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Introduction Mineral trioxide aggregate (MTA) can induce differentiation of the dental pulp cells into odontoblast-like cells and generate a dentin-like mineral structure. The mechanisms underlying MTA-induced odontoblastic differentiation in human dental pulp cells (HDPCs) are not completely understood. The purpose of this study was to evaluate the effect of nifedipine as calcium channel blocker on MTA-induced odontoblastic differentiation in HDPCs. Methods HDPCs extracted from maxillary supernumerary incisors and third molars were directly cultured on MTA with or without nifedipine in the culture medium. Cell growth and expression of odontoblastic differentiation markers were determined by using methyl-thiazol-diphenyl-tetrazolium assay and reverse transcription–polymerase chain reaction analysis, respectively. Phosphorylation of mitogen-activated protein kinase was measured by Western blotting, and calcium deposition was assessed by using alizarin red S staining. Results MTA at a concentration of 1 mg/mL significantly up-regulated the expression of dentin sialophosphoprotein and dentin matrix protein-1 and enhanced mineralized nodule formation. However, nifedipine attenuated the MTA-induced odontoblastic differentiation in HDPCs. In addition, MTA-induced mineralization was blocked by inhibition of extracellular signal-regulated kinase (ERK), p38, and Jun N-terminal kinase (JNK) by using U0126, SB203580, and SP600125, respectively. Furthermore, phosphorylation of ERK and JNK in response to MTA was inhibited when the medium was supplemented with nifedipine. Conclusions This study showed that calcium ions released from MTA play an important role in odontoblastic differentiation of HDPCs via modulation of ERK and JNK activation.

Daily use of probiotic chewing gum might have a beneficial effect on oral health, and it is important that the viability of the probiotics be maintained in this food product. In this study, we examined the stability of probiotic chewing gum containing Weissella cibaria. We evaluated the effects of various factors, including temperature and additives, on the survival of freeze-dried probiotic W. cibaria powder. No changes in viability were detected during storage at 4℃ for 5 months, whereas the viability of bacteria stored at 20℃ decreased. The stability of probiotic chewing gum decreased steadily during storage at 20℃ for 4 weeks. The viability of the freeze-dried W. cibaria mixed with various additives, such as xylitol, sorbitol, menthol, sugar ester, magnesium stearate, and vitamin C, was determined over a 4-week storage period at 20℃. Most of the freeze-dried bacteria except for those mixed with menthol and vitamin C were generally stable during a 3-week storage period. Overall, our study showed that W. cibaria was more stable at 4℃ than that at 20℃. In addition, menthol and vitamin C had a detrimental effect on the storage stability of W. cibaria. This is the first study to examine the effects of various chewing gum additives on the stability of W. cibaria. Further studies will be needed to improve the stability of probiotic bacteria for developing a novel probiotic W. cibaria gum.

