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A retrospective clinical study of mandibular advancement splint therapy for obstructive sleep apnoea – a 7 year review
e290
E-Poster Presentation
References
A retrospective clinical study of mandibular advancement splint therapy for obstructive sleep apnoea – a 7 year review
McFadden, L. R., & Rishiraj, B. (2001). Treatment of temporomandibular joint ankylosis: a case report. J Can Dent Assoc, 67, 659–663. Manganello-Souza, L. C., & Mariani, P. B. (2003). Temporomandibular joint ankylosis: report of 14 cases. Int J Oral Maxillofac Surg, 32, 24–29.
S. Spencer ∗ , A. Cheng, P. Sambrook, A. Goss
http://dx.doi.org/10.1016/j.ijom.2015.08.325 A novel tumor suppressor of axon guiding chemorepulsant semaphorin3a in oral squamous cell carcinoma X. Song 1,2,∗ , Z. Wang 1,2 , J. Chen 1,1 , H. Wu 1,2 , J. Cheng 1,1 , J. Ye 1,2 , X. Ding 1,2 , Y. Wu 1,2 1
Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China 2 Department of Oral and Maxillofacial Surgery, Affiliated Hospital of Stomatology, Nanjing Medical University, Nanjing China Background: Class 3 semaphorins (Sema 3s) are a large group of secreted axon guidance molecules. Increasing studies have shown that Sema3s may act either as tumour suppressor or oncogene in various cancer types. However, little is known in terms of Sema3A in oral squamous cell carcinoma (OSCC). Objectives: To elucidate the role of Sema3A, an axon guiding chemorepulsant in nerve development, in the growth and progression of oral squamous cell carcinoma. Methods: Sema3A was examined in 100 cases of human oral squamous cell carcinoma specimens, 20 cases of normal oral mucosa and cell lines SCC9, CAL27 and HN6 with immunohistochemistry and Western blotting. MTT assay, flow cytometry, cell adhesion and migration, and xenografts were used to evaluate biological significance of Sema3A. Results: Sema3A was significantly reduced in oral squamous cell carcinoma tissues comparing with normal oral mucosa. Overexpression of Sema3A resulted in increased apoptosis, reduced proliferation, adhesion to fibronectin, and migratory capability as well as reduced G2-phase population while increased S-phase population. Cyclin D1, D3 and CDK6 expression were also reduced after Sema3A was over-expressed. In mechanism, we found NF-kb pathway was involved in Sema3A induced growth inhibition and impairment of cancer cell invasion. While transfection of siRNA targeting Sema3A in OSCC cells results in a more progressed growth and invasion as well as elevated NFkb signalling pathway. In addition, in transplanted nude mice, Sema3A overexpression exhibited diminished tumorigenesis and increased apoptisis. Conclusions: Endogenous Sema3A acts as a suppressor of the growth and invasion of human oral squamous cell carcinoma. Acknowledgments: This work is supported in part by the National Natural Science Foundation of China (81402236) and A Project Funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD, 2014-37). http://dx.doi.org/10.1016/j.ijom.2015.08.326
Royal Adelaide Hospital, Adelaide, Australia Background: The gold standard for management of OSA is CPAP therapy, which often provides excellent control. However, many patients fail to tolerate CPAP therapy. A recent Cochrane Review1 found that MAS therapy is effective in improving subjective sleepiness and AHI, but is not as effective as CPAP in reducing AHI. It recommends that MAS therapy be offered to those suffering from mild symptomatic OSA, and patients who have not been able to tolerate CPAP therapy. Objectives: This retrospective clinical audit aims to identify the OSA severity and patient characteristics of those referred to the South Australian Oral and Maxillofacial Surgery Unit for MAS therapy and ascertain the outcomes of MAS therapy for this group. Methods: The audit included patients who received a MAS between 2008 and 2014 in the South Australian OMS Department for the management of OSA. Data collected included certain patient characteristics such as BMI, polysomnography results (baseline and MAS-in-situ), splint type and subjective outcomes such as ESS. Conclusions: Mandibular advancement therapy for obstructive sleep apnoea provides an improvement in patient RDI/AHI. However, the response to MAS is variable and for more severe cases of OSA the response to MAS therapy is limited.
Reference Lim, J., Lasserson, T. J., Fleetham, J., & Wright, J. J. (2009). Oral appliances for obstructive sleep apnoea. Cochrane Database Syst Rev, (3).
http://dx.doi.org/10.1016/j.ijom.2015.08.327 Is maxillary morphology affected by the commonly occurring mutations in FGFR3 gene? V. Sreenivas Prasad ∗ , B.R. Prasad, M.S. Ravi Nitte University, Mangalore, India Background: Most current researches in relation to genetic control of facial growth and development are concentrating on the role of Hox genes and Growth factors. Mutations in several FGFs and FGFRs were found to cause a variety of bone/osteo-genic diseases. More than 97% of achondroplacia cases were reported to be caused by one of two mutations G1138A and G1138C, in exon 10 of the FGFR3. Objectives: These commonly occurring SNP sites were targeted in our study to evaluate whether they are responsible for maxillary growth in the selected subjects. Material and methods: We analyzed the genomic DNA of 30 subjects having Prognathic Maxilla, 30 individuals having Retrognathic Maxilla and compared them with that of 30 individuals having normal maxilla. Genomic DNA was extracted from serum using HiPuraTM Forensic Sample Genomic DNA Purification Kit as per the manufacturer’s instructions. A programmable gradient Thermo cycler (Corbett) was used for standardization of PCR conditions for FGFR3 Forward and Reverse primers. Agarose Gel Electrophoresis was used to detect the PCR products. The PCR products were digested with Mspl and Sfcl (Thermo Scientific) in separate tubes and visualized under UV Trans-illuminator.
