This document discusses gingival inflammation and its stages. It begins by defining inflammation and the cardinal signs. It then discusses the general aspects of inflammation including vascular and cellular events. It outlines the cells involved in inflammation and their roles. The document defines gingivitis and discusses some studies on the topic. It describes the initiation and stages of gingival inflammation from the initial lesion to the advanced lesion. It discusses the cells and molecules involved at each stage and concludes by discussing assessment of gingival inflammation using image analysis.
Sepsis is a generalized infection caused by bacteria entering the bloodstream and overwhelming the body's defenses. It can result from various infections or invasive medical procedures. Key factors in its pathogenesis include bacterial toxins that trigger an overproduction of cytokines, which cause systemic inflammatory response and multi-organ dysfunction. Treatment involves identifying and treating the infection source, administering antibiotics and other measures to support organ function, and modulating the immune response.
This document discusses gingival inflammation and gingivitis. It begins by defining inflammation and describing the cardinal signs. It then outlines the stages of gingivitis from initial to established to advanced/periodontitis. Microorganisms attached to teeth secrete enzymes that damage tissues and widen junctional epithelium, allowing bacterial products to access connective tissue and activate immune cells. Studies showed that not practicing oral hygiene led to plaque buildup and gingivitis within 10-21 days. Gingivitis is characterized by redness, swelling, bleeding and is prevalent worldwide. The document discusses features, course, distribution and systemic influences of gingival inflammation.
This document defines and describes different types of immunodeficiencies. It discusses primary and secondary immunodeficiencies, listing some common examples like DiGeorge's Syndrome. It then summarizes the main features of deficiencies in antibodies, T cells, neutrophils, and complement. Finally, it briefly discusses acquired immunodeficiency syndrome (AIDS) caused by HIV infection.
This document discusses macrophages, their role in health and disease. It covers the development and differentiation of macrophages, their functions in the body including phagocytosis and cytokine production, and their involvement in various diseases such as chronic infections, atherosclerosis, and malignancies. It also describes several diseases of macrophages themselves, including histiocytic disorders like Gaucher's disease, Niemann-Pick disease, and Langerhans cell histiocytosis.
Infection- microbiology and pathology in orofacial infectionPunam Nagargoje
INTRODUCTION
Oral and maxillofacial infections are commonly caused by teeth they are referred as odontogenic infections.
The etiological agents may be bacteria viruses or fungi.
The infection may spread directly from the tooth or secondary infections of cyst or tumours or infection of surgical wound or by contaminated needles.
Infection may be defined as invasion and multiplication of microorganisms in body tissues, especially that causing local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response.
Aerobic bacteria
Gram positive cocci –
Streptococcus species
S.Milleri
S.sanguis
S.Salivarius
S.Mutans
Staphylococcus species
Gram negative cocci –
Neisseria spp.
- N. subflava
N. sicca
Gram positive rods-
Dipetheroids
Lactobacillus spp
Gram negative rods-
Moraxella catarrhalis
Actinobacilllus actinomycetemcomitans
Campylobacter spp.
Capnocytophaga spp.
Eikenella corodens
Helicobactor pylori
Anaerobic bacteria
Gram positive cocci –
Peptococcus species
Pepto Streptococcus species
Gram pasitive bacilli –
Actinomycosis spp
Eubacterium spp
Gram negative species-
veillonella spp.
Gram negative bacilli-
Bacteroids
Prevotella species
Porphyromonas species
Fusobacterium
There are three stages in progression of acute odontogenic infections
Stage I – Innoculation
Stage II – Cellulitis
Stage III – Abscess
Stage IV – Space infection
TYPES
Acute stage - 3 forms
1.Abscess
2.cellulitis
3.fulminating infection
FULMINATING INFECTIONS
Here the infection involves secondary spaces involving vital structures.
Chronic stage
C/c fistulous tract or sinus formation
Abscesses neglected for a long time may discharge intraorally or extra orally
Spread of oral infection
Routes of spread
Direct continuity through tissues
By lymphatics to the lymph nodes.From lymph nodes to tissues results in secondary areas of cellulitis or tissue space abscess.
