The gingiva provides three lines of defense against pathogens:
1. The epithelial surface acts as a mechanical and chemical barrier. Tight junctions between keratinocytes and antimicrobial peptides in epithelial layers prevent pathogen entry.
2. Components in saliva and gingival crevicular fluid (GCF) maintain tissue health and help remove debris from the sulcus. GCF is an inflammatory exudate containing enzymes, electrolytes, and host/bacterial compounds.
3. The gingival tissue mounts an innate and adaptive immune response. Langerhans cells and neutrophils present in the junctional epithelium phagocytose pathogens, while T cells and antibodies provide acquired immunity. Together,
Defense mechanisms of gingiva 4 th seminarHema Duddukuri
The document summarizes the various defense mechanisms of the gingiva. It begins by classifying the defense mechanisms into nonspecific and specific categories. The nonspecific category includes host-microbial symbiosis, tissue resistance via anatomical factors and the mucous barrier, saliva, and the gingival crevicular fluid. It then discusses each of these mechanisms in more detail, focusing on their roles, compositions, and relationships to periodontal health and disease. The document concludes by stating that despite various challenges, the gingiva remains healthy thanks to these innate defense systems.
The document discusses gingival crevicular fluid (GCF), including its history of study over 50 years, mechanisms and factors affecting its production, methods of collection, composition, and clinical significance. GCF is a serum-like fluid found in the gingival sulcus that can be assessed to provide diagnostic information about periodontal health and disease. The document outlines the anatomy of the gingival crevice and epithelium, as well as various methods that have been used to collect and analyze GCF components.
The document discusses the defense mechanisms of the gingiva that help it withstand various adverse environmental conditions. There are nonspecific and specific defense mechanisms. Nonspecific mechanisms include the anatomical structure of the gingiva, the mucous barrier formed by saliva and gingival crevicular fluid, and tissue resistance. Specific mechanisms include the host-microbial symbiosis provided by beneficial commensal bacteria and the local inflammatory response. Saliva plays an important role through its antibacterial factors such as antibodies, enzymes, and buffers that help maintain pH and protect against pathogens. The gingival crevicular fluid also acts as a permeable barrier, with its production increased during inflammation. These defense mechanisms work together to keep the
This document discusses the development of the periodontium, which includes the cementum, periodontal ligament, alveolar bone, and gingiva. It describes how the tooth germ develops from the enamel organ and dental papilla through stages of growth. Root formation is induced by Hertwig's epithelial root sheath, which regulates the development of cementum, periodontal ligament, and alveolar bone through cellular differentiation and protein signaling. The periodontium develops through reciprocal interactions between the enamel organ and dental follicle mesenchyme.
The junctional epithelium is a non-keratinized stratified squamous epithelium that forms an attachment to the tooth surface. It develops from the reduced enamel epithelium during tooth eruption. The junctional epithelium acts as a barrier against oral pathogens and allows for host defense mechanisms to reach the gingival sulcus. It has a rapid turnover rate of 4-6 days and can quickly regenerate after injury. The attachment to enamel is mediated by hemidesmosomes in the epithelial cells that are connected to the internal basal lamina on the tooth surface. Disruption of this attachment can initiate periodontal pocket formation and disease.
Gingival Crevicular Fluid (GCF/ Sulcular Fluid)Sk Aziz Ikbal
This document provides an overview of gingival crevicular fluid (GCF). It discusses the history and pioneering researchers in the field. J. Waerhaug in 1950 focused on the anatomy of the gingival sulcus and its transformation during periodontitis. GCF forms via two mechanisms - increased permeability of blood vessels or as an inflammatory exudate. The document outlines the composition of GCF, including cells, electrolytes, proteins, and metabolic products. Finally, it discusses the clinical significance of GCF and how certain components can serve as diagnostic markers for periodontal disease.
The document discusses aging changes that occur in the periodontium. Key points:
- With aging, the gingival epithelium thickens due to acanthosis. Connective tissue ridges become more prevalent in young individuals while papillae predominate in old individuals.
- The periodontal ligament has greater elastic fibers, decreased vascularity and cellular elements, and altered collagen with aging. Alveolar bone shows increased osteoporosis and irregular surfaces facing the ligament.
- Subgingival plaque in older adults contains more enteric rods and pseudomonads, and increased pathogens like P. gingivalis. Periodontitis is associated with increased risk of conditions like diabetes, coronary
The gingiva provides three lines of defense against pathogens:
1. The epithelial surface acts as a mechanical and chemical barrier. Tight junctions between keratinocytes and antimicrobial peptides in epithelial layers prevent pathogen entry.
2. Components in saliva and gingival crevicular fluid (GCF) maintain tissue health and help remove debris from the sulcus. GCF is an inflammatory exudate containing enzymes, electrolytes, and host/bacterial compounds.
3. The gingival tissue mounts an innate and adaptive immune response. Langerhans cells and neutrophils present in the junctional epithelium phagocytose pathogens, while T cells and antibodies provide acquired immunity. Together,
Defense mechanisms of gingiva 4 th seminarHema Duddukuri
The document summarizes the various defense mechanisms of the gingiva. It begins by classifying the defense mechanisms into nonspecific and specific categories. The nonspecific category includes host-microbial symbiosis, tissue resistance via anatomical factors and the mucous barrier, saliva, and the gingival crevicular fluid. It then discusses each of these mechanisms in more detail, focusing on their roles, compositions, and relationships to periodontal health and disease. The document concludes by stating that despite various challenges, the gingiva remains healthy thanks to these innate defense systems.
The document discusses gingival crevicular fluid (GCF), including its history of study over 50 years, mechanisms and factors affecting its production, methods of collection, composition, and clinical significance. GCF is a serum-like fluid found in the gingival sulcus that can be assessed to provide diagnostic information about periodontal health and disease. The document outlines the anatomy of the gingival crevice and epithelium, as well as various methods that have been used to collect and analyze GCF components.
The document discusses the defense mechanisms of the gingiva that help it withstand various adverse environmental conditions. There are nonspecific and specific defense mechanisms. Nonspecific mechanisms include the anatomical structure of the gingiva, the mucous barrier formed by saliva and gingival crevicular fluid, and tissue resistance. Specific mechanisms include the host-microbial symbiosis provided by beneficial commensal bacteria and the local inflammatory response. Saliva plays an important role through its antibacterial factors such as antibodies, enzymes, and buffers that help maintain pH and protect against pathogens. The gingival crevicular fluid also acts as a permeable barrier, with its production increased during inflammation. These defense mechanisms work together to keep the
This document discusses the development of the periodontium, which includes the cementum, periodontal ligament, alveolar bone, and gingiva. It describes how the tooth germ develops from the enamel organ and dental papilla through stages of growth. Root formation is induced by Hertwig's epithelial root sheath, which regulates the development of cementum, periodontal ligament, and alveolar bone through cellular differentiation and protein signaling. The periodontium develops through reciprocal interactions between the enamel organ and dental follicle mesenchyme.
The junctional epithelium is a non-keratinized stratified squamous epithelium that forms an attachment to the tooth surface. It develops from the reduced enamel epithelium during tooth eruption. The junctional epithelium acts as a barrier against oral pathogens and allows for host defense mechanisms to reach the gingival sulcus. It has a rapid turnover rate of 4-6 days and can quickly regenerate after injury. The attachment to enamel is mediated by hemidesmosomes in the epithelial cells that are connected to the internal basal lamina on the tooth surface. Disruption of this attachment can initiate periodontal pocket formation and disease.
Gingival Crevicular Fluid (GCF/ Sulcular Fluid)Sk Aziz Ikbal
This document provides an overview of gingival crevicular fluid (GCF). It discusses the history and pioneering researchers in the field. J. Waerhaug in 1950 focused on the anatomy of the gingival sulcus and its transformation during periodontitis. GCF forms via two mechanisms - increased permeability of blood vessels or as an inflammatory exudate. The document outlines the composition of GCF, including cells, electrolytes, proteins, and metabolic products. Finally, it discusses the clinical significance of GCF and how certain components can serve as diagnostic markers for periodontal disease.
