E-Mail Alert

Add your e-mail address to receive forthcoming issues of this journal:

Journal Browser

Journal Browser

Special Issue "Pain in Osteoporosis: From Pathophysiology to a Therapeutic Approach"

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Endocrinology & Metabolism".

Deadline for manuscript submissions: 1 November 2019

Special Issue Editor

Guest Editor
Dr. Daniela Merlotti

Researcher, Department of Medicine Surgery and Neurosciences, University of Siena, Italy
E-Mail
Interests: metabolic bone disorders, osteoporosis, Paget’s disease of bone, rare bone diseases

Special Issue Information

Dear Colleagues,

Osteoporosis (OP) is the most common metabolic bone disease. It has become a major public health problem in many countries due to the increase in life expectancy. It has been estimated that, by the year 2025, more than 30 million women and men aged > 65 years will be affected by osteoporosis in the EU. Fractures occur in patients with OP after low energy traumas, and, particularly, hip fractures may be a significant cause of mortality. Pain, functional loss, social isolation, and emotional disturbances may negatively affect patients’ general well-being and quality of life. Vertebral fractures (VFs) represent a typical finding in patients with osteoporosis, with up to 12% of postmenopausal women having at least one vertebral deformity, most of which are osteoporotic VFs. These women show a higher risk of further vertebral and other osteoporotic fractures, impairing health status. Osteoporotic fractures carry a high social burden, and sites typically include the femoral neck, vertebrae, and distal forearm. Chronic pain, disability, and impaired quality of life secondary to fractures are commonly observed in patients with osteoporosis, leading to increased financial costs. Although osteoporosis is known as a silent disease affecting aging populations, its primary symptom remains pain. Acute pain is reported by patients with osteoporosis-related fractures, but chronic pain, mainly back pain, is also a characteristic of severe osteoporosis. Pain is associated not only with fractures but also with bodily changes in patients with osteoporosis that may include sensory, affective, and cognitive aspects. Chronic pain leads to progressive loss of independence and the need for long-term care, especially in the elderly. Pain prevention is linked to the appropriate treatment of osteoporosis, and pain management in patients with osteoporosis requires a multidimensional approach to preserve and improve quality of life. The present Special Issue aims to the main causes of pain in patients with osteoporosis and suggest possible strategies for its management, treatment, and prevention.

Dr. Daniela Merlotti
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Osteoporosis
  • Musculoskeletal pain
  • Vertebral fractures
  • Sarcopenia
  • Bisphosphonate treatment
  • Pain management
  • Quality of life

Published Papers (1 paper)

View options order results:
result details:
Displaying articles 1-1
Export citation of selected articles as:

Research

Open AccessArticle
Inhibition of Osteoclastogenesis by Thioredoxin-Interacting Protein-Derived Peptide (TN13)
J. Clin. Med. 2019, 8(4), 431; https://doi.org/10.3390/jcm8040431
Received: 21 February 2019 / Revised: 22 March 2019 / Accepted: 27 March 2019 / Published: 29 March 2019
PDF Full-text (1796 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Overactivated osteoclasts lead to many bone diseases, including osteoporosis and rheumatoid arthritis. The p38 MAPK (p38) is an essential regulator of the receptor activator of nuclear factor-κB ligand (RANKL)-mediated osteoclastogenesis and bone loss. We previously reported TAT conjugated thioredoxin-interacting protein-derived peptide (TAT-TN13) as [...] Read more.
Overactivated osteoclasts lead to many bone diseases, including osteoporosis and rheumatoid arthritis. The p38 MAPK (p38) is an essential regulator of the receptor activator of nuclear factor-κB ligand (RANKL)-mediated osteoclastogenesis and bone loss. We previously reported TAT conjugated thioredoxin-interacting protein-derived peptide (TAT-TN13) as an inhibitor of p38 in hematopoietic stem cells (HSCs). Here, we examined the role of TAT-TN13 in the differentiation and function of osteoclasts. TAT-TN13 significantly suppressed RANKL-mediated differentiation of RAW 264.7 cells and bone marrow macrophages (BMMs) into osteoclasts. TAT-TN13 also inhibited the RANKL-induced activation of NF-κB and nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), leading to the decreased expression of osteoclast-specific genes, including tartrate-resistant acid phosphatase (TRAP) and Cathepsin K. Additionally, TAT-TN13 treatment protected bone loss in ovariectomized (OVX) mice. Taken together, these results suggest that TAT-TN13 inhibits osteoclast differentiation by regulating the p38 and NF-κB signaling pathway; thus, it may be a useful agent for preventing or treating osteoporosis. Full article
(This article belongs to the Special Issue Pain in Osteoporosis: From Pathophysiology to a Therapeutic Approach)
Figures

Figure 1

J. Clin. Med. EISSN 2077-0383 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top