Yasuyuki Michi

Tokyo Medical and Dental University, Edo, Tōkyō, Japan

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Publications (14)24.17 Total impact

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    ABSTRACT: Chronic osteomyelitis of the jaw (COMJ) is one of the most intractable diseases among head and neck infections. Antimicrobial agents are routinely administered for COMJ without sufficient bacterial information, resulting in frequent treatment failures. To improve our knowledge on the bacterial aetiology of COMJ and assist in the development of effective treatments, we performed comprehensive analysis of the microbiome. Sixteen patients with 4 clinical types of COMJ (i.e. 4 with suppurative osteomyelitis, 3 with osteoradionecrosis of the jaw, 4 with primary chronic osteomyelitis, and 5 with bisphosphonate-related osteonecrosis of the jaw) were enrolled in this study. Bone samples were subjected to bacterial community comparisons using 16S rRNA gene pyrosequencing. As a result, we clarified that COMJ was caused by far more diverse bacterial species (a total of 12 phyla, 163 genera) than previously reported. Moreover, the bacterial structures in COMJ changed dramatically with the disease stages and condition of the affected bone. Multiple correlation analyses revealed that sequestration and bone exposure could affect the community structure. Based on these factors, we reclassified COMJ into 3 clinical stages: I, inflamed or sclerotic bone without exposure; II, sequestrum without exposure; and III, exposed sequestrum. In stage II, the bacterial diversity was significantly lower, and the anaerobe genera Fusobacterium, Tannerella (formerly Bacteroides), and Porphyromonas were more abundant than observed during other stages. Because these bacteria habitually reside in any clinical stage, they were considered as the core microbiome of COMJ. Targeting these bacteria should lead to the development of effective preventions and cures. This article is protected by copyright. All rights reserved.
    Clinical Microbiology and Infection 09/2013; · 4.58 Impact Factor
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    ABSTRACT: We report a case of hemangiopericytoma of the soft palate of 60-year-old patient, who noticed a mass of the soft palate and experienced difficulty in speaking. We found a pediculate, hard, elastic mass measuring 38 mm (cross-sectional diameter). Computed tomography (CT) scans and dynamic magnetic resonance imaging (MRI) confirmed irregularly shaped mass and revealed a heterogeneous internal composition, consistent with vascular tumors. We excised the tumor under general anesthesia. Histopathological diagnosis was based on positive immunoreactivity of CD99 and vimentin and weak, positive staining of CD34. Three and half years following tumor excision, there is no recurrence or metastasis.International Journal of Oral Science (2013) 5, doi:10.1038/ijos.2013.25; published online 24 May 2013.
    International Journal of Oral Science 05/2013; · 2.72 Impact Factor
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    ABSTRACT: Plinabulin (NPI-2358) is a novel microtubule-depolymerizing agent. In HeLa cells, plinabulin arrests the cell-cycle at M phase and subsequently induces mitotic catastrophe. To better understand the effects on this compound on the cell-cycle, we used the fluorescent ubiquitination-based cell cycle indicator (Fucci), which normally enables G1 and S/G2/M cells to emit red and green fluorescence, respectively. When HeLa-Fucci cells were treated with 50nM plinabulin, cells began to fluorescence both green and red in an unusual pattern; most cells exhibited the new pattern after 24h of treatment. X-irradiation efficiently induced G2 arrest in plinabulin-treated cells and significantly retarded the emergence of the unusual pattern, suggesting that entering M phase is essential for induction of the pattern. By simultaneously visualizing chromosomes with GFP-histone H2B, we established that the pattern emerges after nuclear envelope breakdown but before metaphase. Pedigree assay revealed a significant relationship between the unusual expression and mitotic catastrophe. Nocodazole, KPU-133 (a more potent derivative of plinabulin), and paclitaxel also exerted similar effects. From these data, we conclude that the unusual pattern may be associated with dysregulation of late M phase-specific E3 ligase activity and mitotic catastrophe following treatment with anti-microtubule agents.
