This review begins with an overview of the Bmp2 gene's chromosomal neighborhood and then summarizes and evaluates known regulatory mechanisms and inducers.

10 Review American Society of Biomechanics Journal of Biomechanics Award 2013: cortical bone tissue mechanical quality and biological mechanisms possibly underlying atypical fractures. 2015

Geissler, Joseph R / Bajaj, Devendra / Fritton, J Christopher. ·Department of Orthopaedics, New Jersey Medical School, Rutgers University, 205 S. Orange Avenue, Newark, NJ 07103, USA; Joint Program in Biomedical Engineering, Rutgers Biomedical and Health Sciences, and the New Jersey Institute of Technology, Newark, NJ, USA. Electronic address: geissljr@rutgers.edu. · Department of Orthopaedics, New Jersey Medical School, Rutgers University, 205 S. Orange Avenue, Newark, NJ 07103, USA. Electronic address: devendrabajaj@gmail.com. · Department of Orthopaedics, New Jersey Medical School, Rutgers University, 205 S. Orange Avenue, Newark, NJ 07103, USA; Joint Program in Biomedical Engineering, Rutgers Biomedical and Health Sciences, and the New Jersey Institute of Technology, Newark, NJ, USA. Electronic address: chris.fritton@rutgers.edu. ·J Biomech · Pubmed #25683519.

ABSTRACT: The biomechanics literature contains many well-understood mechanisms behind typical fracture types that have important roles in treatment planning. The recent association of "atypical" fractures with long-term use of drugs designed to prevent osteoporosis has renewed interest in the effects of agents on bone tissue-level quality. While this class of fracture was recognized prior to the introduction of the anti-resorptive bisphosphonate drugs and recently likened to stress fractures, the mechanism(s) that lead to atypical fractures have not been definitively identified. Thus, a causal relationship between these drugs and atypical fracture has not been established. Physicians, bioengineers and others interested in the biomechanics of bone are working to improve fracture-prevention diagnostics, and the design of treatments to avoid this serious side-effect in the future. This review examines the mechanisms behind the bone tissue damage that may produce the atypical fracture pattern observed increasingly with long-term bisphosphonate use. Our recent findings and those of others reviewed support that the mechanisms behind normal, healthy excavation and tunnel filling by bone remodeling units within cortical tissue strengthen mechanical integrity. The ability of cortical bone to resist the damage induced during cyclic loading may be altered by the reduced remodeling and increased tissue age resulting from long-term bisphosphonate treatment. Development of assessments for such potential fractures would restore confidence in pharmaceutical treatments that have the potential to spare millions in our aging population from the morbidity and death that often follow bone fracture.

11 Review Risk of fracture and the concomitant use of bisphosphonates with osteoporosis-inducing medications. 2015

Nyandege, Abner N / Slattum, Patricia W / Harpe, Spencer E. ·Market Access Solutions LLC, Raritan, NJ, USA. · Virginia Commonwealth University School of Pharmacy, Richmond, VA, USA. · Midwestern University Chicago College of Pharmacy, Downers Grove, IL, USA sharpe@midwestern.edu. ·Ann Pharmacother · Pubmed #25667198.

