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At least 19 recordsLinked to original sources
PubMed1995

Ameloblastic fibrosarcoma of the jaws. A clinicopathologic and DNA analysis of five cases and review of the literature with discussion of its relationship to ameloblastic fibroma.

Ameloblastic fibrosarcoma, the malignant counterpart of the ameloblastic fibroma, is a rare odontogenic tumor characterized by benign epithelium and a malignant fibrous stroma. We have compared nuclear DNA content of five ameloblastic fibrosarcomas and three ameloblastic fibromas by image analysis. The three ameloblastic fibromas were diploid, whereas 1 of 5 ameloblastic fibrosarcomas was aneuploid. There was no correlation with histologic grade and aneuploidy. These five new cases were also added to a review of the literature, bringing the total cases of reported ameloblastic fibrosarcomas to 51. The ameloblastic fibrosarcoma occurs at a later age (mean, 27.5 years) compared with reported ameloblastic fibromas (mean, 14.6 to 22 years), which supports a step-wise malignant transformation. There was histologic documentation that 44% of ameloblastic fibrosarcomas developed in ameloblastic fibromas. In view of this data and of the reported cumulative recurrence rate of 18.3% for ameloblastic fibroma, it is recommended that ameloblastic fibromas be treated with complete surgical excision and long-term follow up rather than simple curettage or enucleation.

Adolescent↗
PubMed1977

On the effect of vinblastine on ameloblasts of rat incisors in vivo. 2. Protracted effect on secretory ameloblasts. A light microscopical study.

The effects of vinblastine sulphate at a dosage of 0.2 mg per 100 g body weight on the secretory ameloblasts of rat incisors were studied 3, 6 and 24 hours and 3 and 7 days after administration of the drug. The vinblastine affected the secretion profoundly, caused a reduction in size of the cells and death of many ameloblasts. Most of the surviving ameloblasts restored initially-induced loss of polarity. Many also resumed secretion and deposition of enamel matrix. The Tomes' processess were extremely sensitive to vinblastine and all matrix deposited after administration of the drug appeared abnormal in structure. Ameloblasts not resuming secretory activity were less than half the size (height) of normal cells. In some areas all the ameloblasts were destroyed with the exception of a varying number of surviving ameloblasts parts consisting only of a nucleus and a small amount of cytoplasm. The ameloblasts which had re-established secretory activity, and most of the ameloblasts which had not, retained their ability to transform into transporting ameloblasts. Large amounts of ameloblast debris present 3 and 6 hours after administration of the vinblastine were effectively engulfed and digested by the cells of the striatum intermedium within 24 hours.

Ameloblasts↗
PubMed1977

On the effect of vinblastine on ameloblasts of rat incisors in vivo. 3. Acute and protracted effect on differentiating ameloblasts. A light microscopical study.

The acute effect of vinblastine sulphate at a dosage of 0.2 mg per 100 g body weight on ameloblasts in the progress of differentiation in rat incisors, and the ability of these cells to develop into secretory ameloblasts after exposure to the drug, were studied under the light microscope. In the early stages of differentiation (exclusively dividing cells) no changes were seen. In more advanced stages of differentiation the cell apices were altered and the nuclei normally placed near the cell base were located at all levels in the ameloblast layer. These changes were reversible and the cells developed into secretory ameloblasts of normal appearance and function. Ameloblasts in the most advanced stage of differentiation in which secretion had begun were severely damaged, and the mature secretory ameloblast population derived from these cells was decimated and produced enamel matrix with abnormal structure. It is concluded that differentiating ameloblasts are relatively invulnerable to vinblastine, whereas in secretory ameloblasts the organelles directly engaged in the secretory processes are particularly exposed to damage from the drug.

Ameloblasts↗
PubMed2005

Malignant transformation of ameloblastic fibroma to ameloblastic fibrosarcoma: case report and review of the literature.

INTRODUCTION: Ameloblastic fibrosarcoma is a rare malignant odontogenic tumour and is regarded as the malignant counterpart of the ameloblastic fibroma. The epithelial component remains benign, but the mesenchymal component becomes malignant. The diagnosis is made by histopathology. PATIENT: The case of a 26-year-old man who underwent curettage of an ameloblastic fibroma and died of an ameloblastic fibrosarcoma is presented, and the course of malignant transformation is analysed retrospectively. CONCLUSION: One-third of ameloblastic fibrosarcoma cases seem to have developed from recurrent ameloblastic fibromas. Knowledge of the malignant potential in the mesenchymal spindle cells of ameloblastic fibroma will assist in determining the management of these benign tumours, and may prevent malignant transformation to ameloblastic fibrosarcoma.