항생제 사용에 따라 구강내 세균들이 가지게 되는 내성의 발현이 문제가 될 수 있다. 어린이 치면세균막에서 치주질환의 원인균들과 흔히 사용하고 있는 항생제들에 대한 내성유전자의 출현율을 알아보고자 중합효소연쇄반응을 이용하여 조사하였다. 1. 치주질환 원인균의 출현율은 F. nucleatum 95.4%, T. forsythia 55.2% 이었으며, P. gingivalis 40.2%, A. actinomycetemcomitans 5.7%, T. denticola는 3.4% 순이었다. 2. 항생제 내성유전자의 출현율 조사에서 cephalosporin 분해효소인 cfxA는 100%에서 발견되었으며 ${\beta}$ -lactam 분해효소인 $bla_{TEM}$ 과 tetracycline 내성유전자인 tet(M)도 100%의 출현율을 보였다. tet(Q)는 88.5%, ${\beta}$ -lactam 분해효소인 $bla_{SHV}$ 는 29.9%, macrolide계 내성 ermF유전자는 87.4%, vancomycin 내성 vanA는 48.5%의 출현율을 보였다. Aminoglycoside에 대한 복합 내성을 보이는 aacA-aphD와 meticillin 내성유전자 mecA는 9.2%로 가장 낮은 출현율을 보였다. 3. 치주질환 원인균과 항생제 내성유전자와의 관련성 조사에서 T. forsythia와 $bla_{SHV}$ 간에 그리고 P. gingivalis와 vanA간 에 유의한 상관성이 있었다. 항생제 내성유전자 tet(Q)와 ermF (0.514)간에 중등도의 상관성을 나타내었으며, mecA와 vanA (0.25)간에 유의한 상관성을 나타내었다. 건강한 어린이들의 치면세균막에 다양한 치주질환 원인균들과 항생제 내성유전자들이 존재하며, 상호 관련성을 가지고 존재함을 보여주었다. 【The purpose of this study was to assess the prevalence of periodontopathic bacteria and resistance determinants from oral biofilm of children. Subgingival dental plaque was isolated from 87 healthy children, and PCR was performed to determine the presence of 5 periodontal pathogens including P. gingivalis, T. forsythia, T. denticola, F. nucleatum, A. actinomycetemcomitans, and nine resistance genes including tet(Q), tet(M), ermF, aacA-aphD, cfxA, $bla_{SHV}$ , $bla_{TEM}$ , vanA, mecA. 1. The prevalence of F. nucleatum, T. forsythia. and P. gingivalis was 95.4%, 55.2%, and 40.2%, respectively. In addition. the prevalence of A. actinomycetemc omitans was 5.7%, while T. denticola was 3.4%. 2. In analysis of antibiotic resistance determinants. cfxA, $bla_{TEM}$ and tet(M) were detected in all the samples tested. It was also found that the prevalence of tet(Q) showing tetracycline resistance. $bla_{SHV}$ associated with resistance to ${\beta}$ -lactams, ermF exhibiting erythromycin resistance, and, vanA resulting vancomycin resistance was 88.5%, 29.9% 87.4%, and 48.5%, respectively. The aacA-aphD gene showing resistance to aminoglycosides and mecA gene harboring methicillin resistance exhibited the lowest prevalence with 9.2%. 3. In a correlation analysis between periodontopathic pathogens and antibiotic resistance determinants, it was found that there was a significant correlation between T. forsythia and $bla_{SHV}$ . Also, P. gingivalis and vanA showed a correlation. Finally, tet(Q) and ermF showed a significant correlation (phi: 0.514) while mecA and vanA also showed a correlation(phi: 0.25).】

(−)-Epigallocatechin-3-gallate (EGCG) has been reported to inhibit cellular proliferation and induce apoptosis in a range of cancer cells. This study examined the cytotoxicity of EGCG glucoside on human laryngeal epidermoid carcinoma Hep2 cells. The EGCG glucoside treatment decreased the cell viability in Hep2 cells. Furthermore, EGCG glucoside caused apoptotic morphological changes with chromatin condensation and nuclear fragmentation, as observed by a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and activated caspase-3 immunohistochemisty. However, the EGCG glucoside did not induce the production of reactive oxygen species (ROS), suggesting that oxidative stress is not involved in the apoptotic response. EGCG glucoside induces apoptosis in Hep2 cells through not the generation of ROS, but the activation of caspase-3.

(-)-Epigallocatechin-3-gallate (EGCG), a major green tea polyphenol, was tested for in vitro cytotoxicity against human laryngeal epidermoid carcinoma of the larynx Hep2 cells. EGCG-induced apoptotic cell death accompanied by a change in the cell cycle. However, EGCG did not result in caspase activation, nor did a caspase inhibitor block cell death. Furthermore, EGCG caused no change in the intracellular levels of reactive oxygen species (ROS). The levels of p53 were increased in the EGCG-treated cells, with a corresponding decrease in Bcl-2 and Bid protein levels as well as an increase in the Bax level. In addition, EGCG induced the cytoplasmic release of cytochrome c from the mitochondria accompanied by a decreased mitochondrial membrane potential, and subsequently upregulated translocation of apoptosis-inducing factor (AIF) and endonuclease G (EndoG) into the nucleus during the apoptotic process. Taken together, these findings indicate that the p53-mediated mitochondrial pathway and the nuclear translocation of AIF and EndoG play a crucial role in EGCG-induced apoptosis of human laryngeal epidermoid carcinoma Hep2 cells, which proceeds through a caspase-independent pathway.

