gingival hyperplasia,Normal anatomy of the gingiva
The Role of Epithelial-Mesenchymal Transition Process in Gingival Hyperplasia
Fibroblasts Collagen Production and Histological Alterations in Hereditary Gingival Fibromatosis
Inflammatory gingival hyperplasia is an inflammatory restraint to local irritant correlating with the gingiva; the irritant could be microbial like plaque and calculus.
Clinically present as deep red or bluish, considerably friable and fine with smooth glossy surface and commonly bleed easily [1].
These conditions are presented with the epithelial to mesenchymal transition (EMT), where the basal lamina show disruptions and epithelial cells migrate into connective tissue and change their phenotypes to fibroblast-like cells [12].
Clinical significance of junctional epitheliumJignesh Patel
The junctional epithelium forms the border between the tooth surface and gingival sulcus. It acts as a barrier against pathogenic bacteria through rapid turnover and the expression of antimicrobial molecules. Loss of integrity in the junctional epithelium can initiate pocket formation in periodontitis as bacteria colonize the exposed tooth surface. The junctional epithelium has a remarkable ability to regenerate after injury or probing within a few days through rapid cell division. Maintaining a healthy junctional epithelium is important to prevent periodontal diseases from developing at this site of bacterial accumulation.
1. The document describes a case report of a 29-year old male patient who presented with pain in the upper front tooth region. Radiographs revealed an angular bone defect on both sides of tooth #11.
2. To treat the defect, biodentin was placed in the labial cervical vertical groove and platelet-rich fibrin (PRF) mixed with bone graft was placed in the bony defect. An amniotic membrane was also placed.
3. Follow-up 3 months later showed reduced probing depth from 10mm to 3mm, clinical attachment level gain from 7mm to 5mm, and bone fill of the defect from 11mm to 4mm. The treatment successfully regenerated bone and
Atypical ameloblastoma – an enigma in diagnosis review of literature and rep...Quách Bảo Toàn
This case report describes an atypical ameloblastoma presenting diagnostic challenges. Histologically, the lesion showed features of both benign and malignant ameloblastoma. While areas displayed typical ameloblastoma characteristics, other areas showed epithelial dedifferentiation like cellular pleomorphism and atypical mitoses. However, these atypical features were not sufficient to classify it as ameloblastic carcinoma. The case was therefore diagnosed as an atypical ameloblastoma and close follow up was recommended due to its ambiguous nature between benign and malignant pathology. The report also briefly reviews the classification and literature on odontogenic malignancies.
This document discusses periodontal pockets, including their classification, clinical features, pathogenesis, and histopathology. Periodontal pockets are pathologically deepened gingival sulci that are a key feature of periodontal disease. They can form via gingival enlargement or destruction of supporting tissues. Histologically, the soft tissue wall shows edema, inflammation and sometimes fibrosis or ulceration. Bacteria may accumulate in the pocket and invade tissues. The pocket represents an area of ongoing healing and destruction in response to the bacterial challenge.
Nano-composite scaffolds based on electrospun nanofibers have gained great attention due to their ability to emulate natural extracellular matrix (ECM) that affects cell survival, attachment and reorganization.
Promoted protein absorption, cellular reactions, activation of specific gene expression and intracellular signaling, and high surface area to volume ratio are also important properties of nanofibrous scaffolds.
Moreover, several bioactive components, such as bioceramics and functional polymers can be easily blended into nanofibrous matrixes to regulate the physical-chemical-biological properties and regeneration abilities.
Simultaneously, functional growth factors, proteins and drugs are also incorporated to regulate cellular reactions and even modify the local inflammatory microenvironment, which benefit periodontal regeneration and functional restoration
Inflammatory gingival hyperplasia is an inflammatory restraint to local irritant correlating with the gingiva; the irritant could be microbial like plaque and calculus.
Clinically present as deep red or bluish, considerably friable and fine with smooth glossy surface and commonly bleed easily [1].
These conditions are presented with the epithelial to mesenchymal transition (EMT), where the basal lamina show disruptions and epithelial cells migrate into connective tissue and change their phenotypes to fibroblast-like cells [12].
Clinical significance of junctional epitheliumJignesh Patel
The junctional epithelium forms the border between the tooth surface and gingival sulcus. It acts as a barrier against pathogenic bacteria through rapid turnover and the expression of antimicrobial molecules. Loss of integrity in the junctional epithelium can initiate pocket formation in periodontitis as bacteria colonize the exposed tooth surface. The junctional epithelium has a remarkable ability to regenerate after injury or probing within a few days through rapid cell division. Maintaining a healthy junctional epithelium is important to prevent periodontal diseases from developing at this site of bacterial accumulation.
1. The document describes a case report of a 29-year old male patient who presented with pain in the upper front tooth region. Radiographs revealed an angular bone defect on both sides of tooth #11.
2. To treat the defect, biodentin was placed in the labial cervical vertical groove and platelet-rich fibrin (PRF) mixed with bone graft was placed in the bony defect. An amniotic membrane was also placed.
3. Follow-up 3 months later showed reduced probing depth from 10mm to 3mm, clinical attachment level gain from 7mm to 5mm, and bone fill of the defect from 11mm to 4mm. The treatment successfully regenerated bone and
Atypical ameloblastoma – an enigma in diagnosis review of literature and rep...Quách Bảo Toàn
This case report describes an atypical ameloblastoma presenting diagnostic challenges. Histologically, the lesion showed features of both benign and malignant ameloblastoma. While areas displayed typical ameloblastoma characteristics, other areas showed epithelial dedifferentiation like cellular pleomorphism and atypical mitoses. However, these atypical features were not sufficient to classify it as ameloblastic carcinoma. The case was therefore diagnosed as an atypical ameloblastoma and close follow up was recommended due to its ambiguous nature between benign and malignant pathology. The report also briefly reviews the classification and literature on odontogenic malignancies.
This document discusses periodontal pockets, including their classification, clinical features, pathogenesis, and histopathology. Periodontal pockets are pathologically deepened gingival sulci that are a key feature of periodontal disease. They can form via gingival enlargement or destruction of supporting tissues. Histologically, the soft tissue wall shows edema, inflammation and sometimes fibrosis or ulceration. Bacteria may accumulate in the pocket and invade tissues. The pocket represents an area of ongoing healing and destruction in response to the bacterial challenge.
Nano-composite scaffolds based on electrospun nanofibers have gained great attention due to their ability to emulate natural extracellular matrix (ECM) that affects cell survival, attachment and reorganization.
Promoted protein absorption, cellular reactions, activation of specific gene expression and intracellular signaling, and high surface area to volume ratio are also important properties of nanofibrous scaffolds.
Moreover, several bioactive components, such as bioceramics and functional polymers can be easily blended into nanofibrous matrixes to regulate the physical-chemical-biological properties and regeneration abilities.
