CONTENTS:
Introduction
Some basic terminologies
Definition
Rational for use in dentistry
Effects of growth factors at various levels
Mode of action of growth factors
Receptors for growth factors
Common features of growth factors
Classification of growth factors
Type of growth factors and actions
Conclusion
References
INTRODUCTION:
Periodontal diseases result in destruction of periodontal tissues, including cementum, bone, and periodontal ligament (PDL), with eventual tooth loss if left untreated.
Traditional Method……Elimination of bacterial pathogens + Modulation of host response leads to Arrest / Slow disease progression.
Better understanding of the disease at the cellular and molecular level as well as events involved in tissue development, healing and regeneration has Improved therapies with Arrest Of Disease Progression & Ultimate goal is to regenerate the periodontal tissues.
SOME BASIC TERMINOLOGIES :
Repair:
Healing of a wound by tissue that does not fully restore the architecture or function of the part. (AAP, Glossary of periodontal terms, PAL). Repair simply restores the continuity of the diseased marginal gingiva and reestablishes a normal gingival sulcus at the same level on the root as the base of the preexistent periodontal pocket. This process called healing by scar, arrests bone destruction without necessarily increasing bone height (caranza).
Regeneration:
Is the growth and differentiation of new cells and intercellular substances to form new tissues or parts. Regeneration takes place by growth from the same type of tissue that has been destroyed or from it’s precursor. This is termed as wear and tear repair.
Reattachment:
The term has been used in past to refer to the restoration of the marginal periodontium.
As per (AAP-92) it is defined as the reunion of epithelial and connective tissues with root surfaces and bone such as occur after an incision or injury. It should not be confused with new attachment.
New attachment: is the embedding of new periodontal ligament fibers into new cementum and the attachment of the gingival epithelium to a tooth surface previously denuded by disease.
Epithelial adaptation:
Differs from new attachment in that it is the close apposition of the gingival epithelium to the tooth surface without complete obliteration of the pocket.
PERIODONTAL REGENERATION is defined as the restoration of lost periodontium or supporting tissues and includes formation of new alveolar bone, new cementum and new periodontal ligament.
There is a need, however, to improve the predictability of regenerative therapies.
This need has led to increased efforts, to establish the specific cells, factors, delivery systems, flap design, and host responses required for enhancing outcome of regenerative therapies.
Growth factors are proteins that bind to cell surface receptors and regulate cellular proliferation, differentiation, and other functions. They include transforming growth factor beta (TGF-β), epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and fibroblast growth factors (FGFs). TGF-β in particular is important for bone homeostasis and is produced in its inactive form, requiring activation before exerting its effects on cells. Growth factors signal through membrane receptors and regulate gene expression.
This document discusses various growth factors and their roles in periodontal tissues and regeneration. It defines growth factors and their modes of action. It then classifies and describes several important growth factors in detail, including PDGF, TGFs, BMPs, CTGF, FGFs. It discusses the use of growth factors like PDGF and BMPs in therapies and delivery methods.
This document summarizes matrix metalloproteinases (MMPs), a family of enzymes that degrade the extracellular matrix and are involved in tissue remodeling. It groups MMPs into collagenases, gelatinases, stromelysins, matrilysins, membrane-type MMPs, and others. For each group, it lists the MMP names and their protein substrates. It also describes two pathways for activating MMPs at the cell surface, and discusses transcriptional regulation, activation of precursors, substrate specificity, inhibitors like TIMPs and α2-macroglobulins, and classes of pharmacological MMP inhibitors.
Tissue engineering aims to recreate healthy tissues to replace diseased or damaged ones. There are three basic steps: obtaining cells, putting them on a scaffold to incubate, and implanting the new tissue. Sources for periodontal tissue engineering include dental pulp stem cells, periodontal ligament stem cells, and dental follicle stem cells. Signaling molecules like growth factors are incorporated into scaffolds to facilitate their sustained release and support cell proliferation and differentiation. Scaffolds provide a structure for cell adhesion, migration, and production of extracellular matrix. Recent advances include antimicrobial and bioactive membranes, electrospun membranes, and platelet-rich fibrin membranes. Tissue engineering opens new possibilities for periodontal regeneration and restoration of oral function.
This document discusses potential biomarkers for periodontal disease. It begins by defining biomarkers and explaining their advantages over traditional diagnostic methods. It then explores various categories of biomarkers, including microbiological markers like bacterial species and their products, as well as immune and inflammatory markers like cytokines. Specific biomarkers that have shown promise are discussed, such as GCF levels of PGE2, AST, and IgG subclasses. The document also notes challenges with biomarkers, like the polymicrobial nature of periodontal disease making it difficult to choose single bacterial species markers. Overall, the document provides a comprehensive overview of the types of biomarkers studied for periodontal disease and their potential for diagnosis and monitoring disease activity.
reactive oxygen species in periodontal diseaseSuhani Goel
This document summarizes the role of reactive oxygen species (ROS) and antioxidants in periodontal tissue destruction. It defines key terms like free radicals, oxidative stress, and antioxidants. It describes the major ROS molecules like superoxide, hydrogen peroxide, and hydroxyl radicals. These molecules are produced endogenously through metabolic pathways and phagocytosis, and can cause tissue damage by oxidizing lipids, proteins, and DNA. This oxidative damage disrupts cellular functions and structures. The document also discusses how ROS induce transcription factors and cytokine release to promote inflammation. Maintaining the pro-oxidant/antioxidant balance is important for periodontal health.
Influence of steroid hormones on the periodontiumNida Sumra
This document discusses the influence of steroid hormones on the periodontium. It covers the classification of hormones, including steroid hormones like corticosteroids, androgens, progesterone and estrogen. It describes how these hormones can influence the periodontium through effects on bone metabolism, inflammation, collagen synthesis and more. Factors like gender, age and hormone supplementation levels are discussed in terms of their interactions with the periodontal effects of sex hormones.
Growth factors are proteins that bind to cell surface receptors and regulate cellular proliferation, differentiation, and other functions. They include transforming growth factor beta (TGF-β), epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and fibroblast growth factors (FGFs). TGF-β in particular is important for bone homeostasis and is produced in its inactive form, requiring activation before exerting its effects on cells. Growth factors signal through membrane receptors and regulate gene expression.
This document discusses various growth factors and their roles in periodontal tissues and regeneration. It defines growth factors and their modes of action. It then classifies and describes several important growth factors in detail, including PDGF, TGFs, BMPs, CTGF, FGFs. It discusses the use of growth factors like PDGF and BMPs in therapies and delivery methods.
This document summarizes matrix metalloproteinases (MMPs), a family of enzymes that degrade the extracellular matrix and are involved in tissue remodeling. It groups MMPs into collagenases, gelatinases, stromelysins, matrilysins, membrane-type MMPs, and others. For each group, it lists the MMP names and their protein substrates. It also describes two pathways for activating MMPs at the cell surface, and discusses transcriptional regulation, activation of precursors, substrate specificity, inhibitors like TIMPs and α2-macroglobulins, and classes of pharmacological MMP inhibitors.
Tissue engineering aims to recreate healthy tissues to replace diseased or damaged ones. There are three basic steps: obtaining cells, putting them on a scaffold to incubate, and implanting the new tissue. Sources for periodontal tissue engineering include dental pulp stem cells, periodontal ligament stem cells, and dental follicle stem cells. Signaling molecules like growth factors are incorporated into scaffolds to facilitate their sustained release and support cell proliferation and differentiation. Scaffolds provide a structure for cell adhesion, migration, and production of extracellular matrix. Recent advances include antimicrobial and bioactive membranes, electrospun membranes, and platelet-rich fibrin membranes. Tissue engineering opens new possibilities for periodontal regeneration and restoration of oral function.
This document discusses potential biomarkers for periodontal disease. It begins by defining biomarkers and explaining their advantages over traditional diagnostic methods. It then explores various categories of biomarkers, including microbiological markers like bacterial species and their products, as well as immune and inflammatory markers like cytokines. Specific biomarkers that have shown promise are discussed, such as GCF levels of PGE2, AST, and IgG subclasses. The document also notes challenges with biomarkers, like the polymicrobial nature of periodontal disease making it difficult to choose single bacterial species markers. Overall, the document provides a comprehensive overview of the types of biomarkers studied for periodontal disease and their potential for diagnosis and monitoring disease activity.
reactive oxygen species in periodontal diseaseSuhani Goel
This document summarizes the role of reactive oxygen species (ROS) and antioxidants in periodontal tissue destruction. It defines key terms like free radicals, oxidative stress, and antioxidants. It describes the major ROS molecules like superoxide, hydrogen peroxide, and hydroxyl radicals. These molecules are produced endogenously through metabolic pathways and phagocytosis, and can cause tissue damage by oxidizing lipids, proteins, and DNA. This oxidative damage disrupts cellular functions and structures. The document also discusses how ROS induce transcription factors and cytokine release to promote inflammation. Maintaining the pro-oxidant/antioxidant balance is important for periodontal health.
Influence of steroid hormones on the periodontiumNida Sumra
This document discusses the influence of steroid hormones on the periodontium. It covers the classification of hormones, including steroid hormones like corticosteroids, androgens, progesterone and estrogen. It describes how these hormones can influence the periodontium through effects on bone metabolism, inflammation, collagen synthesis and more. Factors like gender, age and hormone supplementation levels are discussed in terms of their interactions with the periodontal effects of sex hormones.