Interactions between periodontal bacteria and human oral epithelial cells can lead to the activation and expression of a variety of inflammatory mediators in epithelial cells. Fusobacterium nucleatum is a filamentous human pathogen that is strongly associated with periodontal diseases. This study examined the effects of methyl gallate (MG) and gallic acid (GA) on the production of inflammatory mediators, interleukin (IL)-6 and IL-8, by oral epithelial cells stimulated by F. nucleatum. In a real-time reverse transcription-polymerase chain reaction and an enzyme-linked immunosorbent assay, live F. nucleatum induced high levels of gene expression and protein release of IL-6 and IL-8. The effects of MG and GA were examined by treating KB oral epithelial cells with MG and GA and stimulating them with F. nucleatum. MG and GA inhibited significantly the increases in the IL-6 and IL-8 gene and protein levels in a dose-dependent manner. These Compounds also inhibited the growth of F. nucleatum. No visible effects of MG and GA on the adhesion and invasion of KB cells by F. nucleatum were observed. In conclusion, both MG and GA inhibit IL-6 and IL-8 production from F. nucleatum-activated KB cells.

Nitric oxide (NO) is a major factor contributing to the loss of neurons in ischemic stroke, demyelinating diseases, and other neurodegenerative disorders. NO not only functions as a direct neurotoxin, but also combines with superoxide (O 2 − ) by a diffusion-controlled reaction to form peroxynitrite (ONOO − ), a species that contributes to oxidative signaling and cellular apoptosis. However, the mechanism by which ONOO − induces apoptosis remains unclear, although subsequent formation of reactive oxygen species (ROS) has been suggested. The aim of this study was to further investigate the triggers of the apoptotic pathway using O 2 − scavenging with light irradiation to block ONOO − production. Antiapoptotic effects of light irradiation in sodium nitroprusside (SNP)-treated SH-SY5Y cells were assayed by reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, DNA fragmentation, flow cytometry, Western blot, and caspase activity assays. In addition, NO, total ROS, O 2 − , and ONOO − levels were measured to observe changes in NO and its possible involvement in radical induction. Cell survival was reduced to approximately 40% of control levels by SNP treatment, and this reduction was increased to 60% by low-level light irradiation. Apoptotic cells were observed in the SNP-treated group, but the frequency of these was reduced in the irradiation group. NO, O 2 − , total ROS, and ONOO − levels were increased after SNP treatment, but O 2 − , total ROS, and ONOO − levels were decreased after irradiation, despite the high NO concentration induced by SNP treatment. Cytochrome c was released from mitochondria of SNP-treated SH-SY5Y cells, but not of irradiated cells, resulting in a decrease in caspase-3 and -9 activity in SNP-treated cells. Finally, these results show that 635-nm irradiation, by promoting the scavenging of O 2 − , protected against neuronal death through blocking the mitochondrial apoptotic pathway induced by ONOO − synthesis.

Objective This study examined the expression pattern of the Deleted-in-colorectal-carcinoma (DCC) gene in developing rat tooth germs. Methods Rat pups at 4, 7 and 10 d postpartum were used in this study. Reverse transcription-polymerase chain reaction (RT-PCR) and immunofluorescent localization were used to determine the level of DCC expression during tooth development. Results There was more than 2-fold higher level of DCC mRNA in the rat 2nd maxillary molar tooth germs on 10 d postpartum, which was the root stage, than in the rat 3rd maxillary molar tooth germ, which was at the cap/early bell development stage. In addition, the levels of DCC mRNA in the 2nd maxillary molar germs at 4, 7 and 10 d postpartum increased gradually according to tooth development. Interestingly, immunoreactivity against DCC was specifically detected in the differentiating ameloblasts. DCC was observed in the lateral and apical sides of the newly differentiating and secretory stage ameloblasts. Afterwards, DCC was localized only in the apical side of the maturation stage ameloblasts, not in the lateral side. Conclusion DCC is expressed in the differentiating ameloblasts, which suggests that this molecule plays a crucial role in amelogenesis.