Simultaneously, functional growth factors, proteins and drugs are also incorporated to regulate cellular reactions and even modify the local inflammatory microenvironment, which benefit periodontal regeneration and functional restoration
Nano-composite scaffolds based on electrospun nanofibers have gained great attention due to their ability to emulate natural extracellular matrix (ECM) that affects cell survival, attachment and reorganization.
Promoted protein absorption, cellular reactions, activation of specific gene expression and intracellular signaling, and high surface area to volume ratio are also important properties of nanofibrous scaffolds.
Moreover, several bioactive components, such as bioceramics and functional polymers can be easily blended into nanofibrous matrixes to regulate the physical-chemical-biological properties and regeneration abilities.
Simultaneously, functional growth factors, proteins and drugs are also incorporated to regulate cellular reactions and even modify the local inflammatory microenvironment, which benefit periodontal regeneration and functional restoration
The document discusses diagnosis and treatment of peri-implant disease. It begins by introducing the history of dental implants and defines peri-implant mucositis and peri-implantitis. The main causes are bacterial infection and biomechanical overload. Treatment involves non-surgical and surgical approaches to arrest disease progression and maintain the implant site. The document then examines the histology and microbiology of healthy and diseased peri-implant tissues.
Periodontal pockets form due to a pathological deepening of the gingival sulcus caused by the apical migration of the junctional epithelium and destruction of underlying periodontal tissues. Plaque accumulation leads to an inflammatory response, detachment of the junctional epithelium, and migration along the root surface. This establishes an open communication between the pocket and connective tissue, allowing bacterial invasion and continued bone resorption and pocket deepening. Histopathology shows extensive proliferation of the lateral pocket epithelium, an inflamed and infiltrated connective tissue, and numerous neutrophils.
Advanced reconstructive technologies for periodontal tissue repairLuis Kabrera
This document discusses advanced technologies for regenerating periodontal tissues. It begins by defining regenerative periodontal therapy and identifying common indications. It then reviews periodontal wound healing, noting it involves inflammation, granulation tissue formation, and remodeling. The focus is on comparing advanced regenerative concepts using growth factors and gene therapy to conventional techniques. While clinical success remains limited, research aims to simplify and enhance rebuilding of periodontal support through new barrier membranes, growth factors, and gene delivery approaches.
This document provides an overview of the microscopic anatomy of the gingiva. It describes the different layers of the gingival epithelium including the oral epithelium, sulcular epithelium, and junctional epithelium. It also discusses the cellular components and layers of the connective tissue below the epithelium. Key structures are described like desmosomes, hemidesmosomes, and tonofilaments that provide connections between epithelial cells and attachment to underlying tissues. The functions of the different epithelial layers and their roles in barrier function and wound healing are also summarized.
This document summarizes a study investigating the role of microRNA-302 in regulating retinal epithelial cell fate by targeting the TGF-β type II receptor. The study demonstrates that microRNA-302 promotes pluripotency in ARPE cells in vitro by regulating TGF-β signaling and epigenetic changes. It also shows that small molecules DZNEP and SB431542 can induce pluripotency by attenuating pathways involved in cell differentiation, supporting the potential for microRNAs and small molecules in regenerative medicine and therapeutics for diseases like diabetic retinopathy.
This document summarizes recent research on the biology of intestinal immunoglobulin A (IgA) responses. It discusses how the gut mucosa generates massive amounts of noninflammatory IgA antibodies through both T cell-dependent and T cell-independent pathways operating in Peyer's patches and other intestinal sites. Peyer's patches contain germinal centers that promote B cell class switching to IgA with help from T cells and cytokines like TGF-β. The follicle-associated epithelium over Peyer's patches contains M cells that deliver antigens to dendritic cells, which initiate Th2 responses important for IgA production. Intestinal epithelial cells educate dendritic cells via TSLP cytokine to promote noninflammatory immune induction including IgA
This document discusses skin and oral mucosal substitutes that have been developed for use in wound closure and reconstructive surgery. It describes several types of substitutes, including cultured epithelial sheets composed of autologous keratinocytes (Epicel), dermal substitutes made of materials like collagen or fibroblasts embedded in a matrix (Integra, Dermagraft), and bilayer substitutes combining an epithelial layer with an underlying dermal layer (Apligraf). The document outlines the requirements and challenges for engineering substitutes to replace skin and mucosal tissue, as well as the clinical applications and limitations of existing substitute technologies.
JC AMNIOTIC MEMEBRAME IN PREPROSTHETIC SURGERYMalaM67
This study evaluated the effectiveness of lyophilized amniotic membrane (AM) in healing intraoral surgical defects in 15 patients. AM was grafted onto surgical defects after excision of oral precancerous lesions. Parameters like operability, haemostasis, pain control, epithelialization and infection were evaluated. AM showed good adherence to wounds and facilitated epithelialization. It was found to be an effective and cost-effective material for healing intraoral surgical defects, though it may not prevent scarring for extensive defects. The study concluded that lyophilized AM is useful for immediate coverage of small intraoral surgical defects.
Periodontal disease results from a complex interplay between subgingival biofilm and the host immune-inflammatory response. While several bacteria are found in periodontal pockets, no single organism causes the disease. The pathogenesis involves the host response to the bacterial challenge, which can remain at a low, asymptomatic level or progress to tissue destruction if left unchecked. Understanding these disease processes is important for developing improved treatment strategies.
GENETIC MOLECULAR BASIS OF TTOTH DEVELOPMENT padmini chiaydu
The document discusses tooth development which begins with thickening of the dental epithelium. Signals from the epithelium induce condensation of the underlying mesenchyme. Distinct anatomical parts of the tooth form through sequential bud, cap, and bell stages as the enamel organ convolutes further. Tooth shape and position are controlled by homeobox genes expressed in the mesenchyme. Five major classes of morphogens (BMPs, FGFs, Wnts, Hedgehog proteins, TNF proteins) regulate tooth morphogenesis through epithelial-mesenchymal interactions and cytodifferentiation in a temporal and spatial manner. These signaling pathways and transcription factors are important for tooth tissue engineering and regeneration approaches in endodontics.
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.
Periodontitis is a chronic multifactorial disease characterized by an inflammation of the periodontal tissue mediated by the host,
which is associated with dysbiotic plaque biofilms, resulting in the progressive destruction of the toothsupporting apparatus and loss of periodontal attachment [1, 10].
