Osteoporosis, inflammation and ageing

Osteoporosis is a condition characterized by low bone mass and increased bone fragility, putting patients at risk of fractures, which are major causes of morbidity substantially in older people. Osteoporosis is currently attributed to various endocrine, metabolic and mechanical factors. However, emerging clinical and molecular evidence suggests that inflammation also exerts significant influence on bone turnover, inducing osteoporosis. Numerous proinflammatory cytokines have been implicated in the regulation of osteoblasts and osteoclasts, and a shift towards an activated immune profile has been hypothesized as important risk factor. Chronic inflammation and the immune system remodelling characteristic of ageing, as well as of other pathological conditions commonly associated with osteoporosis, may be determinant pathogenetic factors. The present article will review the current perspectives on the interaction between bone and immune system in the elderly, providing an interpretation of osteoporosis in the light of inflamm-ageing

Pathophysiology of age-related diseases

A Symposium regarding the Pathophysiology of Successful and Unsuccessful Ageing was held in Palermo, Italy on 7-8 April 2009. Three lectures from that Symposium by G. Campisi, L. Ginaldi and F. Licastro are here summarized. Ageing is a complex process which negatively impacts on the development of various bodily systems and its ability to function. A long life in a healthy, vigorous, youthful body has always been one of humanity's greatest dreams. Thus, a better understanding of the pathophysiology of age-related diseases is urgently required to improve our understanding of maintaining good health in the elderly and to program possible therapeutic intervention

Who needs education on LGBTQIA+ healthcare inclusion?

ABSTRACTThe topic of education on healthcare needs and equity of care for LGBTQIA+ populations is an extremely current issue. There is a demand for education on these topics not only from medical and other health sciences students but also from established healthcare professionals. Given this widespread educational deficiency, it is natural to ask whether the teaching class is prepared to satisfy these requests or in turn needs training on these issues and above all whether it is capable of transmitting attention and sensitivity on the issues of inclusion and equality in needs of healthcare

Psoriasis Induced by Anti-Tumor Necrosis Factor Alpha Agents: A Comprehensive Review of the Literature

Tumor necrosis factor alpha inhibitors revolutionized the management of patients affected by autoimmune diseases such as inflammatory bowel diseases, rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis and psoriasis. The biologic agents targeted to blockade TNF-a, like infliximab, adalimumab, certulizumab pegol, etanercept and golimumab have a good safety profile however, with increasing , broader and prolonged use, could expose to an increased risk of adverse reactions included a wide spectrum of dermatological conditions of different etiology and morphology. Among these, of particular interest the development of skin immune-mediated diseases that seem to be the consequence of the paradoxical inflammation induced by anti-TNF-a therapy. The majority of these lesions are identified as psoriasiform with three main morphologies and different frequency: pustular psoriasis, signs of psoriasis and guttate, although among others, with less frequency erythrodermic or inverted psoriasis may be observed.The increased incidence of these dermatological immune-mediated lesions highlight the importance of the skin as a main target of the side effect of anti-TNFa agents, while the immunopathogenetic hypothesis of these paradoxical effects are quite intriguing.The aim of this review is to collect and to analyse  existing knowledge to better understand the pathogenetic mechanism of these complications  and suggest new fields of investigation,  to improve therapeutic strategies of autoimmune diseases and prevent and / or better address such complication.</p

Solar urticaria, a disease with many dark sides: is omalizumab the right therapeutic response? Reflections from a clinical case report

Solar urticaria is a rare type of photodermatosis that significantly reduces the quality of life of the subjects affected, with a risk of anaphylaxis should the entire body be exposed to the sun. Patients are forced to modify and limit their normal activities, and since the symptoms are triggered by exposure to sun, which is difficult if not impossible to avoid in everyday life, a safe and effective therapy appears to be essential

Inflamm-ageing and lifelong antigenic load as major determinants of ageing rate and longevity.

none4noneDe Martinis M; Franceschi C; Monti D; Ginaldi L.De Martinis M; Franceschi C; Monti D; Ginaldi L

Does allergy break bones? Osteoporosis and its connection to allergy

Osteoporosis and allergic diseases are important causes of morbidity, and traditionally their coexistence has been attributed to causality, to independent processes, and they were considered unrelated. However, the increasing knowledge in the field of osteoimmunology and an increasing number of epidemiological and biological studies have provided support to a correlation between bone and allergy that share pathways, cells, cytokines and mediators. If the link between allergic pathology and bone alterations appears more subtle, there are conditions such as mastocytosis and hypereosinophilic or hyper-IgE syndromes characterized by the proliferation of cells or hyper-production of molecules that play a key role in allergies, in which this link is at least clinically more evident, and the diseases are accompanied by frank skeletal involvement, offering multiple speculation cues. The pathophysiological connection of allergy and osteoporosis is currently an intriguing area of research. The aim of this review is to summarize and bring together the current knowledge and pursue an opportunity to stimulate further investigation.SCOPUS: re.jinfo:eu-repo/semantics/publishe