Background and Objectives: Inhibition of cyclooxygenase (COX) and prostaglandin E2 (PGE2) protects cells against cell injury in specific pathophysiological situations: inflammation and oxidative stress. Although the antiinflammatory effects have been reported in clinical fields for specific wavelength irradiation during wound healing, the physiological mechanism has not been clarified yet. The aim of the present study is to investigate the antiinflammatory mechanism of 635 nm light-emitting-diode (LED) irradiation compared with existing COX inhibitors. Study Design/Materials and Methods: The present study investigated anti-inflammatory effects of 635 nm irradiation on PGE2 release, COX and phospholipase A2 (PLA2) expression, and reactive oxygen species (ROS) dissociation in arachidonic acid (AA)-treated human gingival fibroblast (hGF). These results were compared with their existing COX inhibitors: indomethacin and ibuprofen. The PGE2 release was measured by enzyme immunoassay, the COX expression was measured by western blot and reverse transcriptase polymerase chain reaction (RT-PCR), and ROS level was measured by flow cytometry, laser scanning confocal microscope and RTPCR. Results: Results showed that 635 nm irradiation and existing COX inhibitors inhibit expression of COX and PGE2 release. Unlike indomethacin and ibuprofen, 635 nm irradiation leads to a decrease of ROS levels and mRNA expression of cytosolic phospholipase A2 (cPLA2) and secretary phospholipase A2 (sPLA2). Conclusion: Taken together, 635 nm irradiation, unlike indomethacin and ibuprofen, can directly dissociate the ROS. This inhibits cPLA2 ,s PLA 2, and COX expression, and results in the inhibition of PGE2 release. Thus, we suggest that 635 nm irradiation inhibits PGE2 synthesis like COX inhibitor and appears to be useful as an anti-inf lammatory tool. Lasers Surg. Med. 39:614–621, 2007. 2007 Wiley-Liss, Inc.

Nitric oxide (NO) is associated with many pathophysiology of the central nervous system including brain ischemia, neurodegeneration and inflammation. Epigallocatechin gallate (EGCG) is a major compound of green tea polyphenol that has shown the protective activity against neuronal diseases. This study examined the effect of EGCG on NO-induced cell death in PC12 cells. The administration of sodium nitroprusside (SNP), a NO donor, decreased the cell viability and induced apoptosis showing characterization such as cell shrinkage and chromatin condensation as well as subG1 fraction of cell cycles. EGCG inhibited the cytotoxicity and apoptotic morphogenic changes induced by SNP. EGCG attenuated the production of reactive oxygen species (ROS) by SNP, and ameliorated the SNP-induced Bax to Bcl-2 expression ratio leading to apoptosis. In addition, EGCG prevented the release of cytochrome c from the mitochondria into the cytosol as well as the upregulation of the voltage-dependent anion channel (VDAC), a cytochrome c releasing channel, in the mitochondria of SNP-treated cells. EGCG abrogated the activation of caspase-9, caspase-8 and caspase-3 induced by SNP. These results demonstrate that EGCG has a protective effect against SNP-induced apoptosis in PC12 cells by scavenging ROS and modulating the signal molecules associated with cytochrome c, caspases, VDAC and the Bcl-2 family. These findings suggest that EGCG might be a natural neuroprotective substance.

Porphyromonas gingivalisis one of the suspected periodontopathic bacteria. The lipopolysaccharide (LPS) ofP. gingivalisis a key factor in the development of periodontitis. Inflammatory cytokines play important roles in the gingival tissue destruction that is a characteristic of periodontitis. Macrophages are prominent at chronic inflammatory sites and are considered to contribute to the pathogenesis of periodontitis. Xylitol stands out and is widely believed to possess anticaries properties. However, to date, little is known about the effect of xylitol on periodontitis. The aim of the present study was to determine tumor necrosis factor alpha (TNF-α) and interleukin-1β (IL-1β) expression when RAW 264.7 cells were stimulated withP. gingivalisLPS (hereafter, LPS refers toP. gingivalisLPS unless stated otherwise) and the effect of xylitol on the LPS-induced TNF-α and IL-1β expression. The kinetics of TNF-α and IL-1β levels in culture supernatant after LPS treatment showed peak values at 1 h (TNF-α) and 2 to 4 h (IL-1β), respectively. NF-κB, a transcription factor, was also activated by LPS treatment. These cytokine expressions and NF-κB activation were suppressed by pretreatment with pyrrolidine dithiocarbamate (an inhibitor of NF-κB). Pretreatment with xylitol inhibited LPS-induced TNF-α and IL-1β gene expression and protein synthesis. LPS-induced mobilization of NF-κB was also inhibited by pretreatment with xylitol in a dose-dependent manner. Xylitol also showed inhibitory effect on the growth ofP. gingivalis.Taken together, these findings suggest that xylitol may have good clinical effect not only for caries but also for periodontitis by its inhibitory effect on the LPS-induced inflammatory cytokine expression.

