These results suggest that cellular proliferation and death is regulated in association with apoptosis-related proteins in the lining epithelia of OKCs, and subsequently those cysts are seen as cystic lesions but not as tumor masses.

This review summarizes the biological properties of the junctional epithelium, focusing on its developmental aspects, wide intercellular spaces and desmosomes, dense granules, permeability barrier, phagocytotic activity, adhesive structures and nerve terminals. It also discusses the morphology and functions of long junctional epithelium and peri-implant epithelium. Junctional epithelium is derived from the reduced enamel epithelium during tooth development. Apoptosis occurs in the border between oral and reduced enamel epithelia during tooth eruption. Junctional epithelium expresses a cytokeratin-19 immunoreaction, suggesting that this protein is a consistent differentiation marker. Wide intercellular spaces, which contain neutrophils and nerve endings, are formed as there are fewer desmosomes than in the oral epithelium. Dense, membrane-bound granules in the epithelium might correspond with membrane-coating granules, as revealed by their shape, components and freeze-fracture images. Junctional epithelium with high permeability contains exogenously expressed alpha-defensins, while stratified epithelia contain endogenously expressed beta-defensins. The phagocytotic activity in this epithelium remains unclear. Integrin-alpha6beta4 and laminin-5 form a complex in the tooth surface internal basal lamina. Long junctional epithelium created experimentally attaches to the cementum surface by hemidesmosomes and basal lamina. The peri-implant epithelium differs in proliferation and in adhesive structure from the normal junctional epithelium. In conclusion, wide intercellular spaces and poorly developed desmosomes are closely correlated with a permeable nature. There is still uncertainty over the phagocytotic activity of the epithelium. Integrin-alpha6beta4 and laminin-5 form a significant complex in the internal basal lamina. Junctional epithelium receives a rich sensory nerve and has a high rate of cell turnover. Long junctional epithelium can be produced rapidly during wound healing, due to high proliferative activity. Peri-implant epithelium might be a poorly adhered and permeable epithelium.

Hertwig's epithelial root sheath (HERS) degenerates immediately after root dentin is formed. However, odontogenic tumors or cysts may originate from residual cells, although little is known about how HERS proliferates and disappears. This study investigated whether cell death is provoked in the tissues surrounding the root during eruption of the rat upper molar. We employed the TdT-mediated-dUTP nick end labeling (TUNEL) method and transmission electron microscopy (TEM) to observe the morphological features of cell death. We examined the activity of cell proliferation immunohistochemically using proliferative cell nuclear antigen (PCNA) and the continuity of HERS using polyclonal keratin antibody (PK). Cell death resembling apoptosis and apoptotic bodies phagocytosed by neighboring mesenchymal cells were detected in only a few cells by both TUNEL and TEM. We also found cells with electron-lucent cytoplasm which contained dilated or ruptured mitochondria and remarkably dilated rough endoplasmic reticulum (rER) which lay sparsely along the root. These cells seemed to be dead HERS cells based on their ultrastructural features, location, and stage. PCNA-positive cells were found in the apical end of the HERS cells, fibroblasts of the periodontal ligament, and odontoblasts. PK reacted with HERS; however, PK-positive cells partially disappeared after the 15th postnatal day when the root dentin had formed slightly. These results may indicate that HERS cells migrate into the periodontal ligament or die immediately after root dentin is formed and that various types of cell death such as apoptosis and cytoplasmic type occur in the tissues surrounding the root during tooth development.

The purposes of this study were to investigate the distribution of cytokeratins in the different tissue types of ameloblastoma and to discuss the histogenesis of this tumor. CK19 and CK8, which are markers for odontogenic epithelium, reacted positively to the constituting cells in all types of ameloblastoma. This suggests that all types of ameloblastoma derive from odontogenic epithelium. However, the desmoplastic type diminished the odontogenic characteristics because the basal cells are negative to CK19. Immunoreactions of five kinds of cytokeratin revealed similar results in plexiform, follicular, acanthomatous, and granular cell types. The plexiform type is probably the original type of ameloblastoma; the other types have the characteristics of squamous epithelium, and the follicular, acanthomatous, and granular cell types can develop due to the differentiation of cells of the plexiform type into squamous epithelium.

The results suggest that laminin gamma(2) is secreted as a foothold for cell migration, that integrin beta(4) participates in cell adhesion and that integrin alpha(3) is involved in cell migration in the primary culture cells.