Histological reassessment of the role of bridging fibrosis in the angioarchitectural features associated with lobular distortion of the liver in chronic viral hepatitis

Abstract

Aim:To reassess the role of bridging fibrosis in the lobular distortion of the liver from an angioarchitectural aspect.Methods: Two tissue samples obtained from surgically resected livers with chronic hepatitis and one obtained from an autopsy case with chronic hepatitis were used for the threedimensional observation of angioarchitecture by histological reconstruction.Results: Samples showed bridging fibrosis with various degrees of severity, without cirrhotic changes. Two different types of portal-portal bridging fibrosis were found. In our samples, the type that developed in the bifurcation region of the portal tracts was more common than the type observed between the distal portions originating from different parent portal tracts. The angioarchitecture tended to be generally maintained in these lesions. Concerning portal-central bridging fibrosis, two types were observed. One type developed in the lesion with partial paucity of the third-step portal branches in the portal tract at a relatively early stage of chronic hepatitis. The other type developed in an advanced lesion with a complete loss of the normal angioarchitecture of the parenchymal portion of the portal veins. The former was likely developed after largescale necrosis, such as bridging necrosis, while the latter was presumed to be attributable to portal vein damage associated with long standing chronic inflammation. Conclusion:As has been previously noted regarding lobular angioarchitecture, portal-central bridging fibrosis clearly affects the lobular structure of the liver more than portal-portal bridging fibrosis. Therefore, portal vein damage may be a critical event in the eventual distortion of the lobular structure.

The Role of Vascular Injury and Congestion in the Pathogenesis of Cirrhosis: the Congestive Escalator and the Parenchymal Extinction Sequence

“…Difficulty Identifying Destroyed Tissue Elements The early events in chronic liver disease have been difficult to characterize, as we and others [34] have found, largely because the microvasculature is usually destroyed beyond recognition. Three approaches have allowed progress in this field.…”

Histopathologic diagnosis of chronic viral hepatitis

“…Continued necroinflammatory activity at the limiting plate (interface) destroying periportal parenchyma initiates fibrogenesis in CVH and periportal parenchyma is gradually replaced by fibrous tissue leading to stellate enlargement of the portal tracts ( Figure 4A). Portal-portal fibrous septa is the result of linkage of adjacent fibrotic portal tracts [11]. Episodes of severe lobular necroinflammatory activity involving zone 3 ends up with the formation of portal-central fibrous septa (bridging fibrosis) ( Figure 4B) [12,13].…”