Inflammation appears to have a major role in the development of atherosclerosis. Cyclooxygenase-2 (COX-2) is involved in the inflammatory response via the generation of prostanoids that, in turn, are involved in the production of matrix metalloproteinases (MMPs). This study aimed to investigate atherosclerosis in human aortas for in situ tissue distribution of COX-2, MMPs including MMP-9 and membrane type 1 MMP (MT1-MMP), and tissue inhibitor of metalloproteinase-2 (TIMP-2). Immunohistochemical studies were performed on atherosclerotic lesions of aortas from patients with aortic aneurysms (n = 4) and dissections (n = 3) by using antibodies to COX-2, MMP-9, MT1-MMP, and TIMP-2. Control tissues were obtained from traumatically dissected aortas (n = 2). All specimens from diseased aortas had atherosclerotic lesions ranging from fatty streak to atheromatous plaques. In control, there was no expression of COX-2, MMP-9, and MT1-MMP in all aortic layers. Immunoreactivity for COX-2 was predominantly noted in macrophages and smooth muscle cells (SMCs) of the intima including atherosclerotic plaque itself and the medial layer of the plaque base, as well as in SMCs and endothelial lining of the vasa vasorum in the adventitia. Immunoreactivity for MMP-9 and MT1-MMP was found in the same distribution as that of COX-2. Additionally, the expression of TIMP-2 increased in relation to MMP-9 expression. This study demonstrates that COX-2 is coexpressed with MMP-9 and MT1-MMP, not only by macrophages and SMCs in atherosclerotic lesions, but also in endothelial lining of the vasa vasorum of human aortas. Thus, vascular inflammatory reactions may influence extracellular matrix remodeling by coactivation of MMPs in the development of atherosclerosis and, in turn, the progression of disease.

Advanced atherosclerosis is often associated with dystrophic calcification and remodeling of extracellular matrix of vascular wall. Recently many studies have documented a general relationship between calcification and severity of coronary disease, and discussed the feasibility of electron beam computed tomography for detecting and quantifying the coronary artery calcification in the patients. The present study investigated the expression and the localization of osteopontin, one of noncollagenous bone matrix protein, within the calcified coronary arteries. Autopsy-derived coronary artery specimens were scanned and reconstructed to visualize the pattern of coronary calcification using a novel microscopic computed tomography technique. The localization of the osteopontin were evaluated by immunohistochemial stain with LF7. The present study showed that the pattern of coronary calcification is variable and the expression of osteopontin is localized mainly to calcified lesion. The smooth muscle cells in addition to macrophage expressed osteopontin protein in human coronary atherosclerotic plaques. Soluble osteopontin released near to the sites of vascular calcification may represent an adaptive mechanism aimed at regulating the process of vascular calcification.

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Mesenchymal hamartoma of the chest wall is a rare tumor with about 53 reported cases in the English literature. We reviewed six chest wall mesenchymal hamartomas in four patients, including two cases with multiple lesions, with specific focus on the radiologic and pathologic correlation. All cases occurred in neonates or infants with ages ranging from seven hours to seven months. They were diagnosed with plain chest radiographs (n=6), ultrasonography (n=2), chest CT scan (n=6), whole body bone scan (n=2) and MRI (n=3). All cases except a small one without cystic change showed the typical features of mesenchymal hamartoma radiographically and pathologically. Radiologically they were well-circumscribed masses with solid and cystic components with multiple fluid-fluid levels in association with single or multiple rib destruction or change. The CT scan showed the typical findings of chest wall hamartoma, and the MR showed heterogeneous signal intensities of the mass on T1- and T2-weighted images. The MR also revealed more concisely a secondary aneurysmal bone cyst formation with multiple fluid-fluid levels on the T2-weighted image. Microscopically, they showed alternating areas of cartilaginous islands and primitive appearing mesenchymal proliferation, which corresponded well with the solid component on the radiologic findings. The areas of bone formation and blood-filled cystic spaces matched the calcified or ossified densities and the cystic components, respectively. A small case without cystic change showed peculiar radiological and pathological findings resembling an osteochondroma. In conclusion, mesenchymal hamartoma of the chest wall in infancy is quite rare and sometimes can be misdiagnosed as malignancy due to the bone-destroying radiographic appearance and the highly cellular and mitotically active microscopic features, unless the radiologists and pathologists are aware of the characteristic clinical, radiological, and pathological findings. Imaging studies can usually make a correct diagnosis with good correlation to the pathologic findings.