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Tumor growth requires angiogenesis to develop new blood vessels. This process is regulated by a balance of pro-angiogenic and anti-angiogenic factors. Tumors disrupt this balance by inducing hypoxia and secreting factors like VEGF, which activate the "angiogenic switch" and promote new vessel growth. This allows tumors to recruit blood vessels to supply nutrients and remove waste. Anti-angiogenic therapies aim to block this process by targeting VEGF and its receptors. Drugs like bevacizumab and sorafenib inhibit angiogenesis to limit tumor growth and progression.
This document discusses genetics in tooth development. It begins with an introduction to the stages of tooth development from initiation to root formation. It describes the molecular control of tooth development including key genes such as Msx1, Pax9, Lef1, and Dlx genes. Tooth morphogenesis is controlled by the enamel knot through genes such as Bmp4. The roles of genes in enamel formation including AMELX, ENAM, KLK4 and MMP20 are discussed. Genetics of dentin formation including the role of the DSPP gene in dentinogenesis imperfecta are also summarized. The document provides an overview of the molecular genetics underlying tooth development and malformations.
Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases that degrade extracellular matrix components. MMPs play important roles in tissue remodeling during processes like wound healing and organ development by breaking down collagen, elastin, fibronectin and other matrix proteins. Their activity is regulated by tissue inhibitors of metalloproteinases (TIMPs). Abnormal MMP activity is associated with diseases like cancer, atherosclerosis, and rheumatoid arthritis by facilitating tissue invasion or destruction.
1) BMPs play an important role in tooth development and regeneration by signaling between dental epithelium and mesenchyme. They are expressed in a spatial and temporal sequence that governs tooth patterning and morphogenesis.
2) Progenitor/stem cells found in dental pulp and periodontal ligament have the potential to differentiate into odontoblasts and other dental tissues when exposed to BMPs.
3) The application of BMPs, stem cells, and appropriate extracellular matrix scaffolds could facilitate the regeneration of dental and craniofacial tissues through recapitulating embryonic development pathways.
Proto-oncogenes are normal cellular genes that encode proteins involved in cell proliferation. When mutated, they become oncogenes that encode constitutively active oncoproteins driving increased cell growth. Proto-oncogenes can encode growth factors, growth factor receptors, signal transducers, transcription factors, or cell cycle regulators. Common mutations include RAS mutations in pancreatic cancer, BRAF mutations in melanoma, PI3K mutations in breast cancer, and MYC translocations in Burkitt's lymphoma. These mutations result in constitutive activation of signaling pathways that drive uncontrolled cell proliferation.
This document discusses histochemistry of oral tissues. It defines histochemistry as the qualitative and quantitative assessment of chemicals within cells and tissues. It describes the purpose of histochemistry as coloring structures for identification, locating insoluble materials accurately in tissues, and using materials that do not separate from their environment with high sensitivity. It outlines the main oral tissues studied in histochemistry as connective tissue, epithelial linings, and glandular structures. It provides details on specific histochemical techniques used to study components like glycogen, glyoproteins, proteoglycans, lipids, proteins, nucleic acids, and enzymes in oral tissues.
Cancer arises from normal cells whose nature is permanently changed, causing them to multiply rapidly and not be subject to normal control. Oncogenes are genes capable of transforming normal cells into cancerous cells and result from mutations of normal proto-oncogenes. Both DNA and RNA tumor viruses can transform cells through integration into the host cell DNA, which results in loss of growth control and tumor formation. Retroviruses contain oncogenes (v-onc) that are homologous to cellular proto-oncogenes (c-onc) and can induce transformation after mutation or other changes to the cell's genome.
Tumor growth requires angiogenesis to develop new blood vessels. This process is regulated by a balance of pro-angiogenic and anti-angiogenic factors. Tumors disrupt this balance by inducing hypoxia and secreting factors like VEGF, which activate the "angiogenic switch" and promote new vessel growth. This allows tumors to recruit blood vessels to supply nutrients and remove waste. Anti-angiogenic therapies aim to block this process by targeting VEGF and its receptors. Drugs like bevacizumab and sorafenib inhibit angiogenesis to limit tumor growth and progression.
This document discusses genetics in tooth development. It begins with an introduction to the stages of tooth development from initiation to root formation. It describes the molecular control of tooth development including key genes such as Msx1, Pax9, Lef1, and Dlx genes. Tooth morphogenesis is controlled by the enamel knot through genes such as Bmp4. The roles of genes in enamel formation including AMELX, ENAM, KLK4 and MMP20 are discussed. Genetics of dentin formation including the role of the DSPP gene in dentinogenesis imperfecta are also summarized. The document provides an overview of the molecular genetics underlying tooth development and malformations.
Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases that degrade extracellular matrix components. MMPs play important roles in tissue remodeling during processes like wound healing and organ development by breaking down collagen, elastin, fibronectin and other matrix proteins. Their activity is regulated by tissue inhibitors of metalloproteinases (TIMPs). Abnormal MMP activity is associated with diseases like cancer, atherosclerosis, and rheumatoid arthritis by facilitating tissue invasion or destruction.
1) BMPs play an important role in tooth development and regeneration by signaling between dental epithelium and mesenchyme. They are expressed in a spatial and temporal sequence that governs tooth patterning and morphogenesis.
2) Progenitor/stem cells found in dental pulp and periodontal ligament have the potential to differentiate into odontoblasts and other dental tissues when exposed to BMPs.
3) The application of BMPs, stem cells, and appropriate extracellular matrix scaffolds could facilitate the regeneration of dental and craniofacial tissues through recapitulating embryonic development pathways.
Proto-oncogenes are normal cellular genes that encode proteins involved in cell proliferation. When mutated, they become oncogenes that encode constitutively active oncoproteins driving increased cell growth. Proto-oncogenes can encode growth factors, growth factor receptors, signal transducers, transcription factors, or cell cycle regulators. Common mutations include RAS mutations in pancreatic cancer, BRAF mutations in melanoma, PI3K mutations in breast cancer, and MYC translocations in Burkitt's lymphoma. These mutations result in constitutive activation of signaling pathways that drive uncontrolled cell proliferation.
This document discusses histochemistry of oral tissues. It defines histochemistry as the qualitative and quantitative assessment of chemicals within cells and tissues. It describes the purpose of histochemistry as coloring structures for identification, locating insoluble materials accurately in tissues, and using materials that do not separate from their environment with high sensitivity. It outlines the main oral tissues studied in histochemistry as connective tissue, epithelial linings, and glandular structures. It provides details on specific histochemical techniques used to study components like glycogen, glyoproteins, proteoglycans, lipids, proteins, nucleic acids, and enzymes in oral tissues.
Cancer arises from normal cells whose nature is permanently changed, causing them to multiply rapidly and not be subject to normal control. Oncogenes are genes capable of transforming normal cells into cancerous cells and result from mutations of normal proto-oncogenes. Both DNA and RNA tumor viruses can transform cells through integration into the host cell DNA, which results in loss of growth control and tumor formation. Retroviruses contain oncogenes (v-onc) that are homologous to cellular proto-oncogenes (c-onc) and can induce transformation after mutation or other changes to the cell's genome.
1) Tumors exist within a complex microenvironment consisting of various cell types that influence tumor growth, progression, and metastasis.
2) Chronic inflammation can promote tumor development by increasing genetic mutations while also stimulating angiogenesis and tumor cell proliferation.
3) The tumor microenvironment interacts bidirectionally with cancer cells to encourage processes like angiogenesis, immune suppression, invasion, and metastasis through factors such as TGF-β, VEGF, and cytokines.