Chronic periodontitis is clinically characterized by loss of gingival tissue attachment to the tooth, deepening of the gingival crevice (designated ‘periodontal pocket’ in periodontitis), degradation of the periodontal ligament and loss of alveolar bone 1. This destructive process is associated with the presence of subgingival microbial communities and a dense immuno-inflammatory infiltrate in the periodontium that may lead to tooth loss if not appropriately treated. In gingivitis, a reversible form of periodontal disease that does not result in bone loss, the inflammatory process is restricted to the gingival epithelium and the connective tissue without affecting the deeper compartments of the periodontium 1. However, it should be noted that gingivitis is a major risk factor and a necessary pre-requisite for periodontitis and, moreover, can increase the serum levels of inflammatory biomarkers such as C-reactive protein
This case report describes the surgical treatment of a 36-year-old male patient with an ameloblastoma tumor in the right side of the lower jaw. The tumor was excised via a trapezoidal flap surgery under general anesthesia. Histopathological examination found it to be an acanthomatous ameloblastoma. A reconstruction plate was fixed to prevent mandible fracture. The patient recovered well after surgery and was discharged after 3 days. Ameloblastomas are odontogenic tumors that commonly affect young people and have varying presentations depending on location and histological subtype.
A distinctive oral fibrous proliferation approximating only 2-5% of all benign gingival overgrowths is a unique lesion requiring adequate clinical diagnosis. With no subtle association with chronic irritation, this oral tumor is a diverse lesion. Giant cell fibroma (GCF) requires histopathological examination for its final diagnosis as clinic pathologic features are not sufficient to assess and confirm the lesion. Occurring most commonly during the first three decades of life this asymptomatic pedunculated or sessile lump clinically resembles fibroma and papilloma with no gender predilection. In this paper, we present a unique case of Giant cell fibroma (GCF) in a 4-year-old child.
This document provides information on the classification, diagnosis, and treatment of odontogenic tumors. It begins by classifying odontogenic tumors into three categories based on their origin: tumors of odontogenic epithelium, mixed odontogenic tumors, and tumors of odontogenic ectomesenchyme. Ameloblastoma is then discussed in detail as the most common odontogenic tumor. The document outlines the clinical features, histologic features, diagnosis, and treatment considerations for solid/multicystic ameloblastoma. Complete surgical removal with adequate margins is indicated as the primary treatment approach to prevent recurrence of this locally invasive tumor.
Abstract—This study was aimed to present a case report of a case of peripheral ossifying fibroma which is a rare case. This case was a 30 years non smoker male with the chief complaint of growth of gum tissue, moderately large in the mandibular posterior region. On intraoral examination, a peduncalated growth of 17 x 12 x 6 mm on marginal and attached gingiva with respect to tooth number 47 considerably hard in consistency and movable was seen. The lesion was erythmatous having a smooth non ulcerated surface. It was asymptomatic with no sign of pain. Intra oral periapical radiograph was taken which revealed slight erosion of crest of bone which was later confirmed during surgical excision. The possible reason of crestal bone erosion may be constant pressure of the growth. Differential diagnosis of irritation fibroma, pyogenic granuloma and peripheral giant cell granuloma was considered. However, clinical appearance and consistency was of a hard fibrous growth, which therefore led to a provisional diagnosis of peripheral ossifying fibroma or peripheral odontogenic fibroma.
. HIV-1-infected monocyte–macrophages traverse the BBB and enter the CNS throughout the course of HIV-1 disease. Once in the brain, both free virus and virus-infected cells are able to infect neighboring resident microglia and astrocytes and possibly other cell types.
HIV-1-infected cells in both the periphery and the CNS give rise to elevated levels of viral proteins, including gp120, Tat, and Nef, and of host inflammatory mediators such as cytokines and chemokines.
It has been shown that the viral proteins may act alone or in concert with host cytokines and chemokines, affecting the integrity of the BBB. The pathological end point of these interactions may facilitate a positive feedback loop resulting in increased penetration of HIV into the CNS
. HIV-1-infected monocyte–macrophages traverse the BBB and enter the CNS throughout the course of HIV-1 disease. Once in the brain, both free virus and virus-infected cells are able to infect neighboring resident microglia and astrocytes and possibly other cell types.
HIV-1-infected cells in both the periphery and the CNS give rise to elevated levels of viral proteins, including gp120, Tat, and Nef, and of host inflammatory mediators such as cytokines and chemokines.
It has been shown that the viral proteins may act alone or in concert with host cytokines and chemokines, affecting the integrity of the BBB. The pathological end point of these interactions may facilitate a positive feedback loop resulting in increased penetration of HIV into the CNS
Nano-composite scaffolds based on electrospun nanofibers have gained great attention due to their ability to emulate natural extracellular matrix (ECM) that affects cell survival, attachment and reorganization.
Promoted protein absorption, cellular reactions, activation of specific gene expression and intracellular signaling, and high surface area to volume ratio are also important properties of nanofibrous scaffolds.
Moreover, several bioactive components, such as bioceramics and functional polymers can be easily blended into nanofibrous matrixes to regulate the physical-chemical-biological properties and regeneration abilities.
Simultaneously, functional growth factors, proteins and drugs are also incorporated to regulate cellular reactions and even modify the local inflammatory microenvironment, which benefit periodontal regeneration and functional restoration
The document discusses diagnosis and treatment of peri-implant disease. It begins by introducing the history of dental implants and defines peri-implant mucositis and peri-implantitis. The main causes are bacterial infection and biomechanical overload. Treatment involves non-surgical and surgical approaches to arrest disease progression and maintain the implant site. The document then examines the histology and microbiology of healthy and diseased peri-implant tissues.
Periodontal pockets form due to a pathological deepening of the gingival sulcus caused by the apical migration of the junctional epithelium and destruction of underlying periodontal tissues. Plaque accumulation leads to an inflammatory response, detachment of the junctional epithelium, and migration along the root surface. This establishes an open communication between the pocket and connective tissue, allowing bacterial invasion and continued bone resorption and pocket deepening. Histopathology shows extensive proliferation of the lateral pocket epithelium, an inflamed and infiltrated connective tissue, and numerous neutrophils.
Advanced reconstructive technologies for periodontal tissue repairLuis Kabrera
This document discusses advanced technologies for regenerating periodontal tissues. It begins by defining regenerative periodontal therapy and identifying common indications. It then reviews periodontal wound healing, noting it involves inflammation, granulation tissue formation, and remodeling. The focus is on comparing advanced regenerative concepts using growth factors and gene therapy to conventional techniques. While clinical success remains limited, research aims to simplify and enhance rebuilding of periodontal support through new barrier membranes, growth factors, and gene delivery approaches.
This document provides an overview of the microscopic anatomy of the gingiva. It describes the different layers of the gingival epithelium including the oral epithelium, sulcular epithelium, and junctional epithelium. It also discusses the cellular components and layers of the connective tissue below the epithelium. Key structures are described like desmosomes, hemidesmosomes, and tonofilaments that provide connections between epithelial cells and attachment to underlying tissues. The functions of the different epithelial layers and their roles in barrier function and wound healing are also summarized.
This document summarizes a study investigating the role of microRNA-302 in regulating retinal epithelial cell fate by targeting the TGF-β type II receptor. The study demonstrates that microRNA-302 promotes pluripotency in ARPE cells in vitro by regulating TGF-β signaling and epigenetic changes. It also shows that small molecules DZNEP and SB431542 can induce pluripotency by attenuating pathways involved in cell differentiation, supporting the potential for microRNAs and small molecules in regenerative medicine and therapeutics for diseases like diabetic retinopathy.