Adult↗
PubMed1992

Correlation of the arrangement pattern of enamel rods and secretory ameloblasts in pig and monkey teeth: a possible role of the terminal webs in ameloblast movement during secretion.

Enamel rod architecture and ameloblast arrangement were examined in pig and monkey teeth using light microscopy and scanning and transmission electron microscopy. Enamel rods in the pig teeth were arranged in longitudinal straight rows in the initial enamel layer, in longitudinal wavy rows in the inner enamel layer, and in a staggered pattern in the outer enamel layer. Rod decussation was seen only in the inner layer. Cross-sectioned enamel rods in the pig were arcade-shaped in the initial and inner layers, and mostly round in shape with circular boundaries in the outer layer. Arrangement of secretory ameloblasts at the level of the distal terminal web and Tomes' processes, and shape of Tomes' processes, corresponded to those of the enamel rod in the enamel layers. Distal terminal webs were well developed between straight rows of the ameloblasts forming the initial layer and between wavy rows of the ameloblasts forming the inner layer, and less developed within a row. The filament bundles in the distal terminal webs were also oriented along the rows. However, in the ameloblasts forming the outer layer, which lost their row pattern, distal terminal web filaments were distributed uniformly at the cell periphery. A similar arrangement of wavy rows of ameloblasts at the level of distal terminal web and Tomes' processes was also seen in monkey teeth.

Ameloblasts↗
PubMed1998

Assessment of growth potential by MIB-1 immunohistochemistry in ameloblastic fibroma and related lesions of the jaws compared with ameloblastic fibrosarcoma.

Specimens from two ameloblastic fibromas (including one recurrent case), two ameloblastic fibro-odontomas, and one ameloblastic fibrosarcoma were subjected to investigation by MIB-1 immunohistochemistry in order to elucidate the growth potential of these tumors. MIB-1 labeling indices in the epithelial component of these tumors ranged from 2.9 to 7.5%, whereas those in the mesenchymal component ranged from 1.5 to 13.5%. Of these, labeling indices in the mesenchymal component of the recurrent ameloblastic fibroma and ameloblastic fibrosarcoma were quite high. These findings suggest that evaluation of growth potential in ameloblastic fibroma and related lesions could be of help in understanding tumor aggressiveness and in selecting appropriate surgical procedures.

Adolescent↗
PubMed1978

Fine structure of the secretory and non-secretory ameloblasts in the frog. II. Fine structure of the non-secretory ameloblast.

The non-secretory ameloblasts present at the enamel-free surfaces of maxillary teeth in the frog Rana pipiens were examined by electron microscopy at different stages of tooth development. Their main fine structural features seem to reflect a transport function. During early tooth development, the non-secretory ameloblasts adjacent to odontoblasts and predentin exhibit extensive lateral surface specializations and numerous cytoplasmic vesicles. During late tooth development, the non-secretory ameloblasts adjacent to mineralizing dentin show numerous cellular junctions, well-developed intercellular channels with numerous interdigitating processes and labyrinthine configurations at their distal surfaces. An intact basal lamina is present between the non-secretory ameloblasts and the dentin surface until the dentin becomes fully mineralized. At this stage the adjacent cells no longer exhibit surface specializations. It is suggested that the non-secretory ameloblasts may participate in the mineralization of adjacent dentin at the enamel-free surfaces. This surface dentin becomes fully mineralized at a later stage of development than the underlying dentin.

Ameloblasts↗
PubMed1977

Malignant transformation of ameloblastic fibro-odontoma to ameloblastic fibrosarcoma.

Two cases of malignant transformation of ameloblastic fibro-odontomas are presented, along with a review of the literature on ameloblastic fibrosarcomas. The occurrence of this malignant transformation of ameloblastic fibromas, ameloblastic odontomas, and ameloblastic fibro-odontomas appears to be more frequent than previously thought. This potential transformation alone does not justify radical treatment of all these benign lesions. If there is recurrence accompanied by a histologic pattern change toward a more unorganized fibrous stroma with displacement of the epithelial component, however, then more extensive treatment procedures appear to be indicated.

