ADENOMATOID ODONTOGENIC TUMOR PDF

Adenomatoid odontogenic tumor (AOT), a benign (hamartomatous) lesion of odontogenic origin, is an uncommon tumor which affects mainly. Adenomatoid odontogenic tumor (AOT) is a rare odontogenic tumor which is often misdiagnosed as odontogenic cyst. To acquire additional. Adenomatoid odontogenic tumor is a hamartomous benign neoplasia of odontogenic origin. It appears mostly in young patients and females, the maxillary.

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Study on the origin and nature of the adenomatoid odontogenic tumor by immunohistochemistry. The adenomatoid odontogenic tumor AOT is a clinically benign lesion. Discussions about the AOT hamartomatous or neoplastic nature, and the probable odontogenic epithelial cell it originates from still exist.

Adenomatoid odontogenic tumor – Wikipedia

This research aimed to study and discuss the subject by the immunohistochemical detection of cytokeratins, laminin, collagen IV, PCNA and p53 in 8 tumor samples and 8 dental follicle samples containing reduced enamel epithelium.

The results have shown that CK14 labelling indicated differentiation grades for secreting ameloblasts or ameloblasts in the post-secreting stage in the adenomatoid structure of AOT. Laminin, found on the luminal surface of adenomatoid structures, was compatible with the reduced enamel epithelium during the “protective stage of amelogenesis”. PCNA specifically labelled the spindled areas and peripheral cords of the AOT, indicating that these areas are responsible for tumor growth.

After considerations about pathogenesis, the authors suggested that the nature of AOT is hamartomatous with histogenesis from the reduced enamel epithelium. Odontogenic neoplasms; Adenomatoid odontogenic tumor; Immunohistochemistry. Originating from dental bud tissues and developing preferably in the dental follicles, the adenomatoid odontogenic tumor AOT is undoubtedly accepted as a benign lesion. The issue of its nature being neoplastic or hamartomatous is still object of diverging opinions, generally based on clinical observations and little scientific evidence.

Also, there is no consensus regarding the exact histogenesis of the tumor, with suggestions ranging from the dental lamina to the enamel organ as a whole. InCourtney and Kerr 3 believed it was a hamartoma developmental abnormality of remnant odontogenic epithelium. Carmo and Silva 2 tried to correlate its clinical behavior with the cell proliferation rate assessed by AgNOR histochemistry.

Philipsen and Reichart 14 considered AOT a non-invasive slow-growing benign lesion hamartomatous. For Takahashi, et al. There is no doubt about the AOT origin from the odontogenic epithelium; however the cell directly involved in the pathogenesis is still under discussion.

Mandibular adenomatoid odontogenic tumor: Radiographic and pathologic correlation

Stratum intermedium cells Okada, et al. Electron microscopy studies have revealed the interesting presence of hemidesmosomes in the luminal cell membrane of the duct-like and adenomatoid structures, connecting it to a basal lamina-like material. Membrane-covered vesicles and granules, with electron-dense central portion, were sometimes interpreted as secretion granules producing intraluminal material Lee 9; Hatakyama and Suzuki 7; Schlosnagle and Someren 18; Yamamoto, et al.

Few studies in the literature have used the immunohistochemistry technique to analyze AOTs. The most relevant ones detected substances related to amelogenesis, such as enamelysin Takata, et al. This finding might resemble the basal lamina next to the internal and external epithelium of the enamel organ, or the surface of the reduced enamel epithelium in the enamel maturation stage. Based on clinical observations and histochemical, immunohistochemical and ultrastructural findings in literature, we have adopted the hypothesis of AOT being a simple hamartoma, whose histogenesis would be related to the reduced enamel epithelium.

Thus, our proposal was to establish the participation of the different polypeptides of cytokeratin, laminin, collagen IV, PCNA, and p53 in the cell and tissue structures of AOT, and to compare it with their expression in the reduced odontogenix epithelium and with the immunohistochemical reports of the dental buds.

This may give support to discussions about the existing hypothesis for tumor pathogenesis and biological nature. Paraffin sections of formalin fixed tissue were used for both histological and immunohistochemical evaluation. Hematoxylin-eosin stained sections were made for routine histological examination. Two incubations 5 min. Primary antibodies were then incubated; their sources, concentrations, and times of incubation are listed in Table 1.

The color reaction was developed using a freshly prepared solution of 3,3-diaminobenzidine tetrahydrochloride for 3 min. Finally Mayer’s hematoxylin was used for counterstaining.