ABSTRACT: OBJECTIVE: To review the literature on the concomitant use of bisphosphonates and medications that can influence bone metabolism and potentially attenuate bisphosphonate antifracture efficacy. DATA SOURCES: MEDLINE and CINAHL were searched for articles published in English through December 2014 using the following terms: bisphosphonates, bone density conservation agents, acid-suppressive therapy, levothyroxine, thiazolidinediones (TZDs), selective serotonin reuptake inhibitors (SSRIs), bone fractures. STUDY SELECTION AND DATA EXTRACTION: Studies were included if they reported results of concomitant use of any listed medications with bisphosphonates and risk of fractures and focused on women. Articles that focused generally on the use of one of the listed medications and fractures without explicitly examining the potential antifracture efficacy or attenuation of bisphosphonates were excluded. DATA SYNTHESIS: A total of 6 relevant studies were identified. Four epidemiological studies reported a statistically significant dose-dependent increase in the risk of fractures when bisphosphonates and acid-suppressive drugs were used together. One post hoc analysis of clinical trial data suggested no attenuation of the antifracture effects of bisphosphonates when used concomitantly with acid-suppressive therapy. One study involving bisphosphonates and SSRIs noted a statistically significant association between fracture risk and SSRI use. No study examining TZDs or levothyroxine with bisphosphonates was identified. CONCLUSIONS: Existing research suggests potential attenuation of bisphosphonate antifracture efficacy among patients taking acid-suppressive medications. Based on their pharmacological actions, TZDs, SSRIs, and levothyroxine have similar implications. The paucity of evidence in the literature associating the attenuation of bisphosphonate antifracture efficacy when combined with other medications suggests that further investigation is needed.

12 Review Literature review: The effects of teriparatide therapy at the hip in patients with osteoporosis. 2014

Eriksen, Erik F / Keaveny, Tony M / Gallagher, Eileen R / Krege, John H. ·Department of Endocrinology, Oslo University Hospital, Pb 49596 Nydalen, N-0424 Oslo, Norway. Electronic address: e.f.eriksen@medisin.uio.no. · University of California, Berkeley, Departments of Mechanical Engineering and Bioengineering, 6175 Etcheverry Hall, MC 1740, Berkeley, CA 94720, USA. Electronic address: tmk@me.berkeley.edu. · inVentiv Health Clinical, 504 Carnegie Center, Princeton, NJ 08540, USA. Electronic address: eileen.gallagher@inventivhealth.com. · Lilly USA, LLC, Lilly Technology Center South, Drop Code 5028 Indianapolis, IN 46221, USA. Electronic address: kregejh@lilly.com. ·Bone · Pubmed #25053463.

ABSTRACT: Teriparatide is a skeletal anabolic treatment for patients with osteoporosis at high risk for fracture. Because adequate clinical trials have not yet been conducted to assess the efficacy of teriparatide for reducing the risk of hip fracture, we review here the literature regarding how treatment with teriparatide affects the hip in patients with osteoporosis. Teriparatide increases cancellous bone volume, improves bone architecture, and - uniquely among osteoporosis treatments - increases cortical thickness and cortical porosity. By bone scan and positron emission tomography, teriparatide increases bone formation throughout the skeleton, including the hip. Consistent with these findings, studies using dual-energy X-ray absorptiometry and quantitative computed tomography for longitudinal assessment of changes at the hip have consistently shown increases in areal and volumetric bone mineral density, cortical thickness, and finite element-estimated hip strength in patients treated with teriparatide. Finally, in clinical fracture-outcome trials, treatment with teriparatide has been shown to reduce the risk of nonvertebral fracture, a composite endpoint that includes hip fracture. Taken together, this body of evidence suggests that teriparatide positively affects the hip in patients with osteoporosis.

13 Review Promoting successful aging through effective prevention and management of osteoporosis. 2013

Cavalieri, Thomas A / Noll, Donald R. ·University of Medicine and Dentistry of New Jersey-School of Osteopathic Medicine, One Medical Center Dr, Suite 305, Stratford, NJ 08084-1500, USA. cavalita@umdnj.edu ·J Am Osteopath Assoc · Pubmed #23425934.

ABSTRACT: Successful aging has been described as having 3 components: a low probability of disease and disease-related disability, a capacity for high cognitive and physical function, and active engagement with social and productive activities. Osteopathic physicians play a critical role in the promotion of successful aging through the prevention, early detection, and management of osteoporosis. Not many years ago, osteoporosis was viewed as an age-related disorder for which there was a lack of effective approaches for early intervention and management. Now, that view has changed.