The document discusses aging changes that occur in the periodontium. Key points:
- With aging, the gingival epithelium thickens due to acanthosis. Connective tissue ridges become more prevalent in young individuals while papillae predominate in old individuals.
- The periodontal ligament has greater elastic fibers, decreased vascularity and cellular elements, and altered collagen with aging. Alveolar bone shows increased osteoporosis and irregular surfaces facing the ligament.
- Subgingival plaque in older adults contains more enteric rods and pseudomonads, and increased pathogens like P. gingivalis. Periodontitis is associated with increased risk of conditions like diabetes, coronary
A presentation on the topic of microscopic section of gingiva. This topic is mostly looked on by periodontists. A very important chapter in the speciality in dentistry of periodontology and implantology department. Basic understanding of microscopic features and clinical features of gingiva is an important topic for post graduate as well as undergraduate students in the dental field.
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.
The defense mechanism of gingiva includes GCF, Saliva, epithelial barrier and connective tissue cells. All these protect the periodontium from bacterial invasion.
This document provides an overview of gingival crevicular fluid (GCF), including its historical background, formation, factors affecting flow, permeability of gingival epithelia, methods of collection and estimating volume, typical amount collected, composition, clinical significance, and use of GCF as a biomarker. GCF is the fluid found in the gingival sulcus/crevice and contains cells, electrolytes, enzymes, and other molecules that make it useful for analyzing periodontal health and drug levels in the gingiva. The document discusses various techniques for collecting GCF and analyzing its components to gain clinical insights.
This document provides an overview of viruses and their role in periodontal disease. It begins with definitions of viruses and their classification. It then discusses the structure and life cycle of viruses, how the host responds to viral infections, and specific viruses implicated in periodontal disease like herpes viruses and HIV. The document proposes a model where herpes virus activation in the gingiva can enhance the pathogenic potential of bacteria and contribute to periodontal tissue destruction over time, especially in immunosuppressed individuals. It reviews evidence that herpes viral DNA is detected more frequently in gingival tissue and crevicular fluid from periodontally diseased sites compared to healthy sites.
Host microbial interaction in periodontal diseaseAnushri Gupta
Bacterial Evasion of Host Defense Mechanisms
Immunological Aspects of Microbial Host Interaction
Connective Tissue Alterations:Tissue Destruction in Periodontitis
BONE RESORPTION
Gingival crevicular fluid (GCF) is a serum exudate found in the gingival sulcus. It forms due to an increase in capillary permeability and the osmotic gradient that causes interstitial fluid to accumulate in the sulcus. GCF contains substances from serum, leukocytes, periodontal tissues, and bacteria that can indicate periodontal disease status. It is collected using absorbent paper strips, threads, micropipettes, or lavage to analyze volume and composition. Elevated levels of enzymes, microbes, and metabolic products in GCF have been associated with periodontal tissue destruction.
1. The junctional epithelium is a specialized non-keratinized stratified squamous epithelium that attaches to the tooth surface and forms a collar around the cervical portion.
2. It develops from the reduced enamel epithelium during tooth eruption. The reduced enamel epithelium fuses with the oral epithelium and transforms into the junctional epithelium.
3. The junctional epithelium attaches firmly to the tooth surface through hemidesmosomes of the basal cells (called DAT cells) and an internal basal lamina. This structure is called the epithelial attachment apparatus.
A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
Gingival crevicular fluid (GCF) is a serum transudate that forms in the gingival sulcus. It contains cells, bacteria, serum components, and host mediators that make it useful for periodontal monitoring and diagnosis. GCF forms through increased permeability of blood vessels in the sulcus or through an osmotic gradient. Its composition varies in health and disease, making biomarkers of host enzymes, tissue breakdown products, and inflammatory mediators clinically significant. While non-invasive collection methods exist, contamination and variable recovery pose challenges. Further research on GCF components may aid in diagnosis and monitoring of periodontal disease progression and treatment outcomes.
Periodontal wound healing involves four overlapping phases - exudative, resorptive, proliferative, and regenerative. The proliferative phase includes re-epithelialization, fibroplasia, granulation tissue formation, collagen deposition, angiogenesis, and wound contraction. Growth factors play an important role in regulating periodontal wound healing. Healing after periodontal procedures like scaling and root planing, curettage, ultrasonic curettage, and gingivectomy depends on the extent of tissue disruption and follows a timeline of inflammatory response, epithelial migration, granulation tissue formation, collagen deposition and remodeling.
The document summarizes the development of the periodontium. It discusses how the dental follicle derived from neural crest cells gives rise to cementum, periodontal ligament fibroblasts, and alveolar bone. It also describes the development of the individual tissues - how cementum and periodontal ligament fibers form along the developing root surface, how the gingiva and junctional epithelium develop during tooth eruption, and how alveolar bone develops from the dental follicle to support the tooth socket. The periodontium develops as an integrated unit with interactions between tissues to provide structural support for teeth.
Blood supply,nerve supply and lymphatic drainage of the periodontium finalDr. Neha Pritam
The document discusses the blood supply, nerve supply, and lymphatic drainage of the periodontium. It states that the periodontium receives its blood supply from branches of the internal maxillary artery and its lymphatic drainage involves drainage to local lymph nodes. It also describes the rich nerve supply to the periodontium derived from the trigeminal nerve and its branches. Changes in microcirculation and lymphangiogenesis occur in the periodontium during periodontal disease.
Vitamin E is a fat-soluble vitamin that is naturally occurring antioxidant. It prevents non-enzymatic oxidation of cell components by molecular oxygen and free radicals. This protects cell membrane structure and integrity. Vitamin E works with other antioxidants like vitamins A and C to delay cataract development and protect against heart disease. Deficiency can cause sterility, muscular problems, and blood cell issues while toxicity is rare.
Porphyromonas gingivalis is a gram-negative, anaerobic bacteria that is a major pathogen in periodontal disease. It has several virulence factors that contribute to its role in periodontitis, including a capsule that aids evasion of the immune system, fimbriae that mediate adhesion, and gingipains which are proteolytic enzymes that degrade host proteins and modulate the immune response. P. gingivalis inhabits the gingival crevice and has been strongly associated with progressive bone and tissue destruction in periodontitis. Treatment of periodontal disease can reduce but may not eliminate P. gingivalis from the oral cavity.
JUNCTIONAL EPITHELIUM IN HEALTH & DISEASE-- REGENERATION FOLLOWING SURGERYDr Antarleena Sengupta
This document provides an overview of junctional epithelium, including its structure, development, functions, and clinical significance. Some key points:
- Junctional epithelium forms a collar around the tooth and attaches the gingiva. It is derived from reduced enamel epithelium during tooth development.
- It has a stratified squamous non-keratinizing structure and rapidly turns over cells. The innermost layer of cells directly attach to the tooth surface.
- It plays roles in passive eruption of teeth, acts as a barrier in gingivitis, and its conversion to pocket epithelium is a hallmark of periodontitis development. Loss of its attachment can lead to pocket formation and inflammation.
Porphyromonas gingivalis is a gram-negative, anaerobic bacterium implicated as a primary pathogen in periodontal disease. It produces several virulence factors that allow it to invade tissues, evade the host immune system, and cause damage. These include proteolytic enzymes, lipopolysaccharide, capsular polysaccharides, fimbriae, and outer membrane proteins. Fimbriae aid in adhesion to host cells, while enzymes degrade host proteins and tissues. Capsular polysaccharides and outer membrane structures help resist phagocytosis. P. gingivalis is strongly associated with periodontitis and its virulence factors contribute directly to tissue destruction and immune evasion during infection.
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.
DEFENSE MECHANISM OF GINGIVA-DR JEEVANAND DESHMUKH.pptxDentalYoutube
The document summarizes the defensive mechanisms of gingiva. It discusses four key components: the epithelial surface, gingival crevicular fluid, the initial stages of inflammatory response, and saliva. Regarding the epithelial surface, it describes the junctional epithelium and its role in forming a protective barrier against plaque bacteria while allowing access of immune cells and components. It also notes enzymes and antimicrobial substances produced by junctional epithelial cells. The document then reviews the composition and functions of gingival crevicular fluid, including its role in flushing out bacteria and transporting antibodies and immune cells. It lists several enzymes found in gingival crevicular fluid and their sources and functions. Finally, it briefly mentions
The document discusses the defense mechanisms of the periodontium. It describes the innate and adaptive defense systems. The innate system includes bacterial balance, surface integrity, surface fluids like GCF and saliva, phagocytosis, and the inflammatory response. The adaptive system involves cell-mediated and humoral immunity. Key components that provide protection include the junctional epithelium barrier, antimicrobial peptides and cytokines in GCF, lysozymes and antibodies in saliva, and phagocytic cells like neutrophils and macrophages. Together, these multilayered defenses effectively counter the bacterial challenges in the oral cavity.
