Likely, this process is multifactorial, including vessel obliteration induced by vasculitis,1,29 killing of macrophages and epithelial cells expressing Leishmania antigen, and tissue injury by the inflammatory response.30–32 It is known that metalloproteinase (MMP) genes are highly expressed in the tissue of CL patients and that monocytes secrete high levels of MMP-9.33–35 MMP expression by macrophages may explain our findings of a direct correlation between macrophages and the area of necrosis in CL throughout the disease. This evidence concerns the gene MMP9 and vasculitis.