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.
Bone Morphogenetic Proteins - Role in Periodontal RegenerationDr.Shraddha Kode
This document discusses bone morphogenetic proteins (BMPs), which are signaling molecules that govern tissue development and regeneration. BMPs play an important role in periodontal regeneration and regeneration of other dental tissues. The document outlines the classification, signaling pathways, roles in development, and clinical applications of BMPs, particularly BMP-2 and BMP-7, which have shown efficacy in regenerating bone and periodontal tissues when delivered with appropriate carrier materials. While BMPs show promise for regenerative therapies, further research is still needed to optimize dosage, delivery methods, and carrier materials.
Tissue engineering and periodontal regenerationPrathahini
This document discusses periodontal regeneration and tissue engineering. It defines tissue engineering as recreating healthy tissues to replace diseased ones using principles of cell biology, developmental biology and biomaterials science. The key components of tissue engineering are scaffolds, progenitor cells and biosignals. It discusses various cell types involved in periodontal regeneration like epithelial cells, fibroblasts and blastic cells. Growth factors and molecules important for periodontal regeneration like FGFs, IGFs, BMPs, TGFβ etc. are also summarized. The criteria for evaluating periodontal regeneration and reasons for treatment failures are stated.
role of neutrophils in periodontitis defenders?or offenders?Bhargavi Vedula
This document discusses the role of neutrophils in aggressive and chronic periodontitis. It notes that a significant shift in understanding the pathogenesis of these conditions centers on alterations in neutrophil function, including impaired neutrophil function, primed/hyperactive neutrophils, and concepts under transformation. While functional alterations have been extensively studied, whether neutrophils are inherently defective or progressively damaged remains open to debate. Modulation of the destructive aspects of the host response, such as through low-dose doxycycline or anti-inflammatory lipoxins, shows promise as a treatment approach. Understanding neutrophil function could aid in developing new diagnostic and treatment strategies, with potential to reverse acquired neutrophil defects through mechanical debridement and strategic use of anti
Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases that degrade extracellular matrix components. MMPs play important roles in tissue remodeling during processes like wound healing and organ development by breaking down collagen, elastin, fibronectin and other matrix proteins. Their activity is regulated by tissue inhibitors of metalloproteinases (TIMPs). Abnormal MMP activity is associated with diseases like cancer, atherosclerosis, and rheumatoid arthritis by facilitating tissue invasion or destruction.
Neutrophils play an important role in both oral health and periodontal disease. In oral health, neutrophils help maintain balance through mechanisms like phagocytosis, degranulation, and neutrophil extracellular traps to fight symbiotic bacteria. However, a shift to dysbiotic bacteria due to dental plaque can lead to periodontitis. In periodontitis, dysbiotic bacteria like P. gingivalis and T. denticola interact with neutrophils to inhibit their functions and promote persistent inflammation and tissue damage. This interaction, along with increased recruitment of neutrophils, contributes to chronic inflammation and bone loss in periodontitis. New therapeutic approaches targeting these disease mechanisms show promise for treating periodontitis.
This document discusses the effects of various hormones from the endocrine system on the periodontium. It begins with an introduction to periodontitis and the role of the endocrine system. It then discusses the central endocrine glands of the hypothalamus and pituitary, as well as peripheral glands including the thyroid, parathyroid, pancreas, and adrenal glands. For each gland, it summarizes the hormones secreted and their effects on the periodontium, such as accelerated bone loss from hyperthyroidism, increased tooth loss with hyperparathyroidism, increased risk of periodontitis in diabetes, and reduced immune response from glucocorticoids. Sex steroid hormones from the ovaries and test
The document discusses the effects of hormones from various endocrine glands on the periodontium. It describes how hormones from the hypothalamus and pituitary gland regulate other endocrine glands. It then examines the specific effects of hormones from the adrenal, thyroid, parathyroid, gonads and pancreas on periodontal tissues and the mechanisms by which they may influence periodontal health and disease. It also discusses how gender, age and hormone supplements can impact the effects of sex hormones on the periodontium.
Periodontitis is a chronic infectious inflammatory disease caused by microbes; however the presence of microbes is not enough for the cause of its complex nature of disease. Inflammation is the prime cause of periodontal disease. It commences with the aggregation of pathogenic microbes that induce the host to stimulate a cascade of inflammatory response reactions which in-turn leads to the destruction of the host tissues itself. There is a complex interplay of innate and adaptive immune responses which fights against the pathogens by direct interaction or by release of certain molecules including cytokines.
Cytokines are cell signalling molecules that aid cell to cell communication in immune responses and stimulate the movement of cells towards sites of inflammation, infection and trauma. Cytokine biology reveals that there are some subsets of cytokines which are pro-inflammatory cytokines which stimulate the inflammatory responses and cause tissue destruction.
A periodontist is expected to have a sound basis of the cytokine profile to understand the pathogenesis of periodontitis and also to discover the new treatment modality of anti-cytokine therapy.
Bone morphogenetic proteins in periodontal regenerationDr. Shashi Kiran
This document provides an overview of bone morphogenetic proteins (BMPs). It discusses the history and discovery of BMPs, their structure and classification. The key characteristics and mechanisms of action of BMPs are described, including their role in signaling pathways and spatial/temporal regulation. The document outlines the functions of BMPs in embryogenesis, tooth morphogenesis, and osseoinduction. It also discusses various delivery systems for BMPs, including local protein therapy using both organic matrices like collagen and inorganic matrices like hydroxyapatite.
Toll-like receptors (TLRs) play a key role in the innate immune system by recognizing molecular patterns from pathogens. TLRs are expressed on immune cells like macrophages and dendritic cells. They recognize pathogen-associated molecular patterns and activate signaling pathways that induce inflammatory responses and adaptive immunity. There are 10 human TLRs that recognize different ligands from bacteria, viruses, and fungi. TLR signaling involves either a MyD88-dependent or independent pathway leading to cytokine production and immune cell activation. Dysregulation of TLRs has been implicated in various diseases.
This document provides an overview of platelet concentrates including platelet rich plasma (PRP) and platelet rich fibrin (PRF). It discusses the history of platelet concentrates and their role in wound healing. The techniques for preparing PRP and PRF are described, along with their merits and applications in oral and maxillofacial surgery, periodontology, implantology, endodontics, and other areas. While platelet concentrates show potential for tissue regeneration due to their growth factors, further research is still needed to fully evaluate their clinical effectiveness.
This document discusses the role of viruses in periodontal diseases. It begins by introducing viruses and their structure. It then discusses several important virus families and examples of viruses that can cause oral infections, including herpesviruses like HSV-1, EBV, CMV; papillomaviruses; and picornaviruses. The document reviews the prevalence of herpesviruses detected in samples from patients with gingivitis, aggressive periodontitis, chronic periodontitis, and provides theories on how viruses like CMV may contribute to the pathogenesis of diseases like localized juvenile periodontitis.
Cytokines are small soluble proteins that are important mediators of the inflammatory response. They are produced by immune cells like lymphocytes and monocytes and act as signaling molecules between cells. The document defines cytokines and provides classifications of cytokines. It describes the roles of key cytokines like IL-1 and IL-2 in innate immunity and leukocyte recruitment during the early immune response. Cytokines function through binding to specific cell surface receptors and activating intracellular signaling pathways.
The role of NSAIDs in periodontal disease progressionHope Inegbenosun
This document discusses the role of nonsteroidal anti-inflammatory drugs (NSAIDs) in periodontal disease progression. It outlines that periodontal disease results from the host inflammatory response to bacterial pathogens and involves the production of arachidonic acid metabolites like prostaglandin E2 (PGE2) that promote tissue destruction. NSAIDs inhibit the enzyme cyclooxygenase and thereby reduce PGE2 levels to decrease inflammation and bone resorption. Both animal and human studies show that systemic or local NSAID administration can suppress periodontal disease progression by limiting inflammation and PGE2 production.
The document discusses various chairside diagnostic aids that can be used in periodontal examination. It outlines the limitations of traditional diagnostic methods like clinical and radiographic evaluation. It then describes several advanced diagnostic aids like thermal probes, subtraction radiography. The rationale for developing chairside diagnostic kits is provided which allow immediate reports without specialized equipment. Examples of microbiological, genetic and biochemical chairside test kits are explained in detail, covering their methodology and biomarkers analyzed. Newer diagnostic tests still under development are also mentioned.
Wound healing [including healing after periodontal therapy]Jignesh Patel
The document discusses wound healing and periodontal wound healing in particular. It describes the processes of regeneration and repair. Regeneration involves renewal of tissues through growth of same tissue type, while repair involves replacement of tissues through scar formation. The molecular biology of wound healing is explained, including roles of fibrin clot, growth factors, matrix degradation and connective tissue formation. Healing by primary and secondary intention is also defined. Healing processes following various periodontal procedures like scaling, root planing, flap surgery and implant placement are outlined. Factors influencing wound healing and potential complications are briefly mentioned.
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.
