This document discusses genetic polymorphism and its relationship to periodontal disease. It begins by defining key genetic terms and describes how periodontal disease can be caused by single gene mutations (monogenic disorders) or variations in multiple genes (polygenic disorders). Several specific gene polymorphisms are examined, including genes related to cytokines, receptors, metabolism, and innate immunity. The roles of the IL-1, TNF-α, IL-10 genes and others are summarized. The document also explores several genetic syndromes associated with early-onset periodontitis, such as Papillon-Lefevre syndrome. In conclusion, genetic testing is available to assess patient susceptibility to severe periodontal disease.
This document discusses the genetic factors involved in periodontal disease from multiple perspectives. It begins by establishing that periodontitis is initiated by bacteria but host genetic factors influence the inflammatory response and susceptibility. Several methods for genetic analysis are described, and studies on specific genes and polymorphisms associated with periodontal disease are summarized. The roles of genetics in modulating the subgingival biofilm and in various genetic disorders linked to severe periodontitis are also reviewed. The document concludes by discussing potential applications of genetic knowledge like genetic testing and gene therapy to better understand and treat periodontal disease.
This document summarizes genetic factors associated with periodontitis. It discusses various genetic studies related to chronic and aggressive periodontitis, including studies on gene polymorphisms like IL1, TNF, FCγR, IL10, and others. It also covers genetic terminology, types of genetic studies like twin studies, family studies, case-control studies and genome-wide association studies. Specific gene mutations linked to syndromes associated with periodontitis are mentioned.
Role of genetics in periodontal diseasesAnushri Gupta
Terminologies in Genetics
Genetic study design
genetic syndrome and disease associated with periodontal diseases, heretibility of periodontal disease, gene library, gene therapy
Immuno microbial pathogenesis of periodontal diseaseGanesh Nair
The document provides an overview of the inflammatory response in periodontal disease. It discusses how bacterial virulence factors like lipopolysaccharide activate the host immune system through toll-like receptors and pro-inflammatory cytokines like IL-1β and TNF-α are released, leading to tissue damage. It also describes other microbial products like fimbriae, DNA, and enzymes that stimulate inflammation and host mediators that perpetuate the inflammatory response and cause bone resorption and tissue destruction.
This document summarizes research on oral lichen planus (OLP) and its potential as a preneoplastic inflammatory model. Key points include:
- OLP is a chronic inflammatory oral condition that may carry a 1-2% risk of malignant transformation to oral squamous cell carcinoma.
- Research has explored the role of T-cells, apoptosis, cellular proliferation, p53 expression, chromosomal instability, matrix metalloproteinases, cytokines, and hepatitis C virus infection in the pathogenesis and potential malignant transformation of OLP.
- Further research is needed but OLP shows similarities to other inflammatory conditions like inflammatory bowel disease that are associated with increased cancer risk, supporting its characterization as a potentially pre
Genetics play an important role in periodontal diseases. The document discusses how genetics and environmental factors interact to determine disease severity and progression. Twin studies estimate that genetics account for 40-80% of chronic periodontitis risk, indicating a strong hereditary component. Several genes have been associated with increased risk of chronic and aggressive periodontitis, including genes related to the inflammatory response. Understanding the genetic factors involved can provide insights into disease pathogenesis and potential targets for risk assessment and treatment.
oral lichen planus,,preneoplastic inflammatory modelSharda university
oral lichen planus is a potentialy maligant lession,,so before any treatment planning,its important to know etiology.so i am putting my efforts in this presentation to explain several etiological factors.
This document provides an overview of genetic polymorphism and its relationship to periodontal disease. It begins with definitions of key genetic terms like allele, chromosome, DNA and discusses different types of genetic disorders. It then examines various human gene polymorphisms that have been associated with periodontal diseases, such as IL-1, IL-10, TNF-α, and FcγR gene polymorphisms. The document reviews studies that have investigated the relationship between these polymorphisms and chronic or aggressive periodontitis. It concludes by stating that identifying genetic risk factors could allow for more personalized prevention and treatment approaches for periodontal diseases in the future.
This document discusses the genetic factors involved in periodontal disease from multiple perspectives. It begins by establishing that periodontitis is initiated by bacteria but host genetic factors influence the inflammatory response and susceptibility. Several methods for genetic analysis are described, and studies on specific genes and polymorphisms associated with periodontal disease are summarized. The roles of genetics in modulating the subgingival biofilm and in various genetic disorders linked to severe periodontitis are also reviewed. The document concludes by discussing potential applications of genetic knowledge like genetic testing and gene therapy to better understand and treat periodontal disease.
This document summarizes genetic factors associated with periodontitis. It discusses various genetic studies related to chronic and aggressive periodontitis, including studies on gene polymorphisms like IL1, TNF, FCγR, IL10, and others. It also covers genetic terminology, types of genetic studies like twin studies, family studies, case-control studies and genome-wide association studies. Specific gene mutations linked to syndromes associated with periodontitis are mentioned.
Role of genetics in periodontal diseasesAnushri Gupta
Terminologies in Genetics
Genetic study design
genetic syndrome and disease associated with periodontal diseases, heretibility of periodontal disease, gene library, gene therapy
Immuno microbial pathogenesis of periodontal diseaseGanesh Nair
The document provides an overview of the inflammatory response in periodontal disease. It discusses how bacterial virulence factors like lipopolysaccharide activate the host immune system through toll-like receptors and pro-inflammatory cytokines like IL-1β and TNF-α are released, leading to tissue damage. It also describes other microbial products like fimbriae, DNA, and enzymes that stimulate inflammation and host mediators that perpetuate the inflammatory response and cause bone resorption and tissue destruction.
This document summarizes research on oral lichen planus (OLP) and its potential as a preneoplastic inflammatory model. Key points include:
- OLP is a chronic inflammatory oral condition that may carry a 1-2% risk of malignant transformation to oral squamous cell carcinoma.
- Research has explored the role of T-cells, apoptosis, cellular proliferation, p53 expression, chromosomal instability, matrix metalloproteinases, cytokines, and hepatitis C virus infection in the pathogenesis and potential malignant transformation of OLP.
- Further research is needed but OLP shows similarities to other inflammatory conditions like inflammatory bowel disease that are associated with increased cancer risk, supporting its characterization as a potentially pre
Genetics play an important role in periodontal diseases. The document discusses how genetics and environmental factors interact to determine disease severity and progression. Twin studies estimate that genetics account for 40-80% of chronic periodontitis risk, indicating a strong hereditary component. Several genes have been associated with increased risk of chronic and aggressive periodontitis, including genes related to the inflammatory response. Understanding the genetic factors involved can provide insights into disease pathogenesis and potential targets for risk assessment and treatment.
oral lichen planus,,preneoplastic inflammatory modelSharda university
oral lichen planus is a potentialy maligant lession,,so before any treatment planning,its important to know etiology.so i am putting my efforts in this presentation to explain several etiological factors.
This document provides an overview of genetic polymorphism and its relationship to periodontal disease. It begins with definitions of key genetic terms like allele, chromosome, DNA and discusses different types of genetic disorders. It then examines various human gene polymorphisms that have been associated with periodontal diseases, such as IL-1, IL-10, TNF-α, and FcγR gene polymorphisms. The document reviews studies that have investigated the relationship between these polymorphisms and chronic or aggressive periodontitis. It concludes by stating that identifying genetic risk factors could allow for more personalized prevention and treatment approaches for periodontal diseases in the future.
