Mesenchymal stem cells (MSCs) are often known to have a therapeutic potential in the cell-mediated repair for fatal or incurable diseases. In this study, canine umbilical cord MSCs (cUC-MSCs) were isolated from umbilical cord matrix (n = 3) and subjected to proliferative culture for 5 consecutive passages. The cells at each passage were characterized for multipotent MSC properties such as proliferation kinetics, expression patterns of MSC surface markers and self-renewal associated markers, and chondrogenic differentiation. In results, the proliferation of the cells as determined by the cumulative population doubling level was observed at its peak on passage 3 and stopped after passage 5, whereas cell doubling time dramatically increased after passage 4. Expression of MSC surface markers (CD44, CD54, CD61, CD80, CD90 and Flk-1), molecule (HMGA2) and pluripotent markers (sox2, nanog) associated with self-renewal was negatively correlated with the number of passages. However, MSC surface marker (CD105) and pluripotent marker (Oct3/4) decreased with increasing the number of subpassage. cUC-MSCs at passage 1 to 5 underwent chondrogenesis under specific culture conditions, but percentage of chondrogenic differentiation decreased with increasing the number of subpassage. Collectively, the present study suggested that sequential subpassage could affect multipotent properties of cUC-MSCs and needs to be addressed before clinical applications.

An ultrastructural study was carried out to investigate the nature of an eosinophilic material, having the staining properties of amyloid, in a case of calcifying epithelial odontogenic tumour. At the electron‐microscopical level, the eosinophilic masses consisted of two types of structure which are probably related. The first type appeared as sheets of fine filaments measuring 10–12 nm in diameter. The second type was in the form of aggregates of lamina densa fragments, probably secreted by the tumour epithelium. These fragments appeared to undergo some loss of electron density and became degraded into fine filaments, having similar thickness and electron density to those forming the filamentous masses. It is concluded from this study that the fine filamentous material is a form of amyloid which results from degradation of lamina densa material.