A presentation on the topic of microscopic section of gingiva. This topic is mostly looked on by periodontists. A very important chapter in the speciality in dentistry of periodontology and implantology department. Basic understanding of microscopic features and clinical features of gingiva is an important topic for post graduate as well as undergraduate students in the dental field.
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.
The defense mechanism of gingiva includes GCF, Saliva, epithelial barrier and connective tissue cells. All these protect the periodontium from bacterial invasion.
This document provides an overview of gingival crevicular fluid (GCF), including its historical background, formation, factors affecting flow, permeability of gingival epithelia, methods of collection and estimating volume, typical amount collected, composition, clinical significance, and use of GCF as a biomarker. GCF is the fluid found in the gingival sulcus/crevice and contains cells, electrolytes, enzymes, and other molecules that make it useful for analyzing periodontal health and drug levels in the gingiva. The document discusses various techniques for collecting GCF and analyzing its components to gain clinical insights.
This document provides an overview of viruses and their role in periodontal disease. It begins with definitions of viruses and their classification. It then discusses the structure and life cycle of viruses, how the host responds to viral infections, and specific viruses implicated in periodontal disease like herpes viruses and HIV. The document proposes a model where herpes virus activation in the gingiva can enhance the pathogenic potential of bacteria and contribute to periodontal tissue destruction over time, especially in immunosuppressed individuals. It reviews evidence that herpes viral DNA is detected more frequently in gingival tissue and crevicular fluid from periodontally diseased sites compared to healthy sites.
Host microbial interaction in periodontal diseaseAnushri Gupta
Bacterial Evasion of Host Defense Mechanisms
Immunological Aspects of Microbial Host Interaction
Connective Tissue Alterations:Tissue Destruction in Periodontitis
BONE RESORPTION
Gingival crevicular fluid (GCF) is a serum exudate found in the gingival sulcus. It forms due to an increase in capillary permeability and the osmotic gradient that causes interstitial fluid to accumulate in the sulcus. GCF contains substances from serum, leukocytes, periodontal tissues, and bacteria that can indicate periodontal disease status. It is collected using absorbent paper strips, threads, micropipettes, or lavage to analyze volume and composition. Elevated levels of enzymes, microbes, and metabolic products in GCF have been associated with periodontal tissue destruction.
1. The junctional epithelium is a specialized non-keratinized stratified squamous epithelium that attaches to the tooth surface and forms a collar around the cervical portion.
2. It develops from the reduced enamel epithelium during tooth eruption. The reduced enamel epithelium fuses with the oral epithelium and transforms into the junctional epithelium.
3. The junctional epithelium attaches firmly to the tooth surface through hemidesmosomes of the basal cells (called DAT cells) and an internal basal lamina. This structure is called the epithelial attachment apparatus.
A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
Gingival crevicular fluid (GCF) is a serum transudate that forms in the gingival sulcus. It contains cells, bacteria, serum components, and host mediators that make it useful for periodontal monitoring and diagnosis. GCF forms through increased permeability of blood vessels in the sulcus or through an osmotic gradient. Its composition varies in health and disease, making biomarkers of host enzymes, tissue breakdown products, and inflammatory mediators clinically significant. While non-invasive collection methods exist, contamination and variable recovery pose challenges. Further research on GCF components may aid in diagnosis and monitoring of periodontal disease progression and treatment outcomes.
Periodontal wound healing involves four overlapping phases - exudative, resorptive, proliferative, and regenerative. The proliferative phase includes re-epithelialization, fibroplasia, granulation tissue formation, collagen deposition, angiogenesis, and wound contraction. Growth factors play an important role in regulating periodontal wound healing. Healing after periodontal procedures like scaling and root planing, curettage, ultrasonic curettage, and gingivectomy depends on the extent of tissue disruption and follows a timeline of inflammatory response, epithelial migration, granulation tissue formation, collagen deposition and remodeling.
The document summarizes the development of the periodontium. It discusses how the dental follicle derived from neural crest cells gives rise to cementum, periodontal ligament fibroblasts, and alveolar bone. It also describes the development of the individual tissues - how cementum and periodontal ligament fibers form along the developing root surface, how the gingiva and junctional epithelium develop during tooth eruption, and how alveolar bone develops from the dental follicle to support the tooth socket. The periodontium develops as an integrated unit with interactions between tissues to provide structural support for teeth.
Blood supply,nerve supply and lymphatic drainage of the periodontium finalDr. Neha Pritam
The document discusses the blood supply, nerve supply, and lymphatic drainage of the periodontium. It states that the periodontium receives its blood supply from branches of the internal maxillary artery and its lymphatic drainage involves drainage to local lymph nodes. It also describes the rich nerve supply to the periodontium derived from the trigeminal nerve and its branches. Changes in microcirculation and lymphangiogenesis occur in the periodontium during periodontal disease.
Vitamin E is a fat-soluble vitamin that is naturally occurring antioxidant. It prevents non-enzymatic oxidation of cell components by molecular oxygen and free radicals. This protects cell membrane structure and integrity. Vitamin E works with other antioxidants like vitamins A and C to delay cataract development and protect against heart disease. Deficiency can cause sterility, muscular problems, and blood cell issues while toxicity is rare.
Porphyromonas gingivalis is a gram-negative, anaerobic bacteria that is a major pathogen in periodontal disease. It has several virulence factors that contribute to its role in periodontitis, including a capsule that aids evasion of the immune system, fimbriae that mediate adhesion, and gingipains which are proteolytic enzymes that degrade host proteins and modulate the immune response. P. gingivalis inhabits the gingival crevice and has been strongly associated with progressive bone and tissue destruction in periodontitis. Treatment of periodontal disease can reduce but may not eliminate P. gingivalis from the oral cavity.
JUNCTIONAL EPITHELIUM IN HEALTH & DISEASE-- REGENERATION FOLLOWING SURGERYDr Antarleena Sengupta
This document provides an overview of junctional epithelium, including its structure, development, functions, and clinical significance. Some key points:
- Junctional epithelium forms a collar around the tooth and attaches the gingiva. It is derived from reduced enamel epithelium during tooth development.
- It has a stratified squamous non-keratinizing structure and rapidly turns over cells. The innermost layer of cells directly attach to the tooth surface.
- It plays roles in passive eruption of teeth, acts as a barrier in gingivitis, and its conversion to pocket epithelium is a hallmark of periodontitis development. Loss of its attachment can lead to pocket formation and inflammation.
Porphyromonas gingivalis is a gram-negative, anaerobic bacterium implicated as a primary pathogen in periodontal disease. It produces several virulence factors that allow it to invade tissues, evade the host immune system, and cause damage. These include proteolytic enzymes, lipopolysaccharide, capsular polysaccharides, fimbriae, and outer membrane proteins. Fimbriae aid in adhesion to host cells, while enzymes degrade host proteins and tissues. Capsular polysaccharides and outer membrane structures help resist phagocytosis. P. gingivalis is strongly associated with periodontitis and its virulence factors contribute directly to tissue destruction and immune evasion during infection.
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.