By blood stream-local thrombophlebitis may spread via the veins entering the cranial cavity producing cavernous sinus thrombosis. It may cause septicemia.
Invasion of dental pulp by bacteria after
decay of a tooth
¯
Inflammation, edema & lack of collateral
blood supply
¯
Venous congestion or avascular necrosis
(pulpal tissue death)
¯
Reservoir of bacterial growth(anaerobic)
¯
Periodic egress of bacteria into surrounding
alveolar bone
Factors influencing spread
General factors
Host resistance
Virulance of micro organism
Combination of both
Local factors
Anatomic barriers-
Alveolar bone
Periosteum
IgA preven
Sepsis is a generalized infection caused by bacteria entering the bloodstream and overwhelming the body's defenses. It can result from various infections or invasive medical procedures. Key factors in its pathogenesis include bacterial toxins that trigger an overproduction of cytokines, which cause systemic inflammatory response and multi-organ dysfunction. Treatment involves identifying and treating the infection source, administering antibiotics and other measures to support organ function, and modulating the immune response.
This document discusses gingival inflammation and gingivitis. It begins by defining inflammation and describing the cardinal signs. It then outlines the stages of gingivitis from initial to established to advanced/periodontitis. Microorganisms attached to teeth secrete enzymes that damage tissues and widen junctional epithelium, allowing bacterial products to access connective tissue and activate immune cells. Studies showed that not practicing oral hygiene led to plaque buildup and gingivitis within 10-21 days. Gingivitis is characterized by redness, swelling, bleeding and is prevalent worldwide. The document discusses features, course, distribution and systemic influences of gingival inflammation.
This document defines and describes different types of immunodeficiencies. It discusses primary and secondary immunodeficiencies, listing some common examples like DiGeorge's Syndrome. It then summarizes the main features of deficiencies in antibodies, T cells, neutrophils, and complement. Finally, it briefly discusses acquired immunodeficiency syndrome (AIDS) caused by HIV infection.
This document discusses macrophages, their role in health and disease. It covers the development and differentiation of macrophages, their functions in the body including phagocytosis and cytokine production, and their involvement in various diseases such as chronic infections, atherosclerosis, and malignancies. It also describes several diseases of macrophages themselves, including histiocytic disorders like Gaucher's disease, Niemann-Pick disease, and Langerhans cell histiocytosis.
Infection- microbiology and pathology in orofacial infectionPunam Nagargoje
INTRODUCTION
Oral and maxillofacial infections are commonly caused by teeth they are referred as odontogenic infections.
The etiological agents may be bacteria viruses or fungi.
The infection may spread directly from the tooth or secondary infections of cyst or tumours or infection of surgical wound or by contaminated needles.
Infection may be defined as invasion and multiplication of microorganisms in body tissues, especially that causing local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response.
Aerobic bacteria
Gram positive cocci –
Streptococcus species
S.Milleri
S.sanguis
S.Salivarius
S.Mutans
Staphylococcus species
Gram negative cocci –
Neisseria spp.
- N. subflava
N. sicca
Gram positive rods-
Dipetheroids
Lactobacillus spp
Gram negative rods-
Moraxella catarrhalis
Actinobacilllus actinomycetemcomitans
Campylobacter spp.
Capnocytophaga spp.
Eikenella corodens
Helicobactor pylori
Anaerobic bacteria
Gram positive cocci –
Peptococcus species
Pepto Streptococcus species
Gram pasitive bacilli –
Actinomycosis spp
Eubacterium spp
Gram negative species-
veillonella spp.
Gram negative bacilli-
Bacteroids
Prevotella species
Porphyromonas species
Fusobacterium
There are three stages in progression of acute odontogenic infections
Stage I – Innoculation
Stage II – Cellulitis
Stage III – Abscess
Stage IV – Space infection
TYPES
Acute stage - 3 forms
1.Abscess
2.cellulitis
3.fulminating infection
FULMINATING INFECTIONS
Here the infection involves secondary spaces involving vital structures.
