Peripheral ameloblastoma: biological profile based on 160 cases from the literature.

The present profile of the peripheral ameloblastoma (PA) is based on a literature survey of 160 published tumour cases. The PA is an exophytic growth localized to the soft tissues overlying the tooth-bearing areas of the jaws, the initial diagnosis often being fibrous epulis. In most cases there is no radiological evidence of bone involvement, but a superficial bone erosion--known as cupping or saucerization--may be detected at operation. The PA accounts for 2-10% of all ameloblastomas. The overall average age is 52.1 years, slightly higher for males (52.9 years) than for females (50.6 years). Thus, the PA occurs at a significantly higher age than the intraosseous ameloblastoma (IA; 37.4 years). The male/female ratio amounts to 1.9:1, as opposed to 1.2:1 for the IA. The male/female ratio for the Japanese cases included in this survey is 2.5:1 as opposed to that of non-Japanese cases 1.4:1. As to the location of PA, the maxilla/mandible ratio is 1:2.6. The mandibular premolar region accounts for 32.6% of all sites. Five extra-gingival lesions have been reported under the term PA. As these cases most likely represent salivary gland tumours, they are not accepted under the diagnosis of PA. The odontogenic gingival epithelial hamartoma shows clinical, histological and behavioural features almost identical to the PA, and it is discussed whether this lesion and the PA should be considered one and the same entity. Pathogenetically, two major sources are discussed: remnants of the dental lamina and the oral surface epithelium. Histologically, the PA consists of proliferating odontogenic epithelium exhibiting the same histomorphological cell types and patterns as seen in the IA. The stroma is that of a mature, fibrous connective tissue. The indolent biological behaviour dictates a conservative therapeutical approach. It is discussed whether PA is a true neoplastic counterpart of the IA or rather an odontogenic hamartomatous lesion. Six cases of malignant PA have been reported.

Immunohistochemical detection and distribution of enamelysin (MMP-20) in human odontogenic tumors.

Enamelysin is a tooth-specific protease that was initially isolated from porcine enamel organ and subsequently from human odontoblasts. Since this protease is thought to play important roles in tooth development, the evaluation of enamelysin in odontogenic tumors may aid our understanding of the histogenesis and cell differentiation of such lesions. A monoclonal antibody (203-1C7) was generated against synthesized human enamelysin oligopeptide and was used to assess the immunolocalization of enamelysin in healthy developing tooth germs and various types of odontogenic lesions. In tooth germs, enamelysin expression was detected only in the secretory enamel. Thus, 203-1C7 may serve as an enamel-specific marker in the late stage of enamel matrix development and calcification. In odontogenic lesions, strong enamelysin staining was demonstrated in the immature enamel matrix of ameloblastic fibro-odontomas and odontomas. Furthermore, enamelysin was also detected in globular amyloid masses and calcified foci in calcifying epithelial odontogenic tumors, hyaline droplets, small and large mineralized areas in adenomatoid odontogenic tumors, and a portion of ghost cells in calcifying odontogenic cysts. Positive reactivity was also observed in selected tumor cells in some of these tumors. No intracellular staining for enamelysin was detected in ameloblastomas or the ameloblastic portion of ameloblastic fibro-odontomas. Also, enamelysin was not detected in dentin, dysplastic dentinoid hyaline matrices, and cementum that were present within the tumors examined. Thus, taken together, our results suggest that the enamelysin-specific monoclonal antibody (203-1C7) may be utilized as a marker of early enamel development and that enamelysin may be involved in the pathogenesis of specific odontogenic tumors.

Immunoexpression of transforming growth factor beta in desmoplastic ameloblastoma.