DEFENSE MECHANISM OF GINGIVA-DR JEEVANAND DESHMUKH.pptxDentalYoutube
The document summarizes the defensive mechanisms of gingiva. It discusses four key components: the epithelial surface, gingival crevicular fluid, the initial stages of inflammatory response, and saliva. Regarding the epithelial surface, it describes the junctional epithelium and its role in forming a protective barrier against plaque bacteria while allowing access of immune cells and components. It also notes enzymes and antimicrobial substances produced by junctional epithelial cells. The document then reviews the composition and functions of gingival crevicular fluid, including its role in flushing out bacteria and transporting antibodies and immune cells. It lists several enzymes found in gingival crevicular fluid and their sources and functions. Finally, it briefly mentions
The document discusses the defense mechanisms of the periodontium. It describes the innate and adaptive defense systems. The innate system includes bacterial balance, surface integrity, surface fluids like GCF and saliva, phagocytosis, and the inflammatory response. The adaptive system involves cell-mediated and humoral immunity. Key components that provide protection include the junctional epithelium barrier, antimicrobial peptides and cytokines in GCF, lysozymes and antibodies in saliva, and phagocytic cells like neutrophils and macrophages. Together, these multilayered defenses effectively counter the bacterial challenges in the oral cavity.
Mechanisms of periodontal disease productionTago33347
Bacteria are the primary cause of periodontal disease. To cause damage, bacteria must colonize the gingival crevice, damage the epithelial barrier, and produce substances that cause tissue damage. Key pathogens like Porphyromonas gingivalis produce proteases and other enzymes that degrade collagen and bone, as well as evade host defenses. The immune response also contributes to tissue degradation through the release of cytokines and enzymes from cells like neutrophils and macrophages. Osteoclasts are the main bone resorbing cells, and are activated by factors from bacteria and host tissues to break down bone.
This document provides an overview of host modulation therapy for the treatment of periodontitis. It begins with definitions of key terms and a brief history of the development of the concept of host modulation. The pathogenesis of periodontitis and the host response are then described, focusing on the roles of inflammatory mediators like prostaglandins and matrix metalloproteinases in tissue destruction. The remainder of the document discusses various agents that can be used for host modulation therapy, including NSAIDs, tetracyclines, bisphosphonates, and their mechanisms of action in modulating the host response to reduce periodontal tissue breakdown.
The document discusses the components of the innate immune system. It describes the physical, chemical, biological, and physiological barriers that block pathogens from entering the body. It also explains the cellular responses involving phagocytes that destroy pathogens through phagocytosis. The complement system and inflammatory response are blood proteins and processes that help eliminate pathogens. Key cells of innate immunity discussed are neutrophils, macrophages, dendritic cells, and natural killer cells.
The concise lecture briefly shadows on the functions of saliva placing emphasis on salivary proteins, their function and the acquired pellicle.
Dr Muhammad Danial Khalid
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
This document discusses host modulation therapy for the treatment of periodontitis. It begins with definitions of key terms like host and modulation. It then discusses the history and pathogenesis of periodontitis, focusing on the role of the host immune response. The document outlines several agents used in host modulation therapy, including NSAIDs, which inhibit prostaglandins; agents that block matrix metalloproteinases like tetracycline; and inhibitors of cytokines. It provides details on the mechanisms and effects of these therapeutic agents, with the overall goal of host modulation therapy being to reduce tissue destruction and promote periodontal healing by modulating the harmful aspects of the host immune response.
This document summarizes the major salivary enzymes and their functions. It begins by outlining the chronological discovery of salivary components starting in the 1950s. It then describes the current understanding of salivary proteins' structure-function relationships and conformational requirements. The document discusses the expected network action of the salivary defense system and lists the five primary defense networks involving proteins that agglutinate bacteria, lyse bacterial membranes, and have antifungal and antiviral properties. Finally, it provides details on specific salivary components like defensins, histatins, lactoferrin, and lysozymes that have antimicrobial functions.
The document discusses secondary lymphoid organs in teleost fish. It describes how secondary lymphoid organs like the spleen, gut-associated lymphoid tissue (GALT), gill-associated lymphoid tissue (GIALT), mucosa-associated lymphoid tissue (MALT), and skin-associated lymphoid tissue (SALT) allow for antigen contact, lymphocyte proliferation, and generation of effector and regulatory immune cells. It provides details on the structure and immune functions of the spleen, which contains red and white pulp, ellipsoids, and melanomacrophages that trap antigens and initiate immune responses.
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.
This document summarizes key concepts in periodontal regeneration and tissue engineering. It discusses the appropriate cell types and signals needed for periodontal regeneration, including epithelial cells, fibroblasts, and osteoblasts. Scaffolds provide structure for cell attachment, proliferation and differentiation. Growth factors like BMPs, IGFs, FGFs, and TGF-β play important roles in cell differentiation and bone regeneration. Vascularization is also important to provide nutrients and remove waste. Tissue engineering aims to recreate tissues using the principles of cells, signaling molecules, and biomaterial scaffolds.
The document discusses the key differences between the cell wall and cell membrane in bacteria. The cell wall is the outermost rigid layer composed of peptidoglycan that surrounds the cell membrane. It provides shape and structural integrity to the cell. The inner cell membrane is a fluid phospholipid bilayer that regulates the passage of substances in and out of the cell and helps maintain the cell's potential. It is also the site of many metabolic processes.
The document summarizes key components of the innate immune system. It describes anatomical barriers like skin and mucous membranes that provide a first line of defense. It also outlines physiological barriers such as complement proteins and cytokines that help recruit immune cells. Cellular innate immune cells are discussed including neutrophils, macrophages, and natural killer cells that help eliminate pathogens. The mechanisms of phagocytosis and intracellular killing are summarized including both oxygen-dependent and independent pathways.
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.
A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
Prokaryotic cells lack membrane-bound organelles and have a cytoplasm containing ribosomes, plasmids, and a single circular chromosome. Ribosomes in prokaryotes are smaller than in eukaryotes and differ in composition. Some bacteria contain capsules or slimy glycoalyx layers that help with adhesion and pathogenicity. Flagella and fimbriae aid in motility and adhesion. Spores are resistant structures some bacteria form during unfavorable conditions. Bacteria metabolize nutrients extracellularly and use cellular respiration or fermentation to generate energy.
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the seminar gives a complete analysis of etilogy and pathogenesis involved in digo as well as sequlae of it
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8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
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Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Kat...rightmanforbloodline
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
2. Contents
• Introduction
• Role of epithelium in defense mechanism of gingiva (Structural and
functional aspects)
• Role of gingival crevicular fluid (GCF) in defence mechanism of
gingiva
– Definition
– Composition of GCF
3. – Origin & Function of the cellular components
– Proteolytic host cell enzymes in GCF
– Enzymes from periodontal pathogens
• Role of Leukocytes in Gingival defence
• SALIVA
– Antibacterial Factors
– Salivary antibodies
– Salivary buffers and coagulation factors
– Salivary leukocytes
4. Introduction
• The teeth, the gingival masticatory mucosa,
create a unique environmental challenge
to the protective continuity of gingiva.
• At the interface where the healthy gingiva
meets the tooth surface the structural
continuity is secured by the epithelium .
5. • At the dentogingival junction the micro-organisms form complex
ecological systems that adhere to glycoprotein layer on solid and non-
shedding surfaces and are called as biofilms.
• Since a biofilm is quickly formed on exposed tooth surfaces, the tissue in
the vicinity of this biofilm is constantly challenged.
• Such aggravating external circumstances call for a specialized structural
and functional adaptation for the defence mechanism of gingiva.
6. • Apart from bacterial aggressions gingiva is constantly subjected to
mechanical agressions as well.
• Thus gingiva prepares and protects itself through the fine tuning of
homeostasis. (Kornman W)
• Defence mechanism of gingiva includes four vital components
• epithelial surface
• gingival crevicular fluid
• the initial stages of inflammatory response and
• saliva
7. EPITHELIUM
• Epithelia -first line of defence
• It exhibit considerable differences in histology, thickness and
differentiation suitable for the functional demands of their location.
• The epithelial component of gingiva shows morphologic variations as oral
epithelium, sulcular epithelium and junctional epithelium
8. Possible protective role of the oral epithelium
• An intact epithelial barrier of the gingival, sulcular, and junctional
epithelia under normal conditions is an effective barrier against penetration
of bacterial components and metabolites.
• There is a high turnover rate
replacement of cells and tissue components that are damaged by the
microbial challenge.
removal of bacteria that have colonized the cellular surface and
regeneration of an intact epithelial barrier.
In addition, cells of the oral epithelium contain lysosomes and can exhibit
limited phagocytic activity.
