In the incisors of the WT mice, we observed sequential
ameloblast cell differentiation [i.e., preameloblasts (Fig.
Skin epithelial cells as possible substitutes for
ameloblasts during tooth regeneration.
Other possible causes suggested are: environmen- tal conditions, premature birth, perinatal compli- cations, exposure to dioxine by prolonged breast- feeding, respiratory diseases and oxygen shortage of the
ameloblasts, calcium and phosphate meta- bolic troubles, oxygen starvation associated to low birth weight and febrile childhood diseases.
In marsupials, tubules are described as hollow spaces formed by the course of
ameloblasts, occurring within or outside of prisms, and sometimes continuous with dentine tubules across the enamel-dentine junction (Boyde and Lester, 1967).
Development of enamel is a complex organized process, where the
ameloblasts lay down the enamel rods in an undulating and inter-twining path.
When this complex sequence of cytological and physico-chemical events is disrupted by genetic or environmental factors the function of the
ameloblast may be disrupted perma- nently or temporarily.12 This results in the formation of enamel exhibiting qualitative or quantitative defects that may range from a complete absence of enamel to a normal thickness or no change in structure except for a slight abnormality in colour.3 The type of defect is dependent on the stage of amelogenesis at the time of the disturbance.4
From contemporary understanding of
ameloblast development and maturation, these stem cells are located in the outer enamel epithelium (OEE) and the stellate reticulum (SR) of the labial cervical loop.
C) Anti-enamelisin (Chemicon International, USA), second antibody: Qdot Secondary Antibody 525 conjugate (Molecular Probes, USA), it can be observed the disposition of the enamelisin around the mantle dentin that is mineralized just as the
ameloblast and stronger than the odontoblast (red).
It is the consequence of insults to the highly specialised and vulnerable
ameloblast cells, apparently during the later mineralisation phase of amelogenesis resulting in defective enamel with significantly increased protein content [Farah et al., 2010; Mangum et al., 2010].
Ameloblastoma is an odontogenic tumour of epi-thelial origin and is composed of
ameloblast like cell.1 It is a benign locally invasive tumour with tendency to infiltrate beyond observed radiographic and clinical margins.
Incisional biopsy of the lesion was performed and microscopic examination revealed odontogenic epithelial cells proliferating in broad anastomosing cords showing presence of peripheral tall columnar
ameloblast like cells with reverse nuclear polarity and central stellate reticulum like cells.
Amelogenesis has been divided into three major stages of the
ameloblast life cycle, namely secretory, transition, and maturation.
Effects of a macrolide antibiotic on enamel formation in rat incisors--primary lesion of
ameloblast at the transition stage.