Desmoplastic ameloblastoma (DA) is an unusual subtype of ameloblastoma histologically characterized by the pronounced collagenized stroma. In the present study, the immunolocalization of transforming growth factor beta (TGF-beta), one of the most potent local factors for modulating extracellular matrix formation, was observed in DA in order to study its participation in the stromal desmoplasia. Seven cases of DA, including a "hybrid" lesion, were studied together with ten cases of ordinary follicular and plexiform ameloblastomas as the control. In contrast to ordinary ameloblastomas, marked immunoexpression was observed in all DAs but one. In the "hybrid" lesion, TGF-beta was not expressed in the area of follicular ameloblastoma but in that of DA. These results show that TGF-beta produced by tumor cells of DA plays a part in the desmoplastic matrix formation.

Immunohistochemical demonstration of an enamel sheath protein, sheathlin, in odontogenic tumors.

Enamel proteins can be useful markers for assessment of the functional differentiation of neoplastic epithelium and the nature of extracellular matrices in odontogenic tumors. In the present study, we examined immunohistochemical localization of sheathlin, a recently cloned enamel sheath protein, in various odontogenic tumors to evaluate functional differentiation of tumor cells and the nature of hyalinous or calcified matrices in odontogenic neoplasms. Distinct immunolocalization of sheathlin was observed in the immature enamel of the tooth germ at the late bell stage. Secretory ameloblasts facing the enamel matrix also showed positive staining in their cytoplasm. Definite localization of sheathlin was demonstrated in the enamel matrix in odontogenic tumors with inductive dental hard tissue formation such as ameloblastic fibroodontomas and odontomas. Immunoexpression of sheathlin was, furthermore, demonstrated in eosinophilic droplets in solid nests of adenomatoid odontogenic tumor (AOT) and ghost cells in the epithelial lining of calcifying odontogenic cyst (COC). In AOT, cells facing the eosinophilic droplets also expressed the protein in their cytoplasm. There was neither intracellular staining for sheathlin in the tumor cells nor extracellular staining in the matrix of ameloblastomas and calcifying epithelial odontogenic tumors. Dentin, dysplastic dentin-like hyaline material and cementum in the tumors examined were negative for sheathlin. These results show that immunodetection of sheathlin is a useful marker for functional differentiation of secretory ameloblasts and enamel matrix, which is often hard to differentiate from other hard tissues in odontogenic tumors. Our findings from the view point of sheathlin expression support that the tumor cells of ameloblastomas do not attain full differentiation into functional ameloblasts. It is very interesting that epithelial cells in odontogenic tumors can differentiate into functional ameloblasts without induction by odontogenic mesenchyme, as shown by immunoexpression of sheathlin in eosinophilic droplets within solid epithelial sheets in AOT and ghost cells in the epithelial lining of COC where inductive participation of mesenchymal cells was most unlikely.

Ghost cells in calcifying odontogenic cyst express enamel-related proteins.

The so-called ghost cell is a unique cell type occurring in a variety of odontogenic and non-odontogenic lesions. However, the true nature of ghost cells has not been determined. In the present study, we examined the immunoreactivity of ghost cells in calcifying odontogenic cysts and dermal calcifying epitheliomas, with antibodies against amelogenin, enamelin, sheath protein (sheathlin) and enamelysin, in an attempt to clarify the nature of this unique cell. The cytoplasm of ghost cells in calcifying odontogenic cysts demonstrated distinct immunolocalization of the enamel-related proteins, while similar in the calcifying epitheliomas of the skin showed a negative reaction. The results indicate that the ghost cells in calcifying odontogenic cysts, as opposed to ghost cells in dermal calcifying epitheliomas, contain enamel-related proteins in their cytoplasm accumulated during the process of pathological transformation.

Reduced expression of p27(Kip1) correlates with an early stage of cancer invasion in oral squamous cell carcinoma.