Wound healing is a complex process involving regeneration and repair. It consists of three overlapping phases - inflammatory, proliferative, and remodeling. In the inflammatory phase, coagulation and platelet aggregation form a fibrin clot and recruit inflammatory cells. The proliferative phase involves re-epithelialization through keratinocyte migration and proliferation. Fibroblasts are activated and form granulation tissue through angiogenesis and collagen deposition. Myofibroblasts aid wound contraction in the final remodeling phase. Growth factors influence each phase of wound healing after periodontal and oral procedures.
Cell growth can refer to the increase in cell size and organelles during interphase (G1 and G2 phases) or the growth of a cell population through cell division (M phase). The cell cycle consists of G1, S, G2, and M phases, separated by gap phases G1 and G2. Growth factors such as EGF, TGF-α, HGF, and PDGF act as ligands that bind to cell surface receptors and transmit signals to regulate the cell cycle. These signals activate intracellular pathways using second messengers to induce transcription factors that drive expression of genes controlling cell cycle progression and cell growth.
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.
Bone Morphogenetic Proteins - Role in Periodontal RegenerationDr.Shraddha Kode
This document discusses bone morphogenetic proteins (BMPs), which are signaling molecules that govern tissue development and regeneration. BMPs play an important role in periodontal regeneration and regeneration of other dental tissues. The document outlines the classification, signaling pathways, roles in development, and clinical applications of BMPs, particularly BMP-2 and BMP-7, which have shown efficacy in regenerating bone and periodontal tissues when delivered with appropriate carrier materials. While BMPs show promise for regenerative therapies, further research is still needed to optimize dosage, delivery methods, and carrier materials.
Tissue engineering and periodontal regenerationPrathahini
This document discusses periodontal regeneration and tissue engineering. It defines tissue engineering as recreating healthy tissues to replace diseased ones using principles of cell biology, developmental biology and biomaterials science. The key components of tissue engineering are scaffolds, progenitor cells and biosignals. It discusses various cell types involved in periodontal regeneration like epithelial cells, fibroblasts and blastic cells. Growth factors and molecules important for periodontal regeneration like FGFs, IGFs, BMPs, TGFβ etc. are also summarized. The criteria for evaluating periodontal regeneration and reasons for treatment failures are stated.
role of neutrophils in periodontitis defenders?or offenders?Bhargavi Vedula
This document discusses the role of neutrophils in aggressive and chronic periodontitis. It notes that a significant shift in understanding the pathogenesis of these conditions centers on alterations in neutrophil function, including impaired neutrophil function, primed/hyperactive neutrophils, and concepts under transformation. While functional alterations have been extensively studied, whether neutrophils are inherently defective or progressively damaged remains open to debate. Modulation of the destructive aspects of the host response, such as through low-dose doxycycline or anti-inflammatory lipoxins, shows promise as a treatment approach. Understanding neutrophil function could aid in developing new diagnostic and treatment strategies, with potential to reverse acquired neutrophil defects through mechanical debridement and strategic use of anti
Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases that degrade extracellular matrix components. MMPs play important roles in tissue remodeling during processes like wound healing and organ development by breaking down collagen, elastin, fibronectin and other matrix proteins. Their activity is regulated by tissue inhibitors of metalloproteinases (TIMPs). Abnormal MMP activity is associated with diseases like cancer, atherosclerosis, and rheumatoid arthritis by facilitating tissue invasion or destruction.
Neutrophils play an important role in both oral health and periodontal disease. In oral health, neutrophils help maintain balance through mechanisms like phagocytosis, degranulation, and neutrophil extracellular traps to fight symbiotic bacteria. However, a shift to dysbiotic bacteria due to dental plaque can lead to periodontitis. In periodontitis, dysbiotic bacteria like P. gingivalis and T. denticola interact with neutrophils to inhibit their functions and promote persistent inflammation and tissue damage. This interaction, along with increased recruitment of neutrophils, contributes to chronic inflammation and bone loss in periodontitis. New therapeutic approaches targeting these disease mechanisms show promise for treating periodontitis.
This document discusses the effects of various hormones from the endocrine system on the periodontium. It begins with an introduction to periodontitis and the role of the endocrine system. It then discusses the central endocrine glands of the hypothalamus and pituitary, as well as peripheral glands including the thyroid, parathyroid, pancreas, and adrenal glands. For each gland, it summarizes the hormones secreted and their effects on the periodontium, such as accelerated bone loss from hyperthyroidism, increased tooth loss with hyperparathyroidism, increased risk of periodontitis in diabetes, and reduced immune response from glucocorticoids. Sex steroid hormones from the ovaries and test
The document discusses the effects of hormones from various endocrine glands on the periodontium. It describes how hormones from the hypothalamus and pituitary gland regulate other endocrine glands. It then examines the specific effects of hormones from the adrenal, thyroid, parathyroid, gonads and pancreas on periodontal tissues and the mechanisms by which they may influence periodontal health and disease. It also discusses how gender, age and hormone supplements can impact the effects of sex hormones on the periodontium.
Periodontitis is a chronic infectious inflammatory disease caused by microbes; however the presence of microbes is not enough for the cause of its complex nature of disease. Inflammation is the prime cause of periodontal disease. It commences with the aggregation of pathogenic microbes that induce the host to stimulate a cascade of inflammatory response reactions which in-turn leads to the destruction of the host tissues itself. There is a complex interplay of innate and adaptive immune responses which fights against the pathogens by direct interaction or by release of certain molecules including cytokines.
Cytokines are cell signalling molecules that aid cell to cell communication in immune responses and stimulate the movement of cells towards sites of inflammation, infection and trauma. Cytokine biology reveals that there are some subsets of cytokines which are pro-inflammatory cytokines which stimulate the inflammatory responses and cause tissue destruction.
A periodontist is expected to have a sound basis of the cytokine profile to understand the pathogenesis of periodontitis and also to discover the new treatment modality of anti-cytokine therapy.
Bone morphogenetic proteins in periodontal regenerationDr. Shashi Kiran
This document provides an overview of bone morphogenetic proteins (BMPs). It discusses the history and discovery of BMPs, their structure and classification. The key characteristics and mechanisms of action of BMPs are described, including their role in signaling pathways and spatial/temporal regulation. The document outlines the functions of BMPs in embryogenesis, tooth morphogenesis, and osseoinduction. It also discusses various delivery systems for BMPs, including local protein therapy using both organic matrices like collagen and inorganic matrices like hydroxyapatite.
Toll-like receptors (TLRs) play a key role in the innate immune system by recognizing molecular patterns from pathogens. TLRs are expressed on immune cells like macrophages and dendritic cells. They recognize pathogen-associated molecular patterns and activate signaling pathways that induce inflammatory responses and adaptive immunity. There are 10 human TLRs that recognize different ligands from bacteria, viruses, and fungi. TLR signaling involves either a MyD88-dependent or independent pathway leading to cytokine production and immune cell activation. Dysregulation of TLRs has been implicated in various diseases.
This document provides an overview of platelet concentrates including platelet rich plasma (PRP) and platelet rich fibrin (PRF). It discusses the history of platelet concentrates and their role in wound healing. The techniques for preparing PRP and PRF are described, along with their merits and applications in oral and maxillofacial surgery, periodontology, implantology, endodontics, and other areas. While platelet concentrates show potential for tissue regeneration due to their growth factors, further research is still needed to fully evaluate their clinical effectiveness.
This document discusses the role of viruses in periodontal diseases. It begins by introducing viruses and their structure. It then discusses several important virus families and examples of viruses that can cause oral infections, including herpesviruses like HSV-1, EBV, CMV; papillomaviruses; and picornaviruses. The document reviews the prevalence of herpesviruses detected in samples from patients with gingivitis, aggressive periodontitis, chronic periodontitis, and provides theories on how viruses like CMV may contribute to the pathogenesis of diseases like localized juvenile periodontitis.
Cytokines are small soluble proteins that are important mediators of the inflammatory response. They are produced by immune cells like lymphocytes and monocytes and act as signaling molecules between cells. The document defines cytokines and provides classifications of cytokines. It describes the roles of key cytokines like IL-1 and IL-2 in innate immunity and leukocyte recruitment during the early immune response. Cytokines function through binding to specific cell surface receptors and activating intracellular signaling pathways.
The role of NSAIDs in periodontal disease progressionHope Inegbenosun
This document discusses the role of nonsteroidal anti-inflammatory drugs (NSAIDs) in periodontal disease progression. It outlines that periodontal disease results from the host inflammatory response to bacterial pathogens and involves the production of arachidonic acid metabolites like prostaglandin E2 (PGE2) that promote tissue destruction. NSAIDs inhibit the enzyme cyclooxygenase and thereby reduce PGE2 levels to decrease inflammation and bone resorption. Both animal and human studies show that systemic or local NSAID administration can suppress periodontal disease progression by limiting inflammation and PGE2 production.
The document discusses various chairside diagnostic aids that can be used in periodontal examination. It outlines the limitations of traditional diagnostic methods like clinical and radiographic evaluation. It then describes several advanced diagnostic aids like thermal probes, subtraction radiography. The rationale for developing chairside diagnostic kits is provided which allow immediate reports without specialized equipment. Examples of microbiological, genetic and biochemical chairside test kits are explained in detail, covering their methodology and biomarkers analyzed. Newer diagnostic tests still under development are also mentioned.
