Microfasciculation: a morphological pattern in leprosy nerve damage.

AIMS: To study Microfasciculation, a perineurial response found in neuropathies, emphasizing its frequency, detailed morphological characteristics and biological significance in pure neural leprosy (PNL), post-treatment leprosy neuropathy (PTLN) and non-leprosy neuropathies (NLN). METHODS AND RESULTS: Morphological characteristics of microfascicles were examined via histological staining methods, immunohistochemical expression of neural markers and transmission electronmicroscopy. The detection of microfasciculation in 18 nerve biopsy specimens [12 PNL, six PTLN but not in the NLN group, was associated strongly with perineurial damage and the presence of a multibacillary inflammatory process in the nerves, particularly in the perineurium. Immunoreactivity to anti-S100 protein, anti-neurofilament, anti-nerve growth receptor and anti-myelin basic protein immunoreactivity was found within microfascicles. Ultrastructural examination of three biopsies showed that fibroblast-perineurial cells were devoid of basement membrane despite perineurial-like NGFr immunoreactivity. Morphological evidence demonstrated that multipotent pericytes from inflammation-activated microvessels could be the origin of fibroblast-perineurial cells. CONCLUSIONS: A microfasciculation pattern was found in 10% of leprosy-affected nerves. The microfascicles were composed predominantly of unmyelinated fibres and denervated Schwann cells (SCs) surrounded by fibroblast-perineurial cells. This pattern was found more frequently in leprosy nerves with acid-fast bacilli (AFB) and perineurial damage while undergoing an inflammatory process. Further experimental studies are necessary to elucidate microfascicle formation.

A quantitative and morphometric study of tryptase-positive mast cells in cutaneous leprosy lesions.

While mast cells are known to induce differences in the matrix structures, microvascular patterns, and immune responses in a number of diseases, the possible role of mast cells in these same processes over the spectrum of leprosy has not yet been investigated. Thus, ascertaining the possible influence of mast cells in the outcome of the anti-leprosy response to Mycobacterium leprae is of major importance. In this study, 51 cutaneous biopsies of leprosy patients were stained with anti-tryptase antibody in order to quantify mast cells in leprosy lesions and compare the number and size of these cells in all the forms of leprosy. Biopsies were grouped according to an adapted Ridley-Jopling clinical-immunological classification (17 T, 17 B and 17 L). It was found that the L (lepromatous leprosy) group had the lowest dermal mast cell density values among the three groups studied. Furthermore, the average mast cell cross-sectional area was significantly higher in the L in comparison to the B (borderline-borderline) and T (tuberculoid) biopsies, suggesting mast cell functional differences within the groups. The higher mast cell density in the T and B groups was considered indirect evidence of the role of mast cells in the activated immune response to M. leprae infection.

The diagnosis of leprosy among patients with symptoms of peripheral neuropathy without cutaneous lesions: a follow-up study

Forty-four patients with neuritic leprosy were individually followed for periods ranging from 4 months to almost 4 years for the purpose of ascertaining the presence and/ or absence of leprosy. The neural symptoms presented were sensory impairment (41), parasthesia (28), nerve enlargement (22), nerve tenderness (20), paresia (20), amyotrophy (8). Leprosy was diagnosed in ten out of the total number of patients studied. Leprosy was confirmed by the appearance of reactional neuritis (4), reversal reaction (2), biopsy of the hypoesthesic area (3) and the appearance of non-reactional cutaneous lesion. We reported an experience in the diagnosis of neuritic leprosy and its most frequent clinical presentation with which clinicians have to be acquainted. We can also state that the clinical follow-up was an effective strategy for the diagnosis of the disease when diagnostic facilities are not available or have not confirmed the diagnosis