    Biochemical and Biophysical Research Communications 10/2012; · 2.28 Impact Factor
  • Journal of oral and maxillofacial surgery: official journal of the American Association of Oral and Maxillofacial Surgeons 08/2012; 70(11):e679-82. · 1.58 Impact Factor
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    ABSTRACT: To explore the mechanism of bone destruction associated with oral cancer, we identified factors that stimulate osteoclastic bone resorption in oral squamous cell carcinoma. Two clonal cell lines, HSC3-C13 and HSC3-C17, were isolated from the maternal oral cancer cell line, HSC3. The conditioned medium from HSC3-C13 cells showed the highest induction of Rankl expression in the mouse stromal cell lines ST2 and UAMS-32 as compared to that in maternal HSC3 cells and HSC3-C17 cells, which showed similar activity. The conditioned medium from HSC3-C13 cells significantly increased the number of osteoclasts in a co-culture with mouse bone marrow cells and UAMS-32 cells. Xenograft tumors generated from these clonal cell lines into the periosteal region of the parietal bone in athymic mice showed that HSC3-C13 cells caused extensive bone destruction and a significant increase in osteoclast numbers as compared to HSC3-C17 cells. Gene expression was compared between HSC3-C13 and HSC3-C17 cells by using microarray analysis, which showed that CXCL2 gene was highly expressed in HSC3-C13 cells as compared to HSC3-C17 cells. Immunohistochemical staining revealed the localization of CXCL2 in human oral squamous cell carcinomas. The increase in osteoclast numbers induced by the HSC3-C13-conditioned medium was dose-dependently inhibited by addition of anti-human CXCL2-neutralizing antibody in a co-culture system. Recombinant CXCL2 increased the expression of Rankl in UAMS-32 cells. These results indicate that CXCL2 is involved in bone destruction induced by oral cancer. This is the first report showing the role of CXCL2 in cancer-associated bone destruction.
    Biochemical and Biophysical Research Communications 07/2012; 424(3):456-61. · 2.28 Impact Factor
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    ABSTRACT: Calcifying cystic odontogenic tumors are benign tumors, characterized by the presence of ghost cells and calcified materials. We evaluated clinical characteristics of calcifying cystic odontogenic tumors in 21 cases at the Maxillofacial Surgery, Tokyo Medical and Dental University Hospital, between January 1979 and December 2006. Of the 21 lesions that were studied, 12 were observed in male patients, and 9 in female patients. The median age was 13.0 years (range, 4-69 years). Of the 21 lesions, 11 were located in the maxilla (intraosseous), 9 in the mandible (intraosseous), and 1 in the lower gingiva (extraosseous). Radiographically, 18 lesions appeared as unilocular radiolucencies, and 2 lesions as multilocular radiolucencies. Impacted teeth were observed in 15 cases. In 20 cases, the lesions were treated by enucleation. The follow-up duration ranged from 2 years, 5 months to 28 years, 8 months, and in 1 case, the lesion recurred and showed a malignant transformation 2 years 10 months after the treatment. Histopathologically, the lining epithelium consisted of cuboidal or columnar odontogenic cells. Ghost cells were frequently calcified, and the tissue was hardened. In 14 cases, the tumor was associated with odontoma.
    Kōkūbyō Gakkai zasshi. The Journal of the Stomatological Society, Japan 03/2012; 79(1):26-33.
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    ABSTRACT: We investigated the effects of acerogenin A, a natural compound isolated from Acer nikoense Maxim, on osteoblast differentiation by using osteoblastic cells. Acerogenin A stimulated the cell proliferation of MC3T3-E1 osteoblastic cells and RD-C6 osteoblastic cells (Runx2-deficient cell line). It also increased alkaline phosphatase activity in MC3T3-E1 and RD-C6 cells and calvarial osteoblastic cells isolated from the calvariae of newborn mice. Acerogenin A also increased the expression of mRNAs related to osteoblast differentiation, including Osteocalcin, Osterix and Runx2 in MC3T3-E1 cells and primary osteoblasts: it also stimulated Osteocalcin and Osterix mRNA expression in RD-C6 cells. The acerogenin A treatment for 3days increased Bmp-2, Bmp-4, and Bmp-7 mRNA expression levels in MC3T3-E1 cells. Adding noggin, a BMP specific-antagonist, inhibited the acerogenin A-induced increase in the Osteocalcin, Osterix and Runx2 mRNA expression levels. These results indicated that acerogenin A stimulates osteoblast differentiation through BMP action, which is mediated by Runx2-dependent and Runx2-independent pathways.
