Langerhans cell histiocytosis of the jaws: A report of ten cases with an analysis of the mechanism of eosinophilic infiltration Y. Objective: Langerhans cell histiocytosis (LCH) frequently presents eosinophilic infiltration. Here we report ten cases of LCH that involved the jaws and our investigation of the mechanism underlying eosinophilic infiltration in LCH. Method: We evaluated the CCL-11/eotaxin-1 expression of LCH cells via immunohistochemical staining. Toluidine blue staining was used to inspect the densities of mast cells, with ten periapical granuloma specimens serving as a control group. Results: Every patient was classified as having single-system LCH, even though acute lymphoblastic leukemia occurred in one patient during LCH treatment. The ratio of mandible to maxilla LCH was 5:1. The jaw lesions were the earliest manifestation in seven patients with multifocal LCH. Toluidine blue staining revealed that the number of mast cells in LCH lesions was not significantly higher than in periapical granulomas. However, upon immunohistochemical examination, most of the patients showed diffuse positivity for eotaxin-1 in LCH cells, while few eosinophils/ T cells were immunoreactive. Conclusion: We surmise that the eotaxin-1 expression of LCH cells may be relevant to eosinophilic infiltration in LCH. Further studies of the eotaxin-1 functions including its influence on the immature state of LCH cells may be needed to understand the pathogenesis of LCH as well as the role of tissue eosinophilia in LCH. Method: We report a case of SANT in 53 years-old man presented with abdominal discomfort and pain in a left lumbal region. Abdominal computed tomography scan revealed a massive haematoma extended from spleen to the enlarged left kidney and left retroperitoneal space. The patient also had a spontaneous rupture of right kidney 2 years ago. Results: Macroscopically, the cut surface of spleen showed multiple well circumscribed red brown nodules. Microscopically, SANT consists of multiple well-circumscribed angiomatoid nodules showing plump endothelial cells and extravasated erythrocytes. Nodular formations are surrounded by a variable lymphoplasmacytic infiltrate, spindle cells and collagenous stroma. Immunohistochemical staining displayed endothelial phenotype that resembled splenic capillaries (CD34+/CD31+/CD8−). Expression of CD68 was also present. Conclusion: The differential diagnosis of SANT includes splenic hamartoma, inflammatory myofibroblastic tumor, littoral cell angioma and hemangioendothelioma. It has been postulated that SANT represents a peculiar hamartomatous transformation of splenic red pulp in response to an exaggerated nonneoplastic stromal proliferation. SANT has a benign clinical course and splenectomy has been supposed as curative.