The document summarizes the immune mechanisms in the gingiva. The gingival defense system includes innate immunity components like toll-like receptors, complement system, and natural killer cells. It also contains adaptive immunity components like humoral and cell-mediated immunity. Toll-like receptors are expressed by various cells and recognize pathogen patterns to initiate signaling pathways that result in inflammatory responses. The gingival crevicular fluid contains enzymes, proteins, antibodies, cytokines, and cellular components that help fight infection and promote healing in the gingiva.
Innate immuntity in periodontal ligament and significance ofHudson Jonathan
This document provides an overview of innate immunity and the role of Toll-like receptors (TLRs) in periodontal diseases. It describes how TLRs recognize bacterial ligands and activate immune responses through signaling pathways. TLRs help maintain oral health by limiting microbial invasion, but excessive TLR signaling can lead to tissue destruction during periodontal disease. The document also discusses the potential clinical significance of TLRs as biomarkers for periodontal disease diagnosis and prognosis monitoring.
This document discusses epigenetics and its role in human disease. It begins with an introduction to epigenetics, explaining that epigenetic processes can alter gene expression without changing DNA sequence. It then discusses some key epigenetic mechanisms like DNA methylation and histone modifications. It provides examples of how epigenetic changes are implicated in several diseases, such as neurological disorders, autoimmune diseases, diabetes, and cancer. The document concludes by noting that epigenetic therapies are being explored for diseases like cancer, and that combining epigenetic drugs with immunotherapy shows promise in treating various cancer types.
Toxoplasma Gondii.
Toxoplasmosis - Congenital Toxoplasmosis
The transition between tachyzoites and bradyzoites.
T.gondii as an Epigenator.
Immune Response Pathway.
Behavior Changer by T.gondii infection.
The document provides an overview of innate immunity, including:
- Innate immunity is the first line of defense and includes physical, chemical, and biological barriers as well as cellular and humoral components.
- Cellular components include phagocytes such as macrophages and granulocytes that recognize, engulf, and kill pathogens through receptors and cellular responses.
- Humoral components include cytokines, chemokines, and the complement system.
- Innate immunity helps stimulate the adaptive immune response through antigen presentation and release of inflammatory signals.
1. The document discusses the role of cyclin D1 in regulating cell cycle progression and its implications in tumor initiation, maintenance, progression and metastasis through altering cell adhesion, migration, redox balance and drug resistance.
2. Cyclin D1 disrupts redox balance by producing reactive oxygen species and regulates cell cycle progression from G1 to S phase.
3. It also regulates cell adhesion and migration by stabilizing F-actin fibers and enhancing chemotaxis and inflammation.
Genetics and periodontal disease
Patients with periodontitis show inflammatory destruction of the supporting tissues around the teeth. Loss of connective tissue and collagen in the gingiva is characteristic, along with loss of periodontal ligament and resorption of alveolar bone. Thus the tooth roots become exposed to the oral environment, and the root and root cementum are colonized with a bacterial biofilm, which can calcify to form dental calculus. The chronicity and mostly slow progression of this disease results in tooth mobility, loss of chewing function, esthetic disturbances and, ultimately, if left untreated, tooth exfoliation. Moreover, periodontal inflammation has systemic effects; it can induce low grade systemic inflammation, which has negative effects on other organs.
Periodontitis is a complex chronic inflammatory disease with nonlinear progression that is caused by various factors each playing a role simultaneously and interacting with each other. The various factors determine the immune fitness of a subject. The host exists in a symbiotic relationship with the oral microbiome to maintain homeostasis. Loss of homeostasis results from loss of the host balance and an aberrant host response. This aberrant host response can manifest as a hyper‐ or hyporesponsiveness and/or lack of sufficient resolution of inflammatory reactions. The consequent chronic inflammation elicits changes in the ecology of the subgingival environment providing favorable conditions for the overgrowth of pathobionts that further propagate periodontal inflammation. The factors that determine immune fitness include: (a) genetic factors and epigenetic factors; (b) lifestyle factors; (c) comorbidities; (d) local or dental factors and factors that act randomly; and (e) pathobionts in a dysbiotic subgingival biofilm. Variants in at least 65 genes to date have been suggested as being associated with periodontitis based on genome‐wide association studies and candidate gene case control studies. Interestingly, reports have found pleiotropy between periodontitis and cardiovascular diseases. To date, 4 genetic loci are shared between coronary artery disease and periodontitis. The shared genes suggest that periodontitis is not causally related to atherosclerotic diseases, but rather both conditions are sequelae of similar (the same?) aberrant inflammatory pathways. In addition to variations in genomic sequences, epigenetic modifications of DNA can affect the genetic blueprint of the host responses.
This document discusses host modulation therapy for periodontal disease. It begins with an introduction to host modulation therapy, defining it as aiming to reduce tissue destruction and stabilize or regenerate the periodontium by modifying the host response. It then discusses the historical perspective and development of the concept of host modulation therapy. A key part of the rationale for host modulation therapy is to restore the balance of pro-inflammatory and anti-inflammatory mediators in the host response to periodontal pathogens. The document classifies host modulation therapies and discusses mechanisms including modulation of arachidonic acid metabolites, bone remodeling, matrix metalloproteinases, and cytokines.
The document discusses genome evolution in bacterial pathogens. It describes two main ways that phenotypic similarities can evolve between species: parallel evolution where similar mutations arise independently, and collateral evolution where alleles are shared between populations. It provides examples of how pathogenic strains like Shigella arose from E. coli through plasmid acquisition and phenotypic convergence. The document also summarizes key points from a workshop on bacterial pathogen origin and evolution, including the four main forms of genome evolution and the role of horizontal gene transfer in transmitting virulence genes.
This document discusses genetics in relation to periodontitis. It provides background on genetic study designs like segregation analysis, twin studies, and linkage/association studies that are used to identify genes associated with periodontal diseases. Specific genes linked to aggressive periodontitis are mentioned, including mutations in the alkaline phosphatase, cathepsin C, and CD18/CD11 genes. Studies finding autosomal dominant and recessive inheritance of aggressive periodontitis in different populations are summarized. The role of HLA antigens and IL-1 gene polymorphisms in periodontitis susceptibility is also briefly covered.
ROLE OF NEUTROPHILS IN HEALTH & DISEASE.pptxjasmine918783
Neutrophils are the most abundant white blood cells and form the first line of defense against pathogens. They are formed in the bone marrow through a process called granulopoiesis regulated by G-CSF and migrate to sites of infection. Neutrophils phagocytose and kill microbes via oxidative and non-oxidative mechanisms. Disorders can cause quantitative or qualitative neutrophil defects, resulting in increased susceptibility to infection. Periodontal disease is more severe and widespread in patients with neutrophil disorders due to impaired host response and bacterial modulation of neutrophil functions.
Genetic polymorphisms are normal variations that occur in more than 1% of the population. Single nucleotide polymorphisms are the most common type, involving a change in a single DNA base pair. Polymorphisms can occur in coding and regulatory regions, and may affect protein function or expression levels. The interleukin-1 gene cluster contains polymorphisms that have been associated with increased severity of periodontitis, where individuals with certain IL-1 genotypes experience more rapid bone and tissue loss around teeth. Understanding genetic predispositions can help with early detection and prevention of more serious disease.
host microbial interaction and toll like receptorsSaiBaba790008
This document provides an overview of host-microbial interactions in periodontitis. It discusses the microbial, immunological, and molecular aspects of this interaction. On the microbial side, it describes how bacteria can adhere to and invade host tissues, as well as evade the host immune response. It also explains how bacteria can directly or indirectly cause tissue damage through virulence factors and enzymes. On the immunological side, it discusses the role of pattern recognition receptors like Toll-like receptors and NOD-like receptors in recognizing microbial patterns and initiating inflammation. It also summarizes the acute bacterial challenge phase where the epithelium responds to bacteria and the early stages of the immune response.
