Leprosy is a chronic infection caused by an intracellular microorganism. Genetic predisposition to both disease susceptibility and to host immunological response has been postulated for many years. The aim of this study was to determine whether there is HLA-linked susceptibility to leprosy and its different types. HLA-class I (A, B, C) and II (DR, DQ) antigen frequencies in 80 patients with leprosy (35 borderline lepromatous, 25 lepromatous, 15 borderline tuberculoid, five tuberculoid) were compared with those in 120 healthy individuals. HLA-class I antigens A9, A10, A32, B5, B21, Bw4, Bw6, Cw1, Cw2 and HLA-class II antigens DR9, DR10, DRw52, DQ1, DQ3 were found to be significantly more frequent in patients with leprosy, whereas HLA-class I antigens A3, B44, B49 and HLA-class II antigen DQ5 were so in controls. However, there was no significant difference in HLA-class I and II antigen frequencies between subtypes of leprosy. HLA-A null antigen was found to have weak expression in patients with leprosy. In conclusion, factors other than HLA-class I and class II antigens may have a more critical role in the pathophysiology of leprosy infection in man.
Synovial chondromatosis is a rare benign condition arising from the synovial membrane of the joints, synovial sheaths or bursae around the joints. Primary synovial chondromatosis typically affects the large joints in the third to fifth decade of life. The purpose of this case report is to document this rare synovial pathology, which required open synovectomy and debridement to eradicate it. In our case, the biggest sized SOC was 20x19x6 cm, although there were many joint mice. Our case had the biggest SOC ever extracted, which to the best of my knowledge has not been reported earlier.
The histopathological assessment of Oral Lichen Planus (OLP) and oral lichenoid lesions is relatively subjective. The distinguishing criteria established by WHO effectively reproducible when all selection criteria were fulfilling but sometimes fail to provide a reliable diagnosis. The aim of the present study was to evaluate mast cell counts and their distribution among OLP and lichenoid lesions. The density and localization of mast cells was examined in 22 patients with a diagnosis of OLP (11 patients) or oral lichenoid reactions (11 patients) by c-kit/CD117 immunohistochemical and toluidine blue histochemical staining. Data were analyzed using either the Kruskal-Wallis or Mann-Whitney U tests. No significant difference in the total number of mast cells was observed between the two groups (P = 0.599); however, a significant difference was observed in mast cell counts between reticular and junctional zones (P<0.05). The findings of the present study suggest that mast cells play a key role in the pathogenesis of oral inflammation; however, the ability of mast cell measurements to reliably differentiate between lichen planus and other lichenoid mimickers was limited as the number of mast cells was found to be increased in both the conditions.
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