Down-regulation of p27(Kip1) has been reported to correlate with poor survival of various carcinoma patients including oral squamous cell carcinomas (OSCCs). It is still unclear, however, at what stage of oral carcinogenesis the down-regulation of this protein occurs. In this study, therefore, we evaluated immunoexpression of p27(Kip1) protein in 17 cases of oral epithelial dysplasia and succeeding invasive OSCC in the same patient. We reported here that 88% cases showed high p27(Kip1) expression in dysplastic lesions, whereas 82% cases of succeeding invasive OSCC exhibited reduced expression. The reduction of p27(Kip1) expression was also observed in 16 of 19 (84%) early invasive lesions and well correlated with Ki-67 expression which is good indicator of cell proliferation. We also investigated immunoexpression of p53 protein of which abnormality has been known to occur during the early stage of OSCC development. Overexpression of p53 protein was demonstrated in 29% of dysplastic lesions, 42% of early invasive and 71% of invasive OSCCs. These findings suggest that abnormalities of both p53 and p27(Kip1) are involved in the carcinogenesis of OSCC, but they seem to play their role at different stages of oral cancer development, respectively. Reduced expression of p27(Kip1) may concern the cancer invasion directly or indirectly as well as abnormal proliferation.

p27Kip1 accumulation by inhibition of proteasome function induces apoptosis in oral squamous cell carcinoma cells.

Ubiquitin-mediated proteolysis controls intracellular levels of various cell cycle regulatory proteins, and its inhibition has been shown to induce apoptosis in proliferating cells. In the present study, we examined induction of apoptosis in oral squamous cell carcinoma (OSCC) cells by treatment with specific proteasome inhibitors, carbobenzoxy-L-leucyl-L-leucyl-L-norvalinal and lactacystin. In all three OSCC cell lines examined, apoptotic changes such as apoptotic body formation and DNA fragmentation were observed at various degrees after 24 h of the carbobenzoxy-L-leucyl-L-leucyl-L-norvalinal or lactacystin treatment. HSC2 cells showed the most prominent apoptotic changes among the cell lines examined and demonstrated the highest level of accumulation of p27Kip1 protein after the treatment with proteasome inhibitor. Reduced expressions of cyclin D1 and phospho pRb were also observed after the treatment with proteasome inhibitor. Moreover, 12 h of treatment with the proteasome inhibitor inhibited cdk2/cyclin E kinase activity and increased the ratio of the cell cycle population at the G1 phase. The proteasome inhibitor led to inhibition of cell cycle progression. In addition, activation of CPP32 and reduced expression of Bcl-2 were observed. Because apoptosis induced by the proteasome inhibitor was inhibited by treatment with antisense p27Kip1 oligonucleotide, accumulation of the p27Kip1 protein might play an important role in the apoptosis induced by proteasome inhibitor. The present results suggest that inhibition of proteasome function may be used as a possible target of novel therapy for OSCC.

So-called 'hybrid' lesion of desmoplastic and conventional ameloblastoma: report of a case and review of the literature.

So-called 'hybrid' lesion of ameloblastoma, which is composed of desmoplastic ameloblastoma and conventional follicular/plexiform ameloblastoma, is an unusual variant of ameloblastoma and only eight cases of 'hybrid' lesion have been published in the English literature. To enhance knowledge of this interesting tumor, we add a case of 'hybrid' lesion that occurred in the right mandible of a 48-year-old Japanese male. Radiographic examination disclosed a honeycomb appearance at the anterior alveolar region, combined with a unicystic radiolucency in the molar region of the mandibular body. Histologically, the former showed microscopic features of desmoplastic ameloblastoma and the latter those of follicular ameloblastoma with focal granular cell transformation. The lesion was enucleated with curettage of surrounding bone and the lesional cavity was marsupialized. Although tumor tissues reappeared at 3, 5, 7 and 14 months after the surgery, the patient has remained disease free for 11 years after the last vaporization by CO2 laser of the recurred tumor. Many more cases of 'hybrid' lesion are needed to clarify the clinicopathological, histopathological and biological characteristics of this interesting variant of ameloblastoma.

Clinical and histopathological analyses of desmoplastic ameloblastoma.