Wound healing [including healing after periodontal therapy]Jignesh Patel
The document discusses wound healing and periodontal wound healing in particular. It describes the processes of regeneration and repair. Regeneration involves renewal of tissues through growth of same tissue type, while repair involves replacement of tissues through scar formation. The molecular biology of wound healing is explained, including roles of fibrin clot, growth factors, matrix degradation and connective tissue formation. Healing by primary and secondary intention is also defined. Healing processes following various periodontal procedures like scaling, root planing, flap surgery and implant placement are outlined. Factors influencing wound healing and potential complications are briefly mentioned.
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.
Wound healing is a complex process involving regeneration and repair. It consists of three overlapping phases - inflammatory, proliferative, and remodeling. In the inflammatory phase, coagulation and platelet aggregation form a fibrin clot and recruit inflammatory cells. The proliferative phase involves re-epithelialization through keratinocyte migration and proliferation. Fibroblasts are activated and form granulation tissue through angiogenesis and collagen deposition. Myofibroblasts aid wound contraction in the final remodeling phase. Growth factors influence each phase of wound healing after periodontal and oral procedures.
Cell growth can refer to the increase in cell size and organelles during interphase (G1 and G2 phases) or the growth of a cell population through cell division (M phase). The cell cycle consists of G1, S, G2, and M phases, separated by gap phases G1 and G2. Growth factors such as EGF, TGF-α, HGF, and PDGF act as ligands that bind to cell surface receptors and transmit signals to regulate the cell cycle. These signals activate intracellular pathways using second messengers to induce transcription factors that drive expression of genes controlling cell cycle progression and cell growth.
Growth Factors in the Human Body: A Conceptual Update_Crimson PublishersCrimsonpublishersCJMI
Growth factors are signaling molecules that stimulate cell growth, proliferation, and differentiation. They were originally discovered through their effects on cell and tissue growth in culture. Growth factors act through paracrine, autocrine, or endocrine signaling and can be divided into families based on their structure and function. Some major growth factor families include transforming growth factor beta (TGF-β) and insulin-like growth factor. Growth factors play roles in processes like wound healing but can also contribute to diseases such as cancer, diabetes, and liver fibrosis when their regulation is abnormal.
This document discusses mammalian cell culture and the role of growth factors. It provides details on epidermal growth factor (EGF), fibroblast growth factor (FGF), and platelet-derived growth factor (PDGF). Two case studies are summarized that examine the effects of depriving cells of EGF and the role of PDGF and IGF-1 in activating Schwann cells. The document concludes with references used.
Cancer develops through a process called carcinogenesis where normal cells are transformed into cancer cells through genetic and epigenetic mutations. These mutations activate oncogenes and inactivate tumor suppressor genes, altering the biochemistry of the cell and causing uncontrolled cell growth. The mutations disrupt the typical cell division and growth factor signaling pathways, leading cells to proliferate autonomously without dependence on external growth signals. Common alterations include overproduction of growth factors, changes to growth factor receptors and intracellular signaling proteins, and autocrine signaling loops.
The document discusses several growth factors including epidermal growth factor (EGF), fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), and erythropoietin. It describes how these growth factors function to regulate cell growth, differentiation, and survival by binding to cell surface receptors and activating intracellular signaling pathways. Specific examples of their roles in wound healing, angiogenesis, and fetal development are provided.
Cellular and molecular biology of cementum Satya Kurada
As cementum is one of the hard tissues of the Periodontium which is now being challenging structure to the researcher's, Effort is put forth in understanding the molecular and cellular level of the Cementum. The information is collected from one of the articles from Perio 2000 and also from the slide share forum.
This powerpoint gives you the gist and hopefully a better understanding for the learners.
basic of oncology awreness to general public for .pptAKBARALISABIR
Growth and differentiation are complex biological processes regulated by genetic and environmental factors. Growth involves an increase in size through cellular processes like cell multiplication, growth of components, and accretion of material. Differentiation is the process by which cells develop specialized phenotypes through regulated gene expression. Key aspects of growth and differentiation include organismal growth, morphogenesis, cell number control, and disorders that arise from deregulation like neoplasia. The precise spatial and temporal control of gene expression underlying differentiation and morphogenesis is critical for proper development and maintenance of tissues and organs.
The document discusses the principles of endocrinology, including the study of glands and hormones, their functional roles, and feedback mechanisms. It describes the major classes of hormones, hormone and receptor families, hormone synthesis and action, and pathologic mechanisms of endocrine disease such as hormone excess, deficiency, and resistance.
The document discusses host modulation therapy for treating periodontal disease. It explains that periodontal disease is caused by an imbalance between proinflammatory and anti-inflammatory host responses to bacterial pathogens. Host modulation therapy aims to restore this balance by reducing destructive aspects of the host response and enhancing protective responses. The document outlines the role of mediators like cytokines, prostaglandins, and matrix metalloproteinases in periodontal tissue destruction. It discusses currently used host modulation therapies like non-steroidal anti-inflammatories and sub-antimicrobial dose doxycycline, which is the only systemically administered therapy approved as an adjunct to scaling and root planing.
There are four main types of promoters that can be used to regulate gene expression in plants:
1. Constitutive promoters direct constant expression in all tissues. The 35S and Ubi promoters are commonly used.
2. Tissue-specific promoters restrict expression to certain tissues like seeds, roots or fruits.
3. Inducible promoters are activated by stimuli like light, chemicals or stress. Examples include light-induced rbcs and heat-induced hsp promoters.
4. Synthetic promoters are assembled from elements of different origins to achieve a defined expression pattern. The 35S promoter has been modified by adding modules to increase its strength.
This document discusses human growth factors and their roles in various processes from the Department of Urology at GRH and KMC in Chennai. It lists the moderators and their roles. Growth factors are defined as signaling molecules that stimulate cellular growth, proliferation, and differentiation. Examples include cytokines and hormones. The document discusses the cell cycle and how growth factors interact with cell surface receptors to affect gene transcription and cell cycle progression. It provides examples of many growth factors including their functions and roles in various conditions.
The study of how genes and gene products interact with dietary chemicals to alter phenotype and, conversely, how genes and their products metabolize nutrients is called nutritional genomics or “Nutrigenomics”.
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Oncogenes encode proteins that promote cell growth and inhibit apoptosis. There are four classes of genes that regulate cell growth: proto-oncogenes, tumor suppressor genes, genes that regulate apoptosis, and genes involved in DNA repair. Oncogenes can be activated by mutations, gene fusions, or amplification and drive cancer progression. The products of oncogenes resemble normal growth factors, growth factor receptors, signal transducers, transcription factors, apoptosis regulators, and chromatin remodelers but endow cells with autonomous growth.
This document provides an overview of endocrinology presented by Kenneth Campbell at Texas A&M University - Corpus Christi from April 12-16, 2004. It defines endocrinology as intercellular chemical communication and discusses endocrine systems, hormones, receptors, transducers, effectors, and feedback systems. It also summarizes the major endocrine glands and hormones, including the hypothalamus and pituitary gland, thyroid, adrenal cortex, growth hormone, pancreas, gonads, prolactin, and calcium homeostasis.
This document discusses nutrigenomics, which is the study of how nutrients and bioactive compounds in food affect gene expression. It provides examples of how different nutrients like carbohydrates, fat, protein, minerals and vitamins can regulate gene expression. Key techniques in nutrigenomics like transcriptomics, proteomics and metabolomics are also summarized. The document outlines several potential applications of nutrigenomics like developing customized feeds tailored to an animal's genotype, selecting nutrients to fine-tune gene activity, and gaining insights into performance and disease.
This document discusses the regulation of genome activity in prokaryotes and eukaryotes. It explains that in prokaryotes like bacteria, gene expression is regulated through operons, which coordinate the expression of genes involved in specific pathways. A key example is the lac operon in E. coli. In eukaryotes, gene expression is more complex and regulated at many stages from chromatin structure to post-translational modification. Epigenetics also plays a role in regulating gene expression and cell differentiation through mechanisms like DNA methylation and histone modification.
Similar to Growth factors and their receptors (20)
CONTENETS
INTRODUCTION.
DEFINITION
TYPES OF WOUND.
PROCESS OF WOUND HEALING.
TYPES OF HEALING WOUNDS
PHASES OF WOUND HEALING
COMPLICATIONS OF WOUND HEALINGS.
FACTORS EFFECTING WOUND HEALING.
ROLE OF SALIVA AND GCF IN ORAL WOUND HEALING
CLINICAL REQUIREMENTS FOR EFFECTIVE HEALING AFTER PERIODONTAL SURGERY
HISTOLOGIC PATTERNS OF WOUND HEALING
HEALING FOLLOWING SCALING & ROOT PLANING
HEALING FOLLOWING CURETTAGE.
HEALING FOLLOWING GINGIVIECTOMY,FRENECTOMY,DEPIGMENTATION.
HEALING FOLLOWING FLAP SURGERY (FULL & PARTIAL THICKNESS).
HEALING FOLLOWING APICALLY REPOSTIONED FLAP.
HEALING FOLLOWING MODIFIED WIDMAN FLAP.
HEALING FOLLOWING FREE GINGIVAL GRAFT.