Epigenetics and cell fate in JIA and pulmonary fibrosis by Jim HagoodSystemic JIA Foundation
This document discusses the potential role of epigenetic mechanisms in idiopathic pulmonary fibrosis (IPF) and juvenile idiopathic arthritis (JIA). It outlines how epigenetic changes like DNA methylation and histone modifications can alter gene expression and cell phenotypes, contributing to diseases like IPF that involve remodeling of lung tissue. Studies have found differential methylation and expression of genes in IPF lung tissue. Epigenetic therapies targeting mechanisms like DNA methylation and histone acetylation may one day help treat IPF and other diseases. The document also discusses how epigenetics may contribute to autoimmunity and JIA, noting differences in T cell methylation profiles between JIA patients and controls.
This document provides an overview of genetics and its relationship to oral health. It discusses how genetics plays a role in common oral conditions like dental caries and periodontitis, as well as rare genetic disorders that can affect the oral cavity. The document outlines Mendel's laws of inheritance and describes how genetic factors contribute to risks for oral diseases. It also classifies and examines specific genetic disorders involving structures in the oral region like the jaws, teeth and oral mucosa.
This document discusses genetics and periodontics. It provides an introduction to genetics concepts like genes, genomes, alleles and genetic testing. It discusses the human genome project and evidence that genetics plays a role in periodontal diseases. Certain genes like IL-1, TNF-α and PGE2 are candidates for influencing periodontal diseases based on their roles in immune-inflammatory processes and bone metabolism. Genetic variations involved in periodontal diseases can be determined through studies of candidate genes, genomic scans and proteomics.
This document discusses how plant polyphenols may help treat Alzheimer's disease by inhibiting NF-κB induced cytokine production. It first provides background on Alzheimer's disease and chronic neuroinflammation. It then describes the role of NF-κB in inflammation and how plant polyphenols could prevent the expression of pro-inflammatory genes regulated by NF-κB. The document proposes that plant polyphenols, due to their anti-inflammatory properties, have the potential to slow Alzheimer's disease progression by inhibiting NF-κB signaling in the brain.
1. Aggressive periodontitis is a rare, severe form of periodontitis typically affecting young individuals under 30 years of age. It is characterized by rapid attachment and bone loss.
2. It is caused by specific pathogens like Aggregatibacter actinomycetemcomitans and has a strong genetic component. Patients often exhibit impaired neutrophil function and hyper-inflammatory responses to bacterial toxins.
3. Aggressive periodontitis is classified into localized and generalized forms depending on the extent of involvement and treated through non-surgical therapies like scaling and root planing along with systemic antibiotics.
The premature ageing disorder Hutchinson - Gilford Progeria syndrome (HGPS) is one of the orphan (rarest) human diseases The Classic type of Progeria is HGPS. In humans hundreds of mutations in LMNA gene have been identified which causes several diseases termed as laminopathies. Products of LMNA gene primarily lamin A and C are key components of the nuclear lamina, a proteinaceous mesh work of inner nuclear membrane. Classic HGPS is caused by a de novo point mutation in exon 11(Residue 1824 C to T) of the LMNA gene which results in the production of mutant lamin A protein termed as 'Progerin'. In particular, progerin accumulation elicits nuclear
morphological abnormalities. HGPS is characterized by the presence of aging associated symptoms, including loss of subcutaneous fat, alopecia, cardiovascular Pathology and death due to myocardial infarction and stroke in childhood. Laboratory findings are unremarkable, with the exception of an increased urinary excretion of hyaluronic acid. Without progerin - specific treatment death occurs at an average age of 14.6 years from accelerated atherosclerosis. Supportive therapy like vitamin supplementation, Nutrini, pro-cal are recommended. Treatment usually includes low dose aspirin, lonafarnib, zoledronic acid, pravastatin, gene therapy and RNA therapy.
This document discusses aggressive periodontitis, including its classification, clinical characteristics, subgroups, epidemiology, pathobiology, risk factors, diagnosis, and treatment considerations. Aggressive periodontitis is characterized by rapid attachment and bone loss. It has two subgroups: localized aggressive periodontitis, which affects a limited number of teeth, and generalized aggressive periodontitis, which affects most teeth. The primary cause is bacterial infection, especially with Aggregatibacter actinomycetemcomitans. Genetics also play a role, as there is often a family history. Diagnosis involves clinical assessment of attachment loss and bone loss, as well as ruling out other conditions. Treatment typically involves scaling and root planing along with
The mandible is the only movable bone of the skull. It is formed by a body and two rami, and is connected to other bones via four ligaments. Two nerves - the inferior alveolar nerve and mental nerve - are related to foramina of the mandible. Two other nerves - the nerve to mylohyoid and lingual nerve - run in grooves of the mandible. The mandible has relationships to various arteries, nerves, and salivary glands.
The document discusses the anatomy of the human skull by presenting different views or "normas" including the frontal, vertical, lateral, external basal, and internal basal views. Each view provides a different orientation to examine the bones that make up the skull, including the mandible.
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Semelhante a Presentation of genetic periodontal.pptx
The document summarizes the immune mechanisms in the gingiva. The gingival defense system includes innate immunity components like toll-like receptors, complement system, and natural killer cells. It also contains adaptive immunity components like humoral and cell-mediated immunity. Toll-like receptors are expressed by various cells and recognize pathogen patterns to initiate signaling pathways that result in inflammatory responses. The gingival crevicular fluid contains enzymes, proteins, antibodies, cytokines, and cellular components that help fight infection and promote healing in the gingiva.
Innate immuntity in periodontal ligament and significance ofHudson Jonathan
This document provides an overview of innate immunity and the role of Toll-like receptors (TLRs) in periodontal diseases. It describes how TLRs recognize bacterial ligands and activate immune responses through signaling pathways. TLRs help maintain oral health by limiting microbial invasion, but excessive TLR signaling can lead to tissue destruction during periodontal disease. The document also discusses the potential clinical significance of TLRs as biomarkers for periodontal disease diagnosis and prognosis monitoring.
This document discusses epigenetics and its role in human disease. It begins with an introduction to epigenetics, explaining that epigenetic processes can alter gene expression without changing DNA sequence. It then discusses some key epigenetic mechanisms like DNA methylation and histone modifications. It provides examples of how epigenetic changes are implicated in several diseases, such as neurological disorders, autoimmune diseases, diabetes, and cancer. The document concludes by noting that epigenetic therapies are being explored for diseases like cancer, and that combining epigenetic drugs with immunotherapy shows promise in treating various cancer types.
Toxoplasma Gondii.
Toxoplasmosis - Congenital Toxoplasmosis
The transition between tachyzoites and bradyzoites.
T.gondii as an Epigenator.
Immune Response Pathway.
Behavior Changer by T.gondii infection.
The document provides an overview of innate immunity, including:
- Innate immunity is the first line of defense and includes physical, chemical, and biological barriers as well as cellular and humoral components.
- Cellular components include phagocytes such as macrophages and granulocytes that recognize, engulf, and kill pathogens through receptors and cellular responses.
- Humoral components include cytokines, chemokines, and the complement system.
- Innate immunity helps stimulate the adaptive immune response through antigen presentation and release of inflammatory signals.