Adolescent↗
PubMed1981

An analysis of the interrelationship of the mixed odontogenic tumors--ameloblastic fibroma, ameloblastic fibro-odontoma, and the odontomas.

The mixed odontogenic tumors--ameloblastic fibroma, ameloblastic fibro-odontoma, and the odontomas--represent a group of lesions of which some are neoplastic and some are hamartomatous. Regarding data on age, sex distribution, and site of occurrence of the various lesions, it was concluded that the ameloblastic fibroma represents a separate entity that does not develop into a more differentiated odontogenic lesion and that the ameloblastic fibro-odontoma is an immature complex odontoma. Moreover, it was noted that the distribution according to site of the ameloblastic fibro-odontoma and complex odontoma was dependent on age, both lesions showing a more posteriorly located site of predilection with increasing age. Finally, it is supposed that age-related factors determine whether an aberrant development of the odontogenic tissues exhibits a hamartomatous or a neoplastic nature.

Adolescent↗
PubMed1995

DNA localization in nuclear fragments of apoptotic ameloblasts using anti-DNA immunoelectron microscopy: programmed cell death of ameloblasts.

Ameloblasts responsible for tooth enamel formation are classified into two different phases: secretion and maturation. At the transition between these secretion and maturation stages, a considerable number of cells die. In this study, we examined the morphology of degenerating ameloblasts by conventional electron microscopy, and DNA cleavage in degenerating ameloblast nuclei by the in situ terminal transferase assay. The results suggest that apoptosis (programmed cell death) in ameloblasts, including DNA ligation is induced at the transitional stage. The nuclear fragments, chromatin condensation and DNA relocation in apoptotic nuclei were examined quantitatively by post-embedding anti-DNA immunogold electron microscopy and the in situ terminal transferase assay combined with electron microscopy. Numerical analysis revealed that immunogold labeling density in the condensed chromatin of apoptotic nuclei was comparable on the average to that in the perinuclear heterochromatin of normal nuclei, and that individual apoptotic nuclear fragments exhibited highly variable to that of normal heterochromatin, to fragments with densities twice as high as that of normal heterochromatin. The in situ terminal transferase assay combined with electron microscopy detected DNA ends exposed by ultrathin sectioning as well as DNA cleavage by a putative endonuclease. In conclusion, the state of the DNA, including its ligation and degeneration, changes gradually during chromatin condensation and nuclear fragmentation of apoptosis.

Ameloblasts↗
PubMed1990

Ameloblastic odontosarcoma (ameloblastic fibro-odontosarcoma) in the mandible.

A case of ameloblastic odontosarcoma (ameloblastic fibro-odontosarcoma) originating in the mandible is reported. The patient was a 23-year-old Japanese male with diffuse swelling of the mandible from the left premolar to the ramus region. A biopsy specimen showed the histopathological features of ameloblastic fibrosarcoma. Histologic examination of the surgical specimen revealed various amounts of dysplastic dentin and dentinal matrix which were closely associated with both mesenchymal and epithelial components throughout the lesion. In addition, a small amount of abortive enamel matrix, which was in close contact with ameloblastoid cells of epithelial nests, was found by extensive sampling of the resected specimen. Therefore the present case was diagnosed as ameloblastic odontosarcoma. After 2 years, the patient died of uncontrollable local recurrence and extension to the cranial base.

Adult↗
PubMed1977

Light microscopical and ultrastructural observations on the effect of vinblastine on ameloblasts of rat incisors in vivo. I. Short-term effect on secretory ameloblasts.