This document summarizes recent research on the biology of intestinal immunoglobulin A (IgA) responses. It discusses how the gut mucosa generates massive amounts of noninflammatory IgA antibodies through both T cell-dependent and T cell-independent pathways operating in Peyer's patches and other intestinal sites. Peyer's patches contain germinal centers that promote B cell class switching to IgA with help from T cells and cytokines like TGF-β. The follicle-associated epithelium over Peyer's patches contains M cells that deliver antigens to dendritic cells, which initiate Th2 responses important for IgA production. Intestinal epithelial cells educate dendritic cells via TSLP cytokine to promote noninflammatory immune induction including IgA
This document discusses skin and oral mucosal substitutes that have been developed for use in wound closure and reconstructive surgery. It describes several types of substitutes, including cultured epithelial sheets composed of autologous keratinocytes (Epicel), dermal substitutes made of materials like collagen or fibroblasts embedded in a matrix (Integra, Dermagraft), and bilayer substitutes combining an epithelial layer with an underlying dermal layer (Apligraf). The document outlines the requirements and challenges for engineering substitutes to replace skin and mucosal tissue, as well as the clinical applications and limitations of existing substitute technologies.
JC AMNIOTIC MEMEBRAME IN PREPROSTHETIC SURGERYMalaM67
This study evaluated the effectiveness of lyophilized amniotic membrane (AM) in healing intraoral surgical defects in 15 patients. AM was grafted onto surgical defects after excision of oral precancerous lesions. Parameters like operability, haemostasis, pain control, epithelialization and infection were evaluated. AM showed good adherence to wounds and facilitated epithelialization. It was found to be an effective and cost-effective material for healing intraoral surgical defects, though it may not prevent scarring for extensive defects. The study concluded that lyophilized AM is useful for immediate coverage of small intraoral surgical defects.
Periodontal disease results from a complex interplay between subgingival biofilm and the host immune-inflammatory response. While several bacteria are found in periodontal pockets, no single organism causes the disease. The pathogenesis involves the host response to the bacterial challenge, which can remain at a low, asymptomatic level or progress to tissue destruction if left unchecked. Understanding these disease processes is important for developing improved treatment strategies.
GENETIC MOLECULAR BASIS OF TTOTH DEVELOPMENT padmini chiaydu
The document discusses tooth development which begins with thickening of the dental epithelium. Signals from the epithelium induce condensation of the underlying mesenchyme. Distinct anatomical parts of the tooth form through sequential bud, cap, and bell stages as the enamel organ convolutes further. Tooth shape and position are controlled by homeobox genes expressed in the mesenchyme. Five major classes of morphogens (BMPs, FGFs, Wnts, Hedgehog proteins, TNF proteins) regulate tooth morphogenesis through epithelial-mesenchymal interactions and cytodifferentiation in a temporal and spatial manner. These signaling pathways and transcription factors are important for tooth tissue engineering and regeneration approaches in endodontics.
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.
Periodontitis is a chronic multifactorial disease characterized by an inflammation of the periodontal tissue mediated by the host,
which is associated with dysbiotic plaque biofilms, resulting in the progressive destruction of the toothsupporting apparatus and loss of periodontal attachment [1, 10].
Chronic periodontitis is clinically characterized by loss of gingival tissue attachment to the tooth, deepening of the gingival crevice (designated ‘periodontal pocket’ in periodontitis), degradation of the periodontal ligament and loss of alveolar bone 1. This destructive process is associated with the presence of subgingival microbial communities and a dense immuno-inflammatory infiltrate in the periodontium that may lead to tooth loss if not appropriately treated. In gingivitis, a reversible form of periodontal disease that does not result in bone loss, the inflammatory process is restricted to the gingival epithelium and the connective tissue without affecting the deeper compartments of the periodontium 1. However, it should be noted that gingivitis is a major risk factor and a necessary pre-requisite for periodontitis and, moreover, can increase the serum levels of inflammatory biomarkers such as C-reactive protein
This case report describes the surgical treatment of a 36-year-old male patient with an ameloblastoma tumor in the right side of the lower jaw. The tumor was excised via a trapezoidal flap surgery under general anesthesia. Histopathological examination found it to be an acanthomatous ameloblastoma. A reconstruction plate was fixed to prevent mandible fracture. The patient recovered well after surgery and was discharged after 3 days. Ameloblastomas are odontogenic tumors that commonly affect young people and have varying presentations depending on location and histological subtype.
A distinctive oral fibrous proliferation approximating only 2-5% of all benign gingival overgrowths is a unique lesion requiring adequate clinical diagnosis. With no subtle association with chronic irritation, this oral tumor is a diverse lesion. Giant cell fibroma (GCF) requires histopathological examination for its final diagnosis as clinic pathologic features are not sufficient to assess and confirm the lesion. Occurring most commonly during the first three decades of life this asymptomatic pedunculated or sessile lump clinically resembles fibroma and papilloma with no gender predilection. In this paper, we present a unique case of Giant cell fibroma (GCF) in a 4-year-old child.
This document provides information on the classification, diagnosis, and treatment of odontogenic tumors. It begins by classifying odontogenic tumors into three categories based on their origin: tumors of odontogenic epithelium, mixed odontogenic tumors, and tumors of odontogenic ectomesenchyme. Ameloblastoma is then discussed in detail as the most common odontogenic tumor. The document outlines the clinical features, histologic features, diagnosis, and treatment considerations for solid/multicystic ameloblastoma. Complete surgical removal with adequate margins is indicated as the primary treatment approach to prevent recurrence of this locally invasive tumor.
Abstract—This study was aimed to present a case report of a case of peripheral ossifying fibroma which is a rare case. This case was a 30 years non smoker male with the chief complaint of growth of gum tissue, moderately large in the mandibular posterior region. On intraoral examination, a peduncalated growth of 17 x 12 x 6 mm on marginal and attached gingiva with respect to tooth number 47 considerably hard in consistency and movable was seen. The lesion was erythmatous having a smooth non ulcerated surface. It was asymptomatic with no sign of pain. Intra oral periapical radiograph was taken which revealed slight erosion of crest of bone which was later confirmed during surgical excision. The possible reason of crestal bone erosion may be constant pressure of the growth. Differential diagnosis of irritation fibroma, pyogenic granuloma and peripheral giant cell granuloma was considered. However, clinical appearance and consistency was of a hard fibrous growth, which therefore led to a provisional diagnosis of peripheral ossifying fibroma or peripheral odontogenic fibroma.
. HIV-1-infected monocyte–macrophages traverse the BBB and enter the CNS throughout the course of HIV-1 disease. Once in the brain, both free virus and virus-infected cells are able to infect neighboring resident microglia and astrocytes and possibly other cell types.