1. The document discusses the role of cyclin D1 in regulating cell cycle progression and its implications in tumor initiation, maintenance, progression and metastasis through altering cell adhesion, migration, redox balance and drug resistance.
2. Cyclin D1 disrupts redox balance by producing reactive oxygen species and regulates cell cycle progression from G1 to S phase.
3. It also regulates cell adhesion and migration by stabilizing F-actin fibers and enhancing chemotaxis and inflammation.
Genetics and periodontal disease
Patients with periodontitis show inflammatory destruction of the supporting tissues around the teeth. Loss of connective tissue and collagen in the gingiva is characteristic, along with loss of periodontal ligament and resorption of alveolar bone. Thus the tooth roots become exposed to the oral environment, and the root and root cementum are colonized with a bacterial biofilm, which can calcify to form dental calculus. The chronicity and mostly slow progression of this disease results in tooth mobility, loss of chewing function, esthetic disturbances and, ultimately, if left untreated, tooth exfoliation. Moreover, periodontal inflammation has systemic effects; it can induce low grade systemic inflammation, which has negative effects on other organs.
Periodontitis is a complex chronic inflammatory disease with nonlinear progression that is caused by various factors each playing a role simultaneously and interacting with each other. The various factors determine the immune fitness of a subject. The host exists in a symbiotic relationship with the oral microbiome to maintain homeostasis. Loss of homeostasis results from loss of the host balance and an aberrant host response. This aberrant host response can manifest as a hyper‐ or hyporesponsiveness and/or lack of sufficient resolution of inflammatory reactions. The consequent chronic inflammation elicits changes in the ecology of the subgingival environment providing favorable conditions for the overgrowth of pathobionts that further propagate periodontal inflammation. The factors that determine immune fitness include: (a) genetic factors and epigenetic factors; (b) lifestyle factors; (c) comorbidities; (d) local or dental factors and factors that act randomly; and (e) pathobionts in a dysbiotic subgingival biofilm. Variants in at least 65 genes to date have been suggested as being associated with periodontitis based on genome‐wide association studies and candidate gene case control studies. Interestingly, reports have found pleiotropy between periodontitis and cardiovascular diseases. To date, 4 genetic loci are shared between coronary artery disease and periodontitis. The shared genes suggest that periodontitis is not causally related to atherosclerotic diseases, but rather both conditions are sequelae of similar (the same?) aberrant inflammatory pathways. In addition to variations in genomic sequences, epigenetic modifications of DNA can affect the genetic blueprint of the host responses.
This document discusses host modulation therapy for periodontal disease. It begins with an introduction to host modulation therapy, defining it as aiming to reduce tissue destruction and stabilize or regenerate the periodontium by modifying the host response. It then discusses the historical perspective and development of the concept of host modulation therapy. A key part of the rationale for host modulation therapy is to restore the balance of pro-inflammatory and anti-inflammatory mediators in the host response to periodontal pathogens. The document classifies host modulation therapies and discusses mechanisms including modulation of arachidonic acid metabolites, bone remodeling, matrix metalloproteinases, and cytokines.
The document discusses genome evolution in bacterial pathogens. It describes two main ways that phenotypic similarities can evolve between species: parallel evolution where similar mutations arise independently, and collateral evolution where alleles are shared between populations. It provides examples of how pathogenic strains like Shigella arose from E. coli through plasmid acquisition and phenotypic convergence. The document also summarizes key points from a workshop on bacterial pathogen origin and evolution, including the four main forms of genome evolution and the role of horizontal gene transfer in transmitting virulence genes.
This document discusses genetics in relation to periodontitis. It provides background on genetic study designs like segregation analysis, twin studies, and linkage/association studies that are used to identify genes associated with periodontal diseases. Specific genes linked to aggressive periodontitis are mentioned, including mutations in the alkaline phosphatase, cathepsin C, and CD18/CD11 genes. Studies finding autosomal dominant and recessive inheritance of aggressive periodontitis in different populations are summarized. The role of HLA antigens and IL-1 gene polymorphisms in periodontitis susceptibility is also briefly covered.
ROLE OF NEUTROPHILS IN HEALTH & DISEASE.pptxjasmine918783
Neutrophils are the most abundant white blood cells and form the first line of defense against pathogens. They are formed in the bone marrow through a process called granulopoiesis regulated by G-CSF and migrate to sites of infection. Neutrophils phagocytose and kill microbes via oxidative and non-oxidative mechanisms. Disorders can cause quantitative or qualitative neutrophil defects, resulting in increased susceptibility to infection. Periodontal disease is more severe and widespread in patients with neutrophil disorders due to impaired host response and bacterial modulation of neutrophil functions.
Genetic polymorphisms are normal variations that occur in more than 1% of the population. Single nucleotide polymorphisms are the most common type, involving a change in a single DNA base pair. Polymorphisms can occur in coding and regulatory regions, and may affect protein function or expression levels. The interleukin-1 gene cluster contains polymorphisms that have been associated with increased severity of periodontitis, where individuals with certain IL-1 genotypes experience more rapid bone and tissue loss around teeth. Understanding genetic predispositions can help with early detection and prevention of more serious disease.
host microbial interaction and toll like receptorsSaiBaba790008
This document provides an overview of host-microbial interactions in periodontitis. It discusses the microbial, immunological, and molecular aspects of this interaction. On the microbial side, it describes how bacteria can adhere to and invade host tissues, as well as evade the host immune response. It also explains how bacteria can directly or indirectly cause tissue damage through virulence factors and enzymes. On the immunological side, it discusses the role of pattern recognition receptors like Toll-like receptors and NOD-like receptors in recognizing microbial patterns and initiating inflammation. It also summarizes the acute bacterial challenge phase where the epithelium responds to bacteria and the early stages of the immune response.
Epigenetics and cell fate in JIA and pulmonary fibrosis by Jim HagoodSystemic JIA Foundation
This document discusses the potential role of epigenetic mechanisms in idiopathic pulmonary fibrosis (IPF) and juvenile idiopathic arthritis (JIA). It outlines how epigenetic changes like DNA methylation and histone modifications can alter gene expression and cell phenotypes, contributing to diseases like IPF that involve remodeling of lung tissue. Studies have found differential methylation and expression of genes in IPF lung tissue. Epigenetic therapies targeting mechanisms like DNA methylation and histone acetylation may one day help treat IPF and other diseases. The document also discusses how epigenetics may contribute to autoimmunity and JIA, noting differences in T cell methylation profiles between JIA patients and controls.
This document provides an overview of genetics and its relationship to oral health. It discusses how genetics plays a role in common oral conditions like dental caries and periodontitis, as well as rare genetic disorders that can affect the oral cavity. The document outlines Mendel's laws of inheritance and describes how genetic factors contribute to risks for oral diseases. It also classifies and examines specific genetic disorders involving structures in the oral region like the jaws, teeth and oral mucosa.
This document discusses genetics and periodontics. It provides an introduction to genetics concepts like genes, genomes, alleles and genetic testing. It discusses the human genome project and evidence that genetics plays a role in periodontal diseases. Certain genes like IL-1, TNF-α and PGE2 are candidates for influencing periodontal diseases based on their roles in immune-inflammatory processes and bone metabolism. Genetic variations involved in periodontal diseases can be determined through studies of candidate genes, genomic scans and proteomics.
This document discusses how plant polyphenols may help treat Alzheimer's disease by inhibiting NF-κB induced cytokine production. It first provides background on Alzheimer's disease and chronic neuroinflammation. It then describes the role of NF-κB in inflammation and how plant polyphenols could prevent the expression of pro-inflammatory genes regulated by NF-κB. The document proposes that plant polyphenols, due to their anti-inflammatory properties, have the potential to slow Alzheimer's disease progression by inhibiting NF-κB signaling in the brain.
