We performed a systematic literature review to summarize the underlying pathogenic mechanisms by which adipokines influence rheumatological diseases and the resulting clinical manifestations. Increasing evidence display that numerous adipokines may significantly influence the development or clinical course of various rheumatological diseases. Despite the normal anti- or pro-inflammatory role of the cytokines, the serum level varies enormously in various rheumatological diseases. The expression of high levels of pro-inflammatory cytokines such as leptin or visfatin, respectively in systemic lupus erythematosus and in rheumatoid arthritis, represents a negative prognostic factor; other adipokines such as adiponectin, broadly known for their anti-inflammatory effects, showed a correlation with disease activity in rheumatoid arthritis. In the near future pro-inflammatory cytokines may represent a potential therapeutic target to restrain the severity of rheumatological diseases. Further studies on adipokines may provide important information on the pathogenesis of these diseases, which are not yet fully understood. The mechanisms by which adipokines induce, worsen, or suppress inflammatory and degenerative musculoskeletal pathologies and their clinical significance will be discussed in this review.

Objective and design Recently, many studies have shown that the biologically active form of vitamin D-1,25(OH) 2 D-is involved in many biological processes, including immune system modulation, and patients affected by various autoimmune diseases, such as connective tissue diseases (CTD), showed low levels of vitamin D. It is not clear if vitamin D deficiency is involved in the pathogenesis of autoimmune diseases or it is a consequence. Material We carried out a review of literature to summarize the existing connections between 25-OH vitamin D and CTD. Methods We searched for articles on PubMed by keywords: vitamin D, connective tissue diseases, systemic lupus erythematosus, Sjogren's syndrome, systemic sclerosis, undifferentiated connective tissue disease. Results The relationship between vitamin D and CTD is still not very clear, despite many studies having been performed and some data suggest a connection between these diseases and 25-OH vitamin D levels. Conclusions The limitations of the study, such as the heterogeneity of patients, methods used to measure vitamin D serum concentration and other biases, do not lead to unequivocal results to demonstrate a direct link between low vitamin D serum levels and autoimmune diseases. Further studies are needed to resolve conflicting results.

Abstract:: We performed a review of the available literature in order to summarize the pathogenic and clinical connections between HIV infection and rheumatological syndromes. The increasing life expectancy during human immunodeficiency virus (HIV) infection has led to the observation of many rheumatological manifestations over the years in this type of patients. Although the pathological mechanisms are still not fully understood, several rheumatological diseases have been more commonly observed than in the general population especially after the advent of highly active antiretroviral therapy (HAART) and sometimes clinical and serological findings are influenced by the underlying condition which define a characteristic onset or development of the disease. Autoimmune diseases occur during specific stages of the HIV infection, depending on the underlying pathogenic mechanism being mainly influenced by the CD4+ cells count. Several rheumatological diseases show peculiar clinical manifestations influenced by the underlying HIV infection leading to specific features less commonly observed in healthy population. Conversely to pathological findings, broadly HIV-1-neutralizing antibodies (BnAb) observed in several autoimmune diseases such as SLE, could exert a protective part against HIV infection. It is important to evaluate the onset of autoimmune diseases in HIV patients, in order to start the appropriate treatment to avoid harmful events. More studies are needed to enlighten the trend of autoimmune diseases during HIV infection. Pathogenic mechanisms and clinical manifestations of rheumatological diseases during HIV infection will be discussed in this review.

A review of the available literature was performed in order to summarize the existing evidence between osteoblast dysfunction and clinical features in non-hereditary sclerosing bone diseases. It has been known that proliferation and migration of osteoblasts are concerted by soluble factors such as fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), transforming growth factor (TGF), bone morphogenetic protein (BMP) but also by signal transduction cascades such as Wnt signaling pathway. Protein kinases play also a leading role in triggering the activation of osteoblasts in this group of diseases. Post-zygotic changes in mitogen-activated protein kinase (MAPK) have been shown to be associated with sporadic cases of Melorheostosis. Serum levels of FGF and PDGF have been shown to be increased in myelofibrosis, although studies focusing on Sphingosine-1-phosphate receptor was shown to be strongly expressed in Paget disease of the bone, which may partially explain the osteoblastic hyperactivity during this condition. Pathophysiological mechanisms of osteoblasts in osteoblastic metastases have been studied much more thoroughly than in rare sclerosing syndromes: striking cellular mechanisms such as osteomimicry or complex intercellular signaling alterations have been described. Further research is needed to describe pathological mechanisms by which rare sclerosing non hereditary diseases lead to osteoblast dysfunction.