HIV-1-infected cells in both the periphery and the CNS give rise to elevated levels of viral proteins, including gp120, Tat, and Nef, and of host inflammatory mediators such as cytokines and chemokines.
It has been shown that the viral proteins may act alone or in concert with host cytokines and chemokines, affecting the integrity of the BBB. The pathological end point of these interactions may facilitate a positive feedback loop resulting in increased penetration of HIV into the CNS
. HIV-1-infected monocyte–macrophages traverse the BBB and enter the CNS throughout the course of HIV-1 disease. Once in the brain, both free virus and virus-infected cells are able to infect neighboring resident microglia and astrocytes and possibly other cell types.
HIV-1-infected cells in both the periphery and the CNS give rise to elevated levels of viral proteins, including gp120, Tat, and Nef, and of host inflammatory mediators such as cytokines and chemokines.
It has been shown that the viral proteins may act alone or in concert with host cytokines and chemokines, affecting the integrity of the BBB. The pathological end point of these interactions may facilitate a positive feedback loop resulting in increased penetration of HIV into the CNS
Many evidences that CSCs also play a central role in the pathogenesis and progression of carcinomas of the head and neck (HNSCC), including OSCC,have been found.
Early tissue culture studies showed that only a subpopulation of OSCC cells can form expanding tumor colonies, suggesting that human OSCC may contain some form of stem cells and it was subsequently shown that only a small subpopulation of the cells in OSCC corresponds to tumor-initiating cells.
These finding are in accordance with CSCs concept (17,34) that the tumor mass is a mixture of (a) CSCs dividing themselves to feed the tumor's growth, b) transient amplifying cells that divide themselves a few times before maturing into (c) differentiated tumor cells that do not contribute to tumor growth (4).
The isolation of CSCs from oral cancers has mainly been performed with the CD44 marker that was initially used to isolate breast cancer CSCs.
Many evidences that CSCs also play a central role in the pathogenesis and progression of carcinomas of the head and neck (HNSCC), including OSCC,have been found.
Early tissue culture studies showed that only a subpopulation of OSCC cells can form expanding tumor colonies, suggesting that human OSCC may contain some form of stem cells and it was subsequently shown that only a small subpopulation of the cells in OSCC corresponds to tumor-initiating cells.
These finding are in accordance with CSCs concept (17,34) that the tumor mass is a mixture of (a) CSCs dividing themselves to feed the tumor's growth, b) transient amplifying cells that divide themselves a few times before maturing into (c) differentiated tumor cells that do not contribute to tumor growth (4).
The isolation of CSCs from oral cancers has mainly been performed with the CD44 marker that was initially used to isolate breast cancer CSCs.
Clinical Description
Cleidocranial dysplasia (CCD) spectrum disorder is a skeletal dysplasia representing a clinical continuum ranging from classic CCD (triad of delayed closure of the cranial sutures, hypoplastic or aplastic clavicles, and dental abnormalities), to mild CCD, to isolated dental anomalies without other skeletal features [Golan et al 2000]. Most individuals are diagnosed because they have classic features. CCD spectrum disorder affects most prominently those bones derived from intramembranous ossification, such as the cranium and the clavicles, although bones formed through endochondral ossification can also be affected. Cooper et al [2001] recorded the natural history of 90 probands and 56 first- and second-degree relatives; findings highlight the clinical variability of this condition within affected members of the same family who harbor the same pathogenic variant. Roberts et al [2013] reviewed their experience with more than 100 affected individuals in South Africa.
Classic CCD. The most prominent clinical findings in individuals with classic CCD are listed in Suggestive Findings and include: abnormally large, wide-open fontanelles at birth that may remain open throughout life; clavicular hypoplasia resulting in narrow, sloping shoulders that can be opposed at the midline; and abnormal dentition
Further medical problems identified in individuals with CCD spectrum disorder include short stature, skeletal/orthopedic findings, dental complications, ENT complications, endocrine findings, and mild developmental delay.
Molecular Pathogenesis
RUNX2 encodes runt-related transcription factor 2 (RUNX2), a transcription factor involved in osteoblast differentiation and skeletal morphogenesis. RUNX2 is essential for osteoblast differentiation during intramembranous ossification as well as chondrocyte maturation during endochondral ossification [Zheng et al 2005]. RUNX2 contains an N-terminal stretch of consecutive polyglutamine and polyalanine repeats known as the Q/A domain, a runt domain, and a C-terminal proline/serine/threonine-rich (PST) activation domain. The runt domain is a 128-amino-acid polypeptide motif originally described in the Drosophila runt gene that has the unique ability to independently mediate DNA binding and protein heterodimerization [Zhou et al 1999].
The majority of RUNX2 pathogenic variants in individuals with classic CCD affect the runt domain and most are predicted to abolish DNA binding [Lee et al 1997, Mundlos et al 1997, Otto et al 2002]. Pathogenic missense variants cluster at arginine 225 (p.Arg225) of RUNX2, a critical residue for RUNX2 function. In vitro studies have shown that pathogenic missense variants at p.Arg225 interfere with nuclear accumulation of RUNX2.
Hypomorphic RUNX2 alleles with partial loss of protein function, c.90dupC and c.598A>G, are associated with mild CCD, isolated dental anomalies, and significant intrafamilial variability.
Mechanism of disease causation. Loss of function
RUNX2-sp
Cleidocranial dysplasia (CCD) spectrum disorder is a skeletal dysplasia representing a clinical continuum ranging from classic CCD (triad of delayed closure of the cranial sutures, hypoplastic or aplastic clavicles, and dental abnormalities), to mild CCD, to isolated dental anomalies without other skeletal features [Golan et al 2000]. Most individuals are diagnosed because they have classic features. CCD spectrum disorder affects most prominently those bones derived from intramembranous ossification, such as the cranium and the clavicles, although bones formed through endochondral ossification can also be affected. Cooper et al [2001] recorded the natural history of 90 probands and 56 first- and second-degree relatives; findings highlight the clinical variability of this condition within affected members of the same family who harbor the same pathogenic variant. Roberts et al [2013] reviewed their experience with more than 100 affected individuals in South Africa.
Wound healing is a highly dynamic process and involves complex interactions of extracellular matrix molecules, soluble mediators, various resident cells, and infiltrating leukocyte subtypes.
The immediate goal in repair is to achieve tissue integrity and homeostasis
PV is caused by autoantibodies that target cadherins, specifically desmogleins, though there may be some role for desmocollin; thus, this is a type 2 hypersensitivity reaction.[24][25] Acantholysis, or the loss of keratinocyte–keratinocyte adhesion, is interrupted by circulating IgG autoantibodies to intercellular adhesion molecules.[26][27] Acantholysis is seen as a result of the autoantibodies destroying the intracellular connections, leading to bullae that can easily rupture (known clinically as the Nikolsky sign).