14 Review Review of current literature and implications of RANKL inhibitors for oral health care providers. 2013

Epstein, Matthew S / Ephros, Hillel D / Epstein, Joel B. ·Oral and Maxillofacial Surgery Resident, St. Joseph's Regional Medical Center, Paterson, New Jersey. Electronic address: epsteinmatthew@gmail.com. ·Oral Surg Oral Med Oral Pathol Oral Radiol · Pubmed #22901640.

ABSTRACT: Bisphosphonates (BPs) were the first class of drugs commonly used to prevent skeletal-related events (SRE) in patients with osteoporosis, multiple myeloma (MM), or solid tumors with metastases to bone. A new alternative class of agents, receptor activator of nuclear factor kappa-B ligand (RANKL) inhibitors, are now available for use in these indications and have the potential to replace intravenous BPs. This paper presents a review of the current literature on denosumab and its association with osteonecrosis of the jaw (ONJ). Denosumab is a RANKL inhibitor that has recently been approved for the prevention of SRE for the same indications as BPs except for MM. Although the overall frequency of denosumab-related ONJ may be similar or higher than estimates of the occurrence rate of bisphosphonate-related ONJ, evidence continues to support appropriate planning and preventive care can reduce the likelihood of adverse effects, including osteonecrosis.

15 Review Laryngeal ulceration and hemoptysis secondary to inadvertent alendronate overdose: case report and review of the literature. 2012

Hanna, John / Bee, Joseph / Sataloff, Robert T. ·Department of Otolaryngology, St. Peter's University Hospital, New Brunswick, NJ, USA. ·Ear Nose Throat J · Pubmed #23288794.

ABSTRACT: Alendronate is commonly used in the treatment of osteoporosis and other bone diseases. Its drug profile includes many recognized side effects, and the literature includes case reports of esophageal irritation and ulceration. However, little has been published about laryngeal effects. We describe the case of a 77-year-old man who presented with hemoptysis secondary to laryngeal ulceration caused by the inadvertent misuse of alendronate. This case highlights the need for otolaryngologists to be familiar with alendronate and its side effects.

16 Review Complications in patients with alcohol-associated liver disease who undergo liver transplantation. 2012

Gaglio, Paul J / Gaglio, Paul J. ·Rutgers University College of Arts and Sciences, New Brunswick, NJ 08901, USA. pgaglio@montefiore.org ·Clin Liver Dis · Pubmed #23101987.

ABSTRACT: Cirrhosis caused by alcohol-associated liver disease is a common indication for liver transplantation worldwide. Patients with alcohol-associated liver disease who undergo liver transplantation face multiple challenging comorbid medical issues that enhance the potential for perioperative and postoperative complications. Awareness of these issues and appropriate therapeutic intervention may minimize the negative effect of these complications on posttransplantation survival. This article reviews important posttransplantation problems in patients transplanted for alcohol-associated liver disease.

17 Review The effects of osteoclast modifiers on the oral cavity: a review for prescribers. 2012

Epstein, Matthew S / Epstein, Joel B / Ephros, Hillel D. ·Oral and Maxillofacial Surgery Resident, St. Joseph's Regional Medical Center, Paterson, New Jersey, USA. ·Curr Opin Support Palliat Care · Pubmed #22871978.

ABSTRACT: PURPOSE OF REVIEW: Osteonecrosis of the jaw associated with therapeutic osteoclast modifiers is a rare but serious event. The consequences of osteonecrosis can be devastating despite current treatment. With the increase in diversity of agents and significant increase in the prevalence of osteoclast modifiers prescribed by oncologists understanding diagnosis and management of osteoclast modifiers-related osteonecrosis of the jaws (OMRONJ) is necessary. The risk of osteonecrosis when osteoclast modifiers are used for management of osteoporosis is much less than osteoclast modifiers used in the oncology setting. A basic understanding of the oral exam and current management will lead to more effective communication and more effective prevention of devastating OMRONJ. RECENT FINDINGS: An indistinguishable rate of ONJ seen with new therapeutic agents is becoming apparent and relevant preventive therapy and counseling of the patient is indicated. Currently there is no comprehensive clinical guideline that unifies oncologists and oral health providers in the prevention and management of OMRONJ. SUMMARY: Communication and proper planning with each patient's provider is the most effective strategy to prevent OMRONJ. A team composed of an oncologist, oral and maxillofacial surgeon and dentist competent in managing this condition is necessary. An understanding of the cause and development of OMRONJ can give the prescriber an improved perspective to communicate with oral health professional colleagues. Current guidelines emphasize the need for dental management prior to the use of osteoclast modifiers for the prevention and management of osteonecrosis of the jaw.