Desmoplastic ameloblastoma (DA) is an unusual subtype of ameloblastoma characterized by pronounced desmoplastic stroma. There is, however, still argument whether DA is a distinct clinicopathologic entity. To enhance knowledge of DA, 7 cases of DA (7.9%) were retrieved from 89 ameloblastomas field in the Department of Oral Pathology, Hiroshima University School of Dentistry and analyzed clinicopathologically and histopathologically. The mean age of the patients with DA and non-DA at the time of the diagnosis was 40.6 +/- 5.9 years and 33.1 +/- 2.0 years, respectively. The male-to-female ratio was 2.5:1 in DA and 1.8:1 in non-DA. Four (57%) DAs were located in the maxilla where only 6% of the non-DA occurred. Interestingly, all DAs arose in the anterior/premolar area of the jaws and 6 cases were located mainly within the alveolus. None of the DA showed typical radiographic features of ameloblastoma. In 5 DAs, scattered radiopacities were observed in the radiolucent lesion and gave preoperative diagnoses of non-ameloblastomatous lesions or even osteosarcoma. All DAs showed pronounced desmoplastic stroma where there were compressed tumor islands usually lacking a peripheral layer of ameloblastic cells and a central zone of stellate reticulum. There was cystic change within the epithelial nests in 3 DAs and true glandular structures with mucus cells in a case of DA. Tumor islands often infiltrated into marrow spaces of surrounding bone. There was no capsule formation. Recurrence rate was 14% in DA and 20% in non-DA. The present study based on data of DA in the Japanese population supports that DA must be considered as a distinct clinicopathologic entity.

Biosynthesis of glycosaminoglycans and aggrecan by tumor cells in salivary pleomorphic adenoma: ultrastructural evidence.

The present study attempted to discover the sites of synthesis of various glycosaminoglycans (GAGs) and aggrecan in salivary pleomorphic adenoma (PA) with the use of a highly sensitive and specific post-embedding immunogold-silver staining technique at the ultrastructural level. Silver particles representing various GAGs and aggrecan were found to accumulate frequently in the intercellular spaces of non-luminal cells in the epithelial clusters and were dispersed in the myxoid matrix of the mesenchyme-like areas. Furthermore, the non-luminal epithelial cells were demonstrated to contain immunopositive intracytoplasmic vesicles and vacuoles, some of which were of Golgi complex origin. In contrast, intracellular silver particles for hyaluronic acid were mostly attached to the inner surface of the cell membrane. These observations agree well with the current theories of the biosynthesis of GAGs and proteoglycans and provide direct evidence for the production of various GAGs and aggrecan by tumor epithelial cells of PA. Such findings support the ideas that in PA a loss of epithelium occurs by stromalization following epithelial secretion of extracellular matrix substances and transformation of epithelium to mesenchyme represents the basic principle of the tissue heterogeneity in this tumor.

Reduced expression of p27(Kip1) protein in relation to salivary adenoid cystic carcinoma metastasis.

BACKGROUND: Adenoid cystic carcinoma (ACC) is a malignant tumor of salivary gland origin. It tends to grow slowly but shows frequent recurrence and metastasis, ultimately with a poor outcome. Reduced expression of a cyclin-dependent kinase inhibitor, p27(Kip1), has been reported to correlate with poor survival for patients with various types of carcinoma. However, there has been no previous study reported of p27(Kip1) expression in ACC, to the authors' knowledge. METHODS: To evaluate p27(Kip1) as a prognostic marker, the authors examined the immunohistochemical expression of p27(Kip1) protein in 29 ACCs and correlated its expression with clinicopathologic findings. Eleven pleomorphic adenomas (PAs) were also examined to compare the p27(Kip1) expression in benign and malignant salivary gland tumors. RESULTS: All PAs expressed p27(Kip1) at high levels, whereas 83% of ACCs (24 of 29) showed reduced expression of this protein. Furthermore, the expression levels were significantly lower in ACCs with metastasis than in those without metastasis. The authors also examined the expression of p27(Kip1) in 2 ACC cell lines (ACCh and ACC3) by Northern and Western blot analysis to elucidate the possible mechanism of p27(Kip1) reduction in ACC. Both ACCh and ACC3 expressed p27(Kip1) mRNA, but ACCh did not produce p27(Kip1) protein. In ACCh, the expression of p27(Kip1) protein was induced by treatment with a proteasome inhibitor. CONCLUSIONS: Overall, these findings suggest that reduced expression of p27(Kip1) may correlate with the development and progression of salivary ACC and can be an indicator of its malignant behavior. They also suggest that increased proteasome-mediated degradation may play an important role in this reduction of p27(Kip1) expression.