The highly polarized secretory ameloblasts in the incisors of rats fixed by perfusion with glutaraldehyde two or three hours after intravenous administration of vinblastine sulfate at a dosage of 5 mg per 100 g body weight were studied in the light microscope and the electron microscope. The following effects were observed: 1. All cytoplasmic microtubules in the ameloblasts had vanished. This was not accompanied by the appearance of paracrystals of microtubular protein or macrotubules. 2. The ameloblasts preserved their external features of polarized cells but lost their ability to maintain normal orderly segregation of the cell constituents; i.e. their normal internal compartmentalization and polarity had vanished. 3. The ameloblasts lost their capability of directional translocation of the secretory granules towards the cell apex. 4. Secretory granules already translocated to the cell apex regurgitated in the cell and a probably delayed discharge of secretory material had started in abnormal site at the surface. 5. The normal arrangement of ribosomes into polyribosomes on the membranes of the rough endoplasmic reticulum was no longer present; the ribosomes were apparently distributed at random. 6. New secretion was inhibited or brought to a standstill but secretory material already present in the Golgi complex appeared to be transported normally. 7. The centriole had started to develop into a cilium in many of the cells. 8. The number of autophagic vacuoles had increased.

Ameloblasts↗
PubMed1984

Ameloblastic fibrosarcoma in the maxilla, malignant transformation of ameloblastic fibroma.

This report presents a fatal case of ameloblastic fibrosarcoma arising from an ameloblastic fibroma, originating in the maxilla of 19-year-old Japanese male. An analysis of previously reported fatal cases of ameloblastic fibrosarcoma is included. In the course of the disease, the mesenchymal component of ameloblastic fibroma showed a dramatic histopathological transformation into sarcoma following multiple recurrence and the patient died of uncontrollable local infiltration of the cranial base. Although many cases have seemed to show disappearance of the epithelial component as malignant transformation progressed, many benign appearing ameloblastoid epithelial masses were scattered throughout the sarcomatous area even in the fatal stage in the present case. No distant metastases were found at autopsy. During multiple recurrences of the lesion, a little dysplastic dentin which was closely associated with both epithelial and mesenchymal components was found, though it could not be observed in autopsy material. Ultrastructural findings in autopsy material showed that the mesenchymal component consisted of undifferentiated mesenchymal cells, fibroblastic and fibrocytic cells with marked cellular and nuclear pleomorphism and that the epithelial component closely resembled the enamel organ.

Adult↗
PubMed1977

Fine structure of the secretory and nonsecretory ameloblasts in the frog. I. Fine structure of the secretory ameloblasts.

Amelogenesis in the tooth germs of the frog Rana pipiens was examined by electron microscopy at different stages of tooth development. Cellular changes in secretory ameloblasts during this process showed many basic similarities to those in mammalian amelogenesis. Amelogenesis can be divided into three stages based on histological criteria such as thickness of enamel and the relative position of the tooth germ within the continuous succession of teeth. These stages are early, transitional and late. The fine structure of the enamel-secreting cells reflects the functional role of these ameloblasts as primarily secretory in the early stage, possibly transporting in the late stage and reorganizing between the two functions in the transitional stage. In early amelogenesis the cell exhibits well-developed granular endoplasmic reticulum, Golgi complex, microtubules, dense granules, smooth and coated vesicles, lysosome-like bodies in supranuclear and distal portions of the cell and mitochondria initially concentrated in the basal part of the cell. Numerous autophagic vacuoles are observed concomitant with the loss of some cell organelles at the transitional stage. During late amelogenesis the ameloblasts exhibit numerous vesicles, granules, convoluted cell membranes, junctional complexes and widely distributed mitochondria. Toward the end of amelogenesis, cells become oriented parallel to the enamel surface and the number of organelles is reduced. Amelogenesis in the frog is an extracellular process and mineralization seems to occur simultaneously with matrix formation.

Ameloblasts↗
PubMed2000

Specialized basement membrane of monkey maturation stage ameloblasts mediates firm ameloblast-enamel association by its partial calcification.

A basement membrane-like structure associated with the maturation stage ameloblasts of the monkey (Macaca fuscata) tooth germ was examined with high resolution electron microscopy. The tissue was prepared either with or without demineralization. This structure was composed of a lamina lucida-like (lamina lucida) and lamina densa-like (lamina densa) structure. The latter was made up of a fine "cord" network, the major constituent of the basement membrane. It was closely associated with the third layer of a 200 nm wide looser cord network. In specimens without demineralization the third layer and a part of the lamina densa were calcified, and it formed the edge of the enamel. This particular area had a higher electron density, and the size, shape, and arrangement of mineral crystals were different from those of the rest of the enamel. Also, mineralization appeared to be proceeding along the cords. These observations indicate that this dense layer is a highly specialized basement membrane which mediates the firm association of maturation stage ameloblasts with the enamel by means of the mineralization of a part of this basement membrane itself which becomes integrated as a part of the enamel. Also, this highly specialized manner of association is favorable with the reported control of the loss of organic substances in the maturing enamel by maturation stage ameloblasts.

