Ultrastructural changes in blood vessels of peripheral nerves in leprosy neuropathy. II. Borderline, borderline-lepromatous and lepromatous leprosy patients

Abstract

The ultrastructure of blood vessels in endo-, peri- and epineurium was studied in peripheral cutaneous nerve biopsies of 16 borderline (BB), borderline-lepromatous (BL) or lepromatous (LL) leprosy patients some of whom were in reversal reaction. Comparable vessels in nerve biopsies of control cases and vessels in skin lesion biopsises of the leprosy patients were also studied. Vascular changes were found in nerves of all the leprosy patients. The changes were pronounced in endoneurial vessels and affected 1. endothelial continuity and surface structure, 2. basement membranes of endothelium and pericytes, and 3. the vessel lumen. In addition, intra-endothelial (IE)Mycobacterium leprae were a feature in some of the patients. Gaps occurring between endothelial cells and plasma insudation both noticed in vessels of fascicles with early to very early neuropathy suggested extensive leakage which, in all probability, causes early nerve fibre damage. Luminal and abluminal endothelial protrusions, which were frequently observed, may enhance transendothelial transport. Fenestrations and endothelial attenuation, possibly, lead to an increase in vascular permeability. Endothelial phagocytotic activity, particularly in small (epineurial) arteries, appeared to be stimulated, possibly, by circulatingM. leprae. Basement membrane multilayering (a “hyaline zone”) was found peripherally to pericytes, as is the case in tuberculoid leprosy (Boddingius, 1976). In a number of patients, multilayering occurred also peri-endothelially. Perivascular zones, which are thought to initiate or aggravate neuropathological changes by impairment of diffusion of oxygen and nutrients or metabolites, were very wide in endoneurial vessels of patients in reversal reaction and this suggested an immunological aetiology. Partial or total vessel lumen occlusion, seen in advanced lepromatous neuropathy, most likely contributes to final nerve fibre degeneration and endoneurial fibrosis. M. leprae were found intra-endothelially in endoneurial vessels, though only in fascicles with advanced neuropathy whereas bacilli were not seen in vessel lumina. By contrast, in fascicles with relatively early neuropathy, solid (viable) bacilli were frequently encounteredintra-axomally in myelinated fibres. This suggests that, in many instances, primary infiltration ofM. leprae into nerve fascicles may arise from intra-axonal (IA) bacilli which ascend from dermal nerves and are released within main nerve trunks after demyelination of the host fibre.