Silencing of the CD44 gene by CpG methylation in a human gastric carcinoma cell line.

We analyzed 8 human gastric carcinoma cell lines for the expression of CD44 by northern blot analysis and reverse transcription-polymerase chain reaction (RT-PCR), and identified 1 cell line MKN-28 that did not express CD44. In an attempt to clarify the mechanism responsible for the inactivation of CD44 gene expression in this cell line, we investigated the methylation status around the promoter region of CD44 gene by digestion of the DNA with the methylation-sensitive restriction enzyme HpaII. The promoter region of CD44 in MKN-28 revealed hypermethylation, whereas other CD44-positive cell lines did not. Furthermore, treatment of MKN-28 with the demethylating agent 5-azacytidine restored the expression of the gene. These results suggest that CD44 expression is controlled by a DNA hypermethylation mechanism in MKN-28.

Immunohistochemical and histochemical characterization of the mucosubstances of odontogenic myxoma: histogenesis and differential diagnosis.

To discuss the dental origin of odontogenic myxoma and to provide further information for the differential diagnosis between this tumor and myxoid malignant fibrous histiocytoma (MFH) which occasionally occurs in jaw bones, the contents of glycosaminoglycans (GAGs) and proteoglycans (PGs) in the mucosubstances of 15 odontogenic myxomas, 5 myxoid MFH and 3 human fetal tooth germs in the bell stage of development were characterized using histochemical and immunohistochemical methods. Histochemical staining of hyaluronic acid (HA) was undertaken using biotinylated HA binding protein (B-HABP), and immunohistochemical detection was done using a panel of antibodies against chondroitin 6-sulfate (CS-6), chondroitin 4-sulfate (CS-4), dermatan sulfate (DS), keratan sulfate (KS), heparan sulfate (HS), aggrecan, PG-M/versican, decorin and biglycan. In odontogenic myxoma, CS-6, HA and PG-M/versican were observed in the myxomatous matrix of all cases, while KS and HS were seen in none. As for CS-4, DS, aggrecan, decorin and biglycan, only irregular and mild stainings were shown. Consistent and strong positive straining for CS-6, HA and PG-M/versican were seen in dental papilla and provided evidence supporting the origin of this tumor from dental papilla. Except for the constant staining for HA, the myxoid matrix was rarely stained for most GAGs and PGs in myxoid MFH. Immunodetection of CS-6 and PG-M/version with the use of monoclonal antibodies 3-B-3 and 2-B-1 is therefore recommended as a useful tool in differentiating odontogenic myoma from myxoid MFH.

Expression of p53 and p21CIP1/WAF1 proteins in oral epithelial dysplasias and squamous cell carcinomas.

The expression of tumor suppressor gene, p53 and cyclin-dependent kinase inhibitor, p21 in oral epithelial dysplasia and oral squamous cell carcinoma (OSCC) was examined immunohistochemically and its relationship with clinicopathological findings was analyzed. Among 24 epithelial dysplasias, 4 cases (17%) expressed p53 protein and 23 cases (96%) expressed p21 protein. On the other hand, expression of p53 was observed in 64% of OSCCs, and expression of p21 was observed in 77% of OSCCs. In the analyses of the correlation between the expression of p53 and p21 in epithelial dysplasia and OSCC, 79% of epithelial dysplasias were p53-negative and p21-positive, compared to 25% of the OSCCs. p21 expression did not correlate with p53 expression. These results were also demonstrated in OSCC cell lines by western blot analysis. Cumulative survival rate of the patients p53-negative and p21-positive was higher than those p53-positive and p21-negative, those p53-negative and p21-negative and those p53-positive and p21-positive. These findings suggest that p53 expression and p21 negative expression may involve in neoplastic transformation of oral epithelium. In the present study, we did not observe correlation between the expression of p53 and p21 proteins in OSCC. p21 expression may be regulated by p53-independent pathways as well as p53-dependent ones. However, combination of the p21 and p53 expression may be useful as a prognostic marker.