9. • Junctional epithelium (JE) consists of active populations of cells and
antimicrobial functions, which together form the first line of defense
against microbial invasion into tissue .
• Exhibits several unique structural and functional features-:
I. Rapid cell divison
II. Funnelling of JE towards the sulcus (contributes to the flow of epithelial
cells (Schroeder HE,1979) )
III. Internal basal lamina an effective barrier (laminin)
IV. Anti microbial substance by JE cells. (ICAM 1, defensins)
V. Cytokines (IL-8, IL 1 α,IL 1β,TNF )
(Bartold, 2000)
10. i. Contains proteolytic enzymes- Matrix metalloproteinases(MMP)
(Salonen J, 1991).
• Gelatinase B (MMP-9) is one of the most abundant MMPs- degrade type
IV collagen.
• Collagenase-3 (MMP-13) - collagenase-3 degrades collagens type I, III and
IV as well as fibronectin and some proteoglycan this enzyme seems to play
an important role in invasion of periodontal connective tissue.
• Gelatinase A (MMP-2)- in inflamed pocket epithelium and to be important
in epithelial cell migration (Mäkelä M,1991).
11. • Matrilysin (MMP-7) is another epithelial MMP with a broad spectrum of
substrates. It can degrade fibronectin, laminin, type IV collagen, gelatin and
proteoglycan core proteins.
• Matrilysin is expressed only in the suprabasal cells of JE facing the teeth
and in epithelial cell rests of Malassez.
ii. Other serine proteinases include
Lysosomal cysteine
aspartic acid proteinases
Cathepsin D.
Cathepsin C (dipeptidyl aminopeptidase) is an enzyme important in the
intracellular degradation of proteins and activation of serine proteinases
critical to inflammatory responses.
12. iii. Tissue plasminogen activator (t-PA) (Schmid et al.,1991) and its inhibitor
Plasminogen activator inhibitor (Lindberg et al., 2001) have been
detected in the junctional epithelium.
• Tissue plasminogen activator and urokinase is a serine protease which
converts plasminogen to plasmin.
• Plasmin degrades many extracellular matrix proteins and activates many
matrix metalloproteinases (MMPs)-collagenases and mediators of
complement system.
13. iv. Enzyme-rich lysosomes.-Lysosomal bodies are found in large numbers in
the JE, containing enzymes which participate in the eradication of the
bacteria (Langer and Schroeder, 1971).
eg. cysteine proteinases (cathepsin B and H)
neutral proteinases
chymotrypsin-like proteinase . (cathepsin A)
v. Antigen presenting cells, langerhans cells and dendritic cells are also
present(Juhl et al., 1988)
14. • PMNs - central region of the JE and near the tooth surface, intercellular
spaces.
• lymphocytes and macrophages in and near the basal cell layer
• mononuclear leukocytes in intercellular spaces.
vi. The fluid filled intercellular spaces may vary in width, but are wider in
comparison to oral gingival and sulcular epithelium (Schroeder 1970)-
remarkable permeability.
15. • The intercellular spaces of the junctional epithelium provide a pathway for
fluid and transmitting leukocytes. .. represent a host defence system against
the bacterial challenge.
• These spaces are approximately 2–5% of the junctional epithelial volume in
normal conditions and are infiltrated by small numbers of neutrophils,
mononuclear cells and lymphocytes.
• However, during periods of inflammation, these intracellular spaces are
found to contain abundant migrating leukocytes.
16. • In addition, the large intercellular spaces of the junctional epithelium can
be distended and act as reservoirs for the GCF.
• This can prevent the penetration of bacteria into the epithelium and can act
as a diffusion barrier.
• It also functions as a diffusion pathway for the GCF and its components –
such as chemotactic agents, antibodies, complement components and other
host-derived enzymes, and provides them with an entry into sulcus.
• However, under periods of prolonged exposure to bacterial plaque and the
amplification of the inflammatory response, the protective function of the
junctional epithelium starts to erode and the large intercellular spaces allow
the passage of bacteria and their by-products into the host tissues.
17. To summarize
• Junctional epithelium is firmly attached to tooth surface forming an epithelial
barrier against plaque bacteria.
• It allows access of gingival fluid, inflammatory cells and components of
immunologic host defense to gingival margin.
• Cells exhibit rapid turnover, which contributes to host-parasite equilibrium and
rapid repair of damaged tissue.
• Also cells of junctional epithelium have an endocytic capacity equal to that of
macrophages and neutrophils, and this activity may be protective in nature.
(Cho MI, 2000)
18. GCF
• “GCF is an exudate of varying composition found in the sulcus/periodontal
pocket between the tooth and marginal gingiva.”
(Cimasoni G (1983), Embery G(1994))
19. • The studies of Brill ,1958, 1959,1969 postulated that
GCF was an important component of the protective mechanisms of the
crevicular region.
This concept was supported by the flushing effect of GCF
The important role that GCF may have in transporting antibacterial
substances, either of host origin or those introduced into the circulation
such as antibiotics, to the crevicular space was appreciated.
He concluded that stimulation of the gingival margin was important for the
maintenance of gingival health.
23. Alkaline phosphatase
• ALP is a calcium- and phosphate-binding protein and a phosphor-
hydrolytic enzyme. (Bezerra AA, 2010)
• It is a membrane-bound glycoprotein produced by many cells such as
polymorphonuclear leukocytes (PMNLs), osteoblasts, macrophages, and
fibroblasts within the area of the periodontium and gingival crevice.
• This intracellular enzymes are released increasingly from the injured,
damaged cells or dead cells of periodontal tissues into the gingival
crevicular fluid (GCF) and saliva.
(Daltaban O,2006)
24. • Could also be released from bacterial cells.
• ALP is considered to be an important indicator of bone formation and is a
phenotypic marker for osteoblast cells.
• The pH optimum for alkaline phosphatase activity is 9.0. (Mobley DN,
1984)
25. Acid phosphatase
• Acid phosphatase a lysosomal enzyme, used to free attached phosphoryl
groups from other molecules seein in polymorphonuclear leukocytes (PMNLs),
fibroblasts and has high activity in bone resorbing cells such as Osteoclast and
macrophages. (Yajima, 1986)
• Acid phosphatase is stored in lysosomes and functions when these fuse
with endosomes, which are acidified while they function; therefore, it has an
acid pH optimum. (Henneberry, 1969).
• Seen in Odland bodies.
• The pH optimum for acid phosphatase activity is 4.8-5.8. (Mobley DN, 1984)
26. Cathepsin
• It Is a serine endopeptidase contained in the azurophil granules of human
PMNs.
• Also called chymotrypsin like, because it attacks a number of synthetic
substrates typical for chymotrypsin and is inhibited by the same inhibitors.
• It has an optimum pH of 7.5 and a molecular weight of about 20,000.
• This Enzyme has been shown to hydrolyze hemoglobin and fibrinogen,
casein and collagen. (Starkey PM, 1976)
27. Elastase
• Elastase is a serine endopeptidase that can degrade both collagneous and
non collagenous extra cellular matrix proteins.
• It is released at sites of inflammation.
• The levels of this enzyme in GCF have been noted to increased with
development of gingivitis as well at sites of established periodontitis.
• In addition, the levels of neutrophil elastase have been found to decrease
following treatment of affected periodontal sites. (Meyle J, 1992)
• Longitudinal studies have indicated that GCF levels of neutrophil elastase
have some of further breakdown.
28. Cellular Elements
• Cellular elements found in GCF include
-Bacteria : Despite having constitution similar to the neighbouring plaque,
the actual number of bacteria isolated from GCF do not increase with
increasing plaqueaccumulation.
- Desquamated epithelial cells
- Erythrocytes
- Leukocytes
29. Leukocytes
• Leukocytes are detected in both clinically healthy and diseased tissues.
(Attstrom et al., 1970).
• In 1960, Sharry & Krasse determined -
-47% of all cells obtained from the gingival sulcus were leukocyte
-major route of entry into the oral cavity was via the gingival sulcus.
30. • PMN cells are found in the
-intercellular spaces of JE
-along the tooth surface - Adjacent to plaque
-base of the sulcus > coronally
• Attström et al, 1970 - one of the first study (gingival sulcus)
• Differential count of 95–97% neutrophils
1–2% lymphocytes
2–3% macrophages cells.