1. Aggressive periodontitis is a rare, severe form of periodontitis typically affecting young individuals under 30 years of age. It is characterized by rapid attachment and bone loss.
2. It is caused by specific pathogens like Aggregatibacter actinomycetemcomitans and has a strong genetic component. Patients often exhibit impaired neutrophil function and hyper-inflammatory responses to bacterial toxins.
3. Aggressive periodontitis is classified into localized and generalized forms depending on the extent of involvement and treated through non-surgical therapies like scaling and root planing along with systemic antibiotics.
The premature ageing disorder Hutchinson - Gilford Progeria syndrome (HGPS) is one of the orphan (rarest) human diseases The Classic type of Progeria is HGPS. In humans hundreds of mutations in LMNA gene have been identified which causes several diseases termed as laminopathies. Products of LMNA gene primarily lamin A and C are key components of the nuclear lamina, a proteinaceous mesh work of inner nuclear membrane. Classic HGPS is caused by a de novo point mutation in exon 11(Residue 1824 C to T) of the LMNA gene which results in the production of mutant lamin A protein termed as 'Progerin'. In particular, progerin accumulation elicits nuclear
morphological abnormalities. HGPS is characterized by the presence of aging associated symptoms, including loss of subcutaneous fat, alopecia, cardiovascular Pathology and death due to myocardial infarction and stroke in childhood. Laboratory findings are unremarkable, with the exception of an increased urinary excretion of hyaluronic acid. Without progerin - specific treatment death occurs at an average age of 14.6 years from accelerated atherosclerosis. Supportive therapy like vitamin supplementation, Nutrini, pro-cal are recommended. Treatment usually includes low dose aspirin, lonafarnib, zoledronic acid, pravastatin, gene therapy and RNA therapy.
This document discusses aggressive periodontitis, including its classification, clinical characteristics, subgroups, epidemiology, pathobiology, risk factors, diagnosis, and treatment considerations. Aggressive periodontitis is characterized by rapid attachment and bone loss. It has two subgroups: localized aggressive periodontitis, which affects a limited number of teeth, and generalized aggressive periodontitis, which affects most teeth. The primary cause is bacterial infection, especially with Aggregatibacter actinomycetemcomitans. Genetics also play a role, as there is often a family history. Diagnosis involves clinical assessment of attachment loss and bone loss, as well as ruling out other conditions. Treatment typically involves scaling and root planing along with
Semelhante a Presentation of genetic periodontal.pptx (20)
The mandible is the only movable bone of the skull. It is formed by a body and two rami, and is connected to other bones via four ligaments. Two nerves - the inferior alveolar nerve and mental nerve - are related to foramina of the mandible. Two other nerves - the nerve to mylohyoid and lingual nerve - run in grooves of the mandible. The mandible has relationships to various arteries, nerves, and salivary glands.
The document discusses the anatomy of the human skull by presenting different views or "normas" including the frontal, vertical, lateral, external basal, and internal basal views. Each view provides a different orientation to examine the bones that make up the skull, including the mandible.
The trigeminal nerve is the 5th cranial nerve and is a mixed nerve, mainly sensory and motor. It has three main branches: the ophthalmic, maxillary, and mandibular nerves. The maxillary nerve originates from the trigeminal ganglion and courses through the cranial cavity, pterygo-palatine fossa, floor of the orbit, and face, where it terminates and provides branches. The mandibular nerve is also a mixed nerve that originates from the trigeminal ganglion and courses through the cranium, middle ear, and face, where it terminates and provides several sensory and motor branches to structures in the face and oral cavity.
The document discusses the anatomy of the human skull by outlining four different views or "normas" - the frontal, vertical, lateral, and basal views. It also mentions that the skull is composed of multiple bones and references both the external and internal basal views.
This document provides information on human anatomy terms and concepts. It defines three planes of the body used to describe positions (sagittal, coronal, transverse), and anatomical terms like medial, lateral, superior and inferior. It also outlines types of joints (fibrous, cartilaginous, synovial), muscles (skeletal, cardiac, smooth) and movement terms like flexion, extension, and circumduction. Key facts about tissues, bones, and cartilage are summarized.
This document discusses adhesins and receptors involved in dental plaque formation. It describes the composition of dental plaque and the types of plaque. The mechanism of plaque formation involves 5 steps: 1) formation of the acquired pellicle on the tooth surface, 2) bacterial adherence via adhesins binding to receptors in the pellicle, 3) formation of an inter-microbial matrix, 4) bacterial colonization and plaque maturation, and 5) dispersion. Specific adhesins and receptors that facilitate plaque formation are also outlined.
This document discusses the relationship between psychosomatic disorders and periodontal diseases. It outlines several factors that can affect periodontal health, including age, sex, genetics, stress, smoking, diet, parafunctional habits, medication side effects, and oral hygiene. Stress in particular is linked to conditions like necrotizing ulcerative gingivitis. The document also covers ways that psychosomatic disorders may induce oral issues like harmful habits or effects on tissues through the autonomic nervous system. Proper patient evaluation, education, and referral are important for managing oral health issues with potential psychological influences.
This document discusses furcation involvement in multi-rooted teeth. It begins with definitions of furcation involvement from 1950-1968. The primary cause is plaque accumulation leading to inflammation. Local anatomical factors like root trunk length, root form, and furcation anatomy affect the progression of furcation involvement. Clinical diagnosis involves probing the furcation and correlating with radiographs. Treatment depends on the grade of involvement and may include nonsurgical approaches like scaling and root planing or surgical therapies such as osseous resection or extraction.
This document discusses gingival enlargement, including its terminology, classifications, and etiological factors.
It defines gingival enlargement and explains that the terms gingival hyperplasia and hypertrophy are not precise descriptions as they refer to histological diagnoses. Gingival enlargement can be caused by inflammatory conditions, systemic diseases, medications, and other factors.
It classifies gingival enlargement based on its location and distribution in the mouth. It also discusses diagnosing and grading gingival enlargement. The document then examines various etiological factors and pathological changes that can cause gingival enlargement, including inflammatory, drug-induced, and enlargement associated with systemic diseases or
1) The document discusses the relationship between periodontal disease and cardiovascular disease (CVS) and diabetes. It explores the focal infection theory and possible pathways linking oral infections to secondary non-oral diseases.
2) Periodontal disease is associated with increased risk of CVS diseases like atherosclerosis, coronary heart disease, and stroke. It may increase susceptibility through inflammation, endothelial injury, lipid peroxidation, molecular mimicry, and elevated antibodies from oral bacteria.
3) Periodontal disease is also linked to increased risk of diabetes through shared risk factors and inflammation. Periodontal bacteria may enter the bloodstream and stimulate liver proteins that amplify systemic inflammation, worsening insulin resistance.
Hematologic disorders like neutropenia, leukemia, anemia, and thrombocytopenia can influence the periodontium. Neutropenia involves low levels of circulating neutrophils which are important for inflammatory reactions and defense against infection. This makes the tissues more susceptible to destruction from conditions like periodontitis. Leukemia is a cancer of the blood cells that can lead to infiltration of leukemic cells into the gingiva and increased risk of infection. Anemia reduces oxygen delivery and makes tissues more friable. Thrombocytopenia increases risk of bleeding from the gums. Antibody deficiency disorders like agammaglobulinemia compromise immune defenses and can result in early loss of teeth from period
Hyperparathyroidism and diabetes can influence periodontal health in several ways:
1. They can alter immune responses, such as impairing neutrophil function, which helps bacteria evade the immune system and worsen periodontal disease.