HEALING FOLLOWING PEDICLE SOFT TISSUE GRAFT.
HEALING FOLLOWING GTR PROCEDURES.
HEALING FOLLOWING REGENERATIVE AND RESECTIVE OSSEOUS SURGERY.
HEALING FOLLOWING SOCKET PRESERVATION.
HEALING FOLLOWING WILCKODONTICS.
HEALING FOLLOWING IMPLANT PLACEMENT.
HEALING FOLLOWING IMMEDIATE IMPLANT PLACEMENT.
HEALING AFTER ELECTRO CAUTERY.
HEALING AFTER LASER.
HEALING AFTER PIEZO SURGERY.
POTENTIAL ROLE OF FACTORS IN PERIODONTAL WOUND HEALING
INVITRO MODELS FOR EVALUATION OF PERIODONTAL WOUND HEALING
EVALUATION OF HEALING
HEALING INDEX.
APPLIED CLINICAL ASPECTS AND RECENT ADVANCES TO ENHANCE WOUND HEALING
CONCLUSION.
REFERNCES.
Periodontal Treatment of Medically Compromised Patients [Autosaved].pptxANIL KUMAR
The world's population is estimated to be over 7.7 billion. [1] Within this mass of humanity is a
substantial number of people who are elderly; the graying of the world's population is predicted to
produce millions of individuals with systemic medical conditions that can affect oral health and
dental treatment. The dental management of these medically compromised patients can be
problematic in terms of oral complications, dental therapy, and emergency care
• Introduction
• Definitions
• Macroscopic Features
• Microscopic Features
• Blood supply
• Nerve supply
• Lymphatic drainage
• Role of epithelium in defence mechanism
• Oxygen consumption of gingiva
• Correlation of Macroscopic with microscopic features
• Conclusion
INTRODUCTION
HISTORY
PRINCIPLES OF WORKING OF A LASER
FUNDAMENTALS OF LASER
CHARACTERISTICS OF LASER
CLASSIFICATION OF LASER
EFFECTS OF LASER ON SOFT AND HARD TISSUES
VARIOUS LASERS AVAILABLE FOR PERIDONTAL USE
APPLICATION OF LASER TREATMENT IN PERIODONTAL THERAPY
ADVANTAGES & DISADVANTAGES OF LASER IN PERIODONTAL THERAPY
LASER PRECAUTIONS
LASER HAZARDS
RECENT ADVANCES
CONCLUSION
INTRODUCTION
DEFINITION
EMBRYOLOGY/DEVEOLPMENT
HISTOLOGY OF SALIVARY GLANDS
CLASSIFICATION OF SALIVARY GALNDS
ANATOMY OF SALIVARY GLANDS
AGE CHANGES
CLINICAL CONSIDERATION
CONCLUSION
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
Introduction
History
Epidemiology AIDS
CDC definition and classification of AIDS
Virus structure
Mode of transmission
Life cycle of HIV
Clinical features-WHO classification
Classification of oral lesions associated with HIV
Periodontal manifestations of HIV
Periodontal management of HIV infected patients
Diagnostic tests
Sterilization and precautions to be taken
Conclusion
Introduction
Definition
Methods to control plaque
History
Mechanical plaque control
Chemical plaque control
Biological method of plaque control
Conclusion
References
The temporomandibular joint (TMJ) connects the jaw bone to the skull. It is a complex synovial joint that allows for movement of the mandible during chewing and talking. The TMJ has both bony and soft tissue components including the condyle, glenoid fossa, articular disc, joint capsule, ligaments and muscles. The TMJ develops late in utero and has a complex anatomy that facilitates its range of motion. Disorders can affect the TMJ resulting in problems like pain, limited movement or locking of the jaw.
This document discusses the relationship between nutrition and periodontal health. It begins with definitions of key terms like diet, nutrition, and malnutrition. It then covers the major classes of nutrients like proteins, carbohydrates, fats, vitamins, and minerals. It discusses how deficiencies in specific nutrients like vitamin C, vitamin D, and calcium can impact periodontal health. It also addresses how nutrition interacts with immunity and oral microorganisms, and can affect the epithelial barrier, wound healing, and periodontal repair processes. In summary, the document outlines the various ways in which nutrition plays a role in both supporting periodontal health and influencing the progression of periodontal disease.
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.
The simplified electron and muon model, Oscillating Spacetime: The Foundation...RitikBhardwaj56
Discover the Simplified Electron and Muon Model: A New Wave-Based Approach to Understanding Particles delves into a groundbreaking theory that presents electrons and muons as rotating soliton waves within oscillating spacetime. Geared towards students, researchers, and science buffs, this book breaks down complex ideas into simple explanations. It covers topics such as electron waves, temporal dynamics, and the implications of this model on particle physics. With clear illustrations and easy-to-follow explanations, readers will gain a new outlook on the universe's fundamental nature.
A Strategic Approach: GenAI in EducationPeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
How to Manage Your Lost Opportunities in Odoo 17 CRMCeline George
Odoo 17 CRM allows us to track why we lose sales opportunities with "Lost Reasons." This helps analyze our sales process and identify areas for improvement. Here's how to configure lost reasons in Odoo 17 CRM
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.
A workshop hosted by the South African Journal of Science aimed at postgraduate students and early career researchers with little or no experience in writing and publishing journal articles.
Introduction to AI for Nonprofits with Tapp NetworkTechSoup
Dive into the world of AI! Experts Jon Hill and Tareq Monaur will guide you through AI's role in enhancing nonprofit websites and basic marketing strategies, making it easy to understand and apply.
This presentation includes basic of PCOS their pathology and treatment and also Ayurveda correlation of PCOS and Ayurvedic line of treatment mentioned in classics.
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.
1. GROWTH FACTORS AND THEIR
RECEPTORS
GUIDED BY
DR K REKHA RANI
(PROF & HOD)
PRESENTED BY
R ANIL KUMAR PG-
II
2. CONTEN
TS
Introduction
Basic terminologies
Definition
Rational for use in dentistry
Classification of growth factors
Effects of growth factors at various cell cycles
Mode of action of growth factors
Receptors for various growth factors
Common features of growth factors
Individual growth factors and their actions
Conclusion
References
3. INTRODUCTION
Periodontal diseases result in destruction of periodontal tissues,
including cementum, bone, and periodontal ligament (PDL), with
eventual tooth loss if left untreated.
Goal of all therapeutic modalities is to Restore Health of Individual.
Traditional Method……Elimination of bacterial pathogens
Modulation of host response
Arrest / Slow disease progression
4. Better understanding of the disease at the cellular and molecular
level as well as events involved in tissue development, healing and
regeneration.
Improved therapies
Arrest Of Disease Progression
Ultimate goal of periodontal therapy
- REGENERATION
5. Basic
terminologies
Repair:
Healing of a wound
by tissue that does
not fully restore the
architecture or
function of the part.
(AAP)
Regeneration
Is the growth and
differentiation of new
cells and
intercellular
substances to form
new tissues or parts.
Reattachment:
it is defined as the
reunion of epithelial
and connective
tissues with root
surfaces and bone
such as occur after
an incision or injury.
New attachment:
is the embedding of
new periodontal
ligament fibers into
new cementum and
the attachment of
the gingival
epithelium to a tooth
surface previously
denuded by disease.
6. • PERIODONTAL REGENERATION is defined as the restoration of lost
periodontium or supporting tissues and includes formation of new alveolar
bone, new cementum and new periodontal ligament.
There is a need, however, to improve the predictability of regenerative
therapies.
This need has led to increased efforts, to establish the specific cells, factors,
delivery systems, flap design, and host responses required for enhancing
outcome of regenerative therapies.
Although significant advances have been made toward understanding the
complexities involved in promoting periodontal regeneration, much remains
to be elucidated.
7. Biologic modifiers are materials or proteins and factors that have the
potential to alter the host tissue, so as to stimulate or regulate the wound
healing process.
Classic examples of biologic modifiers are growth factors.
8. DEFINITION
GROWTH FACTORS: A diverse group of polypeptides that have
important roles in regulation of growth and development of a variety
of organs. – GPT
GROWTH FACTORS: it is a general term used to denote a class of
naturally occurring proteins that function in the body to promote
mitogenesis, migration and metabolic activity. -Alan Polson
9. RATIONALE FOR USE IN DENTISTRY
Periodontal development
Disruption of ERS
Reorganization of cells
Between tooth & bone
Progenitor cells
PDL, Bone, Cementum
Periodontal regeneration
Clot formation
Granulation tissue
Progenitor cells
PDL, BONE,
CEMENTUM
Cells at site of marrow derived cells
tooth development
cell-cell & inflammatory response
cell matrix interactions (GFs &cytokines)
(GFs & cytokines)
Migration/attachment/orientation Migration/attachment/orientation
/proliferation factors / proliferation factors
Differentiation factors Differentiation factors
12. Effect of growth factors at various levels of cell cycle
The most fundamental process of tissue growth and development begins with
cell proliferation.
Cells from different tissues grow and divide at quite different rates.
Cell
proliferation
There are four main phases of cell
cycle:
• S phase (synthesis phase)
• M phase (mitotic Phase)
• G1 and G2 phase (gap phases)
• G0 phase (resting phase)
13. Cell
differentiation
Differentiation is a process by which
undifferentiated cells transform into a specific
type of cell.