    Biochemical and Biophysical Research Communications 02/2011; 406(2):211-7. · 2.28 Impact Factor
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    ABSTRACT: Keratocystic odontogenic tumor is a cystic lesion that behaves more aggressively than other jaw cysts. One of its characteristic histologic features is a parakeratinized uniform layer of lining epithelium. A jaw cyst lined with orthokeratinized epithelium is called an orthokeratinized odontogenic cyst. These keratinized jaw cysts are thought to be separate entities, although their histopathogenesis has not been fully assessed. To better understand these lesions, we performed comprehensive immunohistochemical profiling of the keratin expression of each. Orthokeratinized odontogenic cysts expressed keratin 1, keratin 2, keratin 10, and loricrin, suggesting differentiation toward normal epidermis. Keratocystic odontogenic tumors expressed keratin 4, keratin 13, keratin 17, and keratin 19, which is a unique expression pattern reminiscent of a mucosal squamous epithelium and an epithelial appendage. In neonatal rat tooth germ, cells strongly positive for keratin 17 and keratin 19 were observed, specifically in the dental lamina, implying the origin of keratocystic odontogenic tumor. GLI2, a downstream effector of hedgehog signaling, was significantly expressed in keratocystic odontogenic tumor and basal cell carcinoma, accompanied with robust expression of keratin 17, mammalian target of rapamycin, and BCL2. The expression of these GLI2- or keratin 17-related factors was not significantly observed in orthokeratinized odontogenic cysts. These findings provide evidence to support the viewpoint that keratocystic odontogenic tumor and orthokeratinized odontogenic cyst are separate entities, and furthermore suggest their characteristic histology, pathogenesis, and biological behaviors.
    Human pathology 12/2010; 41(12):1718-25. · 3.03 Impact Factor
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    ABSTRACT: To determine whether staining with iodine solution provides an efficient criterion for determining the area of resection for the lesions surrounding squamous cell carcinoma (SCC) and leukoplakia of the tongue, we determined the optimum density of iodine solution and staining procedure and analyzed the color of lightly stained lesions (LSLs) in relation to the histopathologic findings. Sixty-five patients with SCC or leukoplakia of the tongue were divided into two groups: lesions stained with 3% Lugol solution and restained with either 5% Lugol solution (n=38) or 10% iodine glycerin (n=27). Among the lesions stained with 5% Lugol solution, significant differences were found in all color values. Color difference values (DeltaE*ab) using 3% and 5% Lugol solutions were significantly different between epithelial hyperplasia/mild epithelial dysplasia and moderate to severe dysplasia (P < 0.05). According to the evaluations of five clinicians in 46 LSLs, a distinctive boundary was most often obtained using 5% Lugol solution. These results suggest that the most effective method for obtaining a clear boundary and distinguishing moderate to severe dysplasia from mild or no epithelial dysplasia according to the measured color value was to stain with 3% followed by 5% Lugol solution.
    Journal of medical and dental sciences 12/2009; 56(4):123-30.
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    ABSTRACT: Microvascular free flap transfers have become a preferred reconstructive technique; however, rare complications may still prove devastating. This study reviewed 213 consecutive freetissue transfers in order to assess the incidence and causes of complications in patients undergoing microvascular free flap reconstruction in the oral and maxillofacial region. In most cases, reconstruction was undertaken after resection of a malignant tumor. The flap donor sites were the radial forearm (n=111), rectus abdominis (n=88), scapula (n=13), and latissimus dorsi (n=1). The superior thyroid artery and the external jugular vein were commonly used as recipient vessels for anastomosis. The overall flap success rate was 99%. There were 7 cases of postoperative vascular thrombosis (6 venous and 1 arterial), constituting 3.3% of the entire series. Five flaps were salvaged, representing a 71.4% successful salvage rate in cases of vascular complications. Most of the successful salvage attempts were made within 24 hours of the end of the initial operation, and the successful salvage rate for re-exploration was 100%. Finally, the total flap loss rate was 0.9% and the partial flap loss rate was 2.3%. We conclude that early re-exploration should be the first choice for management of vascular compromised flaps. Complications at the donor site occurred in 17 cases (8.0%), the most common complication of which was partial skin graft loss after harvesting a radial forearm flap (n=10; 9.0%). Recipient and donor site morbidity was limited and considered acceptable.
