Implications for pathogenesis of patterns of injury in small- and medium-sized-vessel vasculitis.

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Abstract
The different pathologic features of different types of necrotizing vasculitis indicate that there are different pathogenic mechanisms causing the injury. The pathogenic mechanisms for medium-sized-vessel vasculitis are most effective at causing injury in arteries and are not effective at causing injury in smaller vessels. The predilection of medium-sized-vessel vasculitis for bifurcations may relate to the increased expression of adhesion molecules and increased numbers of intimal macrophages at these sites. The preferential involvement of small vessels by small-vessel vasculitis may relate to the requirement for close apposition between leukocytes and endothelial cells for the pathogenic mechanisms to be operational. The pathology of the necrotizing vasculitis of Kawasaki disease is most consistent with a primary role for monocytes/macrophages and T lymphocytes in the acute injury. The pathology of the necrotizing vasculitis of polyarteritis nodosa and small-vessel vasculitis, including ANCA-vasculitis, is most consistent with a primary role for neutrophils and monocytes in the acute injury.

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