31. • Wilton et al. 1976 focused predominately on the populations of
leukocytes, and established that of 8.8% of total mononuclear
18% - macrophages
24% were T lymphocytes
58% were B lymphocytes.
T-cell : B-cell ratio of 1: 2.7 ( opposite situation peripheral blood)
• Localization + persistent emigration-chemotactic factors
bacteria, host-derived chemotactic factors
32. • Under inflamed conditions, 60% or more of the JE space can be occupied
by neutrophils.
• Initial explanations for the elevation of PMN cell counts in the presence of
inflammation α sulcular fluid flow.
• However, 2.1-fold increase of neutrophils the GCF flow increased almost
5.5-fold during the same period ( Kowashi et al, 1980). It was concluded-
both are two distinct phenomena & migration of inflammatory cells is
directed along gradients of chemoattractants
33. • Once in the sulcus, PMNs begin to create a ‘leukocyte wall’ along the
margins of plaque mass.
• kinetics of leukocytic emigration (Attström & Egelberg, 1970)
radiolabeled PMNs
-appeared in the gingival sulcus 20–30min after being present in the blood
- a peak neutrophil concentration within the sulcus after 1h.
34. • crevicular PMNs are capable of phagocytosis + extracellular killing of
pathogens(‘suicidal’ action). (Scully ,1982)
• Reports identifying possible defects in gingival crevicular PMNs,
- decreased responsiveness to chemotactic substances
- loss of the ability to adhere or migrate
- and reductions in phagocyte activity and intracellular killing
(Miyazaki 1997)
35. • Major events in leukocyte lifecycle
Generation of acute phase signals- C5a
Migration –chemoattaractants factors
Phagocytosis of microbial invaders
Killing of bacteria
36. The potent enzymatic in PMNs act as ‘double-edge sword’, functioning to
protect the host from microbial invaders but also contributing to the host tissue
destruction.
37. • Three potent enzymes that affect the tissues of the periodontium are
collagenase, elastase, and gelatinase.
• In addition, crevicular PMNs are capable of producing pro-inflammatory
mediators directly.
• Other Cellular components-
Macrophages (2–3%) -Phagocytes
-APC
-Enhance the
antimicrobial actions
of PMNs.
-sources of pro-
inflammatory
cytokines.
T lymphocytes Humoral
B lymphocytes
1–2%
plasma cells.
38. Electrolytes in GCF
• Potassium, sodium, and calcium have been studied in GCF. Most studies
have shown a positive correlation of calcium and sodium concentrations
and the sodium-to-potassium ratio with inflammation.
(Kaslick RS, Mandel ID, Chasens AJ, 1970)
39. Organic Compounds in GCF
• Both carbohydrates and proteins have been investigated.
• Glucose hexosamine and hexuronic acid are two of the compounds found
in GCF.
• Blood glucose levels do not correlate with GCF glucose levels; glucose
concentration in GCF is 3-4 times greater in serum due to
- metabolic activity of adjacent tissues,
- local microbial flora.
(Hara K et al., 1969)
• The total protein content of GCF is much less than that of serum. No
significant correlations have been found between the concentration of
proteins in GCF and the severity of gingivitis, pocket depth, or extent of
bone loss.
(Solis Gaffar MC et al., 1980)
40. Proteolytic host cell enzymes in GCF
• A variety of enzymes that degrade proteins, proteoglycans, lipids and
carbohydrates have been detected in GCF.
• Enzymes, especially proteinases that have a role in periodontal tissue turnover
in health and in the tissue destruction that characterizes diseases of the
periodontium.
• Serine proteinases
• Matrix metalloproteins
• Cysteine & Aspartic proteinases
(These are the enzymes of neutrophils)
41. • Under normal conditions, there is a balance between the amount/activity of
proteolytic enzymes and enzyme inhibitors, thereby keeping the activity of
the secreted enzymes under control. In highly inflamed sites, tissues are
infiltrated with neutrophils and other proteinase-producing inflammatory
cells.
42. • Serine proteinases
Elastase
fibronectin, laminin 1,
Proteoglycans
Fibronectin and type IV
(neutrophil transmigration)
Extensive degradation of
extracellular matrix
Elastase and cathepsin G are
capable of activating
epithelial cells to produce IL-
8, IL-6 and prostaglandin E2
Cathepsin G convert the inactive
angiotensin I to angiotensin II.
regulate vascular permeability
and monocyte chemotaxis
Proteinase-3 collagen type IV, elastin,
vitronectin
43. plasminogen activator large substrate specificity.
Plasmin plays a pivotal role in
fibrinolysis.
degrades extracellular matrix
proteins
activates complement .
convert latent pro-matrix
metalloproteinases into active forms
.
44. Matrix metalloproteins
(GCF and saliva)
collagenase (MMP-8) interstitial collagens,
Leukocyte Collagen types I,
II, III, VII, X
Gelatinase (MMP-9) Gelatinolytic enzyme
degrading several
extracellular matrix
proteins, including
basement
membrane (type IV)
gelatin
fibronectin, vitronectin,
laminin, elastin, aggrecan
MMPS
45. Cysteine & Aspartic proteinases
Cysteine proteinases (Cathepsin S,
L, B, H)
Elastin,
several denatured proteins,
activation of pro-MMPs
prourokinase
Aspartic proteinases (Cathepsin D,
E
Proteoglycans,
several denatured proteins
46. • Enzyme Inhibitors
Specific inhibitors, called serpins, restrict the serine proteinase activity in
tissues.
Both uPA and plasmin have their own specific inhibitors, uPA-inhibitor and
plasmin inhibitor.
TIMPs
Cystatins
47. • Epithelial cell proteinases
i. Matrix metalloproteinases
ii. Other serine proteinases.
iii. aspartic acid proteinases
iv. Tissue plasminogen activator (t-PA) (Schmid et.al.,1991) and its inhibitor
PA1-2
48. • Fibroblast proteinases
Fibroblasts are largely responsible for the turnover of connective tissue in
normally functioning tissues such as gingiva and periodontal ligament.
MMP s
MMP-1 (collagenase-1)
MMP-2 (gelatinase A)
MMP-3 (stromelysin-1)
MMP-13 (collagenase-13)
MT1-MMP (MMP-14).
degrade all the components
of connective tissue, including
different collagen types,
adhesion proteins and
proteoglycans
Serine Proteinases.
Cysteine Proteinases.
Cathepsins B And L
intracellular collagen
degradation of fibroblasts
Aspartic Acid Proteinases.
t-PA
49. collagen-degrading enzymes P. gingivalis,
A.actinomycetemcomitans and
spirochaetes
elastase-like enzyme spirochaetes and Capnocytophaga
species
trypsin-like proteases P. gingivalis, B. forsythus,
T. denticola and other spirochaetes
Chymotrypsin like enzymes
T. denticola and Capnocytophaga
species
aminopeptidases Capnocytophaga species and T.
denticola
dipeptidylpeptidases P. gingivalis, P. intermedia and
Capnocytophaga species
50. Hyaluronidase and
chondroitinase
activities
These could hydrolyze the
GAG
components of
proteoglycans in the ECM
by C. ochracea, F.
nucleatum, P. gingivalis
and T. denticola
Neuraminidase
(sialidase) activity
might attack sialoproteins
in the
epithelium, thereby
increasing its permeability
to
bacterial products
B. forsythus, Prevotella
melaninogenica and
P. gingivalis
phospholipases Damage to the surface of
epithelial
and other cells
Porphyromonas, Prevotella
and
Bacteroides species
acid and
alkaline phosphatase
Porphyromonas,
Prevotella, Bacteroides and
Capnocytophaga
species
51. Products of inflammation in GCF
• Lysozyme
Lysozyme is an enzyme found in tears, nasal, and gastric secretions saliva
and GCF.
It is present in both the basic and azurophil granules of PMNs and cleaves
the £-1-4 glycosidic bonds of bacterial cell wall peptidoglycans and
features as a bactericidal agent.
