Yuka Oku

Meikai University, Saitama, Saitama, Japan

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Publications (9)7.63 Total impact

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    ABSTRACT: The present report describes a rare case of styloid process syndrome with complete bilateral ossification of the stylohyoid ligament. A 20-year-old man was referred to our department because of temporomandibular joint disorder. During the 3 years after his initial visit, several symptoms related to classic styloid process syndrome appeared on the right side while ossification of the right stylohyoid ligament was ongoing. Removal of the right ossified stylohyoid ligament was achieved via the external cervical approach, and the symptoms were resolved after the operation. However, 4 years after the first operation, several symptoms of carotid artery syndrome appeared on the opposite side, and ongoing ossification of the left stylohyoid ligament was evident. Removal of the ossified left stylohyoid ligament was achieved via the same approach as that for the first operation, and the symptoms were resolved completely. The present case suggests that a change in the stylohyoid ligament from a flexible chain to a stiff bone clasp is a decisive cause of styloid process syndrome.
    Journal of Oral and Maxillofacial Surgery, Medicine, and Pathology. 04/2013; 25(2):143–146.
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    ABSTRACT: Objective This report describes the usefulness of two-channel ESS, for which an approach via the oral and nasal cavities is employed. Patients and methods Localization and precise counting of the cystic lesions was evaluated using CT, in order to decide on whether two-channel ESS was indicated. This method was indicated for (1) monocystic cases in which the lesion was in close contact with the lateral and/or inferior wall of the inferior nasal meatus, and (2) multicystic cases in which all the lesions were in close contact with the lateral wall of the nasal meatus. This study included 15 patients (8 males and 7 females), who underwent two-channel ESS for POMC between October 2007 and July 2011. The surgical technique was as follows: to facilitate an easier approach to the cyst wall in the inferior nasal meatus, the inferior nasal turbinate was slightly subluxed medially. Then, endoscopes were inserted via not only the nasal but also the oral cavity to reconfirm the interior of the cystic lesion(s) and to guide the instruments. The cyst wall opening to the nasal cavity was made as large as possible. Results We followed these patients at least for 2 year postoperatively, and the patency rate of the inferior meatal window was 93.3% in this series. Two-channel ESS yielded excellent outcomes. Conclusion On the basis of our results, we conclude that two-channel ESS is a minimally invasive method, and should be regarded as one of the first-choice methods of oral surgery for POMC.
    Journal of Oral and Maxillofacial Surgery, Medicine, and Pathology. 01/2013;
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    ABSTRACT: Heparanase is an endoglycosidase that cleaves heparan sulfate (HS), thus participating in degradation and remodeling of the extracellular matrix (ECM). Heparanase up-regulation is correlated with lymph node and distant metastasis, microvessel density and reduced postoperative survival of cancer patients. In the present study, we carried out an immunohistochemical investigation of heparanase to extend and confirm present knowledge regarding its expression in ameloblastomas (AMs), which are characterized by locally aggressive behavior. Paraffin-embedded tissue specimens of 53 AMs were stained using an antibody against heparanase. Immunohistochemical reactivity for heparanase was detected in 94.3% of the AMs examined. Heparanase was expressed strongly in peripheral columnar cells and slightly in central stellate reticulum-like cells. Small tumor nests and budding epithelial branches showed a stronger staining pattern. Stromal cells were negative for heparanase, or showed diffuse expression. However, an enhanced positive immunoreaction was present specifically near osseous tissue and adjacent to the invasive front of tumor nests. Areas of cystic degeneration showed intense heparanase immunoreactivity. The enzyme may facilitate the function of HS-binding growth factors that elicit an angiogenic response and favor osteoclastogenesis in AM.
    Journal of Oral Science 01/2010; 52(1):39-47.
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    ABSTRACT: The most important clinical features of the keratocystic odontogenic tumor (KCOT) are its potential for locally destructive behavior, a tendency to recur, and its origin in the odontogenic epithelium. The clinical features of KCOT are similar to those of ameloblastoma (AM). Histologically, KCOT is distinguished from jaw cyst with keratinization (orthokeratinized odontogenic cyst; OOC). However, current scientifically based clinical parameters cannot predict any potential for neoplastic behavior, or aggressive and localized invasiveness, in patients with KCOT. We have shown that podoplanin, a lymphatic endothelial marker, is highly expressed in AM. The purpose of this study was to determine the usefulness of podoplanin for reclassification of the odontogenic keratocyst (OKC) from cyst to tumor status. Paraffin-embedded tissue specimens of 57 OKCs (46 KCOTs and 11 OOCs) and 15 dentigerous cysts (DCs) were immunohistochemically examined using antibody against podoplanin. Immunohistochemical reactivity for podoplanin was detected in the cell membrane and cytoplasm of most of the basal and suprabasal layer, areas of budding basal cell proliferation, epithelial nests and peripheral cells of daughter cysts in the stromal connective tissue in KCOTs. In the case of OOC and DC, only cases associated with inflammation were positive for podoplanin. Podoplanin is strongly expressed in KCOTs in comparison with OOCs. The pattern of staining for podoplanin in KCOT could be related to its neoplastic nature, and suggests a role of the protein in tumor invasiveness.
    Journal of Oral Pathology and Medicine 11/2009; 39(1):110-4. · 2.06 Impact Factor