2. Chronic hyperglycemia and hyperparathyroidism can impair collagen structure and function, damaging the integrity of the periodontium.
3. They may qualitatively change the subgingival microbiome, promoting pathogens like Porphyromonas and Prevotella that are linked to periodontitis.
salivary old new dd.pppptx disease and healthMohamedYElZahar
1. Salivary biomarkers can provide non-invasive alternatives to clinical diagnostics for periodontal diseases by detecting bacterial, host, and inflammatory markers. A combination of biomarkers may provide a more accurate assessment than a single marker.
2. Specific salivary biomarkers for periodontal diseases include immunoglobulins directed against periodontal pathogens, salivary enzymes like lysozyme and peroxidase, and ions like calcium. Nonspecific biomarkers include lactoferrin, histatin, fibronectin, and platelet activating factor.
3. Emerging biomarkers include analysis of the salivary proteome, transcriptome, and host genomic factors that influence susceptibility. However, no single biomarker adequately diagnoses
- This document discusses mediators of bone loss, focusing on alveolar bone destruction in periodontal disease. It outlines the cellular mechanisms and local mediators involved in bone remodeling and resorption, including pro-inflammatory cytokines, prostaglandins, and RANKL.
- Diagnostic tools for detecting periodontal bone resorption are discussed, including indirect clinical measures like probing depth and radiographs, which have limitations. Systemic biochemical markers of bone resorption are mentioned as another potential diagnostic method.
- The key cellular players in bone remodeling - osteoblasts, osteoclasts, and osteocytes - are described. Homeostatic balance between bone formation and resorption is maintained through
This document provides an overview of wound healing, its functions, stages, mechanisms, factors affecting it, and complications.
A wound is a break in the integrity of the skin or tissues, which may be associated with disruption of the structure and function.
Healing is the body’s response to injury in an attempt to restore normal structure and functions.
Healing can occur in two ways: Regeneration and Repair
There are 4 phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. This document also describes the mechanism of wound healing. Factors that affect healing include infection, uncontrolled diabetes, poor nutrition, age, anemia, the presence of foreign bodies, etc.
Complications of wound healing like infection, hyperpigmentation of scar, contractures, and keloid formation.
This presentation includes basic of PCOS their pathology and treatment and also Ayurveda correlation of PCOS and Ayurvedic line of treatment mentioned in classics.
This presentation was provided by Steph Pollock of The American Psychological Association’s Journals Program, and Damita Snow, of The American Society of Civil Engineers (ASCE), for the initial session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session One: 'Setting Expectations: a DEIA Primer,' was held June 6, 2024.
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
Main Java[All of the Base Concepts}.docxadhitya5119
This is part 1 of my Java Learning Journey. This Contains Custom methods, classes, constructors, packages, multithreading , try- catch block, finally block and more.
Reimagining Your Library Space: How to Increase the Vibes in Your Library No ...Diana Rendina
Librarians are leading the way in creating future-ready citizens – now we need to update our spaces to match. In this session, attendees will get inspiration for transforming their library spaces. You’ll learn how to survey students and patrons, create a focus group, and use design thinking to brainstorm ideas for your space. We’ll discuss budget friendly ways to change your space as well as how to find funding. No matter where you’re at, you’ll find ideas for reimagining your space in this session.
How to Fix the Import Error in the Odoo 17Celine George
An import error occurs when a program fails to import a module or library, disrupting its execution. In languages like Python, this issue arises when the specified module cannot be found or accessed, hindering the program's functionality. Resolving import errors is crucial for maintaining smooth software operation and uninterrupted development processes.
Strategies for Effective Upskilling is a presentation by Chinwendu Peace in a Your Skill Boost Masterclass organisation by the Excellence Foundation for South Sudan on 08th and 09th June 2024 from 1 PM to 3 PM on each day.
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.
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
This slide is special for master students (MIBS & MIFB) in UUM. Also useful for readers who are interested in the topic of contemporary Islamic banking.
LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UPRAHUL
This Dissertation explores the particular circumstances of Mirzapur, a region located in the
core of India. Mirzapur, with its varied terrains and abundant biodiversity, offers an optimal
environment for investigating the changes in vegetation cover dynamics. Our study utilizes
advanced technologies such as GIS (Geographic Information Systems) and Remote sensing to
analyze the transformations that have taken place over the course of a decade.
The complex relationship between human activities and the environment has been the focus
of extensive research and worry. As the global community grapples with swift urbanization,
population expansion, and economic progress, the effects on natural ecosystems are becoming
more evident. A crucial element of this impact is the alteration of vegetation cover, which plays a
significant role in maintaining the ecological equilibrium of our planet.Land serves as the foundation for all human activities and provides the necessary materials for
these activities. As the most crucial natural resource, its utilization by humans results in different
'Land uses,' which are determined by both human activities and the physical characteristics of the
land.
The utilization of land is impacted by human needs and environmental factors. In countries
like India, rapid population growth and the emphasis on extensive resource exploitation can lead
to significant land degradation, adversely affecting the region's land cover.
Therefore, human intervention has significantly influenced land use patterns over many
centuries, evolving its structure over time and space. In the present era, these changes have
accelerated due to factors such as agriculture and urbanization. Information regarding land use and
cover is essential for various planning and management tasks related to the Earth's surface,
providing crucial environmental data for scientific, resource management, policy purposes, and
diverse human activities.
Accurate understanding of land use and cover is imperative for the development planning
of any area. Consequently, a wide range of professionals, including earth system scientists, land
and water managers, and urban planners, are interested in obtaining data on land use and cover
changes, conversion trends, and other related patterns. The spatial dimensions of land use and
cover support policymakers and scientists in making well-informed decisions, as alterations in
these patterns indicate shifts in economic and social conditions. Monitoring such changes with the
help of Advanced technologies like Remote Sensing and Geographic Information Systems is
crucial for coordinated efforts across different administrative levels. Advanced technologies like
Remote Sensing and Geographic Information Systems
9
Changes in vegetation cover refer to variations in the distribution, composition, and overall
structure of plant communities across different temporal and spatial scales. These changes can
occur natural.
2. CHROMOSOME
A nuclear structure that contains genetic information.
Humans have 46 chromosomes that are arranged in 23
pairs. There are 22 pairs of autosomes and one pair of
sex chromosomes (either XX or XY).
3.
4. GENE
the basic physical and functional unit of heredity. Gene is
segment of DNA on a chromosome. Some genes act as
instructions to make proteins.
5. GENOME
• The entire hereditary information of an organism. This
term refers to all of the genes and other nongene
portions of DNA carried by an individual cell.
6. • Genotype The genetic makeup of an organism or cell as
distinct from its expressed features or phenotype
• Phenotype The observable characteristics displayed by an
organism (e.g., morphology, development, gender, eye
color, physiologic properties, behavior). Phenotype results
from the expression of the organism’s genes as well as
from the influence of environmental factors and
interactions between the two
8. MUTATION :
• It is a very rare
change in a
nucleotide which
doesn’t present in
many individuals
9. POLYMORPHISM
• It is kind of mutation but considered to be a normal
variant when a specific allele exceeds more than >1% of
population
10.
11.