Levels differ b/w gingivitis and periodontitis sites. ( Modeer and Twetman
1979)
52. Lactoferrin
• This is an antimicrobial agent with a distribution in PMNs and secretory fluids
similar to that of lysozyme.
• The antibacterial properties- due to its high affinity for iron, thus locking
available sources required for bacterial growth.
• Lactoferrin increased twofold in GCF in sites showing gingivitis and
periodontitis. ( Friedman et al.,1983)
• It has also been reported that the ratio of lactoferrin to lysozyme may be more
representative and a useful diagnostic assay of periodontal inflammation.
53. Cytokines in GCF
IL-1 Armitage ,1996
IL-2.
IL-6
Cox, 1986
Geivelis et al., 1990
IL-8 Payne et al, 1998
TNF-a Beutler and Cerami, 1990
55. • Eicosanoids: Prostaglandins and Leukotrienes-Prostaglandin E2 (PGE2)
has been found in elevated quantities in GCF.
• GCF levels increases 2- and 3- fold in inflammation and 5- to 6-fold
during periods of active attachment loss and bone resorption. (Offenbacher
et al.,1991)
• LTB4 is elevated in inflamed deeper periodontal tissues.
56. • Immunoglobulins in GCF-Immunoglobulins and antibodies of all isotypes
are generally at low levels in GCF from healthy sites. (Reinhardt et al.
1989)
• GCF IgG1 and IgG4 were significantly elevated in active when compared
to stable sites in periodontitis patients and that both were elevated relative
to serum.
57. Complement activation in GCF
• Numerous complement components have been reported in GCF, derived
from serum and/or local synthesis.
• Healthy gingival sulcus GCF fluid transudate contains both C3 and C4.
• Cleaved C3 is increased in GCF at gingivitis sites .
• chronic periodontitis -Only C3 is activated
• Aggressive Periodontitis - C4a, C3b and C5a ( both pathways)
• Significant amounts of bone-resorbing IL-6 are released by osteoblast-like
cells stimulated by C5a. (Pobanz JM etal 2000).
58. Growth Factors
• Regulate key cellular events in tissue repair, including cell proliferation,
chemotaxis, differentiation, and matrix synthesis
EGF- No significant differences in EGF concentrations were found between
the periodontal disease and control groups
TGF-a significant correlations were found between GCF TGF-a
concentrations and pocket depth measurements, bleeding on probing, and
radiographic bone loss.
(Mogi et al.,1994)
PDGF – (Salcetti et al 1997).
VEGF -(Deckers MM 2000).
59. SALIVA
• Whole saliva is an important physiologic fluid that contains a highly
complex mixture of substances.
• It is secreted primarily by three paired major salivary glands and
secondarily by hundreds of minor salivary glands located below the
mucosal surfaces of the mouth.
• Salivary gland secretions contain locally produced proteins, as well as other
molecules from the systemic circulation.
60. Composition of saliva
• SALIVA -WATER (99.5%) and SOLIDS (0.5%).
• Solids include ORGANIC (0.3%) and INORGANIC (0.2%).
• organic constituents include ptaylin, kallikrein, bradikynin, lysosome ,
immunoglobulin igg, mucin, blood group antigen, nerve growth factor, vit c
and vit k, urea and uric acid, cellular components and gama globulin.
• inorganic constituents include- sodium, chlorine, potassium, calcium,
phosphate, fluoride, magnessium, bicarbonate and thiocynate.
61. • Enzymes in saliva
Derived from the salivary glands, bacteria, leukocytes, oral tissue and
ingested substances; the major enzyme is parotid amylase.
S.E. increased in concentration in periodontal disease are hyaluronidase,
lipase, B-glucuronidase and chondritin sulfatase, amino acid
decarboxylases, catalase, peroxidase and collagenase.
62. • Proteolytic enzymes generated by both host and bacteria. They have been
recognised as contributors to the initiation and progression of periodontal
disease, to combat these enzymes; saliva contains antiproteases that inhibit
cysteine proteases such as cathepsins and anti-leucoproteases that inhibit
elastase.
• Another antiprotease identified as a tissue inhibitor of matrix metalloprotienase
(TIMP) has been shown to inhibit the activity of collagen – degrading enzyme
63. • Antibacterial factor-Saliva contains inorganic and organic factors that
influence bacteria and their products in the oral environment.
• Inorganic factors includes ions and gases, bicarbonate, sodium,
potassium, phosphate, calcium, fluorides, ammonium, and carbon dioxide
• Organic factors include lysozyme, lactoferrin, myeloperoxidase, lacto
peroxidase and agglutinins such as glycoproteins, mucins, Beta-2
macroglobulins, fibronectin, and antibodies.
64. • Lysozyme
• Is a hydrolytic enzyme that cleaves the linkage between structural
components of the glycopeptide (muramic acid)
– found in the cell wall of certain bacteria’s.
• Lysozyme works on gram negative and gram-positive organisms,
Veillonella species and A.A. are some of their targets .
• It probably repels certain transient bacterial invaders of the mouth (Pullock
et al 1985).
65. • The lactoperoxidase-thiocynate system in saliva-Is bactericidal to certain
strains of lactobacillus and streptococcus by preventing the accumulation of
lysin and glutamic acid, both of which are essential for bacterial growth.
• Lactoferrin is effective against Actinobacillus species (Arnold et al 1980).
• Myeloperoxidase -An enzyme similar to salivary peroxidase is released
by leukocytes and is bactericidal for actinobacillus, but has added effect of
inhibiting the attachment of Actinomyces strain to hydroxyapatite.
66. Vitamins
• They are found in saliva, as thiamine, riboflavin, niacin, pyridoxine,
pantothenic acid, biotin, folic acid and vitamin C and B12, and vitamin K
are also reported. Suggested sources of the oil are microbial synthesis and
secretion by salivary gland, food debris, degenerating leukocytes and
exfoliated epithelial cells.
Coagulation factors
• Saliva also contains coagulation factors VIII, XI, X, plasma thromboplastin
antecedent (PTA) and the Hageman factor that hasten blood coagulation
and protect the wounds from bacterial invasion. Presence of an active
fibrinolytic enzyme has also been suggested.
67. • Bacteria
• Bacteria in general and specific species in particular are important in the
etiology of gingivitis and periodontitis(Socransky.1970,Genco et al
1988).Further more detection of certain species in saliva can reflect their
presence in periodontal pockets (Asikainen et al.1991,Umeda et al.1998) Saliva
has also been suggested as an important vector in bacterial transmission
(Greenstein &lamster.1997.therefore analysis of saliva may prove to be an
important approach for detection of pathogenic oral bacteria , and may replace
other more complicated and more invasive sampling methods.
•
68. • Blood group active glycoproteins: mucins and salivary agglutinin two
genetically distinct mucin types, designated MG1 and MG2 (Levine et al,
1987)
• MG1, which displays blood group activity, exists in at least three different
glycoforms, differing in sialic acid and sulphate content, depending on the
glandular source (Veerman et al, 1992).
• MG2 has been found to exist as at least two glycoforms, MG2a and MG2b.
the secretory mucins form hydrophilic viscoelastic gels.
69. • These gels function as barriers, protecting the underlying epithelium against
mechanical damage and preventing direct entrance of noxious agents, including
bacteria and viruses, into the underlying vulnerable epithelium.
• Agglutinin
Salivary agglutinin is a highly glycosylated protein, with a molecular mass of
approximately 340 kDa, that carries blood group active antigen.
Salivary agglutinins are expressed in the serous cells of the submandibular,
sublingual and labial glands (Sharma et al., 1998).
70. • Agglutinin is also synthesized in the serous parotid gland.
• Agglutinin binds to a wide variety of microorganisms, including S. mutans,
S. salivarius and S. sanguis (Ligtenberg et al., 2000),resulting in enhanced
phagocytosis and killing of microorganisms by neutrophils and macro-
phages (Holmskov et al., 1999)
71. Cystatins
• cysteine proteinase inhibitory activity (Shomers et al, 1982).
• Because of their proteinase inhibiting properties, cystatins have been
suggested to play a role in controlling proteolytic activity, either from the
host (released during inflammatory processes) or from microorganisms.
• Cystatin S can inhibit partially proteolytic enzymes released in P. gingivalis
culture medium (Blankenvoorde et al.,1996).
