Langerhans Cells in Feline Foetal Epidermis - Immunohistochemical Study of Spatial Distribution

Langerhans cells belong to the skin-associated lymphatic tissue (SALT). They are antigenpresenting cells derived from monocyte precursors in the bone marrow. The distribution of Langerhans cells was investigated in feline foetuses on day 40 of ontogenesis, in 9 selected body regions: regio intermandibularis, regio axilaris, regio prepubica, regio inguinalis, regio parietalis, regio interdigitalis, regio thoracis, regio sacralis and regio caudalis. Mouse monoclonal antibody against CD1 receptor (epitope CD1a) was applied to localize Langerhans cells in the skin samples. The highest number of Langerhans cells was found in biopsy of the dorsal part of the feline foetuses. Langerhans cells were present particularly among keratinocytes of stratum germinativum (stratum basale and stratum spinosum), scattered or clustered among epidermal cells closing the hair canal in the region close to the hair follicle. Langerhans cells were further located among cells of outer root sheath in the region of hair follicle infundibulum close to ostium of sebaceous glands ductus, some were found also in the upper part of the hair follicle isthmus. Langerhans cells seem to participate in skin disorders related to hypersensitivity and even tumour transformations. Distribution of these cells may play a role in disease predispositions; knowledge of the physiology and pathophysiology of Langerhans cells opens possible targeted treatments in veterinary medicine

Early Regression of the Dental Lamina Underlies the Development of Diphyodont Dentitions

Functional tooth germs in mammals, reptiles, and chondrichthyans are initiated from a dental lamina. The longevity of the lamina plays a role in governing the number of tooth generations. Monophyodont species have no replacement dental lamina, while polyphyodont species have a permanent continuous lamina. In diphyodont species, the dental lamina fragments and regresses after initiation of the second tooth generation. Regression of the lamina seems to be an important mechanism in preventing the further development of replacement teeth. Defects in the complete removal of the lamina lead to cyst formation and has been linked to ameloblastomas. Here, we show the previously unknown mechanisms behind the disappearance of the dental lamina, involving a combination of cell migration, cell-fate transformation, and apoptosis. Lamina regression starts with the loss of the basement membrane, allowing the epithelial cells to break away from the lamina and migrate into the surrounding mesenchyme. Cells deactivate epithelial markers (E-cadherin, cytokeratin), up-regulate Slug and MMP2, and activate mesenchymal markers (vimentin), while residual lamina cells are removed by apoptosis. The uncovering of the processes behind lamina degradation allows us to clarify the evolution of diphyodonty, and provides a mechanism for future manipulation of the number of tooth generations