Aortic dissection is an age-dependent life-threatening cardiovascular disease with high mortality rates. Recent research has shown that inflammation plays an important role in aortic dissection. Inflammatory cells, such as lymphocytes and macrophages, not only increase the expression of proteases and cell adhesion molecules but also release reactive oxygen species. These cells also contribute to apoptosis of smooth muscle cells in the aortic artery, and finally lead to medial degradation. This process has been considered to be the principal mechanism for aortic dissection. Furthermore, changes in systemic inflammatory biomarkers are associated with acute-phase reactions and complications in aortic dissection. These biomarkers are also used to predict the prognosis of aortic dissection and to distinguish acute aortic dissection from other chest pain diseases. In addition, elevated inflammatory cell activity in aortic wall, identified by positron emission tomography/computed tomography, is associated with serious clinical symptoms and leads to a poor clinical outcome in aortic dissection. Such observations may provide us with new sights into the mechanism of aortic dissection. In this review, we discuss the role of inflammation in the development and progression of aortic dissection. Understanding this inflammatory process may provide us with new strategies for pharmacological treatment of aortic dissection.