4) Therapies targeting the tumor microenvironment can impact its composition and make cancer cells more invasive, highlighting the need for combination treatments.
BE UPDATE TO IT,, AS IT IS 3 years back from 2017
Kindly mail me if you feel, needy of this presentation
you can find my mail id @ slide share,,, if not mail me @
sukesh3567@gmail.com.
Good luck
This document discusses cancer metastasis, specifically metastasis to the jaw. It begins by defining cancer metastasis as the process where tumor cells invade nearby tissues and spread via the lymphatic system or bloodstream to form tumors in other parts of the body. The jaw is a relatively rare site of metastasis, accounting for around 1-1.5% of oral malignant tumors. The most common primary sites that metastasize to the jaw are the lungs, breast, kidneys, and bone. Metastasis to the jaw usually presents with pain, difficulty chewing, swelling, and pathological fractures. Radiographs may show osteolytic or osteoblastic lesions depending on the primary tumor type. Histopathological examination is needed for definitive diagnosis of metastatic
Oncogene And Tumor Suppressor Gene
The document discusses oncogenes and tumor suppressor genes. It defines proto-oncogenes as genes involved in cell growth that can become activated oncogenes through mutations. Oncogenes are classified into five groups. Tumor suppressor genes normally inhibit tumor formation but mutations inactivate this function in a two-hit model. Examples discussed include HER2/neu, Ras, Myc, Rb, p53, BRCA1, BRCA2, and APC.
The document summarizes the development of the mandible from the first branchial arch. It begins as Meckel's cartilage, which later develops into the mandibular body, rami, and processes through intramembranous ossification and endochondral ossification guided by secondary cartilages. The mandibular canal and alveolar process also develop during this time. The shape of the mandible changes with age from birth through childhood, adulthood, and old age. Developmental disturbances can result in conditions like agnathia, micrognathia, and macrognathia.
Epithelial and mesenchymal transition in invasion and metastasisAshwini Gowda
This document discusses neoplasia and the process of metastasis. It defines neoplasia as new, uncontrolled growth and describes the hallmarks of cancer cells, including autonomous growth, loss of differentiation, invasion and metastasis. It explains the multi-step process of metastasis, beginning with local invasion of tumor cells into surrounding tissue facilitated by degradation of the extracellular matrix and migration of cells. The document then discusses the vascular dissemination of tumor cells and colonization at distant sites, outlining several theories for how metastatic potential arises in tumors. Key genes and pathways involved in epithelial-mesenchymal transition and the generation of cancer stem cells are also reviewed.
The document summarizes the process of cancer metastasis through the invasion-metastasis cascade. It involves 6 key steps: 1) Localized invasion of primary tumor cells aided by loss of cell adhesion molecules and matrix metalloproteinases. 2) Intravasation of tumor cells into blood vessels assisted by tumor-associated macrophages. 3) Transport of circulating tumor cells protected by platelet emboli. 4) Extravasation of tumor cells from vessels into distant tissues. 5) Formation of dormant micrometastases. 6) Rare colonization of micrometastases into macroscopic tumors limited by the foreign tissue environment. Metastasis suppressor genes and strategies targeting multiple steps simultaneously show promise for preventing cancer spread.
Angiogenesis is the formation of new blood vessels from pre-existing vessels. It involves sprouting, splitting, and remodeling of existing vessels. It supplies oxygen and nutrients and removes waste. Tumors stimulate angiogenesis to grow beyond 2mm3 by producing angiogenic factors like VEGF. Angiogenesis inhibitors like endostatin can restrict tumor growth. Anti-angiogenic therapies cut off the tumor blood supply, while vascular disrupting agents directly damage existing tumor vessels.
Stem cells found in dental tissues such as dental pulp, dental pulp of deciduous teeth, apical papilla, and dental follicle can differentiate into odontoblast cells and have potential applications in dental tissue regeneration and repair. There are several types of dental stem cells that can potentially be used to regenerate dental tissues and whole teeth. Delivery of growth factors has shown potential to induce homing of endogenous stem cells to regenerate dental pulp-like tissue in root canals of extracted human teeth implanted in mice without cell transplantation. Further research is still needed but dental stem cells show promise for applications in dental tissue engineering and whole tooth regeneration.
1. Cancer epigenetics involves heritable changes in gene expression that are not due to changes in DNA sequence. Histone modifications and chromatin remodeling complexes play important roles in cancer development by regulating gene expression and transcription.
2. Many genes that encode histone modifying enzymes are mutated in cancer. Mutations in DNA methyltransferases, histone methyltransferases, and histone demethylases commonly occur in cancers.
3. Targeting epigenetic enzymes and pathways, such as with DNA methyltransferase or histone deacetylase inhibitors, shows promise as cancer therapies. Combination epigenetic and conventional chemotherapy may help reduce drug resistance.
Giant cell lesions can be physiological, occurring normally in tissues like bone marrow and placenta, or pathological. Pathological giant cells are usually formed by the fusion of macrophages and are seen in conditions like granulomas, infections, and foreign body reactions. There are several types of giant cells characterized by their histological appearance and distribution of nuclei, including Langhans', foreign body, and Touton giant cells. Giant cell lesions can also occur in bone and oral mucosa in various inflammatory, infectious, neoplastic, and metabolic conditions. Central giant cell granuloma is a benign bone lesion first described by Jaffe in 1953 as a reparative process consisting of fibrohistocytic proliferation and haemosiderin
The document summarizes updates to the salivary gland section of the 5th edition of the World Health Organization Classification of Head and Neck Tumors, including the description and inclusion of several new entities. Specifically, it introduces sclerosing polycystic adenoma, keratocystoma, intercalated duct adenoma, and striated duct adenoma as new benign entities, as well as microsecretory adenocarcinoma and sclerosing microcystic adenocarcinoma as new malignant entities. It also discusses controversies that remain unresolved, such as the classification of mucinous adenocarcinoma and intraductal carcinoma.
The neural crest is a multipotent population of migratory cells that arises at the border of the neural plate and gives rise to many different cell types. Neural crest cells migrate throughout the embryo along defined pathways and differentiate depending on environmental cues. Cranial neural crest cells contribute to structures of the head like cartilage and bone, and form the tissues of the pharyngeal arches which give rise to parts of the skull and face. Trunk neural crest cells differentiate into tissues like melanocytes, neurons, and adrenal glands. The environment neural crest cells migrate to determines their final fate.
A tumor marker is a substance present in or produced by a tumor or by the tumor’s host in response to the tumor’s presence that can be used to differentiate a tumor from normal tissue or to determine the presence of a tumor based on measurement in the blood or secretions.
Bone is a living tissue that provides structure and support. It can be classified based on shape, development, histology, and composition. The alveolar process forms with tooth development and eruption to support teeth in the jaw. It consists of cortical and cancellous bone layers surrounded by osteoblasts and osteoclasts, which build and resorb bone through various signaling pathways and enzymes.
Genetics in Tooth Development
Introduction
The Molecular Program of Tooth Development
Primary Epithelial Band
Dental Lamina
Vestibular Lamina
Initiation of the Tooth
Genes expressed during tooth development
Developmental signals controlling the position and the number of tooth germs along the oral surface
Homeobox code model
Instructive Signals for Patterning
Tooth Type Determination
Regionalization of Oral and Dental Ectoderm
Bud Stage
Bud-to-Cap Transition
Signaling centres
Applied aspects
The p53 gene is a tumor suppressor gene that regulates the cell cycle and prevents tumor formation. It acts as the "guardian of the genome" by inducing cell cycle arrest or apoptosis in damaged cells. p53 is commonly mutated in cancer, inactivating its normal functions and allowing damaged cells to continue dividing. When p53 is mutated, DNA damage fails to trigger cell cycle arrest, potentially leading to neoplastic transformation. The document discusses p53's role in DNA repair, apoptosis, and cell cycle regulation as well as how it is inactivated through mutations and the cancers most associated with p53 mutations, such as breast, colorectal, liver, lung, and ovarian cancers.