Differentiation brings about structural and
functional changes in the cell which are
necessary for the formation of type of tissue,
e.g., fibroblast for periodontal ligament,
osteoblast for bone, etc.
Growth factors will stimulate or inhibit cell
differentiation, exert their effect through
receptor binding and are thus described as
regulators of the cell cycle.
Growth factors play an important role in the
regeneration of periodontal tissues to stimulate
the migration, proliferation, and differentiation
of various cells that have the capacity to
regenerate the tissues.
14. MODE OFACTION OF GROWTH FACTORS
The mode of action of the growth factor is the way the growth factor is meant
to interact with its target receptor.
Endocrine mode of action
The endocrine mode of action is depicted by hormones (contrary to the
growth factors) whereby they are secreted by one cell type and travel in the
blood stream to a distant target cell to exert their actions. Examples of
hormones having this type of action are parathyroid hormone, growth
hormone, and luteinizing hormone.
Local modes of action are more traditionally associated with the term growth
factor and involve paracrine, autocrine, juxtacrine, and intracrine modes.
15. It involves the production of the factor by one cell secreted in soluble form
outside the cell and then binding to surface receptors on the same cell to evoke
an effect.
e.g., TGF-α which is produced by and acts on epithelial cells, BMPs which are
produced by and act on osteoblastic cells
Autocrine mode of action
16. Paracrine mode of action
The growth factor is secreted by one cell in a soluble manner and binds to
receptors on the target (another) cell to evoke its effects.
e.g., PDGF and TGF, which are produced by platelets and act on target cells
such as lymphocytes and osteoblasts.
17. It is similar to the paracrine mode except that the factor produced by cell of
origin is cell surface bound and requires cell contact by the target cell to evoke
a response.
e.g., stem cell factor
Juxtacrine mode of action
18. It is similar to the autocrine mode in which the factor produced by the cell is
not secreted but acts intracellularly to facilitate the effect.
e.g., parathormone-related protein (PTHrP) in which a portion of the protein
has been shown to translocate to the nucleus to inhibit apoptosis
Intracrine mode of action
19. RECEPTORS FOR VARIOUS GROWTH FACTORS
Growth factors are natural cell products; they cannot diffuse across a cell
membrane and must act by binding to high affinity cell receptors.
For a growth factor to exert its effect, its designated receptor must be present
on the cell membrane in sufficient quantity, orientation, and functional
activity to transmit the appropriate stimuli.
Growth factor receptors can be broadly divided into two categories.
Cell surface receptors
Intracellular receptors.
Cell surface receptors commonly bind to peptide factors that are soluble in
water but not easily transported across the lipophilic cell membrane.
20. Cell surface receptors can be further divided into the following:
G-protein-linked
receptors
• Platelet-derived growth factor
• Parathormone-related protein
Receptor
tyrosine kinases
• Platelet-derived growth factor
• Insulin-like growth factors I and II
• Fibroblast growth factor
Serine threonine
receptor kinases
• Transforming growth factor β
• Bone morphogenetic proteins
21. The intracellular receptors are commonly described for steroids such as.
Vitamin D3
Estrogen
Glucocorticoids.
Steroid receptors have been seen in both the cytoplasm & the nucleus of the
target cells. Once a cell surface receptor has been bound and activated, a
series of second messengers are responsible for evoking a biologic activity.
Four main second messengers are as follows: Adenyl cyclase,
Phospholipase C, Tyrosine kinases & serine threonine receptor kinases.
Protein phosphorylation is a key component of the growth factor activity and
is responsible for mediating changes in cell proliferation and cell
differentiation which are the hallmarks of the growth factor activity.
22.
23. Common features of GFs
• Growth factors are products that are release or activated
when is necessary. This action occurs during the events
such as tissue regeneration or wound healing.
Natural cell
products:
• Except few, growth factors act locally.
Local action:
• Growth the cell membrane, they exert their activity by first
binding to high-affinity cell membrane receptors. The
capacity of cell to respond to growth factors depend on
presence of these factors.
Receptor
activity:
Regulation:
Multifunctional
activity:
Mechanism of
action:
• The production factors is tightly regulated in normal
• Polypeptide growth factors stimulate wide variety of
cellular activities, which include growth, migration,
differentiation and production of extracellular matrix.
• In some cases, GFs can stimulate the same cell that
synthesizes the molecule (autocrine stimulation) or can
affect nearby cells (paracrine stimulation)
24. Platelet-Derived Growth Factor (PDGF)
PDGF was originally purified from human platelets.
PDGF has been found to be produced by various other cells, monocytes,
megakaryocytes, vascular endothelium, smooth muscles cells, and
transformed cells (Ross et al., 1986; Raines et al., 1990).
PDGF contain two polypeptide chains forming three isoforms either as a
homodimer (AA or BB) or as a heterodimer (AB).
PDGF A and B chains are present in gingival epithelium with PDGF-A
playing an important role during early stages of wound healing while
PDGF-B appears later (Green et al., 1997).
The biologic effects of PDGF are mainly initiated via two tyrosine kinase
receptors termed alpha and beta PDGF receptors (Rosenkranz and
kazlauskas 1999) which are differentially expressed by normal and
regenerating periodontal cells indicating that PDGF is involved in complex
pattern in healing events (Parker et al., 2001).
25. Actions
of
PDGF PDGF is a chemoattractant for fibroblasts, leukocytes
and smooth muscle cells. It acts synergistically with
IGF-I, promoting protein synthesis and production of
ECM.
It has mitrogenic effects on osteogenic cells, promoting
their proliferation and migration in the healing area,
promotes synthesis of fibronectin and collagen type I, III
and V & inhibits collagenase and plasminogen activator.
PDGF upregulates the expression of angiogenic
molecule like vascular endothelial growth factor
(VEGF) and hepatocyte growth factor, and also the
proinflammatory cytokine interleukin-6, thereby
indirectly promoting periodontal regeneration.
26. Piche et al (1989) demonstrated that PDGF stimulates the proliferation of
cells from the periodontal ligament and the growth is dependent on the
phenotype of the periodontal ligament cells, osteoblastic phenotypes
proliferate much more than fibroblastic phenotypes.
Matsuda et al (1992) reported also that PDGF has a mitogenic effect on
periodontal ligament fibroblastic cells. These cells show a strong chemotactic
response to PDGF. PDGF-AB stimulates collagen synthesis and PDGF-BB
stimulates proliferation and chemotaxis.
Oates et al (1993) also demonstrated that PDGF-AA and-BB are major
mitogens for human periodontal ligament cells.
Dennison et al (1994) found that PDGF stimulates the proliferation from
periodontal ligament cells than from gingival fibroblasts.
Lynch et al. (1991) treated 13 dogs with human recombinant (rh) PDGF-BB
and IGF-I in methyl cellulose gel. Five weeks after surgery, histological
analysis demonstrated a significant increase in new bone and cementum
formation in the growth factor treated sites over that in control sites
Literature review:
27. Mc Allister et al (1995) showed that the proliferative
responses of PDGF-BB are inhibited by bradikinin in cells of
the peridontium.
Park et al. (1995) conducted a study Guided tissue
regeneration around experimentally created horizontal class
III furcation defects with and without the use of PDGF-BB
(solution) in 6 beagle dogs was studied. The authors found
that after 8 to 11 weeks there was statistically a greater
amount of bone and periodontal ligament formed in the
lesions where PDGF-BB was used in combination with GTR.
Nevins et al (2005) conducted a large-scale,
prospective, blinded, and randomized controlled clinical
trial study and demonstrated that the use of rhPDGF-BB +
β-TCP was safe and effective in the treatment of
periodontal osseous defects.
28.
29.
30.
31. Transforming Growth Factor (TGF)
The TGFs are a family of structurally and functionally unrelated proteins
that have been isolated from normal and neoplastic tissues.
The two best characterized polypeptides from this group of growth factors are
TGF-α and TGF-β.
TGF-α is a 50-aminoacid single-chain protein
with a molecular weight of approximately 5600
Da
It belongs to the epidermal growth factor (EGF)
family of cytokines. It is a mitogenic polypeptide
and secreted protein, which is expressed by
monocytes, keratinocytes, and variou, tumor
cells
EGF and TGF-α are equipotent at inducing in
vitro endothelial cell proliferation and bind
equally to endothelial cell EGF receptor.
It acts synergistically with TGF-ᵦ to stimulate
anchorage independent cell proliferation and
produce a mitogenic response.
32. TGF-ᵦ
multifunctional
structurally
related growth and
differentiation
factors associated
to the
inflammatory
response.
play an important
role in apoptosis,
angiogenesis,
wound healing
and fibrosis.
TGF-ᵦ is encoded
by three different
genes TGF-ᵦ1,
TGF-ᵦ2 and TGF-ᵦ3
,
It is secreted in an
inactive form and
is activated by
proteolysis and
low pH, which are
present during
wound healing.
It is found in
highest
concentrations in
bone and platelets.
dimeric
polypeptide with a
molecular weight
of 25,000 Da and
consists of 2
amino acid chains
linked together by
disulfide bonds.
34. Matsuda et al (1992) saw that TGF-induces inhibitory effects on mitogenic responses of
the periodontal ligament cells. It reveals no chemotactic effect on these cells, however TGF-
stimulates the collagen synthesis.