Chronic stage
C/c fistulous tract or sinus formation
Abscesses neglected for a long time may discharge intraorally or extra orally
Spread of oral infection
Routes of spread
Direct continuity through tissues
By lymphatics to the lymph nodes.From lymph nodes to tissues results in secondary areas of cellulitis or tissue space abscess.
By blood stream-local thrombophlebitis may spread via the veins entering the cranial cavity producing cavernous sinus thrombosis. It may cause septicemia.
Invasion of dental pulp by bacteria after
decay of a tooth
¯
Inflammation, edema & lack of collateral
blood supply
¯
Venous congestion or avascular necrosis
(pulpal tissue death)
¯
Reservoir of bacterial growth(anaerobic)
¯
Periodic egress of bacteria into surrounding
alveolar bone
Factors influencing spread
General factors
Host resistance
Virulance of micro organism
Combination of both
Local factors
Anatomic barriers-
Alveolar bone
Periosteum
IgA preven
The document provides an overview of inflammation, including its definition, etiology, cardinal signs, types (acute and chronic), vascular and cellular events in acute inflammation, mediators, regulation, inflammatory cells, factors affecting acute inflammation, and the fate of acute inflammation. It also discusses chronic inflammation, granulomatous inflammation, comparing acute and chronic inflammation, and dental implications including pulpal infections, periapical infections/inflammation, gingival inflammation, and periodontal inflammation.
Biofilm formation involves the accumulation of microorganisms on surfaces where they form sessile communities encased in an extracellular polymeric substance matrix. Biofilm formation progresses through initial attachment, irreversible attachment aided by EPS production, early development, maturation, and dispersion. Virulence factors and quorum sensing play important roles in biofilm formation. Mature biofilms pose challenges for antibiotic treatment and are implicated in various pathogenic conditions like cystic fibrosis, periodontitis, and device-related infections. Therapeutic strategies aim to target biofilm formation, virulence factors, and quorum sensing.
Periodontitis is caused by bacterial infection of the gums that triggers an inflammatory host response. Bacteria form biofilms in the gingival crevice. This elicits production of inflammatory molecules like IL-1β and TNF-α by immune cells. In susceptible individuals, inflammation is excessive and causes tissue destruction and bone loss. As bone loss progresses, periodontal pockets deepen, increasing pathogen load and further inflammation.
Acute inflammation is the body's initial response to harmful stimuli and involves both vascular and cellular events. The vascular events include increased blood flow, vascular permeability and blood vessel dilation. The cellular events include the recruitment of leukocytes from the bloodstream to the site of injury and their migration into tissues. This is followed by phagocytosis of pathogens and damaged cells by macrophages and neutrophils. Mediators of acute inflammation such as histamine, cytokines and complement proteins are released from cells to promote the inflammatory response. The response and its outcomes can vary depending on factors related to the host and the causative agent.
This document discusses periradicular lesions, which are inflammatory changes that can occur in the tissues surrounding the root apex in response to irritants from infected or inflamed dental pulps. It describes the various irritants that can cause periradicular lesions, including microbes, toxins, mechanical/chemical irritants from root canal procedures. It also discusses the inflammatory process and mediators involved, such as neuropeptides, kinins, cytokines, prostaglandins and leukotrienes. Depending on the nature and extent of the irritants, a variety of tissue changes can result, from transient inflammation to destruction of periradicular tissues.
The document discusses the stages of gingival inflammation. It begins by defining inflammation and providing background on its history. It then discusses 4 stages of gingival inflammation: initial lesion, early lesion, established lesion, and advanced lesion. The initial lesion involves dilation of capillaries and leukocyte recruitment. The early lesion develops within 1 week and may show clinical signs like erythema. The established lesion evolves over months and is characterized by plasma cell predominance. The advanced lesion extends inflammation into alveolar bone, potentially leading to periodontitis in susceptible individuals. Microscopic examination shows features corresponding to the stage of inflammation.