18 Review Transient osteoporosis of pregnancy. 2012

Maliha, George / Morgan, Jordan / Vrahas, Mark. ·Harvard Orthopaedic Trauma Service, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114, USA. gmaliha@princeton.edu ·Injury · Pubmed #22464203.

ABSTRACT: Transient osteoporosis of pregnancy (TOP) is a rare yet perhaps under-reported condition that has affected otherwise healthy pregnancies throughout the world. The condition presents suddenly in the third trimester of a usually uneventful pregnancy and progressively immobilizes the mother. Radiographic studies detect drastic loss of bone mass, elevated rates of turnover in the bone, and oedema in the affected portion. Weakness of the bone can lead to fractures during delivery and other complications for the mother. Then, within weeks of labour, symptoms and radiological findings resolve. Aetiology is currently unknown, although neural, vascular, haematological, endocrine, nutrient-deficiency, and other etiologies have been proposed. Several treatments have also been explored, including simple bed rest, steroids, bisphosphonates, calcitonin, induced termination of pregnancy, and surgical intervention. The orthopedist plays an essential role in monitoring the condition (and potential complications) as well as ensuring satisfactory outcomes for both the mother and newborn.

19 Review Denosumab for the reduction of bone loss in postmenopausal osteoporosis: a review. 2011

Bridgeman, Mary Barna / Pathak, Rolee. ·Ernest Mario School of Pharmacy, Rutgers University, Piscataway, New Jersey. ·Clin Ther · Pubmed #22108301.

ABSTRACT: BACKGROUND: Osteoporosis is a prevalent condition that may lead to increased risks for bone fracture and other morbidities and increased health care costs. Treatment modalities for osteoporosis aim to prevent further bone loss and to reduce the risk for fracture. Denosumab is a human monoclonal antibody developed for use in osteoporosis. It inhibits the receptor activator of nuclear factor κB ligand, a cytokine that mediates osteoclast-mediated bone resorption. OBJECTIVE: The intent of this article was to review the clinical pharmacology, pharmacokinetic and pharmacodynamic properties, efficacy, and tolerability of denosumab in the prevention and treatment of postmenopausal osteoporosis. METHODS: The MEDLINE and MEDLINE In-Process & Other Non-Indexed Citations databases were searched for English-language reviews, abstracts, presentations, and clinical trials of denosumab in humans, published from 1995 through July 2011. Search terms included denosumab, osteoporosis, RANK ligand, and bone resorption. Available data were evaluated, and relevant clinical data were selected for inclusion. RESULTS: Three Phase II and 4 Phase III studies that evaluated the efficacy of denosumab in postmenopausal women were identified. In a Phase III study, the percentage change from baseline in bone mineral density (BMD) was significantly greater with denosumab compared with placebo (+6.5% vs -0.6%, respectively; P < 0.0001). In another Phase III trial, the cumulative prevalence of vertebral fractures was significantly lower with denosumab compared with placebo (2.3% vs 7.2%; 95% CI, 0.26-0.41; P < 0.001). Denosumab treatment was associated with significantly greater changes in BMD at the total hip (+4.5% vs +3.4%; P < 0.0001) and distal radius (+1.1% vs +0.6%; P = 0.0001) compared with alendronate. Adverse events reported with the use of denosumab have included back pain (34.7%); pain in the extremities (11.7%); general musculoskeletal pain (7.6%); elevated cholesterol (7.2%); inflammation of the bladder (5.9%); and dermatologic conditions including dermatitis, eczema, and rashes (combined prevalence, 10.8%). Serious adverse events have included hypocalcemia (1.7%), pancreatitis (0.2%), and severe infection (0.2%). Several cases of osteonecrosis of the jaw have also been reported. CONCLUSIONS: Based on the data from the available literature, denosumab is an efficacious and well-tolerated treatment for postmenopausal osteoporosis.