Oates et al (1993) compared the mitogenic activity of TGF- with interleukin-1 and
PDGF in fibroblast cells derived from the periodontal ligament, and saw that TGF-
is a weak mitogen compared to PDGF. They supported a role for TGF- as a regulator
of the mitogenic response to PDGF.
Dennison et al (1994) showed that TGF- and PDGF show a significantly greater
increase in proliferation of periodontal ligament cells than in gingival fibroblasts.
Selvig et al. (1994) studied the effects of topical application of a combination of IGF-II, b-
FGF and TGF- ß in a collagen sponge to treat experimentally created fenestration defects in
4 beagle dogs. Histometric analysis showed no differences in fibroblast and collagen density
between control and growth factor defects up to 14 days after surgery. Bone regeneration
was significantly greater in control than in growth factor defects.
35. Bone Morphogenetic Proteins (BMPs)
The name BMP was given in 1965 by Urist.
BMPs are a group of regulatory glycoproteins that are members of the TGF-β
superfamily.
They help in numerous cellular functions including development,
morphogenesis, cell proliferation, apoptosis and ECM synthesis.
The main action of BMPs is to commit undifferentiated pluripotent cells to
differentiate into cartilage and bone forming cells (Ripamonti and Reddi,
1994; Wozney,1992).
More than 20 BMP-related proteins have been identified, several of which
induce bone formation.
36. They act as mitogens on undifferented mesenchymal cells and osteoblast
precursor.
BMPs induce bone formation, whereas other growth factors such as TGF-ᵦ 1
and PDGF do not.
BMPs have an anabolic effect on periodontal tissue through the stimulation
of osteoblastic differentiation in human periodontal ligament (PDL) cells
(Eickholz et al., 2007).
BMP 2-12 singly initate de novo endochondral bone formation (Celeste et
al., 1990; Urist, 1965).
They induce the expression of osteoblast phenotype (i.e. increase in alkaline
phosphatase activity in bone cells).
Act as chemoattractants for mesenchymal cells and monocytes as well as
bind to extracellular matrix collagen type-IV (Paralkar et al., 1990).
Properties of BMPs
37. Role of BMPs in periodontal regeneration
• Bowers et al. (1991) found that while osteogenin (BMP-3) augments new bone and cementum
deposition around submerged teeth, it does not significantly enhance new bone or cementum
formation around non-submerged teeth. Using demineralized freeze-dried bone or allografts,
some better results have been reported.
• Sigurdsson et al., (1995) and Kinoshita et al., (1997) successfully achieved periodontal
regeneration in dogs using rhBMP-2 and a systemic carrier.
• Clinical trials using rhBMP-2 in an absorbable collagen sponge carrier (Howell et al., 1997;
Cochran et al., 2000) have yielded encouraging results with the protein and the carrier well
tolerated, locally and systemically
• Cochran LD et al(1999) studied the effects of rhBMP-2 on stimulation of bone formation
around endosseous dental implants. It was demonstrated that a bone differentiation factor
significantly stimulates bone formation in peri-implant bone defect in canine mandible. The
results also demonstrated that rhBMP-2 can be used to stimulate bone growth both around and
onto the surface of endosseous dental implants placed in sites with extended peri-implant
osseous defects.
38.
39.
40.
41.
42. Fibroblast Growth Factors (FGF)
These are family of structurally related strongly heparin binding peptides
that have been implicated in healing and regeneration.
• FGF-1 has an isoelectric range of 5.6-6.0 and a molecular
weight of approximately 15,000 Da.
• This protein functions as a modifier of endothelial cell
migration and proliferation, as well as angiogenic factor.
• FGF-1 is considered to function in several important
physiological and pathological processes, such as
embryonic development, morphogenesis, angiogenesis and
wound healing
Fibroblast growth factor-1
(FGF-1)/acidic FGF (a FGF)
• FGF-2 has an isoelectric point of approximately 9.6 and
has a molecular weight in the range of 16,000-18,000 Da.
• It has low molecular weight (LMW) and high molecular
weight (HMW) isoforms.
• LMW FGF-2 is primarily cytoplasmic and functions in an
autocrine manner, whereas HMW FGF-2 is nuclear and
exert activities through intracrine mechanism (Arese et al.,
1999).
Fibroblast growth factor-2
(FGF-2)/ basic FGF (b FGF)
43. Action of FGF
a.At
cellular
level
A competence growth factor is the one which stimulate resting cells in G0 phase to enter the cell
cycle in G1 phase.
It is found in association with the ECM in the basement membranes and is attached to hepran
sulphate, which provide protection from degradation and allows it to maintain it biological
potential.
During
wound
healing
The FGF-1, FGF-2 and keratronocyte growth factor (KGF) are primary FGFs involved in wound
healing.
They stimulate proliferation of most of the major cell type involved in wound healing including
vascular endothelial cells, fibroblasts, keratinocyte and chondrocytes.
Angiogenes
is
FGF-2 has ability to induce all steps necessary for new blood vessel formation both in vivo and in
vitro. It regulates the production of collagen type-I and laminin by PDL cells.
FGF-1 stimulates endothelial cell proliferation which enhances new blood vessel proliferation in
healing area.
Effect on
PDL cell
They have chemotactic and mitogenic effects on PDL cells.
Due to overall effects, they play vital role in periodontal regeneration.
44. Terranova et al (1989) demonstrated that b-FGF stimulates human endothelial and periodontal
ligament cell migration and proliferation, and that the combination with an attachment protein,
fibronectin, further enhances periodontal ligament cell chemotaxis.
Takayama et al (2001) The gelatinous carrier alone or the carrier containing 0.1 or 0.4%
human recombinant FGF-2 was topically applied to the defects and compared with no
treatment. Eight weeks after application, the periodontal regeneration in those defects was
analyzed. In all FGF-2-treated sites, significant periodontal regeneration was dose-
dependently observed in greater amounts than in the carrier treated or non-treated
sites.(beagle dogs).
Murakami et al (2003) study- beagle dogs in furcation defects . Twelve furcation class II bone
defects were surgically created in six beagle dogs, then recombinant bFGF (30 lg/site) +
gelatinous carrier was topically applied to the bony defects. Six weeks after application,
periodontal regeneration was analyzed. Topical application of bFGF can enhance considerable
periodontal regeneration in artificially created furcation class II bone defects of beagle dogs.
Tamura et al (2018) conducted a study on periodontal regeneration using gelatin hydrogels
incorporating basic fibroblast growth factor in intra bony defects and concluded that topical
application of bFGF/gelatin hydrogel may promote periodontal regeneration in cases of chronic
periodontitis with infrabony defects.
45.
46. Insulin-like growth factors (IGFs)
IGFs are first described in 1957 by Salmon and Daughaday (Salmon et al.,
1957).
They are family of mitogenic proteins that control growth, differentiation and
maintenance of differentiated function, in numerous tissues.
The IGF family include three ligands (insulin, IGF-I and IGF-II), their
corresponding cell surface receptors (IR, IGF-IR, and IGF-IIR), and atleast six
IGFbinding proteins (IGFBPs).
It is mainly produced by liver, smooth muscle and placenta , and are carried
in plasma as complex with a specific binding protein.
47. Insulin-like growth
factor-I (IGF-I)
IGF-I is a 70-amino acid
protein with a molecular
weight of 7649 Da and
anisoelectric point of
8.4
It has endocrine,
paracrine and autocrine
effect
It is mainly produced by
liver but virtually every
tissue is able to secrete
IGF-I for
autocrine/paracrine
purposes.
Insulin-like growth
factor-II (IGF-II)
IGF-II[also known as
multiplication
stimulating activity
(MSA)] is a 67- amino
acid neutral peptide
with a molecular weight
of 7471 Da.
IGF-II binds to IGF-II
receptor (IGF-IIR),to
IGF-IR and weakly to
insulin receptor.
. The effect of IGF-II on
metabolism of gingival
fibroblasts is still
uncertain.
48. • Play important role in fetal growth and differentiation.
• IGF-I plays important role in T-lymphocytes development and
function. It can increases the number of CD4+ CD8+ immature T-
cells, promotes T-cells survival proliferation, chemotaxis and
maturation (Tu et al., 2000).
Growthanddevelopment
• It is powerful chemoattractant of fibroblasts and it lead to
periodontal regeneration by stimulating the formation of
mesenchymal tissues including collagen, bone and cementum
(Skottner et al., 1989).
• It upregulates cementoblast mitogenesis, phenotypic gene
expression, and mineralization (Saygin et al., 2007).
Effect at cellular level
• IGF-I is an important factor involved during wound healing
because it is mitogenic for keratinocytes and a potent
chemotactic agent for vascular endothelial cells. Its levels are
increased at healing sites suggesting that its presence is requires
for adequate wound healing(Werner and Grose, 2003).
Role in wound healing
Effect on periodontal ligament cells
Actions of IGF-I
• One study demonstrated the mitogenic effects of IGF-I on
PDL fibroblastic cells and concluded that a synergistic
effect result from using a combination of PDGF-AB and
IGF-I.