This document provides an overview of salivary gland tumors. It discusses that salivary gland tumors are heterogeneous and most are benign. The majority originate in the parotid glands. Pleomorphic adenoma is the most common benign tumor and occurs most often in the parotid glands. The document describes the histopathology and classification of various salivary gland tumors including pleomorphic adenoma, adenoid cystic carcinoma, and mucoepidermoid carcinoma. It also discusses the genetics and hypothesized cells of origin for different salivary gland neoplasms.
This presentation provides an overview of the training and career path to become an EMT. It discusses taking science and medical courses, volunteering at hospitals for hands-on experience, enrolling in EMT classes to choose a medical field, and being ready for the job with all acquired knowledge and skills. The presentation also touches on responding to complex situations, dealing with death and injuries, working hours and payment, and finding the career rewarding and inspirational.
This document discusses the phases and cellular processes involved in wound healing. It describes three phases - inflammatory, proliferative, and maturation. The inflammatory phase involves hemostasis, recruitment of inflammatory cells, and production of growth factors. The proliferative phase involves angiogenesis, fibroplasia, and re-epithelialization to form granulation tissue. The maturation phase involves remodeling of scar tissue and collagen. Local and systemic factors that can impact wound healing are also discussed.
1) Tumors exist within a complex microenvironment consisting of various cell types that influence tumor growth, progression, and metastasis.
2) Chronic inflammation can promote tumor development by increasing genetic mutations while also stimulating angiogenesis and tumor cell proliferation.
3) The tumor microenvironment interacts bidirectionally with cancer cells to encourage processes like angiogenesis, immune suppression, invasion, and metastasis through factors such as TGF-β, VEGF, and cytokines.
4) Therapies targeting the tumor microenvironment can impact its composition and make cancer cells more invasive, highlighting the need for combination treatments.
BE UPDATE TO IT,, AS IT IS 3 years back from 2017
Kindly mail me if you feel, needy of this presentation
you can find my mail id @ slide share,,, if not mail me @
sukesh3567@gmail.com.
Good luck
This document discusses cancer metastasis, specifically metastasis to the jaw. It begins by defining cancer metastasis as the process where tumor cells invade nearby tissues and spread via the lymphatic system or bloodstream to form tumors in other parts of the body. The jaw is a relatively rare site of metastasis, accounting for around 1-1.5% of oral malignant tumors. The most common primary sites that metastasize to the jaw are the lungs, breast, kidneys, and bone. Metastasis to the jaw usually presents with pain, difficulty chewing, swelling, and pathological fractures. Radiographs may show osteolytic or osteoblastic lesions depending on the primary tumor type. Histopathological examination is needed for definitive diagnosis of metastatic
Oncogene And Tumor Suppressor Gene
The document discusses oncogenes and tumor suppressor genes. It defines proto-oncogenes as genes involved in cell growth that can become activated oncogenes through mutations. Oncogenes are classified into five groups. Tumor suppressor genes normally inhibit tumor formation but mutations inactivate this function in a two-hit model. Examples discussed include HER2/neu, Ras, Myc, Rb, p53, BRCA1, BRCA2, and APC.
The document summarizes the development of the mandible from the first branchial arch. It begins as Meckel's cartilage, which later develops into the mandibular body, rami, and processes through intramembranous ossification and endochondral ossification guided by secondary cartilages. The mandibular canal and alveolar process also develop during this time. The shape of the mandible changes with age from birth through childhood, adulthood, and old age. Developmental disturbances can result in conditions like agnathia, micrognathia, and macrognathia.
Epithelial and mesenchymal transition in invasion and metastasisAshwini Gowda
This document discusses neoplasia and the process of metastasis. It defines neoplasia as new, uncontrolled growth and describes the hallmarks of cancer cells, including autonomous growth, loss of differentiation, invasion and metastasis. It explains the multi-step process of metastasis, beginning with local invasion of tumor cells into surrounding tissue facilitated by degradation of the extracellular matrix and migration of cells. The document then discusses the vascular dissemination of tumor cells and colonization at distant sites, outlining several theories for how metastatic potential arises in tumors. Key genes and pathways involved in epithelial-mesenchymal transition and the generation of cancer stem cells are also reviewed.
The document summarizes the process of cancer metastasis through the invasion-metastasis cascade. It involves 6 key steps: 1) Localized invasion of primary tumor cells aided by loss of cell adhesion molecules and matrix metalloproteinases. 2) Intravasation of tumor cells into blood vessels assisted by tumor-associated macrophages. 3) Transport of circulating tumor cells protected by platelet emboli. 4) Extravasation of tumor cells from vessels into distant tissues. 5) Formation of dormant micrometastases. 6) Rare colonization of micrometastases into macroscopic tumors limited by the foreign tissue environment. Metastasis suppressor genes and strategies targeting multiple steps simultaneously show promise for preventing cancer spread.
Angiogenesis is the formation of new blood vessels from pre-existing vessels. It involves sprouting, splitting, and remodeling of existing vessels. It supplies oxygen and nutrients and removes waste. Tumors stimulate angiogenesis to grow beyond 2mm3 by producing angiogenic factors like VEGF. Angiogenesis inhibitors like endostatin can restrict tumor growth. Anti-angiogenic therapies cut off the tumor blood supply, while vascular disrupting agents directly damage existing tumor vessels.
Stem cells found in dental tissues such as dental pulp, dental pulp of deciduous teeth, apical papilla, and dental follicle can differentiate into odontoblast cells and have potential applications in dental tissue regeneration and repair. There are several types of dental stem cells that can potentially be used to regenerate dental tissues and whole teeth. Delivery of growth factors has shown potential to induce homing of endogenous stem cells to regenerate dental pulp-like tissue in root canals of extracted human teeth implanted in mice without cell transplantation. Further research is still needed but dental stem cells show promise for applications in dental tissue engineering and whole tooth regeneration.
1. Cancer epigenetics involves heritable changes in gene expression that are not due to changes in DNA sequence. Histone modifications and chromatin remodeling complexes play important roles in cancer development by regulating gene expression and transcription.
2. Many genes that encode histone modifying enzymes are mutated in cancer. Mutations in DNA methyltransferases, histone methyltransferases, and histone demethylases commonly occur in cancers.
3. Targeting epigenetic enzymes and pathways, such as with DNA methyltransferase or histone deacetylase inhibitors, shows promise as cancer therapies. Combination epigenetic and conventional chemotherapy may help reduce drug resistance.
Giant cell lesions can be physiological, occurring normally in tissues like bone marrow and placenta, or pathological. Pathological giant cells are usually formed by the fusion of macrophages and are seen in conditions like granulomas, infections, and foreign body reactions. There are several types of giant cells characterized by their histological appearance and distribution of nuclei, including Langhans', foreign body, and Touton giant cells. Giant cell lesions can also occur in bone and oral mucosa in various inflammatory, infectious, neoplastic, and metabolic conditions. Central giant cell granuloma is a benign bone lesion first described by Jaffe in 1953 as a reparative process consisting of fibrohistocytic proliferation and haemosiderin
The document summarizes updates to the salivary gland section of the 5th edition of the World Health Organization Classification of Head and Neck Tumors, including the description and inclusion of several new entities. Specifically, it introduces sclerosing polycystic adenoma, keratocystoma, intercalated duct adenoma, and striated duct adenoma as new benign entities, as well as microsecretory adenocarcinoma and sclerosing microcystic adenocarcinoma as new malignant entities. It also discusses controversies that remain unresolved, such as the classification of mucinous adenocarcinoma and intraductal carcinoma.
