Osteopenia | EPFL Graph Search

Are you an EPFL student looking for a semester project?

Work with us on data science and visualisation projects, and deploy your project as an app on top of GraphSearch.

Osteopenia, known as "low bone mass" or "low bone density", is a condition in which bone mineral density is low. Because their bones are weaker, people with osteopenia may have a higher risk of fractures, and some people may go on to develop osteoporosis. In 2010, 43 million older adults in the US had osteopenia. Unlike osteoporosis, osteopenia does not usually cause symptoms, and losing bone density in itself does not cause pain. There is no single cause for osteopenia, although there are several risk factors, including modifiable (behavioral, including dietary and use of certain drugs) and non-modifiable (for instance, loss of bone mass with age). For people with risk factors, screening via a DXA scanner may help to detect the development and progression of low bone density. Prevention of low bone density may begin early in life and includes a healthy diet and weight-bearing exercise, as well as avoidance of tobacco and alcohol. The treatment of osteopenia is controversial: non-pharmaceutical treatment involves preserving existing bone mass via healthy behaviors (dietary modification, weight-bearing exercise, avoidance or cessation of smoking or heavy alcohol use). Pharmaceutical treatment for osteopenia, including bisphosphonates and other medications, may be considered in certain cases but is not without risks. Overall, treatment decisions should be guided by considering each patient's constellation of risk factors for fractures. Many divide risk factors for osteopenia into fixed (non-changeable) and modifiable factors. Osteopenia can also be secondary to other diseases. An incomplete list of risk factors: Age: bone density peaks at age 35, and then decreases. Bone density loss occurs in both men and women Ethnicity: European and Asian people have increased risk Sex: women are at higher risk, particularly those with early menopause Family history: low bone mass in the family increases risk Tobacco use Alcohol use Inactivity – particularly lack of weight-bearing or resistance activities Insufficient caloric intake – osteopenia can be connected to female athlete triad syndrome, which occurs in female athletes as a combination of energy deficiency, menstrual irregularities, and low bone mineral density.

About this result

This page is automatically generated and may contain information that is not correct, complete, up-to-date, or relevant to your search query. The same applies to every other page on this website. Please make sure to verify the information with EPFL's official sources.

Related publications (1)

Related concepts (15)

Related lectures (16)

Osteopenia

Estrogen (medication)

An estrogen (E) is a type of medication which is used most commonly in hormonal birth control and menopausal hormone therapy, and as part of feminizing hormone therapy for transgender women. They can also be used in the treatment of hormone-sensitive cancers like breast cancer and prostate cancer and for various other indications. Estrogens are used alone or in combination with progestogens. They are available in a wide variety of formulations and for use by many different routes of administration.

Hormone replacement therapy

Hormone replacement therapy (HRT), also known as menopausal hormone therapy or postmenopausal hormone therapy, is a form of hormone therapy used to treat symptoms associated with female menopause. These symptoms can include hot flashes, vaginal atrophy, accelerated skin aging, vaginal dryness, decreased muscle mass, sexual dysfunction, and bone loss or osteoporosis. They are in large part related to the diminished levels of sex hormones that occur during menopause. Estrogens and progestogens are the main hormone drugs used in HRT.

Effect of Patient Diversity on Inverted Pertrochanteric Fracture Treatment ME-314: Concurrent engineering project

Explores the impact of patient diversity on the treatment of inverted pertrochanteric fractures.

Osteoporosis Overview BIO-450: Molecular endocrinology

Covers bone remodeling, hormone effects, menopause impact, and osteoporosis treatments.

Bone Mineral Density: Glenoid Thickness Analysis ME-314: Concurrent engineering project

Explores methods to improve glenoid bone mineral density analysis using CT scans.

T Cell Costimulation Molecules CD80/86 Inhibit Osteoclast Differentiation by Inducing the IDO/Tryptophan Pathway

Mario Michael Zaiss, Zhen Chen

Bone resorption is seminal for the physiological remodeling of bone during life. However, this process needs to be strictly controlled; excessive bone resorption results in pathologic bone loss, osteoporosis, and fracture. We describe a control mechanism of bone resorption by the adaptive immune system. CD80/86, a pair of molecules expressed by antigen-presenting cells and involved in T cell costimulation, act as negative regulator for the generation of bone-resorbing osteoclasts. CD80/86-deficient mice were osteopenic because of increased osteoclast differentiation. CD80/86-deficient osteoclasts escaped physiological inhibition by CTLA-4 or regulatory T cells. Mechanistically, engagement of CD80/86 by CTLA-4 induced activation of the enzyme indoleamine 2,3-dioxygenase (IDO) in osteoclast precursors, which degraded tryptophan and promoted apoptosis. Concordantly, IDO-deficient mice also showed an osteopenic bone phenotype with higher numbers of osteoclast precursors and osteoclasts. Also, IDO-deficient mononuclear cells escaped the anti-osteoclastogenic effect of CTLA-4. This molecular mechanism was also present in humans because targeting CD80/86 by abatacept, a CTLA-4-immunoglobulin fusion protein, reduced, whereas blockade of CTLA-4 by ipilimumab antibody enhanced, the frequency of peripheral osteoclast precursors and osteoclastogenesis. In summary, these data show an important role of the adaptive immune system, in particular T cell CD80/86 costimulation molecules, in the physiological regulation of bone resorption and preservation of bone mass, as well as affect the understanding of the function of current and future drugs fostering or blocking the effects of CTLA-4 in humans.

Amer Assoc Advancement Science2014