Interplay between Hypoxia, Inflammation and Adipocyte Remodeling in the Metabolic Syndrome

Obesity, a major social and health problem in many countries, is due to the accumulation of white adipose tissue in subcutaneous and visceral depots. The discovery of adipocytes capacity of synthesis of numerous adipocytokines and growth factors and the cross talk between adipocytes and cells of the adipose stromo-vascular fraction had highlighted the role of adipose tissue dysfunction in obesity. In visceral obesity the unbalanced synthesis of pro- and anti-inflammatory adipocytokines contributes to the development of the metabolic syndrome which cumulates the factors that increase the risk for ischemic heart disease and cerebral stroke. Adipose tissue accumulation is associated with a state of chronic inflammation, and local hypoxia is considered its underlying cause due to the hypertrophic or/and the hyperplasic growth of the fat pad. Adipose tissue hypoxia is one of the first pathophysiological changes and was placed as a missing link between obesity and low-grade inflammation present in the metabolic syndrome. Hypoxia is a major trigger for adipose tissue remodeling including adipocyte death, inflammation, tissue fibrosis, and angiogenesis. Recently, the role of hypoxia in brown adipose tissue dysfunction, a tissue presumed as the biologic counterbalance of the metabolic disturbances in human obesity, is discussed

Innate Immune Response as a New Challenge in Periodontal Inflammation

Gingivitis and periodontitis are induced by numerous pathogenic microbiota hosted in the subgingival biofilm that first trigger the innate immune response. Innate immune response is part of a homeostatic system which is the first line defence and defines the host inherited resistance to infection. Both genetic and environmental factors are involved in variable individual susceptibility to inflammation of periodontal tissues. That is why, although more than 600 bacterial species have been detected in the periodontal plaque, the type of bacteria incriminated in the development of the inflammation is still unclear. Moreover, in the last decade gene polymorphisms have been largely recognised as important conditions associated with increased susceptibility to periodontal diseases. Manipulating the immune response by the development of drugs that inhibit adverse host reactions and promote beneficial effects might be of therapeutic or prophylactic importance. This work intends to assess the importance of Toll-like receptors as main effectors of the innate immune response in the triggering, maintenance and progression of periodontal inflammation, as well as of the involvement of synthetic molecules targeting TLR signalling pathways in treating periodontal diseases