The neural crest is a multipotent population of migratory cells that arises at the border of the neural plate and gives rise to many different cell types. Neural crest cells migrate throughout the embryo along defined pathways and differentiate depending on environmental cues. Cranial neural crest cells contribute to structures of the head like cartilage and bone, and form the tissues of the pharyngeal arches which give rise to parts of the skull and face. Trunk neural crest cells differentiate into tissues like melanocytes, neurons, and adrenal glands. The environment neural crest cells migrate to determines their final fate.
A tumor marker is a substance present in or produced by a tumor or by the tumor’s host in response to the tumor’s presence that can be used to differentiate a tumor from normal tissue or to determine the presence of a tumor based on measurement in the blood or secretions.
Bone is a living tissue that provides structure and support. It can be classified based on shape, development, histology, and composition. The alveolar process forms with tooth development and eruption to support teeth in the jaw. It consists of cortical and cancellous bone layers surrounded by osteoblasts and osteoclasts, which build and resorb bone through various signaling pathways and enzymes.
Genetics in Tooth Development
Introduction
The Molecular Program of Tooth Development
Primary Epithelial Band
Dental Lamina
Vestibular Lamina
Initiation of the Tooth
Genes expressed during tooth development
Developmental signals controlling the position and the number of tooth germs along the oral surface
Homeobox code model
Instructive Signals for Patterning
Tooth Type Determination
Regionalization of Oral and Dental Ectoderm
Bud Stage
Bud-to-Cap Transition
Signaling centres
Applied aspects
The p53 gene is a tumor suppressor gene that regulates the cell cycle and prevents tumor formation. It acts as the "guardian of the genome" by inducing cell cycle arrest or apoptosis in damaged cells. p53 is commonly mutated in cancer, inactivating its normal functions and allowing damaged cells to continue dividing. When p53 is mutated, DNA damage fails to trigger cell cycle arrest, potentially leading to neoplastic transformation. The document discusses p53's role in DNA repair, apoptosis, and cell cycle regulation as well as how it is inactivated through mutations and the cancers most associated with p53 mutations, such as breast, colorectal, liver, lung, and ovarian cancers.
This document provides an overview of salivary gland tumors. It discusses that salivary gland tumors are heterogeneous and most are benign. The majority originate in the parotid glands. Pleomorphic adenoma is the most common benign tumor and occurs most often in the parotid glands. The document describes the histopathology and classification of various salivary gland tumors including pleomorphic adenoma, adenoid cystic carcinoma, and mucoepidermoid carcinoma. It also discusses the genetics and hypothesized cells of origin for different salivary gland neoplasms.
This presentation provides an overview of the training and career path to become an EMT. It discusses taking science and medical courses, volunteering at hospitals for hands-on experience, enrolling in EMT classes to choose a medical field, and being ready for the job with all acquired knowledge and skills. The presentation also touches on responding to complex situations, dealing with death and injuries, working hours and payment, and finding the career rewarding and inspirational.
This document discusses the phases and cellular processes involved in wound healing. It describes three phases - inflammatory, proliferative, and maturation. The inflammatory phase involves hemostasis, recruitment of inflammatory cells, and production of growth factors. The proliferative phase involves angiogenesis, fibroplasia, and re-epithelialization to form granulation tissue. The maturation phase involves remodeling of scar tissue and collagen. Local and systemic factors that can impact wound healing are also discussed.
The document analyzes post-translational modifications (PTMs) of alpha-tubulin in three breast cancer cell lines - MCF10a, MCF7 and MDA-MB-231 - which represent different stages of cancer progression and an epithelial-to-mesenchymal transition (EMT). Western blot and microscopy analysis found increased levels of acetylated and detyrosinated alpha-tubulin in the more invasive MCF7 and MDA-MB-231 cell lines compared to the less invasive MCF10a cell line. This suggests PTMs are associated with, but not directly regulatory of, cancer progression and EMT-like events. Further study of PTMs may provide diagnostic tools to assess metastatic cancer potential.
Pentoxifylline as an Adjunct to Antimicrobial Therapy to Reduce Length of Sta...Philip Yinger
This document presents background information on neonatal sepsis and proposes a randomized controlled trial to investigate the efficacy of adjunctive pentoxifylline therapy in reducing length of stay among preterm infants with blood culture-confirmed sepsis. Neonatal sepsis is associated with significant morbidity, mortality, and socioeconomic burden. While antimicrobial therapy is the standard of care, adjunctive therapies that modulate the immune response show promise in improving outcomes. Pentoxifylline inhibits pro-inflammatory cytokines and may reduce organ dysfunction, improving cardiovascular function and tissue perfusion. The proposed study would compare length of stay outcomes between infants receiving pentoxifylline plus antimicrobials versus placebo plus antimicrobials.
Transformation and transfection allow the genetic alteration of cells through the introduction of foreign DNA. Transformation refers specifically to bacteria, where naked DNA fragments can be taken up through natural competence or artificial methods like heat shock or electroporation. Transfection applies to eukaryotic cells, using techniques like lipofection to introduce DNA through membrane pores. Common methods to transform plants include Agrobacterium infection, particle bombardment, and electroporation. These techniques generate genetically modified cells and organisms.
Deferential diagnosis of mesothelial proliferations and neoplasmsSvetoslav Bardarov
This document discusses the differential diagnosis of mesothelial proliferations and neoplasms. It provides background on the mesothelium, including its embryology, morphology, and functions. Reactive mesothelial hyperplasia is described. The case involves a 60-year-old female with ascites, for which the differential diagnosis includes papillary mesothelial hyperplasia, well differentiated papillary mesothelioma, tubulo-papillary mesothelioma, and low-grade adenocarcinoma. Immunostains and morphology are used to distinguish between epithelial and mesothelial lesions. The final diagnosis is low-grade papillary serous adenocarcinoma of the peritoneum based on
This document summarizes a study comparing the efficacy of pentoxifylline to placebo in the treatment of oral submucous fibrosis (OSF). OSF is a premalignant condition characterized by fibrosis of the oral cavity and restricted mouth opening. The study included 62 patients with OSF who were randomly assigned to receive either pentoxifylline or a placebo for 7 months. Outcomes including symptoms, mouth opening, and fibrosis were assessed. The results showed greater improvement in symptoms and signs for the pentoxifylline group compared to the placebo group, with few side effects reported. The study concluded that pentoxifylline may be an effective treatment for OSF.
This document discusses epithelial-mesenchymal transition (EMT) and its role in cancer metastasis. It summarizes findings from a study using a triple-transgenic mouse model of breast cancer metastasis that found: 1) Primary tumor cells disseminated and formed metastases while maintaining their epithelial phenotype, not undergoing EMT. 2) Inhibiting EMT with miR-200 had no effect on metastasis. 3) Non-EMT tumor cells were sensitive to chemotherapy, whereas mesenchymal cells were resistant. The study provides evidence that EMT may not be required for cancer metastasis in this model.