E-Poster Presentation
References
A retrospective clinical study of mandibular advancement splint therapy for obstructive sleep apnoea – a 7 year review
McFadden, L. R., & Rishiraj, B. (2001). Treatment of temporomandibular joint ankylosis: a case report. J Can Dent Assoc, 67, 659–663. Manganello-Souza, L. C., & Mariani, P. B. (2003). Temporomandibular joint ankylosis: report of 14 cases. Int J Oral Maxillofac Surg, 32, 24–29.
S. Spencer ∗ , A. Cheng, P. Sambrook, A. Goss
http://dx.doi.org/10.1016/j.ijom.2015.08.325 A novel tumor suppressor of axon guiding chemorepulsant semaphorin3a in oral squamous cell carcinoma X. Song 1,2,∗ , Z. Wang 1,2 , J. Chen 1,1 , H. Wu 1,2 , J. Cheng 1,1 , J. Ye 1,2 , X. Ding 1,2 , Y. Wu 1,2 1
Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China 2 Department of Oral and Maxillofacial Surgery, Affiliated Hospital of Stomatology, Nanjing Medical University, Nanjing China Background: Class 3 semaphorins (Sema 3s) are a large group of secreted axon guidance molecules. Increasing studies have shown that Sema3s may act either as tumour suppressor or oncogene in various cancer types. However, little is known in terms of Sema3A in oral squamous cell carcinoma (OSCC). Objectives: To elucidate the role of Sema3A, an axon guiding chemorepulsant in nerve development, in the growth and progression of oral squamous cell carcinoma. Methods: Sema3A was examined in 100 cases of human oral squamous cell carcinoma specimens, 20 cases of normal oral mucosa and cell lines SCC9, CAL27 and HN6 with immunohistochemistry and Western blotting. MTT assay, flow cytometry, cell adhesion and migration, and xenografts were used to evaluate biological significance of Sema3A. Results: Sema3A was significantly reduced in oral squamous cell carcinoma tissues comparing with normal oral mucosa. Overexpression of Sema3A resulted in increased apoptosis, reduced proliferation, adhesion to fibronectin, and migratory capability as well as reduced G2-phase population while increased S-phase population. Cyclin D1, D3 and CDK6 expression were also reduced after Sema3A was over-expressed. In mechanism, we found NF-kb pathway was involved in Sema3A induced growth inhibition and impairment of cancer cell invasion. While transfection of siRNA targeting Sema3A in OSCC cells results in a more progressed growth and invasion as well as elevated NFkb signalling pathway. In addition, in transplanted nude mice, Sema3A overexpression exhibited diminished tumorigenesis and increased apoptisis. Conclusions: Endogenous Sema3A acts as a suppressor of the growth and invasion of human oral squamous cell carcinoma. Acknowledgments: This work is supported in part by the National Natural Science Foundation of China (81402236) and A Project Funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD, 2014-37). http://dx.doi.org/10.1016/j.ijom.2015.08.326
Royal Adelaide Hospital, Adelaide, Australia Background: The gold standard for management of OSA is CPAP therapy, which often provides excellent control. However, many patients fail to tolerate CPAP therapy. A recent Cochrane Review1 found that MAS therapy is effective in improving subjective sleepiness and AHI, but is not as effective as CPAP in reducing AHI. It recommends that MAS therapy be offered to those suffering from mild symptomatic OSA, and patients who have not been able to tolerate CPAP therapy. Objectives: This retrospective clinical audit aims to identify the OSA severity and patient characteristics of those referred to the South Australian Oral and Maxillofacial Surgery Unit for MAS therapy and ascertain the outcomes of MAS therapy for this group. Methods: The audit included patients who received a MAS between 2008 and 2014 in the South Australian OMS Department for the management of OSA. Data collected included certain patient characteristics such as BMI, polysomnography results (baseline and MAS-in-situ), splint type and subjective outcomes such as ESS. Conclusions: Mandibular advancement therapy for obstructive sleep apnoea provides an improvement in patient RDI/AHI. However, the response to MAS is variable and for more severe cases of OSA the response to MAS therapy is limited.
Reference Lim, J., Lasserson, T. J., Fleetham, J., & Wright, J. J. (2009). Oral appliances for obstructive sleep apnoea. Cochrane Database Syst Rev, (3).
http://dx.doi.org/10.1016/j.ijom.2015.08.327 Is maxillary morphology affected by the commonly occurring mutations in FGFR3 gene? V. Sreenivas Prasad ∗ , B.R. Prasad, M.S. Ravi Nitte University, Mangalore, India Background: Most current researches in relation to genetic control of facial growth and development are concentrating on the role of Hox genes and Growth factors. Mutations in several FGFs and FGFRs were found to cause a variety of bone/osteo-genic diseases. More than 97% of achondroplacia cases were reported to be caused by one of two mutations G1138A and G1138C, in exon 10 of the FGFR3. Objectives: These commonly occurring SNP sites were targeted in our study to evaluate whether they are responsible for maxillary growth in the selected subjects. Material and methods: We analyzed the genomic DNA of 30 subjects having Prognathic Maxilla, 30 individuals having Retrognathic Maxilla and compared them with that of 30 individuals having normal maxilla. Genomic DNA was extracted from serum using HiPuraTM Forensic Sample Genomic DNA Purification Kit as per the manufacturer’s instructions. A programmable gradient Thermo cycler (Corbett) was used for standardization of PCR conditions for FGFR3 Forward and Reverse primers. Agarose Gel Electrophoresis was used to detect the PCR products. The PCR products were digested with Mspl and Sfcl (Thermo Scientific) in separate tubes and visualized under UV Trans-illuminator.