Introduction Cutaneous leishmaniasis is endemic in Sri Lanka. The immunopathogenesis of these lesions in Sri Lankans has not been documented. Objectives To classify skin lesions into histological groups, to assess parasitic load, density of each inflammatory cell type and necrosis and to characterise the lymphocytic reaction in cutaneous leishmaniasis in comparison to leprosy. Methods Skin biopsies from 31 patients with demonstrable amastigotes in smears or tissue sections were studied. The lesions were classified by two independent observers into four distinct histological groups based on different cell types in the inflammatory infiltrate and formation of granulomata. Parasitic load and the presence of necrosis were recorded. Immunohistochemical staining for CD45RO and CD20 for counting T and B cells respectively was done. Results Histological groups of cutaneous leishmaniasis ranging from group I-IV were similar to that of the spectrum in leprosy ranging from lepromatous to tuberculoid leprosy. The histological groups from I-IV showed a significant inverse relationship with the mean parasitic index. Necrosis was not a prominent feature. The mean percentage of T cells in the histological spectrum from group I-IV in leishmaniasis was similar to the spectrum from lepromatous to tuberculoid leprosy. Mean percentage of T cells were 20.1% in group I, 20.5% in group II, 33.8% in group III and 47.8% in group IV. Lepromatous, borderline tuberculoid and tuberculoid leprosy had 21.3%, 33.4% and 48.0% T cells respectively. Conclusion Cutaneous leishmaniasis is a spectral disease similar to leprosy. The mean percentage T cells from group I-IV were similar to those in the spectrum of leprosy and mean percentage B cells varied in a narrow range.

Because the majority of ST can lead to malocclusion, especially in mixed dentition, awareness, early detection, and timely clinical intervention of ST are recommended.

No abstract

Amelogenesis imperfecta (AI) is a hereditary disorder which alters the enamel formation of the teeth by exhibiting the changes in quality and quantity of the enamel. The varieties of clinical presentations range from hypoplastic, hypomaturation to hypocalcified with the combination of different genetic mutations. It can present in both deciduous and permanent dentitions. The diagnosis of AI depends on clinico-pathological correlation by excluding other structural disorders of enamel such as fluorosis and chronological hypoplasia. Therefore, the knowledge of AI is related to its clinical features, radiological and histological findings, genetic mutations and treatment options are utmost important during the management of AI. The following review article will address the diagnostic and management perspectives of AI.

No abstract