A growing body of evidence shows that compounds of plant origin have the ability to prevent cancer. The fruit of gardenia, Gardenia jasminoides Ellis (Rubiaceae), has long been used as a food additive and herbal medicine, and its pharmacological actions, such as protective activity against oxidative damage, cytotoxic effect, and anti-inflammatory and anti-tumor activity, have already been reported.The purpose of the present study was to investigate the presence of DNA topoisomerase 1 inhibitor in various solvent fractions of Gardenia extract and examine the induction of oral cancer cell death upon treatment with Gardenia extract.The methanol extract of Gardenia was partitioned with n-hexane, dichloromethane, ethyl acetate, n-butanol, and water.In the DNA topoisomerase 1 assay, n-hexane and dichloromethane fractions inhibited topoisomerase 1 and led to a decrease in the cell viability of KB cells. The dichloromethane fraction (0.1 mg/mL) also showed 77% inhibition of cell viability in KB cells compared with HaCaT cells. Treatment with dichloromethane fraction led to apoptotic cell death as evidenced by flow cytometric analysis and morphological changes. In addition, treatment with Gardenia extract dichloromethane fraction led to the partial increase of caspase-3, caspase-8 and caspase-9 activities and the cleavage of poly (ADP-ribose) polymerase.Taken together, these results suggest that the dichloromethane fraction from Gardenia extract induces apoptotic cell death by DNA topoisomerase 1 inhibition in KB cells. These findings suggest the possibility that Gardenia extract could be developed as an anticancer modality.

The interaction between Lactobacillus reuteri, a probiotic bacterium, and oral pathogenic bacteria have not been studied adequately. This study examined the effects of L. reuteri on the proliferation of periodontopathic bacteria including Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum, Porphyromonas gingivalis, and Tannerella forsythia, and on the formation of Streptococcus mutans biofilms. Human-derived L. reuteri strains (KCTC 3594 and KCTC 3678) and rat-derived L. reuteri KCTC 3679 were used. All strains exhibited significant inhibitory effects on the growth of periodontopathic bacteria and the formation of S. mutans biofilms. These antibacterial activities of L. reuteri were attributed to the production of organic acids, hydrogen peroxide, and a bacteriocin-like compound. Reuterin, an antimicrobial factor, was produced only by L. reuteri KCTC 3594. In addition, L. reuteri inhibited the production of methyl mercaptan by F. nucleatum and P. gingivalis. Overall, these results suggest that L. reuteri may be useful as a probiotic agent for improving oral health.

Zinc has antimicrobial activity and zinc salts including zinc chloride (ZnCl(2)) have been used for the control of oral malodor. In this study, we hypothesized that pyrrolidine dithiocarbamate (PDTC), a zinc ionophore, may enhance antimicrobial efficacy of ZnCl(2). The bactericidal effectiveness of ZnCl(2) alone (0.5-8 mM) or in combination with PDTC (1 or 10 microM) was evaluated by in vitro short (1 h) time-killing assays against Fusobacterium nucleatum and Porphyromonas gingivalis. Only a slight viability decrease was observed with ZnCl(2) or PDTC alone after 1-h incubation. By contrast, combination of ZnCl(2) and PDTC could achieve a more than 100-fold viability reduction compared with ZnCl(2) or PDTC alone in F. nucleatum and P. gingivalis. Therefore, PDTC greatly enhanced the bactericidal activity of ZnCl(2) against the oral malodor-producing bacteria. These results suggest that use of PDTC may be useful for enhancing bactericidal activity of antimalodor regimens of zinc salts.

Introduction The purpose of this study was to investigate the change of lip-line cant (LLC) after 1-jaw orthognathic surgery in mandibular asymmetry patients. Methods Preoperative and postoperative data of 22 patients having 1-jaw orthognathic surgery, with menton deviation over 2° before the surgery, were our subjects. LLC was measured in the preoperative and postoperative frontal photographs, and its change was correlated with various craniofacial measurements obtained from preoperative and postoperative frontal cephalograms and maxillofacial 3-dimensional computed tomography images. Results Although these subjects had 2.4° of LLC on average before surgery, LLC improved to 0.5° after surgery, and the change (1.9°) was statistically significant. In the correlation analysis, preoperative LLC showed positive correlations with menton deviation and mandibular anterior occlusal plane cant. In the correlation analysis of LLC change, it had positive correlations with preoperative LLC and mandibular anterior occlusal plane cant and preoperative and postoperative change of menton deviation. Conclusions These results suggest that LLC is present with chin deviation, even without significant maxillary canting, and can be improved considerably by 1-jaw surgery alone.