Periodontitis in the house musk shrew (Suncus murinus): a potential animal model for human periodontal disease.

BACKGROUND: Our understanding of periodontal diseases has been facilitated greatly by the use of animal models. However, no animal model has been identified that truly reflects the disease seen in humans. Suncus murinus, a rat-sized laboratory house musk shrew, has received attention as a valuable animal model due to ease of handling. In the studies described here, periodontal conditions in Suncus murinus were evaluated to determine the usefulness of the shrew as an experimental model for understanding various aspects of periodontal diseases. METHODS: Periodontal tissues of 34 Suncus murinus (18 to 430 days old) were examined macroscopically, morphometrically, histologically, and ultrastructurally. RESULTS: Dentition pattern is I3/1, C1/1, P2/1, M3/3. Spontaneous gingival swelling with accumulation of plaque was observed in more than two-thirds of animals older than 200 days. Morphometric analysis of alveolar bone demonstrated a pattern of bone loss that correlated closely with animal age. Histologically, periodontal lesions varying from gingivitis to periodontitis, similar to those observed in humans, were noted. Marked infiltration of lymphocytes and plasma cells in the connective tissue was noted, usually not seen in periodontal lesions of rodents. Although osteoclastic alveolar bone resorption was noted, active bone resorption was not a frequent feature in specimens obtained from chronic inflammatory lesions. Ultrastructurally, degradation of collagen fibers in the inflamed area and ingestion of collagen fibrils by fibroblasts in the deeper connective tissue were often seen. CONCLUSIONS: These results indicate the potential utility of Suncus murinus as a model to study periodontal disease; e.g., chronic nature of the inflammatory periodontal lesions, similar to those in humans, as well as other advantages including size and ease of handling and housing of these animals.

Immunohistochemical evaluation of the small and large proteoglycans in pleomorphic adenoma of salivary glands.

This study investigated the immunolocalization of small and large proteoglycans (PGs), including decorin, biglycan, PG-M/versican and aggrecan, in salivary pleomorphic adenoma (PA) using monoclonal and polyclonal antibodies. In addition, a polyclonal antibody, A0082, recognizing blood vessels was also used to help identify truly mesenchymal tissues in PA. Decorin reactivity was detected only in tumor capsule and interstitial tissue of non-neoplastic salivary gland, but not in the tumor tissue. Biglycan was frequently revealed throughout the matrix of small chondroid regions and in the peripheral portion of larger chondroid regions. PG-M/versican was mainly localized to the truly mesenchymal tissues in PA and the innermost portion of tumor capsule. On the contrary, aggrecan was extensively expressed in the non-luminal epithelial areas as well as in the myxoid and chondroid areas, but not in the truly mesenchymal tissues. These findings suggest that aggrecan is the most widely distributed PG in PA and may be produced mainly by non-luminal tumor cells. The absence of aggrecan from the truly mesenchymal tissues argues against its origin from this source. Both aggrecan and biglycan may play important roles in the chondroid differentiation and morphogenesis of PA.

Proliferative activity of calcifying odontogenic cysts as evaluated by proliferating cell nuclear antigen labeling index.