This document discusses sepsis, including definitions, pathophysiology, clinical features, diagnosis, and management. It defines sepsis as a life-threatening condition caused by a dysregulated immune response to infection leading to organ dysfunction. The pathophysiology involves a dysregulated inflammatory response and coagulation system. Signs and symptoms may include altered vital signs and organ dysfunction. Diagnosis involves identifying infection source through cultures and biomarkers. Treatment involves prompt antibiotics, fluid resuscitation, and supportive care based on Surviving Sepsis Campaign guidelines.
The document summarizes key components and mechanisms of the innate immune system in periodontal diseases. The innate immune system provides non-specific defenses and includes intact epithelial barriers, fluids like saliva and GCF, the complement cascade, cell signaling molecules, vasoactive peptides, adhesion molecules, and phagocytic cells like neutrophils and macrophages. These components work together to recognize pathogens, initiate inflammation, and promote pathogen elimination through mechanisms like phagocytosis, helping to maintain periodontal health.
3er Curso Latino Americano de Cicatrización Avanzada en Heridas (I)Karen Pulido
The document discusses various bacterial pathogens commonly found in wounds such as Streptococcus pyogenes, Staphylococcus aureus, and Streptococcus agalactiae. It describes the virulence factors and strategies used by these bacteria to evade the immune system, including the production of biofilms. The summary also outlines approaches to reducing bacterial bioburden in wounds through cleansing, debridement, and judicious use of antibiotics while supporting the host's natural immune response.
Acute inflammation is characterized by five signs: redness, heat, swelling, pain, and loss of function. It involves both vascular and cellular events over a short period of time. The vascular events include increased blood flow and permeability, which leads to fluid leakage. The cellular events involve leukocyte recruitment to the site through adhesion molecules and chemotaxis, followed by activation and phagocytosis of microbes. Acute inflammation can manifest morphologically as serous, fibrinous, purulent or hemorrhagic inflammation. It typically resolves through resolution or repair, but can also lead to suppuration or progress to chronic inflammation.
This document summarizes the stages of gingival inflammation. It begins with initial inflammation seen as vascular changes like dilated capillaries. Early inflammation occurs within 1 week, shown microscopically as PMN infiltration. Established inflammation happens after 2-3 weeks of plaque accumulation and is characterized by B and T lymphocyte accumulation and plasma cell domination. Advanced inflammation involves bone loss and widespread tissue damage. The document provides histological details of the progression from healthy gingiva to advanced periodontitis.
Immunology Lecture day 1 ADDU section DElla Navarro
1. The document provides an overview of immunology and the immune system, including the inflammatory process, anatomy and physiology of the immune system, and different types of immune responses.
2. It discusses the immune system in detail, including the different white blood cells, lymphoid tissues, types of immunity, immune response types, stages of immune response, and immunoglobulins.
3. The document also covers primary and secondary immunodeficiencies like HIV/AIDS, and provides the stages and diagnosis of HIV infection.
This document discusses and classifies acute and subacute osteomyelitis. It begins by defining osteomyelitis as a bone or bone marrow infection. It then classifies osteomyelitis based on timing of onset (acute <2 weeks, subacute 2-6 weeks, chronic >6 weeks) and method of spread (exogenous or hematogenous). Key points include: acute osteomyelitis most commonly spreads hematogenously while staphylococcus aureus is the most common cause; subacute osteomyelitis has an indolent course and is often an incidental finding on imaging. Treatment involves antibiotics, surgery if abscess or lack of response, and immobilization.
Inflammation is the body's protective response to injury or infection that involves increased blood flow, swelling, heat, pain, and loss of function. The document outlines the general considerations of inflammation including its definition, causes, and cardinal signs. It then discusses the major events of acute inflammation including vascular changes, exudation of fluid, and recruitment and activation of leukocytes. Finally, it classifies inflammation into acute and chronic types and further classifies acute inflammation based on the type of exudate produced (serous, fibrinous, suppurative, hemorrhagic).
The document summarizes the stages of gingivitis:
1) The initial lesion involves vascular changes like dilated capillaries. Microscopically there are acute inflammatory changes beneath the junctional epithelium.