This study examined the prevalence of oral microbes in the saliva of oncological patients and healthy subjects. PCR was used to assess the frequency of oral microbes including 3 cariogenic bacteria, 5 periodontopathic bacteria and 4 Candida species in the saliva of 104 oncological patients and 52 healthy subjects. Among these microorganims, Streptococcus mutans, Fusobacterium nucleatum and Candida albicans were most frequently detected in both groups. There were no significant differences in the prevalence of cariogenic bacteria between the patient and healthy groups, whereas significant differences in the frequency of Porphyromonas gingivalis and Tannerella forsythia were observed between the two groups (p ＜ 0.05). The prevalence of all five periodontopathogens was higher in the healthy group than in the patient group. The prevalence of C. albicans in patients was significantly higher than that of healthy group (p ＜ 0.05). In conclusion, there were significant differences in the prevalence of P. gingivalis, T. forsythia and C. albicans between the oncological patient group and healthy group.

The objective of this study was to analyze quantitatively whether Weissella cibaria could affect the proliferation of five periodontopathic bacteria, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Aggregatibacter actinomycetemcomitans, and Fusobacterium nucleatum, after incubation for 8~48 h. In addition, by using real-time PCR with a dual-labeled probe, each growth of bacteria was examined under different growth media conditions. The proliferation of periodontopathic bacteria was significantly inhibited by W. cibaria after incubation for 24~48 h (p ＜ 0.05), whereas the growth of W. cibaria was not affected by these pathogenic bacteria. The growth of P. gingivalis, T. forsythia and T. denticola significantly increased in each growth media after incubation for 24 h (p ＜ 0.05), as compared to the culture in mixed growth media. However, no differences in the growth of five periodontopathic bacteria were observed between each growth media and mixed media after incubation for 48 h. The growth and pH of W. cibaria culture significantly were changed in MRS after incubation for 24~48 h (p ＜ 0.05), as compared to the bacterial culture in mixed growth media. The pH of P. gingivalis and F. nucleatum culture significantly was changed in both growth media and mixed media after incubation for 24~48 h (p ＜ 0.05). Our data indicate that W. cibaria significantly inhibits the proliferation of five periodontopathic bacteria and each growth of bacteria is quantitatively analyzed under various media conditions by real-time PCR.

Backgound Oropharyngeal cancer (OPC) associated with human papilloma virus (HPV OPC) shows better treatment outcomes than non-HPV OPC. We investigated the expression of p53, β-tubulin, bcl-2 and ERCC 1, which are well-known biomarkers to predict the chemotherapy response, according to HPV status in OPC patients. Methods Patients who treated with at least 2 cycles of induction chemotherapy followed by concurrent chemoradiotherapy for locally advanced oropharyngeal cancer were reviewed. HPV PCR and immunohistochemical stain was done in paraffin embedded tumor tissue and evaluated the relation with the chemotherapy response and survival outcomes according to HPV status. Results Seventy-four patients were enrolled for this study and all patients received induction chemotherapy with docetaxel, 5-FU and cisplatin. After induction chemotherapy, complete response (CR) was shown in 22 patients (30%) and partial response (PR) in 46 patients (62%). HPV + was detected in 21 patients (28%), while 35 patients (47%) showed p16+ expression by IHC analysis. p16 positive patients showed better overall response, PFS and OS than p16 negative patients. p53 and class III beta-tubulin expression were significantly higher in HPV- and p16- than HPV + and p16+ patients. Conversely, bcl-2 expression was greater in HPV + or p16+ than HPV- or p16- patients. ERCC1 expression did not differ significantly according to HPV status. In multivariate analyses, early T stage (p = 0.036) and good PS (PS 0) (p = 0.029) showed a better 3Y-PFS rate, and low p53 expression (p = 0.012) and complete response after induction chemotherapy (p = 0.026) were highly associated with 3Y-OS rate. Low expression of p53 and p16 positive patients showed significantly prolonged OS than others (p = 0.010). Conclusion P53, class III beta-tubulin and bcl-2 were differently expressed in OPC according to HPV status and present study suggested the underlying mechanism of better response to chemotherapy in case of HPV OPC than non-HPV OPC. Among these biomarkers, p53 is the strongest prognostic marker in OPC and p53 in addition to p16 support the rationale to study of de-escalation strategy for OPC.