Ameloblasts↗
PubMed1990

An estimation of ameloblast generation time and of the ameloblast proliferative compartment of guinea pig teeth.

The generation time of inner enamel epithelial cells has been estimated by many investigators using rodent and lagomorph teeth but the results have varied. In the present study of guinea pig molars, the inner enamel epithelial cell generation time (Tc) and its fractions (Ts, Tg2, Tm and Tg1) were calculated. Previous investigators have attempted to determine the extent of the proliferative compartment of inner enamel epithelial cells using the position of mitotic figures as their guide, but results have been inconsistent. It appears that this has been due to the small percentage of mitotic figures among the cell population and the difficulty of visualising them. In the present study, a novel approach was used to determine the extent of the inner enamel epithelial cell proliferative compartment which was not based on the position of mitotic figures, but on the calculation of other generation time fractions. It was found that the proliferative compartment extended for approximately 47 cells occlusally from the synthetic compartment. The results also showed that there was no evidence of stem cells in the ameloblast columns and hence, ameloblasts depended on their cell supply from the stem cell compartment apical to the ameloblast columns.

Ameloblasts↗
PubMed1980

Ultrastructure of the ameloblast-stratum intermedium border during ameloblast differentiation.

The molar tooth germs of newborn mice were isolated and the zone of ameloblast differentiation studied with the electron microscope. Special attention was paid to the changes that occur in the contacts such as desmosomes, tight junctions and close attachments associated with cell interdigitations between the inner enamel epithelium (IEE) and the stratum intermedium (SI) cells from the beginning of differentiation to the onset of enamel secretion. These changes are accompanied by variations in the width and configuration of the intercellular space separating the two cell layers. The terminal web persists from the beginning of cell elongation to the appearance of Tomes's process. Through its attachment to the zonulae adherentes, a terminal web-lateral junction system is created which stabilizes the differentiating ameloblasts. Also the SI cell layer is interpreted as a stabilizer for the IEE layer, particularly during the differentiation phase. This interpretation does not conflict with information that the SI cells transport materials required for enamel secretion.

Ameloblasts↗
PubMed2000

Immunohistochemical expression of neural tissue markers (neuron-specific enolase, glial fibrillary acidic protein, S100 protein) in ameloblastic fibrodentinoma: a comparative study with ameloblastic fibroma.

Formalin-fixed paraffin-embedded sections of three cases of ameloblastic fibrodentinoma (AFD) were studied by the avidin-biotin-peroxidase complex method using antibodies against neuron-specific enolase (NSE), glial fibrillary acidic protein (GFAP) and S100 protein and the results were compared with those in ameloblastic fibroma (AF). A striking histopathological characteristic of AFD was the formation of abortive dentin with various degrees of maturation at the epithelial-mesenchymal tissue interface. Central cells of enamel organ-like epithelia with various stages of abortive dentin induction in AFD were generally positive for NSE. Dental lamina-like epithelial cells also showed positive staining in some areas. No cells were positive for NSE in AF. Positive staining for GFAP was observed in the juxta-epithelial mesenchymal tissue of the formation stage of immature dentin with various numbers of entrapped cells in AFD, but GFAP staining was negative in other mesenchymal and epithelial tissues at other stages. In AF, no GFAP-positive cells were found. There were a few S100 protein-positive cells found in the foci of epithelial components in both AFD and AF. Mesenchymal cells showing a dendritic or spindle shape were positive for S100 protein in some areas of AFD and AF. Although such cells in the mesenchymal component of pigmented AFD were more numerous than in non-pigmented AFD and AF, their distribution pattern in the former condition was basically similar to that in the latter. Although the present results, obtained from conventional immunohistochemical procedures, do not directly reflect the expression of neural crest-derived cells in the dentinogenesis of AFD, such results do not disprove the possibility of the expression of neural proteins probably related to neural crest-derived cells in dentinogenesis under certain pathologic conditions in odontogenic mixed tumors. Such a phenomenon may also occur during dentinogenesis in other odontogenic mixed tumors and in normal tooth differentiation, but at an undetectable level.

Adult↗