72. Von Ebner glands protein (VEGh)
• VEGh is a salivary protein secreted by the Von Ebner glands located around
the circumvallate and foliate papillae of the tongue.
• Originally it has been assumed that VEGh was involved in the perception of
bitter taste.
• However, later it was demonstrated that VEGh can act as inhibitor of cysteine
proteinases (Van't Hof et al., 1997).
• Evidence has also been produced that VEGh can act as an oxidative-stress
induced scavenger of peroxidation products (Redl et al., 1999)
• The ubiquitous presence of VEGh in various secretions, including saliva, tears
and semen, would indeed favour a more general role, e.g. as an antiviral agent.
73. secretory leucocyte proteinase inhibitor (SLPI)
• Another example of salivary protein with more than one function is the
Secretory Leukocyte Proteinase Inhibitor (SLPI).
• This protein is an inhibitor of serine proteinases (designated a serpin),
including neutrophil elastase, chymotrypsin and Cathepsin G.
• In addition to its proteinase inhibitory properties, SLPI has antimicrobial
and antiviral properties.
74. TIMPS: tissue inhibitors of metalloproteinases
• In parotid and submandibular secretions TIMP-1 has been identified, a member
of the family of tissue inhibitors of matrix metalloproteinases (MMPs)
• Considering their potent inhibitory action against MMPs, including
collagenase, gelatinase and stromelysin, TIMPs are thought to play an
important role in turnover and remodelling of the extracellular matrix.
• other unique functions of TIMPs have been reported, including erythroid
potentiating activity, cell growth-promoting activity, and stimulation of
osteoclastic bone resorption (Murate and Hayakawa 1999).
• Interestingly, the latter activity could not be ascribed to merely their inhibitory
effect on matrix proteolysis,indicating that TIMPs, like VEGh and SLPI, are
multifunctional proteins.
75. Extra-parotid glycoprotein (EP-GP)
• EP-GP is another example of a protein that originally had been implicated
in the formation of the dental pellicle, because of its high affinity for
hydroxyapatite (Rathman et al., 1989).
• The ubiquitous presence in mucosal secretions pointed to a more general
protective role for EP-GP, a concept that was supported by the observation
that this protein binds to microorganisms (Schenkels et al.,1997) as well as
to the CD4 receptor on monocytes(Autiero et al., 1997; Gaubin et al.,
1999).
76. Chromogranin A
• Chromogranin A is a major protein in adrenal chroma•ffin cells and
adrenergic neurons.
• In humans, a prompt elevation of salivary chromogranin A-like
immunoreactivity is found in psychosomatic stresses (Nakane et al., 1998).
• Vasostatin-1, the natural N-terminal chromogranin A-derived fragment in
bovine sequence, displays antibacterial activity against Gram-positive
bacteria at micromolar concentrations and is also able to kill a large variety
of filamentous fungi and yeast cells (Lugardon et al., 2000).
77. Conclusion
• Various component act in defense of gingiva. eg. Gingival epithelium,
sulcular fluid and saliva.
• These component through various mechanism & enzymes resist against the
mechanical & bacterial aggressions & maintain the gingiva normal healthy
state.
• The origin, the composition and the clinical significance of these
components are now known with more precision and have significantly
helped our understanding of the pathogenesis of periodontal disease.
78. References
• Caranza’s Clinical Periodontology. Defense Mechanisms of the Gingiva,
10th edition, Elsevier Publisher. Ch-20 Pg no. 344.
• Bosshardt DD, Lang NP. The Junctional Epithelium: from Health to
Disease J Dent Res 2005;84: 9-20
• Esha V, Apurv J. Defense mechanisms of gingiva. J Orofac Res 2014;
4:111-14.
• Dale BA. Periodontal epithelium: A newly recognized role in health and
disease. Periodontal 2000 2002; 30:70-8
79. • Pollanen Marja T, Salonen J, Uitto V. Structure and function of tooth-
epithelial interface in health and disease. Periodontol 2000 2003;31:12-31.
• Uitto V, Christopher M. Proteolytic host cell enzymes in gingival crevice
fluid. Periodontol 2000 2003,31:77–104
• Barrey M, Stephen W. Proteolytic and hydrolytic enzymes from putative
periodontal pathogens: characterization, molecular genetics, effects on host
defenses and tissues and detection in gingival crevice fluid. Periodontol
2000 2003; 31:105–124
• Ferguson DB. Current diagnostic uses of saliva J Dent Res 1987;66:420-
4.
• Kaufman E. The diagnostic applications of saliva – a review. Crit Rev
Oral Biol Med 2002;13:197-212.
Editor's Notes
ORAL (OUTER EPITHELIUM)
-0.2-0.3 mm in thickness.
-It is keratinized or parakeratinized, and it functions in the mechanical defense of the periodontium.
SULCULAR EPITHELIUM
- thin, non-keratinized stratified squamous epithelium, without rete pegs and it extends from the coronal limit of the junctional epithelium to the crest of the gingival margin.
The turnover rate of the oral sulcular epithelium has been estimated as 10–14days, while that of the junctional epithelium is around 4–6days (Attström R. 1985).
Gingival epithelial cells-physical barrier against infection and underlying ging attachment by resp to bacteria by prolifer, different, alt of cell signaling ultimately cell death and alter tissue homeostasis- produce cytokines IL-1 and 8, growth factors, defensins hbD 1, 2, LL 37, adhesion molecules and enzymes.
Protect deeper struct by prolif and differentiation
exfoliation must occur at an extremely high rate (Loe and Karring ,1969 ; Listgarten ,1972). Distinct phenotype of DAT cells...b/c
of permissive and instructive signals. Also, the DAT cells migrate towards the sulcus bottom.
ICAM is a ligand expressed by macrophages, lymphocytes, vascular endo-bind to leukocyte integrin molecules and localise them to site of injury. Induced by IL1 and TNF.
Defensins are small cysteine rich cationic molecules, 18-45 amino acids, assist in killing phagocytosed bact by binding to mcrobial cell membrane and forming pore like defects-efflux of essential ions and nutrients. Expressed in neutrophils and epithelial cells.
Since the DAT cells are connected to the basal lamina via hemidesmosomes, a remodeling of the epithelial attachment
must occur.
Yet low power defense-lack odland bodies and low glycolytic enzyme activity
from IBL.
A significant number of the DAT cells are, like the basal cells along the connective tissue, capable of synthesizing DNA, which demonstrates their mitotic activity (Salonen JI ,1997).
Cell membrane of leucocytes and JE cells
Adhesion b/w JE cells
Guidance of PMN through JE
proliferation, Stimulation and co regulation of activated T cells
Cell receptor for different bacteria-therefore interactions alteration of JE
Inter cellular adhesion molecule 1(ICAM 1)
Cell membrane of JE cells
Cell –cell interactions in inflammatory reactions
Guiding PMN towards sulcus bottom
Lymphocyte function antigen3(LFA3)
Cell membrane of JE cells
Cell –cell interactions in inflammatory Reactions
Controls leucocyte migration to inflammatory sites
MMP produced by neuto fibro, macro
By gerome gross and Charles lapiere 1962
Found in lysososoems-degrade cellular polypeptides and therby role in cellular turnover, cathepsin K secreted by osteoclasts.
I J not there l1 l2, o s wz
A serine
B h c cysteine
D e aspartyl
Found in lysososoems-degrade cellular polypeptides and therby role in cellular turnover, cathepsin K secreted by osteoclasts.
I J not there l1 l2, o s wz
A serine
B h c cysteine
D e aspartyl
Oxygen dependent-NADPH (to generate superoxide) converted to H2O2 bactericidal
MPO H2O2 to hypochlorous acid more potent
Or independent of MPO to OH(fenton or haber weiss)) and singlet oxygen ROS, in macrphage
Non-oxygen dependent NADPH independent by defensins, permeability increasing, lysosomal hydrolases
Besides discharge-IL 2 6, TNF, PG, PAF, oxygen metabolites.
Up to now, for instance, none of the multiple components analyzed in the fluid has improved clinical judgment of the rate of progress of gingivitis and periodontitis or of the rate of repair of these conditions.