This document summarizes several types of benign soft tissue tumors including fibroma, fibromyoma/leiomyoma, lipoma, chondroma, and haemangioma. Fibroma arises from fibrous tissue and presents as a capsulated, oval mass. Fibromyoma originates from smooth muscle and presents as a firm, rounded mass in the uterus or GI tract. Lipoma arises from fatty tissue and presents as a soft, lobulated, yellow mass. Chondroma arises from cartilage and presents as a hard, lobulated mass in bones. Haemangioma is a malformed blood vessel tumor that presents as vascular spaces filled with blood.
This document summarizes a study comparing the efficacy of Pentoxifylline to placebo in the treatment of oral submucous fibrosis (OSF). OSF is a premalignant condition caused by chewing areca nut and characterized by fibrosis in the mouth restricting opening. The study involved randomly assigning 62 patients with OSF to receive either Pentoxifylline or a placebo for 7 months. Outcomes like mouth opening, symptoms, and signs of OSF were evaluated and compared between the two groups at baseline and over 18 months of follow-up.
The document discusses cell adhesion and migration. It outlines four classes of cell junctions: anchoring junctions, occluding junctions, channel-forming junctions, and signal-relaying junctions. Anchoring junctions like adherens junctions and desmosomes connect cells to each other and transmit stresses through connections to the cytoskeleton. Tight junctions form seals between cells and separate membrane domains. Cadherins are important cell adhesion molecules that mediate calcium-dependent cell-cell adhesion through homophilic binding. Regulation of cadherins and other cell adhesion molecules controls processes like epithelial-mesenchymal transition that are important for tissue development and cancer metastasis.
The document discusses wound healing and classification. It describes the phases of wound healing as inflammatory, proliferative, and remodeling. The inflammatory phase begins immediately after wounding and lasts 2-3 days, involving vasoactive amines, growth factors, and inflammatory cells. The proliferative phase lasts from days 3 to 3 weeks, involving fibroblast activity, collagen production, angiogenesis, and re-epithelialization. The remodeling phase begins during proliferation and lasts up to 2 years, involving collagen remodeling and maturation. Healing is classified as primary intention for clean wounds or secondary intention for infected wounds. Factors like age, obesity, smoking, and malnutrition can affect wound healing.
The document provides guidance on evaluating endometrial biopsy specimens. It discusses that the functionalis layer of the endometrium from the fundus is ideal for diagnosis. Proliferative phase dating is not possible while secretory phase dating is. Findings of fat in the specimen indicates uterine perforation. Endometrial polyps, hyperplasia, and carcinomas are discussed along with mimics. Immunostains can help in certain cases. The clinician should be notified of significant findings and limitations of the specimen.
This document discusses cell transformation, which is a change to a cell's DNA. It describes three methods of transforming cells:
1) Transforming bacteria cells using plasmids containing foreign DNA that can be inserted into the plasmid. The recombinant plasmids can then deliver the DNA into the bacterial cell.
2) Transforming plant cells either by using the bacterium Agrobacterium tumefaciens to transfer recombinant plasmids, or by using a gene gun to inject DNA-coated particles into plant cells.
3) Transforming animal cells by injecting foreign DNA directly into egg nuclei, or using gene replacement to "knock out" an existing gene.
Tooth development proceeds with reciprocal inductive interactions between stomadeum ectoderm and underlying ectomesenchymal cells in a strictly controlled temporal and spatial order.
Well studied at the molecular biologic level, over 300 genes and 100 growth and differentiation factors are implicated in the control of cellular differentiation and crosstalk in dental development that result in structures containing combination of mineralized tissues (enamel, dentine, cementum), soft connective tissues (dental pulp, periodontal ligament), blood vessels, nerves and lymphatics.
Epithelial – Mesenchymal Interactions in Tooth Development.pptxDrPurvaPihulkar
Epithelial mesenchymal interactions (EMIs) are a series of programmed, sequential and reciprocal (complex and multiphase) communications between the epithelium and the mesenchyme with its heterotypic cell population, that result in the differentiation of one or both cell populations.
Odontogenesis is the process of tooth development, which involves both ectodermal and mesenchymal components, being the key elements in the development of teeth.
In order for the tooth to form, an interactive mechanism between these heterotypic cellular populations is required.
For these interactions to occur there should be some or other form of messenger system between epithelium and mesenchyme, further underlining the importance of cell signaling networks and intricacies of physiological growth of an individual.
In the process of embryonic development the ectoderm is composed of surface ectoderm, neural crest and neural tube.
Tooth development proceeds with reciprocal inductive interactions between stomadeum ectoderm and underlying ectomesenchymal cells in a strictly controlled temporal and spatial order.
Well studied at the molecular biologic level, over 300 genes and 100 growth and differentiation factors are implicated in the control of cellular differentiation and crosstalk in dental development that result in structures containing combination of mineralized tissues (enamel, dentine, cementum), soft connective tissues (dental pulp, periodontal ligament), blood vessels, nerves and lymphatics
2000 biologia celular y molecular de la enciakenigal
The document summarizes key aspects of gingival structure and function. It discusses:
1) The gingiva is comprised of epithelial and connective tissue components that differ in location, architecture, composition and function but work together as a unit.
2) The gingival epithelium consists of the oral epithelium, sulcular epithelium, and junctional epithelium, which differ in origin, structure, and cellular composition.
3) The junctional epithelium attaches to the tooth surface and contains migrating leukocytes, while the oral and sulcular epithelia are multilayered and may be parakeratinized.
Hertwig's epithelial root sheath is broken up and separated from the root, allowing differentiation of cementoblasts and formation of cementum. This marks the transition from root formation to development of the periodontium, including the periodontal ligament, cementum, and alveolar bone. Mesenchymal cells in the dental follicle and perifollicular region develop into fibroblasts that synthesize collagen fibers and other proteins to form the principal fiber groups of the periodontal ligament. Homeostasis of the periodontium is maintained by regulators that prevent mineralization and allow proliferation and remodeling of tissues in response to forces.
Chronology of dental development and development of occlusionshilpathaklotra
The document summarizes key stages of dental development and changes in dental arches:
- Tooth development begins with thickening of oral epithelium, forming the primary epithelial band that invades underlying mesenchyme. This forms the dental lamina which serves as the primordium for deciduous teeth.
- Teeth develop through bud, cap, bell, and advanced bell stages. During these stages, the enamel organ and dental papilla form and cells differentiate into ameloblasts and odontoblasts. Enamel knots organize cuspal morphogenesis.
- Root formation begins after crown formation is complete, guided by Hertwig's epithelial root sheath which induces dentin formation and shapes
Growth & development of tooth & tongue/ dental crown & bridge coursesIndian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The document summarizes the development of teeth from early embryogenesis through the stages of tooth formation. It discusses the three germ layers that form during gastrulation and the formation of the neural tube. Tooth development begins with the formation of the dental lamina from oral epithelium. Tooth buds form from outgrowths of the dental lamina and develop through the bud, cap and bell stages. Key cellular and molecular components that regulate tooth morphogenesis are the enamel organ, dental papilla, transcription factors and growth factors.
The junctional epithelium is a non-keratinized stratified squamous epithelium that forms an attachment to the tooth surface. It develops from the reduced enamel epithelium during tooth eruption. The junctional epithelium acts as a barrier against oral pathogens and allows for host defense mechanisms to reach the gingival sulcus. It has a rapid turnover rate of 4-6 days and can quickly regenerate after injury. The attachment to enamel is mediated by hemidesmosomes in the epithelial cells that are connected to the internal basal lamina on the tooth surface. Disruption of this attachment can initiate periodontal pocket formation and disease.
1. The primitive oral cavity is lined by a 2-3 cell thick layered epithelium covering embryonic connective tissue formed from neural crest cells.