A “super-compensation hypothesis” recently submitted by Sinha et al. proposes that additional factors may also play a role in PV.[28] Multiple mechanisms for antibody-induced acantholysis have been suggested, including the induction of signal transduction and the inhibition of adhesive molecule function through steric hindrance, which can trigger cell separation.[29] The pathogenesis of PV has been described in more detail by Hammers et al.[30]
In patients with PV, autoantibodies against desmoglein 1 (Dsg 1) and desmoglein 3 (Dsg 3) is the purported cause.[31] Desmogleins are transmembrane glycoproteins that are an integral part of desmosomes which, in part, are required for cell–cell adhesion via interaction with intermediate filaments. The most common targets of desmoglein for IgG antibodies are the extracellular cadherin domains, which can result in the loss of desmosome-adhesive properties. These signaling pathways trigger endocytosis, depletion, and direct inhibition of Dsg 3 interactions.[32] It is generally believed that the amino portion of the cadherin proteins is most implicated in the pathogenesis of acantholysis leading to PV.[33]
Many animal models have shown that enzymatic inactivation of Dsg 1 and gene deletion of Dsg 3 results in pathology similar to PV.[34][35] This phenomenon was observed to be dose-dependent and suggests that reducing the circulating levels of IgG against Dsg 1 and Dsg 3 can improve patient outcomes.[36] In patients with primarily cutaneous disease, Dsg 1 likely plays a role more superficially, whereas Dsg 3 is more likely to be found in deeper cutaneous structures and mucous membranes.[37][38] The implication is that Dsg 3 can compensate for the absence of Dsg 1 in mucosal structures (thus demonstrating PV in cutaneous lesions only). In contrast, Dsg 1 without Dsg 3 is insufficient to manage mucous membranes or cutaneous lesions alone, implying that Dsg 1 is in lower proportion in mucous membranes.
The binding of antibodies to desmogleins has been confirmed by epitope mapping and is presumed to disrupt desmoglein binding by affecting steric hindrance.[39] Another theory for the pathophysiology of PV is the desmoglein nonassembly depletion hypothesis. This theory suggests that autoantibodies not only bind desmoglein but that they also bind each other, leading to crosslinking and the inability of desmosomes to maintain cell–cell adhesion.[40][41]
PV is caused by autoantibodies that target cadherins, specifically desmogleins, though there may be some role for desmocollin; thus, this is a type 2 hypersensitivity reaction.[24][25] Acantholysis, or the loss of keratinocyte–keratinocyte adhesion, is interrupted by circulating IgG autoantibodies to intercellular adhesion molecules.[26][27] Acantholysis is seen as a result of the autoantibodies destroying the intracellular connections, leading to bullae that can easily rupture (known clinically as the Nikolsky sign).
A “super-compensation hypothesis” recently submitted by Sinha et al. proposes that additional factors may also play a role in PV.[28] Multiple mechanisms for antibody-induced acantholysis have been suggested, including the induction of signal transduction and the inhibition of adhesive molecule function through steric hindrance, which can trigger cell separation.[29] The pathogenesis of PV has been described in more detail by Hammers et al.[30]
In patients with PV, autoantibodies against desmoglein 1 (Dsg 1) and desmoglein 3 (Dsg 3) is the purported cause.[31] Desmogleins are transmembrane glycoproteins that are an integral part of desmosomes which, in part, are required for cell–cell adhesion via interaction with intermediate filaments. The most common targets of desmoglein for IgG antibodies are the extracellular cadherin domains, which can result in the loss of desmosome-adhesive properties. These signaling pathways trigger endocytosis, depletion, and direct inhibition of Dsg 3 interactions.[32] It is generally believed that the amino portion of the cadherin proteins is most implicated in the pathogenesis of acantholysis leading to PV.[33]
Many animal models have shown that enzymatic inactivation of Dsg 1 and gene deletion of Dsg 3 results in pathology similar to PV.[34][35] This phenomenon was observed to be dose-dependent and suggests that reducing the circulating levels of IgG against Dsg 1 and Dsg 3 can improve patient outcomes.[36] In patients with primarily cutaneous disease, Dsg 1 likely plays a role more superficially, whereas Dsg 3 is more likely to be found in deeper cutaneous structures and mucous membranes.[37][38] The implication is that Dsg 3 can compensate for the absence of Dsg 1 in mucosal structures (thus demonstrating PV in cutaneous lesions only). In contrast, Dsg 1 without Dsg 3 is insufficient to manage mucous membranes or cutaneous lesions alone, implying that Dsg 1 is in lower proportion in mucous membranes.
The binding of antibodies to desmogleins has been confirmed by epitope mapping and is presumed to disrupt desmoglein binding by affecting steric hindrance.[39] Another theory for the pathophysiology of PV is the desmoglein nonassembly depletion hypothesis. This theory suggests that autoantibodies not only bind desmoglein but that they also bind each other, leading to crosslinking and the inability of desmosomes to maintain cell–cell adhesion.[40][41]
The primary function of platelets is their role in hemostasis. Briefly, under normal physiological conditions, platelets will adhere to and begin to spread over the surface of subendothelial cells exposed by damage to the vascular endothelium.(1) Adhesion is dependent on the platelet membrane glycoprotein lb complex. The von Willebrand factor (vWF) is required for both adhesion and spreading.
The primary function of platelets is their role in hemostasis. Briefly, under normal physiological conditions, platelets will adhere to and begin to spread over the surface of subendothelial cells exposed by damage to the vascular endothelium.(1) Adhesion is dependent on the platelet membrane glycoprotein lb complex. The von Willebrand factor (vWF) is required for both adhesion and spreading.
Phagocytosis begins with adhesion of the phagocyte surface receptors to the pathogen, which then is internalized into vesicles called phagosomes.
Inside the phagocyte, the phagosome fuses to lysosomes, whose contents are released with consequent digestion and pathogen elimination.
Changes in the oxidase’s gene system components present in phagolysosome membrane lead to disability in respiratory burst and generation of reactive oxygen species (ROS).
Phagocytosis begins with adhesion of the phagocyte surface receptors to the pathogen, which then is internalized into vesicles called phagosomes.
Inside the phagocyte, the phagosome fuses to lysosomes, whose contents are released with consequent digestion and pathogen elimination.
Changes in the oxidase’s gene system components present in phagolysosome membrane lead to disability in respiratory burst and generation of reactive oxygen species (ROS).
Platelets have many functions, including phagocytosis of viruses, latex, immune complexes and iron; maintenance of vascular integrity
by filling gaps that form in the endothelium and by directly supporting endothelial cells; synthesis and release of vWF in humans and some animal species, and fibronectin;
participating in surface adhesion andactivation processess (Caen and Rosa, 1995; Clemetson, 1995; Nurden, 1995);
production and release of potent smooth muscle and endothelial cell proliferating factor( s); and retraction of clots, a process that stabilizes the initial hemostatic plug and activates clot lysis.