20 Review A model for the pathogenesis of bisphosphonate-associated osteonecrosis of the jaw and teriparatide's potential role in its resolution. 2011

Subramanian, Gayathri / Cohen, Harold V / Quek, Samuel Y P. ·PGY1, General Practice Residency Program, New Jersey Dental School-UMDNJ, Newark, NJ 07101, USA. ·Oral Surg Oral Med Oral Pathol Oral Radiol Endod · Pubmed #21821444.

ABSTRACT: OBJECTIVE: The objective of this study was to present a comprehensive model for the pathogenesis of bisphosphonate-associated osteonecrosis of the jaw (BON). STUDY DESIGN: Review of PubMed literature relevant to BON, bisphosphonates (BPs), and bone remodeling. RESULTS: Six case reports of spontaneous resolution of BON lesions following administration of teriparatide (Forteo; Eli Lilly and Co., Indianapolis, IN) were identified. These reports suggest that osteoanabolic therapies may hold promise in BON management. Here we propose that BON pathogenesis is multifactorial and is the combined result of attenuated osteoblastic activity (owing to the patient's underlying disease, e.g., osteoporosis or multiple myeloma), BP-mediated osteoclast toxicity, and the resultant compromised osteoblast-osteoclast interactions during bone remodeling. Consequently, a vicious cycle of ineffective local remodeling results in the persistence of defective bone, compromised tissue perfusion, and if unresolved, ultimately leads to necrosis. CONCLUSIONS: Our model for BON pathogenesis advocates for earlier therapeutic intervention in BON. The biological rationale for teriparatide's efficacy in BON justifies further investigation.

21 Review Identification, diagnosis, and prevention of osteoporosis. 2011

Levine, Jeffrey P. ·Department of Family Medicine and Community Health, UMDNJ-Robert Wood Johnson Medical School, One Robert Wood Johnson Place, CN 19, New Brunswick, NJ 08903-0019, USA. levinejp@umdnj.edu ·Am J Manag Care · Pubmed #21761956.

ABSTRACT: Prevention of osteoporotic fractures is of major importance from a public health perspective. Despite the large burden the disease exacts on individuals and society, not all patients with osteoporosis receive optimal treatment. Since only 1 in 3 patients with osteoporosis is diagnosed, clinicians need to improve their ability to identify patients who are candidates for bone mineral density (BMD) screening. Although limited data exist about the direct correlation between effective screening and fracture morbidity and mortality, it has been proved that increases in fractures are associated with increases in morbidity and mortality. Therefore, identifying patients at risk, making a timely diagnosis, implementing prevention measures (ie, calcium, vitamin D, exercise, fall precautions, etc), and initiating pharmacologic therapy for appropriate patients can all help to minimize fracture risk.

22 Review Nitric oxide and bone. 2010

Wimalawansa, Sunil J. ·Department of Medicine, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ, USA. wimalasu@umdnj.edu ·Ann N Y Acad Sci · Pubmed #20392265.