Data were scored by observing the presence of a brown end odintogenic at the site of the target antigen under a light microscope. Positive controls for each CK and vimentin were used as indicated by the supplier, which labelled, in normal tissues, the following: CK7, 18, 19 glandular epitheliaCK 10, 13 suprabasal cells of epidermisCK 14 basal cells of epidermisand vimentin endothelial cells.

Replacing the primary antibody with TRIS performed negative controls. Tables 2 and 3 summarize the immunohistochemical results obtained using paraffin sections of formalin fixed tissue. The adenomatoid odontogenic tumors presented epithelial proliferation in which cells placed in solid odontogeinc forming sheets, or a nest-and cord-like pattern. Odomtogenic the solid nodules, cells were ovoid and cylindrical, the latter outlining duct-like structures, which contained homogeneous eosinophilic material in the center.

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Sometimes the eosinophilic material showed linear configuration, also outlined by cylindrical cells.

Adenomatoid structures were generally present, which were round with a much wider diameter than the duct-like structures and outlined by low or tall columnar cells. Not rarely did these structures present a thin layer of the eosinophilic material in its internal surface. Interspersed in the solid areas, as if separating them in blocks, there were fusiform and stellated cells resembling the stellate reticulum with thin strands.

Small cuboid or polyhedrical cells formed peripheral cords that tumro seemed oxontogenic fold and overlap, forming compact avenomatoid. In one of the tumors, occasional cell foci with a squamous appearance were observed. Mineralized structures resembling Liesegang rings, dystrophic calcification areas, and other small intercellular eosinophilic hyaline deposition, with shapeless light or dark pinkish appearance, sometimes lamellar and concentric were present.

Adjacent to the tumoral proliferation, a cystic lining formed by stratified pavement epithelium was common. The underlying connective tissue was fibrous, thick, with extensive areas of hemorrhage and discrete inflammatory mononuclear infiltrate. In odontoenic vicinities of the tumor, blood capillary vessels with perivascular hyalinization, ocontogenic delicate connective tissue rich in ground substance were tujor. In the immunohistochemical staining, tumoral epithelial cells were not positive for cytokeratins 7, 13, 18, 19, vimentin and p CK14 was detected in the cords of cubic and peripheral polyhedrical cells, as well as in the fusiform and stellated cells adjacent to the solid areas of the tumor.

Cells forming the adenomatoid structures and the solid areas were not positive in two of the samples and varied in the others Figure 1. It labelled, from weakly to strongly, most of the cells in the solid areas, adenomatoid structures, cords of cubic and polyhedrical cells, and was practically absent or weak in the fusiform cells and in the stellated cells interspersed in the solid areas Figure 2.

The immunohistochemical analysis showed positive results for laminin in the luminal surface of oodontogenic cells bordering the adenomatoid structures, in the small intercellular deposits of lighter eosinophilic material interspersed in the epithelial proliferation of spindled areas and cords, and adenoamtoid the borders between the tumor and connective tissue Figure 3.

The material corresponding to tmuor eosinophilc was negative for laminin. Collagen IV had discrete expression only in the zone of the basal membrane of a few tumors; however, around the neighboring stromal capillary vessels it was noteworthy. The samples of pericoronal flap presented pavement stratified reduced enamel epithelium, with two or three cell layers and, in one of the samples, cubic basal cells and columnar superficial cells, resembling post-secretory ameloblasts.

The immunohistochemical detection of CKs presented intense positivity for CK14 in all epithelial elements Figure 4. The expression was variable for CK13, labelling occasional disperse cells, generally superficial Figure 5.

Weak expression in this same pattern characterized CK19, in three samples. The results for CK7, 18, vimentin, and p53 were negative. Laminin was clearly expressed in the zone of the basal membrane, both of the epithelium and of the blood vessels, a pattern that was followed by collagen IV; however, with weaker expression, not rarely absent adenomatold to the epithelium. PCNA was expressed mainly in the basal epithelial cell nuclei and in some of the suprabasal cells.

The adebomatoid with columnar cells followed this pattern, with rare positive suprabasal cells Figure 6.

Epithelia in inflammatory areas presented disperse positivity. As previously said, we focused on the ultrastructural detail of the presence, in the luminal surfaces of the adenomatoid structures, of hemidesmosomes and a material adenoamtoid to the basal lamina, confirmed histochemically by the presence adenomatoiv laminin.

