To make reproducible diagnoses for oral carcinoma in situ (CIS), combined immunohistochemistry directed at the positioning of squamous cell proliferation (Ki-67) and differentiation (keratin (K) 13 and K19) was used, both of which support histological evaluations by providing biological evidence. Normal/hyperplastic epithelia was defined by K19+ cells only in the first basal layer, K13+ cells in the third basal and upper layers, and sporadic Ki-67+ cells in the second basal layer. These profiles indicated that a proliferating center of the oral epithelium is located in the parabasal cell layer, and K19 and K13 can be regarded as markers for basal and prickle cells, respectively. Epithelial dysplasia was characterized by irregular stratification of Ki-67+ cells and the absence of K19/K13 in proliferating cells. Irregular emerging of K19+ and K13+ cells in proliferating foci with unique stratification of atypical Ki-67+ cells indicated CIS. When the definition was applied, surgical margins in 172 recurrent cases were shown to contain CIS (39.4%) and squamous cell carcinoma (55.8%), indicating that the new diagnostic criteria for CIS reflected clinical behaviors of the cases. The results indicate that oral CIS contain more histological variations, especially those with definite keratinization, than what had been previously defined.
The results indicate that the ECM remodeling steps in OSF are similar to each phase of usual granulation tissue formation. Restricted mouth opening may be a result of loss of variety of ECM molecules including elastin into the homogeneity of collagen type I replacing muscle fibers.
The findings indicate that perlecan is localized in the intercellular space of the oral epithelia, and that it is over-expressed in dysplastic epithelial cells and is deposited in their interepithelial space, which results in the histology of reduction of cellular cohesion.
Recent studies have demonstrated that human dental pulp contains adult stem cells. A pulse of the thymidine analog BrdU given to young animals at the optimal time could clarify where slow-cycling long-term labelretaining cells (LRCs), putative adult stem cells, reside in the pulp tissue. This study focuses on the mapping of LRCs in growing teeth and their regenerative capacity after tooth injuries. Two to seven peritoneal injections of BrdU into pregnant Wistar rats revealed slow-cycling long-term dense LRCs in the mature tissues of born animals. Numerous dense LRCs were postnatally decreased in number and reached a plateau at 4 weeks after birth when they mainly resided in the center of the dental pulp, associating with blood vessels. Mature dental pulp cells were stained with Hoechst 33342 and sorted into (<0.76%) side population cells using FACS, which included dense LRCs. Some dense LRCs co-expressed mesenchymal stem cell markers such as STRO-1 or CD146. Tooth injuries caused degeneration of the odontoblast layer, and newly diVerentiated odontoblast-like cells contained LRCs. Thus, dense LRCs in Electronic supplementary material The online version of this article (
The localization and biosynthesis of basement membrane-type heparan sulfate proteoglycan (HSPG), known as perlecan, were studied in ameloblastomas using surgical tissue sections and cells in primary culture to demonstrate the existence of extracellular matrix (ECM) molecules in the intercellular space of epithelial tissue. HSPG was immunolocalized in the intercellular spaces of stellate reticulum-like cells and small vacuolar structures between basal cells in tumor cell nests as well as in myxofibrous stroma. By means of in-situ hybridization, mRNA signals for the HSPG core were intensely demonstrated in the cytoplasm of basal and parabasal cells of parenchyma. Furthermore, the in-vitro biosynthesis of HSPG core protein by ameloblastoma cells was confirmed using immunofluorescence, immunoprecipitation, and reverse-transcriptase polymerase chain reaction (RT-PCR). The results indicated that ameloblastoma cells synthesize HSPG and deposit it in their intercellular space. The intercellular HSPG might act as a carrier for transport of nutrients to tumor cells within ameloblastomatous foci.
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