49. Blom et al (1992) demonstrated that IGF-I has a mitogenic
effect on fibroblasts originating from various connective
tissues and cell lines, and that IGF-I can stimulate the DNA
synthesis of periodontal ligament fibroblasts.
Matsuda et al (1992) demonstrated that IGF-I has mitogenic
effects on periodontal ligament fibroblastic cells. They showed
that a synergistic effect results from using a combination of
PDGF-AB and IGF-I. IGF-I is chemoattractive to periodontal
ligament cells.
Rutherford et al (1992) also demonstrated that PDGF acts
synergistically with IGF-I to synthesize DNA in periodontal
ligament cells, and found that the corticosteroid
dexamethasone has the same effect as on PDGF.
Cho et al (1994) showed that IGF-I has the ability to induce
premature differentiation of periodontal ligament cells into
osteoblasts and cementoblasts after its application to lesions
and this could lead to ankylosis. IGF-I may be useful for
promoting cementogenesis and or osteogenisis.
50. EGF
The EGF is a
multifunctional
cytokine involved in a
variety of functions,
including epithelial
growth and
differentiation, and
wound healing.
In 1986, Stanley Cohen1
received the Nobel for his
work elucidating the role of
the EGF in the regulation of
cell growth and development.
The major sources of EGF are
urine and salivary glands,
although it also has been
isolated from Brunner's
glands and platelets as well
as from cerebrospinal and
amniotic fluids.
EGF stimulates DNA
synthesis and cell growth in
a large variety of cells,
including those of
epithelial, endothelial and
mesodermal origin.
However, EGF stimulates
prostaglandin production
and induces bone
resorption in cultures of
neonatal mouse calvaria.
It is found in membrane
associated and soluble
form. Both soluble and
membrane associated forms
of EGF are active. Its actions
are activated with its
attachment to epidermal
growth factor receptor (EGF-
R). The EGF-R has 3 major
regions:
1.Extracellular domain which
contains growth factor.
Hydrophobic transmembrane
domain. Cytoplasmic domain
which contains tyrosine
specific protein kinase
Epidermal growth factor (EGF)
51.
52. Vascular endothelial growth factor (VEGF)
VEGF is a potent angiogenic factor and was first described as an essential
growth factor for vascular endothelial cells. It is also known as vascular
permeability factor (VPF). Originally, it was described as endothelial cell-
specific mitogen.
Sources:
Macrophages, Platelets, Keratinocytes & Tumorcells.
VEGF is an important growth factor involved in functions such as bone
formation , hematopoiesis , wound healing, and development.
The VEGF family comprises seven members: VEGF-A, VEGF-B, VEGF-C,
VEGF-D, VEGF-E, VEGF-F, and PIGF (placenta growth factor). All members
have a common VEGF homology domain.
53. Actions:
1. VEGF-A induces angiogenesis by following mechanisms,
2. VEGF-A is chemotactic for macrophages and granulocytes.
3. VEGF-A is involved in vasodilation (indirectly by NO release).
4. VEGF-B is involved in embryonic angiogenesis.
5. VEGF-D is needed for the development of lymphatic vasculature.
6. PIGF is important for vasculogenesis
a. increased migration of endothelial cells.
b. increased mitosis of endothelial cells.
c. increased matrix metalloproteinase activity.
d. creation of blood vessel lumen.
e. creates fenestrations.
54. • Johnson RB et al 1999 speculated that VEGF may be an important factor
in the progression of gingivitis to periodontitis through its role in promoting
the expansion of the vascular network observed in inflammation.
• Pelin Guneri et al (2004) compared VEGF expression in healthy and
periodontally diseased tissues with GCF of healthy and diabetic patients.
• Their study suggested that GCF -VEGF values increased in periodontal sites
of all test groups (DM).
55. Regeneration of the periodontal tissues is a dynamic process
involving cell-to-cell and cell–extracellular matrix interactions.
Growth factors elegantly co-ordinate these interactions resulting in
wound healing and regeneration of tissues.
Combinations of PDGF and IGF have been considered attractive
candidates for regenerative therapies.
With the advent of the recombinant technique it is now possible to
provide large quantities of purified growth factors for use in invivo
studies.
CONCLUSION
56. REFERENCES
Carranza 9th Edition.
Pathologic basis of disease: Robbins & Cotrans 7th Edn
Biologic mediators of periodontal regeneration Perio 2000;1999:40-59
Biology of periodontal connective tissues: Sampath Narayanan & Mark
Bartold
Growth substances: Potential use in periodontics: Western society of
Periodontology Vol:37;3,1989.
Bone Morphogenetic proteins: Background & implications for oral
reconstruction: A review J Clin Periodontol 1997: 24; 355-365.
Dabra S, Singh P. A remarkable role of growth factors in resolving oral and
specific periodontal pathologies: A strategic review. Indian J Dent Res
2011;22:496-7.
57. • Divyanshu Jamwal, Pramod Waghmare, Amit Chaudhari, Nilima Landge and
Ketaki KanadeA review”, International Journal of Current Research. 10, (09),
73439-73444.
• Agarwal A, Singh N, Khan M, Nabi Khan SS, Sahu K, Jadhav SU. Role of
growth factors in bone regeneration. Int J Prev Clin Dent Res 2020;7:69-71.
• Mani R., Mahantesha S., Nandini T.K., Lavanya R. Growth Factors in
Periodontal Regeneration. Journal of Advanced Oral Research / May-Aug
2014 / Vol. 5 No. 2.
• Sidhu J et al. Growth factors in Periodontics. Journal of Advanced Medical
and Dental Sciences Research |Vol. 4|Issue 2| March - April 2016.
• Raja S, Byakod G, Pudakalkatti P. Growth factors in periodontal
regeneration. International journal of dental hygiene. 2009 May;7(2):82-9.
• Cochran DL, Wozney JM. Biological mediators for periodontal regeneration.
Periodontology 2000. 1999 Feb;19(1):40-58.
58. Li F, Yu F, Xu X, Li C, Huang D, Zhou X, Ye L, Zheng L. Evaluation of
recombinant human FGF-2 and PDGF-BB in periodontal regeneration: a
systematic review and meta-analysis. Scientific reports. 2017 Mar 6;7(1):65.
Vandana KL, Singh G, Prakash S, Bhushan KS, Mahajan N. Periodontal
regeneration by application of recombinant human bone morphogenetic
protein-2 in human periodontal intraosseous defects: A randomized
controlled trial. Int J Oral Health Sci 2016;6:11-7.
Cochran DL, Wozney JM. Biological mediators for periodontal regeneration.
Periodontology 2000. 1999 Feb;19(1):40-58.
Murakami S. Periodontal tissue regeneration by signaling molecule (s): what
role does basic fibroblast growth factor (FGF‐2) have in periodontal therapy?.
Periodontology 2000. 2011 Jun;56(1):188-208.
Bosshardt DD, Sculean A. Does periodontal tissue Regeneration really work?
Periodontol 2000 2009; 51: 208–219.
Mac Neil RL, Somerman MJ. Development and regeneration of the
periodontium: parallels and contrasts. Periodontol 2000 1999; 19: 8-20.
59. Caffesse RG, Quinones CR. Polypeptide growth factors and attachment
proteins in periodontal wound healing and regeneration. Periodontol 2000
1993; 1: 69-79.
Cochran DL, Wozney JM. Biological mediators for periodontal regeneration.
Periodontol 2000 1999; 19: 40-58.
Bartold PM, Narayan AS. Biology of the periodontal connective tissue. 1st ed;
Quintessence publishing; USA; 1998: 241-266.
Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant Dentistry,
5th ed; Blackwell Munksgard; Oxford; 2008:541-562.
Moore YR, Dickinson DP, Wikesjo UME. Growth/differentiation factor-5: a
candidate therapeutic agent for periodontal regeneration? A review of pre-
clinical data. J Clin Periodontol 2010; 37: 288–298.
Nevins M, Hanratty J, Lynch SE. clinical results using rhPDGF and
mineralized FDBA in periodontal defects. Int J Periodontics Restorative Dent
2007; 27: 421-427.
60. Rastogi P, Saini H, Singhal R, Dixit J. Periodontal regeneration in deep
intrabony periodontal defect using hydroxyapatite particles with platelet rich
fibrin membrane–a case report. J Oral Biol Craniofacial Res 2011; 1: 41-43.
Christgau M, Moder D, Hiller KA, Dada A, Schmitz G, Schmalz G. Growth
factors and cytokines in autologous platelet concentrate and their correlation
to periodontal regeneration outcomes. J Clin Periodontol 2006; 33: 837–845.
Growth factors. AAP Literature reviews 1999: 189-194.
Raja S, Byakod G, Pudakalkatti P. Growth factors in periodontal
regeneration. Int J Dent Hygiene 2009; 7: 82–89.
Matsuda N, Lin W-L, Kumar MI, Genco RJ. Mitogenic, chemotactic and
synthetic responses of rat periodontal ligament cells to polypeptide growth
factors invitro. J Periodontol 1992;63:515-525.
Okuda K, Kawase T, Momose M, Murata M, Saito Y, Suzuki H et al. Platelet-
rich plasma contains high levels of platelet-derived growth factor and
transforming growth factor-beta and modulates the proliferation of
periodontally related cells in vitro. J Periodontol 2003; 74: 849-857.