Platelets have many functions, including phagocytosis of viruses, latex, immune complexes and iron; maintenance of vascular integrity
by filling gaps that form in the endothelium and by directly supporting endothelial cells; synthesis and release of vWF in humans and some animal species, and fibronectin;
participating in surface adhesion andactivation processess (Caen and Rosa, 1995; Clemetson, 1995; Nurden, 1995);
production and release of potent smooth muscle and endothelial cell proliferating factor( s); and retraction of clots, a process that stabilizes the initial hemostatic plug and activates clot lysis.
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.
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
Diagnostic polymerase chain reaction (PCR) is an extremely powerful, rapid method for diagnosis of microbial infections and genetic diseases, as well as for detecting microorganisms in environmental and food samples.
However, the usefulness of diagnostic PCR is limited, in part, by the presence of inhibitory substances in complex biological samples, which reduce or even block the amplification capacity of PCR in comparison with pure solutions of nucleic acids .
In general, diagnostic PCR may be divided into four steps: (1) sampling, (2) sample preparation, (3) nucleic acid amplification, and (4) detection of PCR products
Diagnostic polymerase chain reaction (PCR) is an extremely powerful, rapid method for diagnosis of microbial infections and genetic diseases, as well as for detecting microorganisms in environmental and food samples.
However, the usefulness of diagnostic PCR is limited, in part, by the presence of inhibitory substances in complex biological samples, which reduce or even block the amplification capacity of PCR in comparison with pure solutions of nucleic acids .
In general, diagnostic PCR may be divided into four steps: (1) sampling, (2) sample preparation, (3) nucleic acid amplification, and (4) detection of PCR products
The etiology of a disease refers to the causative trigger(s), whereas pathogenesis refers to the mechanism(s) by which the disease progresses.
In other words, while the microbial biofilm developing on the tooth surface constitutes a necessary etiological factor, its mere presence is insufficient for the initiation of the disease.
Further risk factors, such as host genetics, lifestyle, stress, and systemic conditions, that dictate the immunopathogenesis are crucial for the transition from a healthy to a diseased state.
More from Romissaa ali Esmail/ faculty of dentistry/Al-Azhar university (20)
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In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
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2. Molecular mechanisms in gingival
enlargement
By
Romissaa Aly
Assistant lecturer of
Oral Medicine,
Periodontology,
Diagnosis and Dental
Radiology (Al-Azhar
University)
3. Content:
Normal anatomy of the gingiva
The Role of Epithelial Mesenchymal
Transition Process in Gingival Hyperplasia
Fibroblasts Collagen Production and
Histological Alterations in Hereditary Gingival
Fibromatosis
4.
5. Classification of oral mucous
membrane
1-Keratenized mucosa ( Masticatory
mucosa)
(A) Gingiva (B) Hard
palate
2- Non-keratenized mucosa (Lining
mucosa)
(A) Firmly
attached
(B) Loosely
attached
Soft
palate lip cheeck Ventral S
tongue
Floor of
mouth
Vestibule
Alveolar
mucosa
3- Specialized mucosa
Dorsal surface of the
tongue
6. Macro-anatomy of the gingiva
Free
gingiva
Free
gingival
groove
Interdental
papilla
Attached
gingiva
Mucogingival
junction
Alveolar
mucosa
7. Histology of gingiva
Stratified squamous
keratenized
epithelium
Lamina
propria
Epithelial rete
peg
C.T papilla
Tall
Numerou
s
Slender
Irregular
No submucosa
11. K.st.sq epith (st.basal) Non-K.st.sq.epith
*The cells are cubiodal, contain large oval nucleus, granular basophilic
cytoplasm
*The cytoplasm contain tonofilaments
Arranged in bundles Remain dispersed
*The cells are closely attached to each other by desmosomes
12. 1- Thickening of the
adjacent cell membrane.
2- A pair of attachment
plaque.
3-
Tonofilaments.
4- An intervening extracellular
structure.
The
desmosomes
14. Basal lamina (Basement membrane)
By EM junction of epithelium and C.T
described as Basal lamina : consistes of
1) Lamina densa (20-120nm)
consists of glycoprotein (laminin)
material run parallel to basal cells
2) Lamina lucida (20-40nm)
Appearently clear zone present between
lamina densa and basal cells
A subepithelial fibers termed (Reticular lamina)
Consists of a system of:
1) Fine argyrophilic reticular fibers
2) special anchoring fibers (small loops of fibers)
Both inserted into lamina densa and reached the
plasma membrane of basal cells mostly in the region of
hemidesmosomes
3) Collagen bundles run through loops of anchoring fibers and thu
interlocked with basal densa to form a flexible attachment
15.
16. The lamina propria
It is the C.T that support the epithelium
It is divided into 2 layers:
1) Papillary layer
2) Reticular layer
17. The Role of Epithelial Mesenchymal
Transition Process in Inflammatory Gingival
Hyperplasia
18. Inflammatory gingival hyperplasia is an
inflammatory restraint to local irritant correlating with
the gingiva; the irritant could be microbial like plaque and
calculus.
Clinically present as deep red or bluish, considerably friable
and fine with smooth glossy surface and commonly bleed easily
[1].
19. Histologically, inflammatory gingival enlargement
characterized by thicking of the epithelium with
increased volume of the connective tissue with
different degree of inflammation and fibrosis [2].
20. Gingival overgrowth usually treated with
traditional periodontal treatment such as scaling and
root planning, but if it include significant fibrotic
component that don't respond to the traditional
treatment so it will be treated by surgical
removal of the excess tissue [3].
21.
22. Content
Definition of EMT
Main features of epithelial and mesenchymal cells
Types of EMT
Major Criteria and Relevant Markers to Detect EMT
Induction and Regulation of EMT
EMT in Fibrosis and Disease
23. EMT is a process in which epithelial cells
migrate in to the connective tissue and
transdifferentiate into fibroblast-like cells, this
occurs as the epithelial cell-cell and cell- extracellular
matrix interactions are destabilized [4].
50. TGF b is considered to be the prototypical cytokine
for induction of EMT because different isoforms mediate
various aspects of EMT in many diverse cellular contexts,
whereas the effects of other EMT inducers are often context
dependent and variable (Sanford et al., 1997; Xu et al., 2009).
51.
52. Treatment of mammary epithelial cells with
repeated low doses of hydrogen peroxide, a protocol
mimicking the chronic inflammation that is common
to many human diseases, leads to a fibroblastlike
phenotype (Mori et al., 2004).
56. Myofibroblasts are present in large numbers in
sites with ongoing inflammation and repair, and effectively
close wounds through the contraction of connective tissue
(Guarino et al., 2009; Hinz, 2010).
57. Myofibroblasts were originally believed to be generated
by proliferation and activation of local fibroblasts
(Barnes and Gorin, 2011; Grillo, 1963).
This was supported by the presence of fibroblasts
positive for proliferation markers at the periphery of
the wound (Grillo, 1963) that acquire smooth muscle
features during wound healing and progressive organ fibrosis
(Barnes and Gorin, 2011).