    International Journal of Oral Science 05/2009; 6(1):46–54. · 2.72 Impact Factor
  • International Journal of Oral and Maxillofacial Surgery - INT J ORAL MAXILLOFAC SURG. 01/2009; 38(5):579-580.
  • International Journal of Oral and Maxillofacial Surgery - INT J ORAL MAXILLOFAC SURG. 01/2009; 38(5):434-434.
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    ABSTRACT: Angiogenesis is an important phenomenon for the growth and metastasis of solid tumors. The present study examined the characterization of angiogenic factors produced by human oral squamous cell carcinoma (oral SCC) cell lines established from lymph node metastatic tumors and primary tumor in different patients. The conditioned medium of HSC3 with the strongest metastatic ability among the examined lines enhanced a tube-forming activity of bovine carotid artery endothelial (BAE) cells in collagen gel cultures. The treatment of HSC3 with anti-vascular endothelial growth factor (VEGF) antibody or anti-basic fibroblast growth factor (bFGF) antibody, either alone or in combination, attenuated the activity of urokinase-type plasminogen activator (uPA) in the endothelial cells stimulated by the conditioned medium of HSC3. In contrast, neither anti-interleukin-8 (IL-8) antibody nor anti-hepatocyte growth factor (HGF beta) antibody affected uPA activity in the endothelial cells. Among these HSC cell lines, HSC3 secreted VEGF with the highest (1.92 +/- 0.24 ng/10(6) cells/24 h) level and bFGF. The level of bFGF secreted by HSC3 was lower than that secreted by BAE cells. Other oral SCC cell lines secreted lower levels of VEGF and undetectable levels of bFGF. By reverse transcriptase-polymerase chain reaction analysis of mRNA the production of VEGF121, VEGF145, VEGF165, VEGF189, and VEGF206 in these cell lines was able to be detected. Moreover, the conditioned medium of HSC3 enhanced the tyrosine phosphorylation and expression of kinase insert domain-containing receptor (KDR/flk-1) in the endothelial cells. These results suggest that oral SCC promotes angiogenesis via expression of VEGF and upregulation of their receptor KDR/flk-1 expression in endothelial cells.
    Oral Oncology 02/2000; 36(1):81-8. · 2.70 Impact Factor
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    ABSTRACT: Objectives:Keratocystic odontogenic tumor (KCOT, formerly known as odontogenic keratocyst) is a benign neoplasm, which arises from odontogenic epithelium. This tumor is a potentially aggressive lesion with a propensity toward recurrence. It arises sporadically or in association with the nevoid basal cell carcinoma syndrome (NBCCS). Orthokeratinized odontogenic cyst (OOC) was originally described as a rare subtype of KCOT; however, this lesion has been categorized as a distinct entity from KCOT, based on the differences in the histological feature and clinical behavior. KCOT is characterized by a lining of parakeratinized stratified squamous epithelium. In contrast, OOC is composed of orthokeratinized squamous epithelium. OOC has no tendency to recur and associate with NBCCS. To understand the characteristics of the cell lineage and differentiation status between KCOT and OOC. Methods:We examined the expression of the major keratins (K1-K20) by immunohistochemistry, using paraffin-embedded archival specimens of 20 cases of KCOT and 18 cases of OOC. Results:The basal layer of both KCOT and OOC expressed K5 and K14 (basal cell keratins). KCOT expressed K4 and K13 (mucosal squamous epithelial keratins), but not in OOC. K17 (an inducible keratin in activated keratinocytes) and K19 (a keratin that is often observed in epithelia of odontogenic lineage) were consistently expressed in KCOT, but not in OOC. In contrast, OOC expressed K1 and K10 (keratins of epidermal keratinocytes) and loricrin (a skin marker) but KCOT was negative. Conclusions:KCOT showed a unique keratin profile that was different from any normal squamous epithelia. In contrast, OOC exhibited the keratin profile comparable to epidermis. These results suggest a different pathogenesis of OOC and KCOT.
    2nd Meeting of IADR Pan Asian Pacific Federation (PAPF) and the 1st Meeting of IADR Asia/Pacific Region 2009;