2. Tooth development involves three overlapping phases: initiation, morphogenesis, and histogenesis, during which dental tissues differentiate.
3. The first sign of tooth development is the formation of a continuous epithelial band around the primitive oral cavity, which divides into vestibular and dental lamina. The dental lamina then invaginates and forms 20 buds for the primary teeth.
The document discusses the development of teeth and surrounding periodontium. It describes how the dental lamina forms and divides into the dental lamina and vestibular lamina. Tooth development is initiated through the interaction of oral epithelium and underlying mesenchyme. Tooth germs form and progress through the bud, cap and bell stages as the enamel organ and dental papilla develop. Signaling molecules regulate tooth patterning and determination of tooth shape.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Development of teeth and developmental defectsVini Mehta
This document provides an overview of tooth development and developmental defects. It begins with the primitive oral cavity and stages of tooth formation from the dental lamina through bell stages. Genes and growth factors involved in odontogenesis are discussed. Enamel, dentin, and root formation include descriptions of ameloblasts, odontoblasts, and Hertwig's epithelial root sheath. Common developmental defects affecting tooth size, shape, number, and structure are presented. The document concludes with prevalence data showing hypodontia and microdontia as the most frequent anomalies.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Development of periodontium. periodonticsGururam MDS
This document provides an overview of tooth and periodontal tissue development. It discusses how neural crest cells give rise to dental and periodontal structures. Tooth development progresses through bud, cap, and bell stages as the enamel organ and dental papilla interact. Cementum, periodontal ligament, and alveolar bone develop during root formation guided by Hertwig's epithelial root sheath. The gingiva develops from both epithelial and connective tissue precursors. Epithelial-mesenchymal interactions are important for maintaining tissue phenotypes and regulating epithelial growth.
The document describes the anatomy and histology of the gingiva. It discusses that the gingiva is divided into free gingiva, interdental gingiva, and attached gingiva. It describes the epithelial layers, basement membrane, gingival fibers, blood supply, and characteristics of normal gingiva such as color, texture, contour, shape, size, and consistency.
Similar to Epithelial-Mesenchymal Transition: At the Crossroads of Development and Tumor Metastasis /orthodontic courses by Indian dental academy (20)
Opportunity for Dentists (BDS/MDS )to relocate to United kingdom -Register as a DENTAL HYGIENIST/ DENTAL THERAPIST without Board exams and after approval you can register in GDC as a DH/DT and start working as a DH/DT Immediately and get paid.
You can complete the whole process in 3-4 months.Salary range for DH/DT is around 2500-3500 Pounds per month.
Eligibility / requirements-
1. An International English Language Testing System (IELTS) certificate
at the appropriate level.(Within 2 yrs of application date )
2: A recent primary dental qualification that has been taught and examined in English..(Within 2 yrs of application date )
3: A recent pass in a language test for registration with a regulatory authority in a country where the first language is English.
If you are interested Please contact us for more details.
1ST, 2ND AND 3RD ORDER BENDS IN STANDARD EDGEWISE APPLIANCE SYSTEM /Fixed ort...Indian dental academy
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals
who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry,
Periodontics and General Dentistry.
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
I –Aligners are made with FDA approved transparent thermoplastic materials using 3D scanning, 3D Printing and finally Trays with Pressure vacuum formers.
Dear Doctor,
Indian Dental Academy Now offers comprehensive online Orthodontics course.
Course includes:
1.whiteboard lecture presentations
2.Case Discussions
3.with hundreds of pictures.
4.Demo on Models
5.Demo on Patients
6. subtitles in your own language
12 months unlimited access and support @350 USD only.
For Demo please visit :www.idalectures.com/preview/
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Thanks & Regards
Indian Dental Academy
--
Indian Dental Academy
Leader in continuing dental education
www.indiandentalacademy.com
skype:indiandentalacademy
+919248678078
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Cytotoxicity of silicone materials used in maxillofacial prosthesis / dental ...Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Diagnosis and treatment planning in completely endntulous arches/dental coursesIndian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Properties of Denture base materials /rotary endodontic coursesIndian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
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Use of modified tooth forms in complete denture occlusion / dental implant...Indian dental academy
This document discusses dental occlusion concepts and philosophies for complete dentures. It introduces key terms like physiologic occlusion and defines different occlusion schemes like balanced articulation and monoplane articulation. The document discusses advantages and disadvantages of using anatomic versus non-anatomic teeth for complete dentures. It also outlines requirements for maintaining denture stability, such as balanced occlusal contacts and control of horizontal forces. The goal of occlusion for complete dentures is to re-establish the homeostasis of the masticatory system disrupted by edentulism.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
This document discusses dental casting investment materials. It describes the three main types of investments - gypsum bonded, phosphate bonded, and ethyl silicate bonded investments. For gypsum bonded investments specifically, it details their classification, composition including the roles of gypsum, silica, and modifiers, setting time, normal and hygroscopic setting expansion, and thermal expansion. It provides information on how the properties of gypsum bonded investments are affected by their composition. The document serves as a comprehensive overview of dental casting investment materials.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
How to Setup Warehouse & Location in Odoo 17 InventoryCeline George
In this slide, we'll explore how to set up warehouses and locations in Odoo 17 Inventory. This will help us manage our stock effectively, track inventory levels, and streamline warehouse operations.
Temple of Asclepius in Thrace. Excavation resultsKrassimira Luka
The temple and the sanctuary around were dedicated to Asklepios Zmidrenus. This name has been known since 1875 when an inscription dedicated to him was discovered in Rome. The inscription is dated in 227 AD and was left by soldiers originating from the city of Philippopolis (modern Plovdiv).
Leveraging Generative AI to Drive Nonprofit InnovationTechSoup
In this webinar, participants learned how to utilize Generative AI to streamline operations and elevate member engagement. Amazon Web Service experts provided a customer specific use cases and dived into low/no-code tools that are quick and easy to deploy through Amazon Web Service (AWS.)
Chapter wise All Notes of First year Basic Civil Engineering.pptxDenish Jangid
Chapter wise All Notes of First year Basic Civil Engineering
Syllabus
Chapter-1
Introduction to objective, scope and outcome the subject
Chapter 2
Introduction: Scope and Specialization of Civil Engineering, Role of civil Engineer in Society, Impact of infrastructural development on economy of country.
Chapter 3
Surveying: Object Principles & Types of Surveying; Site Plans, Plans & Maps; Scales & Unit of different Measurements.
Linear Measurements: Instruments used. Linear Measurement by Tape, Ranging out Survey Lines and overcoming Obstructions; Measurements on sloping ground; Tape corrections, conventional symbols. Angular Measurements: Instruments used; Introduction to Compass Surveying, Bearings and Longitude & Latitude of a Line, Introduction to total station.
Levelling: Instrument used Object of levelling, Methods of levelling in brief, and Contour maps.
Chapter 4
Buildings: Selection of site for Buildings, Layout of Building Plan, Types of buildings, Plinth area, carpet area, floor space index, Introduction to building byelaws, concept of sun light & ventilation. Components of Buildings & their functions, Basic concept of R.C.C., Introduction to types of foundation
Chapter 5
Transportation: Introduction to Transportation Engineering; Traffic and Road Safety: Types and Characteristics of Various Modes of Transportation; Various Road Traffic Signs, Causes of Accidents and Road Safety Measures.
Chapter 6
Environmental Engineering: Environmental Pollution, Environmental Acts and Regulations, Functional Concepts of Ecology, Basics of Species, Biodiversity, Ecosystem, Hydrological Cycle; Chemical Cycles: Carbon, Nitrogen & Phosphorus; Energy Flow in Ecosystems.