The calcifying odontogenic cyst (COC) presents with diverse histological features; thus, several subclassifications have been proposed. To evaluate the significance of the various histological features and subtypes of COC from the perspective of proliferative activity, the proliferating cell nuclear antigen (PCNA) labeling index (LI; the percentage of positive nuclei) was assessed immunohistochemically in 25 cases of COC (21 benign and four malignant). All of the benign cases were of the cystic variety and further subclassified into non-proliferative subtype (NPS; four cases); proliferative subtype (PS; eight cases); and COC associated with odontoma (COCaO, nine cases). The PCNA LI of the malignant COC (65.2+/-5.6) was significantly higher than that of the benign COC (11.6+/-9.0; P = 0.002). Non-proliferative subtype (6.8+/-2.8) showed the lowest PCNA LI and PS (17.2+/-11.2) the highest of among the three subtypes of benign cystic COC (P = 0.028). In nine cases of COCaO, six showed epithelial lining of the non-proliferative type as NPS and the other three had lining with proliferative features as PS. The PCNA LI of the latter COCaO group (14.3+/-6.6) was significantly higher than that of the former (6.1+/-4.3; P = 0.05), as seen between PS and NPS. These results demonstrate that PCNA LI is a possible parameter for differentiating malignant COC from benign COC and, whatever the subtypes, the proliferative features in the lining are the main factor influencing the proliferating activity of COC.

Odontogenic tumors. A demographic study of 759 cases in a Chinese population.

Seven hundred fifty-nine cases of odontogenic tumors retrieved from the files of College of Stomatology, West China University of Medical Sciences were classified according to the World Health Organization's Histological Classification of Odontogenic Tumors and compared with similar reports from other countries. Among these cases, 93.9% of the tumors were benign and 6.1% were malignant. Ameloblastomas predominated (58.6%) with a predilection for the mandible, while odontomas, generally regarded as the most frequent odontogenic tumor in North America, only accounted for 6.7%, the fourth most common tumor in this series. The mandible and the maxilla were divided into eight anatomic regions, and the distribution of each odontogenic tumor type amongst these regions was recorded. The relative incidence of each tumor type, patient age and gender were also compared with data from other selected large series. Geographic differences were noted in the relative incidence of ameloblastoma, odontoma and malignant odontogenic tumors among the Chinese/African, North American and Turkish/German groups. Ameloblastoma and malignant odontogenic tumors are not considered rare in a Chinese population.

Three-dimensional appearance of Langerhans cells in human gingival epithelium as revealed by confocal laser scanning microscopy.

Detailed three-dimensional morphological information of the cell without distortion due to thin sectioning can be obtained from thick sections using a confocal laser scanning microscope. Here that microscope was used to evaluate human gingival Langerhans cells stained with anti-CD1a antibody. Optical sectioning and reconstruction by laser scanning microscopy revealed not only three-dimensional aspects of Langerhans cells but also spatial information on the distribution of their dendritic processes towards the gingival surface. The orientated configuration of those processes may reflect the reaction of the gingival Langerhans cell to the surrounding moist environment containing antigenic stimuli originating in saliva.

Distribution of macrophage lineage cells in rat gingival tissue after topical application of lipopolysaccharide: an immunohistochemical study using monoclonal antibodies: OX6, ED1 and ED2.

To discuss the role of macrophage lineage cells on the periodontal tissue destruction, we immunohistochemically examined the phenotype and the dynamics of macrophage lineage cells 1 or 3 h or 1, 2, 3 or 7 d after topical application of LPS (5 mg/ml in physiological saline) from the rat gingival sulcus using 3 monoclonal antibodies: OX6 (antigen-presenting cells), ED1 (monocytes, macrophages and dendritic cells) and ED2 (resident macrophages). We could detect at least 3 different types of macrophage lineage cells, namely OX6+/ED1+/ED2- dendritic cells and exudate macrophages and ED2+ resident macrophages. After LPS application the majority of macrophage lineage cells accumulated in the subjunctional epithelial area were newly extravasated OX6+/ED1+/ED2- dendritic cells or macrophages. The number of these cells increased progressively with time and reached a maximum level at d 2. On the other hand, number and tissue distribution of ED2+ resident macrophages did not change. These results indicate that several types of macrophage lineage cells exist in rat gingival tissue and suggest that dendritic cells and exudate macrophages transiently accumulated after LPS application are responsible for various host immune response and tissue destruction caused by LPS.