ABSTRACT: Age-associated decrease in nitric oxide (NO) production may be related to an increase in cardiovascular events, sexual dysfunction, and osteoporosis. Relative NO deficiency is a plausible biological basis for NO replacement therapy. Hormone replacement therapy (HRT) enhances local NO production and rectifies NO deficiency in postmenopausal women. However, excess local production of NO aggravates bone destruction in inflammatory arthropathies. In addition to its use in alleviating angina and erectile dysfunction, NO compounds could be a valuable supplemental therapy for chronic conditions including osteoporosis. Estrogen mediates its beneficial effects in bone, in part via the NO/cGMP pathway; hence NO donor therapy is an alternative to estrogen, estrogen agonists-antagonists, and androgen receptor modulator therapy in the prevention and treatment of osteoporosis. Large numbers of animal studies and human pilot studies support the concept of using NO donors for preventing bone loss. Administration of exogenous NO or prolonging endogenous NO activity are practical ways to supplement NO.

23 Review Bisphosphonate-associated osteomyelitis of the jaw: guidelines for practicing clinicians. 2008

Wimalawansa, Sunil J. ·Division of Endocrinology, Metabolism & Nutrition, Department of Medicine, Robert Wood Johnson Medical School, University of Medicine & Dentistry of New Jersey, New Brunswick, New Jersey 08903-0019, USA. wimalasu@umdnj.edu ·Endocr Pract · Pubmed #19158055.

ABSTRACT: OBJECTIVE: To evaluate the literature and discuss the risk factors, mechanisms, pathophysiologic aspects, and recommended management of bisphosphonate-associated osteomyelitis of the jaw (BAOMJ). METHODS: More than 350 published articles, case reports mentioning BAOMJ, and independent histology slides from BAOMJ lesions were reviewed critically. The most pertinent publications are cited and discussed. RESULTS: The incidence of BAOMJ increases after extraction of teeth, dentoalveolar surgical procedures, or recent oral trauma leading to exposed maxillary or mandibular bone. Contributory factors include poor oral hygiene, oral infections, periodontal disease; recent or ongoing corticosteroid administration or chemotherapy; compromised immune status; diabetes or vascular insufficiency; old age; chronic diseases; and malignancies. On average, 1 of every 100,000 patients treated with bisphosphonates orally for osteoporosis or Paget disease of bone may develop BAOMJ-like lesions. Patients with cancer often receive bisphosphonate doses 10 times or higher, and also more frequently, than those used in patients with osteoporosis or Paget disease of bone. Therefore, greater frequency of administration of bisphosphonates, higher dosages, and prolonged use (that is, for more than 2 years) are likely to be factors triggering BAOMJ. CONCLUSION: The association of bisphosphonate therapy with BAOMJ is rare in noncancer patients and is likely to be a class effect that may occur with use of any bisphosphonate. Whether patients with cancer require such a high frequency of intravenously administered bisphosphonates needs to be investigated. Following established guidelines can decrease the risks of BAOMJ in vulnerable patients. Rather than necrotic bone, current evidence supports an infectious and perhaps immunologic underlying cause for BAOMJ. The estimated incidence of BAOMJ among noncancer patients receiving bisphosphonates is about 0.001%, whereas among patients with cancer receiving intravenous bisphosphonate therapy the incidence is between 0.5% and 4%, depending on the dose, frequency, and duration of therapy (on average, approximately 2%). Nevertheless, the benefits of bisphosphonates far outweigh the risks.

24 Review Celecoxib, NSAIDs and the skeleton. 2008

O'Connor, J Patrick / Lysz, Thomas. ·UMDNJ-New Jersey Medical School, Newark, New Jersey 07103, USA. oconnojp@umdnj.edu ·Drugs Today (Barc) · Pubmed #19137124.