12. mutations in a single
gene are both necessary
and sufficient to produce
the clinical phenotype
and to cause the disease
Genetic diseases
Simple mendelian diseases
(monogenic disorders)
Complex genetic diseases
(polygenic disorders)
In complex disorders with multiple causes,
variations in a number of genes encoding
different proteins result in a genetic
predisposition to a clinical phenotype.
Environment and life-style are major
contributors to the pathogenesis of
complex diseases.
The genetic alterations that contribute
to complex diseases are called
polymorphism.
13. • E.g. syndromic periodontitis
(syndromes, which have
periodontal disease
manifestations as part of
syndromic manifestations are
Papillon Lefevre syndrome,
Chediak- Higashi syndrome, Ehler-
Danlos syndrome, cyclic
neutropenia, and leukocyte
adhesion deficiency
Genetic diseases
Simple mendelian diseases
(monogenic disorders)
Complex genetic diseases
(polygenic disorders)
E.g. Non syndromic periodontitis
14.
15. • Periodontitis is a multi-factorial disease. Genetics is
considered a susceptibility factor in relation to
periodontitis. Among the various study designs,
population studies are used to find the frequencies of
polymorphisms of candidate genes, by comparing
between cases and controls.
16.
17. GENETIC SUSCEPTIBILITY TO PERIODONTAL
DISEASE
Periodontitis in Genetic
Syndromes and Other
Diseases
Nonsyndromic
Periodontitis
18.
19. A. IL-1 GENE POLYMORPHISM:
• IL 1 stimulates bone resorption, inhibits collagen
synthesis, stimulates the production of other
inflammatory mediators and metalloproteinases.
• IL-1α and IL-1β are encoded, respectively, by IL1A,
IL1B genes, located near each other on the long arm
(q arm) of chromosome 2 .
1-Cytokine gene polymorphism
20. • IL-1 gene cluster is located on chromosome 2.
Cytokine gene polymorphism
21. • Meta-analyses show that at least two single nucleotide
polymorphisms: IL-1α[−889](rs1800587) and IL-
1β[+3953] (rs1143634), are associated with periodontal
inflammation. Therefore, they can be regarded as
candidate genes involved in further periodontitis risk
assessment (Brodzikowska A et al., 2019).
1-Cytokine gene polymorphism
22. B. TNF- ALPHA GENE POLYMORPHISM
• TNF triggers bone destruction by stimulating osteoclastic activity
and decreasing osteoblastic activity. TNF has been shown to be
involved in periodontitis pathogenesis.
• TNF-alpha (-308 G/A) polymorphisms might not be
associated with the risk of periodontitis, whereas the CT
genotype and the C allele of the TNF-alpha (-1031) T/C
Single nucleotide polymorphism are potential risk factors for
periodontitis in Saudi subjects (Azab E and Elfasakhany F, 2022).
1-Cytokine gene polymorphism
23.
24.
25. C. IL-10 GENE POLYMORPHISMS
• IL-10 gene is located on chromosome 1.
• IL-10 is a protective cytokine in periodontal disease.
• Functional disturbances in IL-10 due to genetic
polymorphisms could be detrimental to host tissue and
linked to periodontal disease susceptibility.
1-Cytokine gene polymorphism
26. OTHER CYTOKINES
• There is some preliminary evidence that genotype with
respect to the IL-2 SNP might be associated with severity
in aggressive periodontitis (Scarrel-Caminaga RM et al., 2002)
• Analysis IL-6 gene polymorphisms in Czech patients with
chronic periodontitis suggested that -572
G/Cpolymorphisms of IL-6 gene might be one of the
protective factors associated with lower susceptibility to
chronic periodontitis (Holla LI et al., 2004)
27. A. FC
R GENE POLYMORPHISMS
• .
2. Receptor and other gene polymorphisms
28. A. FC
R GENE POLYMORPHISMS
• The inflammatory cascade induced by IgG containing immune
complexes is initiated by the IgG Fc receptors on phagocytes.
Efficient clearance of IgG opzonised pathogens by phagocyte FcγR
is crucial for periodontal health. Leukocytes exhibit receptors [R]
for the constant region [Fc] of immunoglobulin molecule.
2. Receptor and other gene polymorphisms
29. A. FC
R GENE POLYMORPHISMS
2. Receptor and other gene polymorphisms
30. A. FC
R GENE POLYMORPHISMS
2. Receptor and other gene polymorphisms
31. A. FC
R GENE POLYMORPHISMS
2. Receptor and other gene polymorphisms
33. B. CYTOKINE AND CHEMOKINE RECEPTOR GENE
POLYMORPHISMS
2. Receptor and other gene polymorphisms
34. C. IMMUNE RECEPTOR GENE POLYMORPHISM
N-FORMYL PEPTIDE RECEPTOR POLYMORPHISMS (FPR)
• The high affinity FMLP receptor (FPR1) of phagocytic cells
interacts with bacterial FMLP and mediates chemotaxis,
degranulation, and superoxide production.
• Zhang et al., studied the prevalence of polymorphisms of the
FMLP receptor gene in localised, generalised, and grade C
periodontitis.
35.
36. A. VITAMIN D RECEPTOR GENE (VDR) POLYMORPHISM
• Vitamin D receptor gene polymorphism has regulatory effects
on bone mineral density and bone turnover.
• Hennig et al., suggested that genetic polymorphism in Taq1
site of VDR gene might be a risk indicator for susceptibility to
Early-onset periodontal diseases (Hennig et al., 1999).
3. METABOLISM – RELATED GENE POLYMORPHISM
37. B. CALCITONIN RECEPTOR POLYMORPHISM
• Calcitonin maintains blood calcium levels and inhibits osteoclats.
• Nosaka et al., 2002 have found that patients with this polymorphism
were 20 times more likely to suffer buccal marginal bone loss than
patients who were calcitonin receptor genotype negative
3. METABOLISM – RELATED GENE
POLYMORPHISM
38. •HUMAN LEUKOCYTE ANTIGENS (HLA )GENE
POLYMORPHISM
• MHC class II molecules (HLA-DP,-DQ,-DR) are expressed on B and T
cells, macrophages and accessory cells for the presence of foreign
peptides .
• HLAs play an important role in the immune response
because they bind some of the peptides of processed
antigens and present them at the surface of
antigenpresenting cells, such as macrophages or dendritic
cells to the T-cell receptor of CD4- or CD8-positive
lymphocytes..
• .
4. Antigen – recognition related gene
polymorphism
39. • HUMAN LEUKOCYTE ANTIGENS (HLA )GENE
POLYMORPHISM
4. Antigen – recognition related gene
polymorphism
40. • HLA GENE POLYMORPHISM
• Studies have suggested that patients with the HLA-DRB1
1501- DQB1 0602 genotype may have an accelerated T
cell response to Porphyromonas. gingivalis and an
increased susceptibility to EOP in Japanese patients
(Takashiba S et al,1999).
4. Antigen – recognition related gene
polymorphism
41. A. TLR2 AND TLR4 GENE POLYMORPHISMS
• Toll-like
receptors are
signal
molecules
essential for
the cellular
response to
bacterial cell
wall
components.
5. POLYMORPHISMS IN THE INNATE IMMUNITY
RECEPTORS
42. A. TLR2 AND TLR4 GENE POLYMORPHISMS
• These polymorphisms have been correlated with
hyporesponsiveness to LPS, sepsis and infection caused by gram
negative bacteria.
• Schroeder et al., suggested that genetic variants of TLR- 4 might
act as risk factor for the development of periodontitis.(Schroeder et al., 2005)
5. POLYMORPHISMS IN THE INNATE IMMUNITY
RECEPTORS
43. B. CD 14 GENE POLYMORPHISM
• CD14 acts as
a co-receptor
(along with
the Toll-like
receptor TLR
4 for the
detection of
bacterial lipop
olysaccharide
(LPS).