Such characteristics are similar to those of the reduced enamel epithelium REE in the protective and maturation stage of amelogenesis, which led us to work on the hypothesis of the origin of AOT from it. It is known that at the end of amelogenesis, post-secretory ameloblasts synthesize a material similar to the basal lamina, which adheres to the newly formed enamel. This stage is called “protective stage of amelogenesis”, which avoids cementoblastic differentiation in the follicle and cementum deposition or “osteodentin” next to the enamel Ten Cate 23 This would justify the capability of AOT cells to secrete enamel odontogeic proteins, such as amelogenin or enamelin shown tumkr the immunohistochemical reactions of Murata, et al.

We can consider in our hypothesis of AOT origin from the REE that the cells in that epithelium had been recently active, producing enamel matrix in the amelogenesis and that some of them might still keep the capacity of synthesis and secretion when forming the AOT. Corroborating this idea is the known influence of the REE on the modifications in the composition of enamel after amelogenesis, in normal conditions, which does not play only the protective role Ten Cate 23 We believe that AOT cells might be able to secrete two types of substances, according to their functional capability: The distinction between these two substances in the routine hematoxylin and eosin staining is possible.

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We described in our results the presence of eosinophilic material in small intercellular deposits, with a shapeless pinkish aspect either lighter or darker, sometimes lamellar, both tunor in the epithelial sheets of the AOT. The former was immunohistochemically positive for laminin, therefore, representing substance of the basal membrane. tukor

The latter did not express laminin and apparently was prone to mineralization, and probably corresponded to the material positive to enamel protein in the study of Takata, et al. As the AOT is an epithelial tumor, it is interesting to analyze histochemically the different types of cytokeratins in it.

They emphasised CK odontoenic present in the inner epithelium of the enamel organ in the early bell stage, which was posteriorly substituted by CK19, when the ameloblasts were completely differentiated. We had an interesting CK14 immunohistochemical profile. In some of the samples, it labelled only cells between the spindled and duct-like odontogdnic, distinguishing two cell populations. The spindled areas and the cylindrical cells of the duct-like structures did not express it.

So, the variation in the expression of CK14 indicated variable differentiations of the tumoral cells. The spindled structures, where the duct-like and adenomatoid structures were located, would form a cell group analogous to post-secretory ameloblasts of the reduced enamel epithelium, surrounded by a second group, constituted by flat fusiform cells, sometimes with morphology similar to that of tymor stellate reticulum.

If we consider the cubic cells of the duct-like and adenomatoid structures analogous to adenomaoid ameloblasts in their early stage, still capable of secreting some enamel protein, the tendency for absence of CK14 is understandable because this also occurred in normal ameloblasts.

Adenomatoid odontogenic tumor, an uncommon tumor

From the moment at which the cells no longer have their secretory function, CK14 is expressed again. This justifies the expression in all epithelial cell elements of other AOTs and in the REE, regardless of the histological characteristics.

Laminin was clearly present in adfnomatoid luminal surface of the adenomatoid structures odontohenic in the lighter eosinophilic intercellular deposits, either focal or linear, which is compatible with the surface of the reduced enamel epithelium during the protective stage of amelogenesis.

Nevertheless, in our REE samples, laminin was not detected in the epithelial surface, probably because the REE in the samples are associated to dentigerous cyst, which would modify its expression. Type IV collagen adenokatoid restricted to the interface between tumor epithelium and stroma.

Nevertheless, the authors believed that some cells of AOT cribriform areas would resemble dental lamina primitive cellswhile others would be histodifferentially more mature secretory phase of odontogenesisdue to a 4 IV chain expression had ocurred on the cribriform areas and hyaline materials.

Case Reports in Dentistry

PCNA results in the REE odomtogenic as expected, with expression restrict to the basal or suprabasal cells or cells scattered in areas in which subepithelial inflammation was present. In the AOT, PCNA revealed that the cells in the spindled areas and in the peripheral daenomatoid were the most proliferative, which could suggest that those sites would be responsible for the tumoral growth.

We could justify the absence of the typical adenomatoid structures in the solid nodules forming sheets because they could have disappeared for having been gradually compressed by the tumoral mass as it evolved. The large adenomatoid structures, resulting from the adeomatoid tridimensional, “tubular” configuration of the columnar cells and cylindrical superficial cells of the REE due to its hamartomatous growth, would be formed in recent tumors, right from their onset.

They would gradually decrease, however, due to compression of the tumoral mass as it grew. The specific PCNA cell labelling in the AOTs, not present in the flat and stellate cells among the spindled areas, helped to rule out a neoplastic nature for the tumor.

As far as the extrafollicular variant, we agree with Philipsen, et al. The hamartomatous lesion would start at the REE and occasionally would not hinder dental timor.