ABSTRACT: Treating acute and chronic musculoskeletal pain is essential for improving healing of traumatic injuries and surgical procedures, and for improving patient quality of life. Physicians are limited primarily to treating musculoskeletal pain with nonsteroidal antiinflammatory drugs (NSAIDs), cyclooxygenase type 2 (COX-2)-selective NSAIDs such as celecoxib, or narcotics. Patients often treat their pain with over-the-counter NSAIDs. Unlike narcotics that target the central nervous system to alleviate pain, NSAIDs inhibit cyclooxygenase activity within the central nervous system and at the peripheral pain site to prevent the conversion of arachidonic acid into prostaglandins. Thus, NSAID use can and does alter certain fundamental processes involved in the normal healing of injured tissues. Cyclooxygenase activity and prostaglandin signaling are critical regulators of normal skeletal metabolism and inflammation related to injury or disease. Since most people only use NSAIDs sporadically to treat pain, few data indicate that short-term or repeated occasional use of NSAIDs is deleterious to skeletal health. However, clinical data suggest that chronic use of celecoxib, may impair normal skeletal function leading to decreased bone mineral density in older male patients. Experimental studies also have documented the negative effects of NSAIDs on healing of skeletal tissues. Fracture healing and tendon-to-bone healing appear to be particularly susceptible to inhibition by celecoxib. Limited retrospective clinical data tends to support the experimental data that COX-2 function is critical for normal bone healing. In contrast, NSAID use and perhaps COX-2-selective NSAID use may be beneficial for healing of other skeletal injuries. In particular, NSAID use does not appear to have a long-term negative effect on the ultimate healing of tendons and ligaments. Indeed, NSAID therapy may inhibit adhesion formation during tendon healing, which leads to a better functional recovery. Certainly, NSAID therapy following acetabular fractures, other hip fractures, or following hip replacement surgery is beneficial for reducing heterotopic ossification that can limit joint mobility. The effects of NSAID or celecoxib therapy on healing of other skeletal tissues is less clear. For instance, clinical data indicates that celecoxib therapy does not impair spinal fusion but experimental data indicates the opposite. Similarly, some reports suggest that NSAID therapy may prevent further erosion of cartilage in certain arthritic conditions while other reports indicate that NSAID treatment will exacerbate cartilage damage. The difference in effects caused by NSAID or celecoxib therapy likely relate to the role cyclooxygenase has in the biology of the injured tissue or its healing response. Differences in pharmacology between NSAIDs, treatment regimens, experimental models and potential off-target effects also may confuse many of these issues. It is clear, however, that cyclooxygenase activity is involved in the healing of many skeletal tissues, either directly or indirectly through modulation of the inflammatory response. Consequently, pharmacological manipulation of cyclooxygenase using NSAIDs or celecoxib can profoundly affect skeletal health.

25 Review Nitric oxide: novel therapy for osteoporosis. 2008

Wimalawansa, Sunil J. ·Regional Osteoporosis Center, Division of Endocrinology, Metabolism and Nutrition, Department of Medicine, Robert Wood Johnson Medical School, New Brunswick, NJ 08903, USA. wimalasu@umdnj.edu ·Expert Opin Pharmacother · Pubmed #19006476.

ABSTRACT: BACKGROUND: Relative nitric oxide (NO) deficiency is responsible for many pathophysiological processes, including in postmenopausal women providing a plausible biological basis for use of NO replacement therapy in humans. Excess or inappropriate local production of NO aggravates bone destruction in some diseases such as septic shock, rheumatoid and other inflammatory arthropathies. RESULTS: A variety of in vitro and in vivo data have revealed the efficacy of nitroglycerin and nitrates on bone cells. Since some part of the beneficial effects of estrogen on bone is mediated via the NO-cGMP pathway, NO donor therapy is an attractive alternative to estrogen therapy to prevent and treat osteoporosis. When the body cannot generate adequate amounts of NO for biological homeostasis, administration of exogenous NO or prolongation of the actions of endogenous NO are practical ways to supplement NO, especially in postmenopausal women. CONCLUSION: Postmenopausal NO deficiency is rectified with hormone replacement therapy, which enhances local production of NO. Declining local NO production secondary to estrogen deficiency in postmenopausal women, and perhaps in older men, could be one of the key reasons for age-related increased incidences of cardiovascular events, sexual dysfunction as well as osteoporosis. Thus, in addition to supplementation of NO compounds in acute situations such as alleviating angina and erectile dysfunction, it could be a valuable addition to the armamentarium of therapies for chronic conditions such as osteoporosis.