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    ABSTRACT: Podoplanin, a mucin-type transmembrane glycoprotein, is specifically expressed by lymphatic but not blood vascular endothelial cells, and is also widely expressed in various specialized cell types throughout the body. Recent studies have demonstrated that it mediates a pathway leading to collective cell migration and invasion in vivo and in vitro. In the present study, we carried out an immunohistochemical investigation of podoplanin to clarify whether it is expressed in human ameloblastomas (AMs), which are characterized by locally aggressive behavior with a high rate of recurrence. In addition, we examined the localization of the epithelial marker E-cadherin and the mesenchymal marker vimentin to clarify whether AMs show epithelial-mesenchymal transition (EMT). Paraffin-embedded tissue specimens of 38 AMs were examined immunohistochemically using antibodies against podoplanin, E-cadherin, and vimentin. Immunohistochemical reactivity for podoplanin was detected in the cell membrane and cytoplasm of most odontogenic tumor epithelial cells in AMs. Podoplanin was expressed strongly in peripheral columnar cells and slightly in central stellate reticulum-like cells. E-cadherin was expressed in central stellate reticulum-like cells and showed decreased expression in peripheral columnar cells. Immunoreactivity for E-cadherin was weak or negative in keratinizing cells of acanthomatous AMs, suggesting terminal differentiation of the tumor cells. Immunohistochemical reactivity for vimentin was found in stromal cells, but partial or no reaction was observed in neoplastic cells. Expression of podoplanin in AMs is considered to be associated with neoplastic odontogenic tissues; this molecule might play a role in the collective cell migration of tumor nests in AMs. The pattern of expression of E-cadherin and vimentin suggests that invasion in AMs occurs in the absence of EMT. The migration and invasion mediated by podoplanin in AMs could be related to cytoskeletal reorganization.
    Journal of Oral Pathology and Medicine 09/2009; 39(1):103-9. · 2.06 Impact Factor
  • Oral Medicine & Pathology. 01/2009; 13(2):71-74.
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    ABSTRACT: In 2005, the WHO Working Group considered odontogenic keratocyst (OKC) to be a tumor and recommended the term keratocystic odontogenic tumor (KCOT), separating the lesion from the orthokeratinizing variant, which is now considered an odontogenic cyst. We analyzed the clinicopathological features of KCOTs encountered over a period of 28 years at Meikai University Hospital. The diagnosis was confirmed by reevaluation of hematoxylin and eosin-stained slides on the basis of the 2005 WHO Classification. Clinical history was also taken into consideration. A total of 183 KCOTs were found, and the two genders were affected almost evenly (51.3% male; 48.7% female; male to female ratio 1.05 to 1). Patient age at the time of diagnosis ranged from 6 to 78 years, with a peak in the third decade of life (mean age: 32.8 years). The mandible was the site of occurrence of 70.5% of tumors; 16.4% occurred in the maxilla and 13.1% in both. Association with the nevoid basal cell carcinoma syndrome (NBCCS) was found in 6.0% of all tumors, and recurrence was found in 13.1% of patients. We found that tumors that initially appeared in the maxilla alone had a higher recurrence rate than those that first appeared in the mandible alone. Pathological examination of KCOT is important to avoid misdiagnosis and provide appropriate treatment and follow-up.
    Journal of Oral Science 07/2008; 50(2):205-12.
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    ABSTRACT: Neural cell adhesion molecule (NCAM) is a type of cell surface glycoprotein and a member of the immunoglobulin superfamily. It has been reported that NCAM may be associated with perineural invasion by malignant salivary gland tumors such as adenoid cystic carcinoma. We have previously demonstrated that NCAM is constitutively expressed in the human salivary gland tumor cell line HSG, in vitro. In the present study, we have aimed to clarify the hypothesis that NCAM-mediated inhibition of salivary gland tumor proliferation is caused by homophilic binding and involves the prevention of signal transduction for perineural invasion using HSG cells. NCAM mRNA and protein expression was found to decrease in a dose-dependent manner upon treatment with the anti-NCAM antibody (MAb NCAM) for 24 h. The MTT assay showed a significant reduction in the number of viable HSG cells. Confocal laser microscopy showed that HSG cells underwent apoptosis after treatment with MAb NCAM. The activation of caspases 3, 7 and 9 was observed in HSG cells after treatment with MAb NCAM, thus confirming that apoptosis was induced by the activated caspases. Apaf-1 activity was also detected in HSG cells in a dose-dependent manner after treatment with MAb NCAM. The up-regulation of TGF-beta1-mediated NCAM expression appeared to lead to the activation of homophilic NCAM binding, further accelerating HSG cell proliferation. In addition, the localization of NCAM in adenoid cystic carcinomas (ACCs) was examined using an immunohistochemical method. NCAM was slightly to moderately positive in 9 of 13 cases (69.2%) of ACC. These findings suggest that NCAM is associated not only with a cell-to-cell adhesion mechanism, but also with tumorigenesis, including growth, development and perineural invasion in human salivary gland tumors.
    Oncology Reports 12/2005; 14(5):1143-9. · 2.30 Impact Factor
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    ABSTRACT: The cylindromatosis (CYLD) gene was originally identified as a tumor suppressor that is mutated in familial cylindromatosis, an autosomal dominant condition that confers a predisposition to multiple tumors of the skin appendages. CYLD has deubiquitinating enzyme activity and inhibits the activation of transcription factor NF-kappaB. Therefore, loss of CYLD function correlates with tumorigenesis. Expression of CYLD has been detected in various organs, but its expression in salivary gland tumor (SGT) is still unknown. Adenoid cystic carcinoma (ACC) is a well known and typical malignant SGT ACC was previously known as cylindroma in view of its marked histological resemblance to dermal cylindroma. In this study, the expressions of CYLD and NF-kappaB mRNA in HSG, a human SGT cell line, were found to be increased by TNF-alpha stimulation. Immunohistochemistry clearly demonstrated the expression of CYLD and NF-kappaB-related factors in ACC tissue.
    In vivo (Athens, Greece) 20(4):467-72. · 1.22 Impact Factor