61. The study was carried out by Lina Ibtesam Khalid
et al 2019 in an effort to determine if EMT operates in the
pathogenesis of inflammatory gingival hyperplasia to serve as
a source of fibroblasts..
J Res Med Dent Sci, 2019, 7 (5):80-84
In this this they were sought to investigate if the
Epithelial mesenchymal transition theory
participitated in the advancement of this benign lesion.
62. Markers of the study:
E-Cadherin is considered as a prototypical epithelial
marker of EMT.
Vimentin is mainly expressed in cells of mesenchymal
origin and it is often used as a marker for epithelial
mesenchymal transition
Alpha smooth muscle actin positive myofibroblast
63. •E-Cadherin is required for the maintenance of
normal intercellular adhesion and barrier integrity in
oral tissues [12].
• Vimentin is one of the most familiar members of
intermediate filaments (IFs), as it is the major IF
protein in mesenchymal cells and it is frequently used as a
developmental marker of cells and tissues [13].
64. The reduction in epithelial expression of E-Cadherin also
called the Cadherin switch has been known to promote
EMT by facilitating weakening of the intercellular
junctions and promoting movement of epithelial cells towards
the connective tissue [6].
Alpha smooth muscle actin positive myofibroblast have
been demonstrated in type 2 EMT [7].
65. To confirm this mechanism, They investigated the
Immuno-histochemical expression of three specific
markers assessing EMT mechanism namely α-SMA,
Vimentin and E-Cadherin.
Alpha-SMA is a putative myofibroblast marker. Since
myofibroblasts are implicated in EMT induced fibrosis they
sought to analyse α – SMA expression in the samples.
66.
67.
68. Material and method:
The study involved 15 tissue blocks of inflammatory
gingival hyperplasia taken from the archives of oral
pathology, laboratory of oral diagnosis department,
collage of dentistry/university of Baghdad.
Immunohistochemical expression of Vimentin, E-
Chdaherin and α-SMA was assessed.
69. The mean number of vimentin& E-Chadherin positive
fibroblast were 51.43% & 48.56%, respectively, so as these
two markers are biomarkers for EMT, it is suggested
that EMT process may be involved at least partly in
the pathogenesis of inflammatory gingival hyperplasia.
Results:
70. Results:
Vimentin and E-Chadherin immunoreactivity of the
connective tissue fibroblasts showed 100% positivity, while
Alpha smooth muscle actin staining was mostly seen
in the endothelial lined blood vessels with a few
myofibroblast with in the connective tissue being
stained positive.
71. so increased expression and activation of TGF-B1 in
inflammatory gingival hyperplasia (14) promote an
epithelial cell plasticity that may progress to
EMT [15].
72. Figure 1: Section of
inflammatory ginigival
hyperplasia showing vimentin
expression in fbroblast cells of
connective tissue (40x)
(A) Positive cytoplasmic
expression of spindle cell
fibroblast.
(B) Negatively stained.
Figure
73. Figure 2: Section of inflammatory ginigival hyperplasia showing
Echadherin expression in fibroblast cells of connective (40x).
(A)Surface epithelia (internal control for E-chadherin) positive
membranous and negative cytoplasmic and nuclear staining.
(B) positive membranous expression of spindle cell fibroblast
74. Figure 3: Section of inflammatory ginigival hyperplasia
showing alpha smooth muscle actin expression in fibroblast
cells of connective tissue(40x). (A) positive cytoplasmic
expression of spindle cell fibroblast.
75. Jeopardized E-Chadherin expression could alter the
cell phenotype from epithelial to fibroblast with
spindle shape morphology [17].
Okada H and coworkers, (2000) have shown that the
epithelial cells migrate from the epithelial layer, travel through
the basement membrane and accumulate in the interstititium
of the tissue; here they eventually get rid of their epithelial
markers and gain a fully fibroblastic phenotype [18,19].
77. Content
Normal anatomy of gingiva
The Role of Epithelial Mesenchymal
Transition Process in Inflammatory
hyperplasia
Fibroblasts Collagen Production and
Histological Alterations in Hereditary Gingival
Fibromatosis
80. Hereditary gingival fibromatosis (HGF), also called
elephantiasis gingivae, hereditary gingival
hyperplasia, and hypertrophic gingiva, is a disorder
characterized by progressive enlargement of the gingiva.
This enlargement results from an increase in the connective
tissue elements of the submucosa and displays different
severities,
Diseases 2019, 7, 39
81. sometimes covering the entire crowns of the teeth
and deforming the palate, thereby creating occlusal and
aesthetic problems, as well as causing difficulties in
speech and mastication.
82. •Thickening of the alveolar ridge rarely appears
at birth, typically initiates with the eruption of
deciduous or permanent dentition, exacerbates during
adolescence, and can persist within adulthood [1].
•However radiographic imaging shows no specific
changes in the teeth or alveolar bone.
83. •HGF may also exhibit an autosomal dominant or recessive
mode of inheritance.
• The recessive pattern usually linked to other
syndromes: Cowden, Jones, Goltz-Gorlin,; and other
systemic diseases: cherubism, hypothyroidism,
chondrodystrophy, growth hormone deficiency craniofacial
dysmorphism or leukemia [3–6].
84. Histologically, HGF shows gingival features relatively
acellular and with an increased amount of randomly
arranged bundles of collagen.
The overlying epithelium may be variable in
thickness and have prominent, elongated rete
ridges extending into the underlying connective
tissue [8].
85. In rare cases, the description includes deposition of
amyloids and islands of odontogenic epithelium [10].
•However, these histological features are
nonspecific, and the diagnosis should be based
on clinical findings and family history [11].
86. •These conditions are presented with the epithelial
to mesenchymal transition (EMT), where the
basal lamina show disruptions and epithelial cells
migrate into connective tissue and change their
phenotypes to fibroblast-like cells [12].
87. Fibroblasts are the key cells involved in the
gingival production of collagen and respond to
the local stress depending on the environmental
conditions.
Therefore, is essential that they have to maintain a good
metabolic statement to respond to all aggressions.
88. Chronic Periodontitis is related to
oxidative stress [14], and previous studies
have found a relationship between oxidative
stress and cyclosporine-induced gingival
overgrowth [15], but to date, no studies have
linked this oxidative stress to HGF.
99. 3.5: Lipid Peroxidation
Lipid peroxidation could be a consequence of basal ROS
overproduction or fewer antioxidants capacity and could
indicate high levels of oxidative stress in gingival fibroblasts
from the father compared to the control and his daughter
(Figure 4D).
100. Conclusions
The histological data showed basal lamina disruption,
epithelial cell migration into connective tissue and a lack of
laminin 5 in their basal membrane.
In vitro results have demonstrated, for the first time,
that collagen synthesis is influenced by an oxidant
and can be restored by an antioxidant in HGF
fibroblasts.