Water Pollution: Water Quality standards, Introduction to Treatment & Disposal of Waste Water. Reuse and Saving of Water, Rain Water Harvesting. Solid Waste Management: Classification of Solid Waste, Collection, Transportation and Disposal of Solid. Recycling of Solid Waste: Energy Recovery, Sanitary Landfill, On-Site Sanitation. Air & Noise Pollution: Primary and Secondary air pollutants, Harmful effects of Air Pollution, Control of Air Pollution. . Noise Pollution Harmful Effects of noise pollution, control of noise pollution, Global warming & Climate Change, Ozone depletion, Greenhouse effect
Text Books:
1. Palancharmy, Basic Civil Engineering, McGraw Hill publishers.
2. Satheesh Gopi, Basic Civil Engineering, Pearson Publishers.
3. Ketki Rangwala Dalal, Essentials of Civil Engineering, Charotar Publishing House.
4. BCP, Surveying volume 1
Elevate Your Nonprofit's Online Presence_ A Guide to Effective SEO Strategies...TechSoup
Whether you're new to SEO or looking to refine your existing strategies, this webinar will provide you with actionable insights and practical tips to elevate your nonprofit's online presence.
How Barcodes Can Be Leveraged Within Odoo 17Celine George
In this presentation, we will explore how barcodes can be leveraged within Odoo 17 to streamline our manufacturing processes. We will cover the configuration steps, how to utilize barcodes in different manufacturing scenarios, and the overall benefits of implementing this technology.
2. REFERENCES
• Epithelial-Mesenchymal Transition in tumor
microenvironment, Jing et al. Cell & Bioscience
2011, 1:29.
• Epithelial-mesenchymal signalling regulating tooth
morphogenesis, Irma Thesleff, Journal of Cell
Science 116, 1647-1648, 2003
• Epithelial-mesenchymal transitions: the importance
of changing cell state in development and disease, J.
Clin. Invest. 119:1438–1449 (2009).www.indiandentalacademy.com
3. • Genetics and tooth anomalies - an update, Oral &
Maxillofacial Pathology Journal, Vol. 4, Jan, 2013.
• Reiterative signaling and patterning during
mammalian tooth morphogenesis, Mechanisms of
Development 92 (2000) 19-29.
• Oral Anatomy, Histology and Embryology – 4th
Edition, Berkovitz.
• Textbook of Oral Anatomy & Histology - 4th Edition,
Tencate.
www.indiandentalacademy.com
4. OVERVIEW OF EPITHELIAL-
MESENCHYMAL TRANSITION
• There are mainly two cell types -epithelial and
mesenchymal.
• Epithelial cells are adherent cells that form coherent
layers.
• Apico-basal polarity,
• Characteristic basally localized basement membrane
that separates the epithelium from other tissues.
www.indiandentalacademy.com
5. • Mesenchymal cells are non-polarized and lack
intercellular junctions, such that they can move as
individual cells throughout the extracellular matrix.
• The epithelial and mesenchymal cell phenotypes are
not irreversible, and during embryonic development,
cells can convert between the epithelial and
mesenchymal states.
www.indiandentalacademy.com
6. INTRODUCTION
• Epithelial-mesenchymal transition (EMT) and its
converse, mesenchymal-epithelial transition (MET),
are concepts first defined by Elizabeth Hay, 40 years
ago.
• EMT is a process, whereby epithelial cell layers lose
polarity and cell-cell contacts and undergo a
dramatic remodeling of cytoskeleton. ( Thiery, 2002)
www.indiandentalacademy.com
7. 3 major changes in cellular phenotype in
EMT
1. Morphological changes from a cobblestone-like
monolayer of epithelial cells with an apical-basal
polarity to dispersed, spindle-shaped mesenchymal
cells with migratory protrusions.
www.indiandentalacademy.com
8. 2. Changes of differentiation markers from cell-cell
junction proteins and cytokeratin intermediate
filaments to vimentin filaments and fibronectin.
3. Functional changes associated with the
conversion of stationary cells to motile cells that
can invade through ECM.
www.indiandentalacademy.com
9. • The epithelial-mesenchymal transition is a highly
conserved cellular program that allows polarized,
immotile epithelial cells to convert to motile
mesenchymal cells.
• This important process was initially recognized during
embryonic development and recently been implicated
in promoting carcinoma invasion and metastasis.
www.indiandentalacademy.com
10. • In this review, the authors have summarized and
compared major signaling pathways that
regulate the epithelial-mesenchymal transitions
during both development and tumor metastasis.
www.indiandentalacademy.com
11. EMT IN DEVELOPMENT
• During development, the EMT program has been
observed to underlie a variety of tissue
remodeling events, including mesoderm
formation, neural crest development, secondary
palate formation.
www.indiandentalacademy.com
12. Mesoderm Formation
• The earliest example of an EMT program
participating in embryogenesis is the formation of
mesoderm from the primitive ectoderm.
• The induction of mesoderm begins in a specific
area of the primitive ectoderm, termed the
primitive streak.
www.indiandentalacademy.com
13. • The first event in mesoderm formation is the
invagination of the epithelial cells.
• This step is characterized by drastic morphological
changes in a small population of epithelial cells.
www.indiandentalacademy.com
14. • Subsequently, these cells undergo mesenchymal
differentiation and migrate along the narrow
extracellular space underneath the ectoderm.
• The newly gained ability for such ectoderm-derived
cells to migrate along and through ECM marks the
completion of the EMT program during gastrulation.
www.indiandentalacademy.com
15. Neural Crest Formation
• The neural crest develops at the
boundary between the neural plate
and the epidermal ectoderm.
• The presumptive neural crest cells
proceed to lose N-cadherin-
mediated cell-cell adhesion while
becoming excluded from the
neural epithelium. www.indiandentalacademy.com
16. • Upregulate genes required for mesenchymal
phenotype and migratory ability.
• High levels of fibronectin and hyaluronan
appear in the presumptive neural crest area
before the onset of migration.
www.indiandentalacademy.com
17. Secondary Palate Formation
• Development of the secondary
palate requires fusion of the
palatal shelves at the midline.
• As the shelves approach one
another from opposite sides of
the developing oral cavity,
epithelial cells covering the tip
of each shelf intercalate and
form the medial epithelial seam.
www.indiandentalacademy.com
18. • Soon after fusion, these medial epithelial cells
undergo an EMT and are integrated into the
mesenchymal compartment of the palate, thereby
completing the program of palatogenesis.
www.indiandentalacademy.com
19. Epithelial-Mesenchymal Interactions During
Tooth Development
Initiation of Tooth Development
• Epithelium is the instructive component of
epithelial-mesenchymal interaction.
I arch epithelium + I arch mesenchyme Tooth germs
II arch epithelium + I or II arch mesenchyme No
www.indiandentalacademy.com
20. • The potential for first arch epithelium to initiate tooth
development only exists in the very early stages of
odontogenesis.
• Thereafter, when first arch mesenchyme is combined
with second arch epithelium, tooth germs are formed.
• This suggests that, after initiation by the oral epithelium,
the ‘control’ of tooth development passes to the
mesenchyme.
www.indiandentalacademy.com
21. Mechanisms responsible for specifying the tooth
forming zones in the oral region and for
controlling tooth number
• The expression of Pitx2 is restricted to dental
epithelium.
• Shh gene expression is restricted to the dental
epithelium at sites of tooth development and appears
to be involved in epithelial-mesenchymal
interactions.
www.indiandentalacademy.com
22. • Wnt helps maintain boundaries between tooth-
forming areas and non-tooth forming regions.