5. POLYMORPHISMS IN THE INNATE IMMUNITY
RECEPTORS
44. B. CD 14 GENE POLYMORPHISM
• CD14 exists in two forms, one anchored to the membrane by
a glycosylphosphatidylinositol (GPI) tail (mCD14), the other a
soluble form (sCD14).
• Increased serum levels of sCD14 have been known to be
associated with periodontitis (Hayashi J, et al, 1999)
• There are contradictory findings from the studies of Holla et al and
Yamazaki et al. which did not find any association between CD14
genome polymorphism and chronic periodontitis(Holla et al., 2002; Yamazaki et
al, 2003)
5. POLYMORPHISMS IN THE INNATE IMMUNITY
RECEPTORS
45. A. CATHEPSIN C GENE POLYMORPHISM
• Cathepsin C is a lysosomal protease present in neutrophils and
macrophages as well as epithelial cells. Hart and co-workers, 2000,
identified and localized a gene on chromosome 11, which is
responsible for a severe form of pre-pubertal periodontitis in a
family of Jordanian descent.
• Other mutations in the CTS C gene have been linked to the
Papillon-Lefevre syndrome, a disease which is also associated with
a severe form of pre-pubertal periodontitis
6. MISCELLANEOUS GENE POLYMORPHISMS
46. B. MMP GENE POLYMORPHISM
6. MISCELLANEOUS GENE POLYMORPHISMS
SNP in gene of MMP-1 promoter region -1607 is associated with
increased risk of Grade C periodontitis.
Another study showed that three MMP polymorphisms had a small
effect on Grade A and B periodontitis.
47. C- POLYMORPHISMS IN GENES ENCODING FOR MYELOPEROXIDASE
(MPO) AND N-ACETYL TRANSFERASE (NAT-2)
• MPO and NAT2 are enzymes participating in the metabolism of
xenobiotics including arylamines from tobacco smoke. MPO is also
implicated in defence against bacterial challenge and
inflammatory tissue destruction.
6. MISCELLANEOUS GENE POLYMORPHISMS
48. C- POLYMORPHISMS IN GENES ENCODING FOR MYELOPEROXIDASE
(MPO) AND N-ACETYL TRANSFERASE (NAT-2)
• Kocher et al. and Meisel et al. conducted studies in Caucasian
population which demonstrated that the N-acetyl transferase slow
phenotype was significantly associated with severity of bone loss
(Kocher et al, 2000;Meisel et al, 2000).
6. MISCELLANEOUS GENE POLYMORPHISMS
49. D. OTHER POLYMORPHISMS
• Other polymorphisms include ACE (Angiotensin converting enzyme), ER2
(Endothelein receptor 2), IL (Interleukin) 2, IL4, IL6, IFN-GR (Interferon gamma
receptor) 1, MMP (Matrix mettaloproteinase)-1, MMP3, MMP9, MPO
(Myeloperoxidase), RAGE (Receptor for advanced glycation end products), TGF
(Transforming growth factor) β, TIMP (Tissue inhibitor of metalloproteinase) 2,
Plasminogen activation, Mannose binding lectin, Osteoprotegrin and TNFR (Tumor
necrosis factor receptor) 2 gene polymorphisms.
• Association between these polymorphisms and periodontal disease is yet to be
proved.
6. MISCELLANEOUS GENE POLYMORPHISMS
50.
51. PERIODONTAL SUSCEPTIBILITY TEST (PST
• Currently, a genetic test is being marked for severe chronic
periodontitis, called periodontal susceptibility test (PST). It
tests for the presence of specific polymorphisms of the IL--
1a and IL-1ß genes. The genotype is determined from a
finger stick blood or saliva samples
52. PERIOPREDICT TEST I
• It examines a person’s genetic makeup to detect risk
factors for severe periodontal disease by measuring
variations in the cytokine Interleukin-1 (IL-1)
• quick, painless, and easily performed in a dentist’s office.
• A genetic sample is obtained from the mouth via a cheek
swab
56. PAPILLON–LEFÈVRE SYNDROME
• Cathepsin C is a lysosomal protease present in neutrophils and
macrophages as well as epithelial cells, found on chromosome
11.
• Cathepsin C gene polymorphism lead to:
Advanced periodontal disease usually affects the primary and
secondary dentition shortly after the teeth erupt, and many
patients become edentulous while in their teens AND Palmar–
plantar keratodermas affect the palms of the hands and the
plantar surfaces of the feet.
59. CHEDIAK-HIGIASHI SYNDROME
• AR
• mutations in the lysosomal trafficking regulator gene (LYST) leading to
Prevention of lysosome fusion with phagosome, decreasing neutrophil
killing
Clinical features:
• albinism, bleeding diathesis, recurrent bacterial infections,
immunodeficiency, and neurological dysfunctions.
• It is believed that neutropenia and congenital neutrophil dysfunction in CHS
lead to bacterial invasion and rapid destruction of periodontal tissues at a
very early age.
61. HYPOPHOSPHATASIA
• rare inherited metabolic disease
• mutations in the ALPL gene (encoding tissue-
nonspecific alkaline phosphatase) result in varying
degrees of enzyme deficiency.
• HPP manifests in a spectrum of symptoms, including
early primary tooth loss (root intact) and alveolar bone
mineralisation defects.
63. EHLER-DANLOS SYNDROME
• autosomal-dominant disorder
characterized by :
• early-onset periodontitis leading to premature loss
of teeth,
• joint hypermobility, and mild skin findings
65. DOWN SYNDROME
• trisomy 21 (presence of all or part of a third copy of chromosome 21)
• generalized grade C Periodontitis
• loss of teeth at an early age.
• Added to immunedeficiency, inadequate control of bacterial
plaque, deficient masticatory function, and alterations in dental
anatomy (short roots)
66.
67. LEUKOCYTE ADHESION DEFICIENCY(LAD)
• Genetic disorder results from an inability to produce or a
failure to normally express an important cell surface integrin
(CD18), which is necessary for leukocytes to adhere to the
vessel wall at the site of infection.
• leukocytes cannot effectively adhere to the vessel wall near
the site of infection, they cannot migrate to the infection
leading to increased bacterial infection.
68. LEUKOCYTE ADHESION DEFICIENCY(LAD)
• Respiratory tract infections and sometimes otitis
media.
• Both the primary and permanent teeth are affected,
often resulting in early tooth loss.
Notas do Editor
In both cases, allele 2 was characterized
by cytosine nucleotide replacement by thymine.
Number is genetic locus
T over c means T substituted by c
Tnf alpha gene polymorphism in promoter area
Fc receptors bind to antibodies that are attached to infected cells or invading pathogens. Their activity stimulates phagocytic or cytotoxic cells to destroy microbes, or infected cells by antibody-mediated phagocytosis or antibody-dependent cell-mediated cytotoxicity
FPR1 is prominently expressed by mammalian phagocytic and blood leukocyte cells where it functions to mediate these cells' responses to the N-formylmethionine-containing oligopeptides which are released by invading microorganisms and injured tissues. thereby initiates innate host immune responses. FMLP stands for N-Formylmethionine-leucyl-phenylalanine
T-cell receptor (TCR) is a protein complex found on the surface of T cells, or T lymphocytes, that is responsible for recognizing fragments of antigen as peptides bound to major histocompatibility complex (MHC) molecules.