“…Etiopathogenesis of EDS is still unclear; molecular defects affecting the synthesis, structure or function of the fibrillar collagens types I, III, and V have been described in EDS (4,10). The diagnosis is based on clinical features; in fact, there are no pathognomonic laboratory tests and no specific pathologic features in most types (4). The diagnosis is full fit by the presence of one of three major criteria (skin hyperextensibility, tissue fragility, and joint hypermobility), while the presence of one or more minor criteria (smooth, velvety skin, subcutaneous spheroids, recurrent joint dislocations or subluxations, chronic limb or joint pain, positive family history of EDS, muscle hypotonia, easy bruising, functional bowel disorders, [functional gastritis and/or irritable bowel syndrome], high, narrow palate, dental crowding, and neurally-mediated hypotension or postural orthostatic tachycardia) is necessary to distinguish a specific type of EDS (4,11,12).…”