• Pax9 and Msx1 genes appear to be required to
enable the tooth germ to progress beyond the bud
stage.
www.indiandentalacademy.com
23. Mechanisms responsible for specifying tooth type
and tooth shape
Which of the two components is more important
for inducing morphogenesis and histogenesis –
the enamel organ or the dental papilla ?
www.indiandentalacademy.com
24. • Culturing dental papilla mesenchyme with
epithelium from the developing foot pad – normal
tooth development.
• Incisor enamel organ is combined with a molar
papilla, the resulting tooth is a molariform and
vice versa.
www.indiandentalacademy.com
25. • The results indicated that, at the cap stage of
tooth development, the principal organizer is
the dental papilla, in terms of both
morphogenesis and histogenesis.
www.indiandentalacademy.com
26. Epithelial-mesenchymal signalling regulating
tooth morphogenesis
• Tooth morphogenesis is an advancing process that is
regulated by sequential and reciprocal interactions
between the epithelial and mesenchymal tissues.
• During which the simple oral ectoderm thickens,
buds, grows and folds to form the complex shape of
the tooth crown.
www.indiandentalacademy.com
27. • During tooth initiation the ectoderm (white) thickens
and forms a placode that buds to the underlying
neural-crest derived mesenchyme (yellow).
www.indiandentalacademy.com
28. • The epithelium signals to the mesenchyme, which
then condenses around the epithelial bud.
• During subsequent morphogenesis the epithelium
folds and grows to surround the dental papilla
mesenchyme (cap stage).
www.indiandentalacademy.com
29. • The final shape of the tooth crown becomes fixed
during the bell stage, when the hard tissue forming
cells of the tooth (odontoblasts and amelobasts)
differentiate at the interface of the epithelium and
mesenchyme and deposit the dentin and enamel
matrices, respectively.
www.indiandentalacademy.com
30. • The signal molecules of several conserved families
mediate cell communication during tooth
development.
• Most of them belong to the transforming growth
factor β (TGFβ), fibroblast growth factor (FGF),
Hedgehog and Wnt families.
www.indiandentalacademy.com
31. • The signals mostly regulate interactions between the
ectoderm and mesenchyme, they also mediate
communication within one tissue layer.
• The genes regulated by the different signals include
transcription factors and signal receptors that regulate
the competence of the cells to respond to the next
signals, and thereby continue the communication
between cells and tissues.
www.indiandentalacademy.com
32. Molecular regulation of tooth development from
initiation to crown morphogenesis
www.indiandentalacademy.com
33. Molecular Regulation of EMT
• A number of distinct signaling pathways that
regulate EMT.
• The extracellular signals responsible for inducing
EMTs and the key transcriptional factors that
respond these signals.
• Such transcription factors function as master
regulators of the EMT programs.
www.indiandentalacademy.com
34. TGF- β Signaling
• Members of the transforming growth factor- β (TGF- β)
superfamily have been implicated as major induction
signals of EMT during almost all of the morphogenetic
events.
• Primary inducer of EMT.
www.indiandentalacademy.com
35. • TGF- β receptors are localized at tight junctions and
directly interact with two important regulators of
epithelial cell polarity and tight-junction assembly,
Par6 and Occludin.
• Phosphorylation of Par6 by TGF- β receptor leads
to a loss of tight junctions and apical-basal
polarity.
www.indiandentalacademy.com
36. The Wnt Signal
• The Wnt pathway is implicated in the initiation and
maintenance of mesoderm formation and neural
crest formation.
• The role of Wnt signaling in heart valve induction is
also well documented.
www.indiandentalacademy.com
37. The Notch Pathway
• Notch signalling has also been implicated in
modulating the EMT program during embryogenesis.
• Notch signalling regulates cranial neural crest cells
indirectly through its effect on expression of BMP
family members.
www.indiandentalacademy.com
38. • Notch signalling is not sufficient and needs to be
co-ordinated with additional signalling inputs in
order to promote an EMT.
www.indiandentalacademy.com
39. Signals from Tyrosine Kinase Receptors
• In addition to TGF-β, several other tyrosine kinase
receptors, including FGF, IGF, EGF family
members, and more recently PDGF, also play critical
roles in regulating EMT-like morphogenetic events
that occur during development.
www.indiandentalacademy.com
40. Transcriptional Regulation
• During the execution of the EMT program, many
genes involved in cell adhesion, mesenchymal
differentiation, cell migration, and invasion are
transcriptionally altered.
• The best-studied transcriptional modulation during
EMT is that involving the E-cadherin gene promoter.
www.indiandentalacademy.com
41. • The functional loss of E-cadherin in an epithelial
cell has been considered a hallmark of EMT.
• Detailed analyses of the human E-cadherin promoter
have identified E-box elements that are responsible
for its transcriptional repression.
www.indiandentalacademy.com
42. • The zinc-finger transcription factor Snail was
found to directly bind to the E-boxes of the E-
cadherin promoter and to repress transcription
of this gene (Batlle et al., Cano et al., 2000).
www.indiandentalacademy.com
43. • Several additional zinc-finger transcription factors
have been found to be capable of repressing E-
cadherin transcription, thereby causing the dissolution
of cell-cell adhesion that occurs during EMT, these
include Slug and two members of the ZEB family of
transcription factors, ZEB1 (dEF1) and ZEB2
(SIP1).
www.indiandentalacademy.com
44. • Recently, E47 and Twist1, widely expressed
bHLH transcription factors, have been shown to
repress E-cadherin transcription directly by
binding to E-boxes in the E-cadherin promoter.
www.indiandentalacademy.com
45. • Like Twist1, two additional embryonic
transcription factors, FOXC2 and Goosecoid have
also been demonstrated to induce EMTs in certain
epithelial cells, while they seem to lack the ability
to directly bind to the E-cadherin promoter.
www.indiandentalacademy.com
46. EMT in Carcinoma Progression and
Metastasis
• In order for carcinoma cells to break away from
neighboring cells to invade adjacent cell layers, these
tumor cells must lose cell-cell adhesion and acquire
motility.
• Loss of E-cadherin has been associated with
carcinoma progression and poor prognosis in various
human tumors.
www.indiandentalacademy.com
47. Molecular Network of Signaling Pathways and Transcription Factors that Regulate the
EMT Program in Carcinoma Cells
www.indiandentalacademy.com
48. Future Perspectives
• Currently, the EMT program is only loosely defined by
certain cell morphological changes, changes of
differentiation markers from epithelial to mesenchymal
patterns, and the functional changes required for cells to
migrate and invade through ECM.
• As such, a clear molecular definition of the EMT
program during both development and tumor metastasis
is still elusive.
www.indiandentalacademy.com
49. • Loss of E-cadherin may be the only consistently
reported molecular change occurring during the
various EMTs.
• Since loss of E-cadherin alone in normal epithelial
cells results in cell death rather than EMT, it appears
that the core EMT molecular program includes more
than E-cadherin repression.
www.indiandentalacademy.com
50. • Identification of the molecular signature of the EMT may
be aided by the recent genomic analyses of the EMT
program occurring in embryogenesis and tumor
progression.
• Such a specific molecular signature of the EMT
program would create the framework for elucidation of
the complete signaling network that regulates the EMT
program.
www.indiandentalacademy.com
51. Shortcomings
• Epithelial mesenchymal interaction during tooth
development has not been included.
• Anomalies due to disturbances in epithelial
mesenchymal interaction- not mentioned.
www.indiandentalacademy.com