2) The early lesion evolves within 1 week, appearing as early gingivitis. Microscopically there is leukocyte infiltration and rete pegs develop in the junctional epithelium.
3) The established lesion involves predominance of plasma cells and B lymphocytes. Microscopically there is widening of intercellular spaces and degradation of collagen around inflammatory cells.
4) The advanced lesion extends into alveolar bone. Microscopically there is widespread tissue damage and
Acute inflammation is characterized by five signs: redness, heat, swelling, pain, and loss of function. The main events of acute inflammation are vascular events like vasodilation and increased permeability, and cellular events involving leukocyte recruitment and activation. This results in an inflammatory cell-rich exudate. Acute inflammation can resolve, repair through regeneration or fibrosis, lead to suppuration or pus formation, or progress to chronic inflammation. Examples include acute appendicitis, meningitis, and pneumonia.
Acute inflammation in pathologic basis of diseasesoyovwipedro2
Acute inflammation is characterized by five signs: redness, heat, swelling, pain, and loss of function. The main events of acute inflammation are vascular events like vasodilation and increased permeability, and cellular events involving leukocyte recruitment and activation. This results in an inflammatory cell-rich exudate. Acute inflammation can resolve, repair through regeneration or fibrosis, lead to suppuration or pus formation, or progress to chronic inflammation. Examples include acute appendicitis, meningitis, and pneumonia.
This document summarizes inflammation and the cellular responses involved. It describes inflammation as the body's protective response to injury that is interwoven with the repair process. The cardinal signs of acute inflammation are described as heat, redness, swelling, pain, and loss of function. Both acute and chronic inflammation involve vascular changes, leukocyte migration, and chemical mediators like histamine, cytokines, and arachidonic acid metabolites. Phagocytosis, granulomatous inflammation, healing, and extracellular matrix remodeling are also summarized.
The thyroid gland is the largest endocrine gland located in the neck. It produces thyroid hormones such as T4 and T3 that regulate metabolism. The thyroid follicles contain colloid made of thyroglobulin, which iodine is attached to in order to produce the hormones. The hormones are then released into circulation and have widespread effects increasing the basal metabolic rate and promoting growth and development. Thyroid hormone production is regulated by TSH from the pituitary gland in a negative feedback loop. Disorders can result from too much or too little thyroid hormone production and affect many body systems.
The document provides an overview of the anatomy and physiology of the visual system. It discusses the major parts of the eye including the sclera, cornea, iris, retina, rods and cones. It describes how light is focused on the retina through the lens system and how visual signals are transmitted via the optic nerve and pathways to the visual cortex. It also covers topics like color vision, accommodation, dark adaptation and various eye movements.
More Related Content
Similar to Gingival inflammation - Dr Priya Jose.pptx
The document provides an overview of inflammation, including its definition, etiology, cardinal signs, types (acute and chronic), vascular and cellular events in acute inflammation, mediators, regulation, inflammatory cells, factors affecting acute inflammation, and the fate of acute inflammation. It also discusses chronic inflammation, granulomatous inflammation, comparing acute and chronic inflammation, and dental implications including pulpal infections, periapical infections/inflammation, gingival inflammation, and periodontal inflammation.
Biofilm formation involves the accumulation of microorganisms on surfaces where they form sessile communities encased in an extracellular polymeric substance matrix. Biofilm formation progresses through initial attachment, irreversible attachment aided by EPS production, early development, maturation, and dispersion. Virulence factors and quorum sensing play important roles in biofilm formation. Mature biofilms pose challenges for antibiotic treatment and are implicated in various pathogenic conditions like cystic fibrosis, periodontitis, and device-related infections. Therapeutic strategies aim to target biofilm formation, virulence factors, and quorum sensing.
Periodontitis is caused by bacterial infection of the gums that triggers an inflammatory host response. Bacteria form biofilms in the gingival crevice. This elicits production of inflammatory molecules like IL-1β and TNF-α by immune cells. In susceptible individuals, inflammation is excessive and causes tissue destruction and bone loss. As bone loss progresses, periodontal pockets deepen, increasing pathogen load and further inflammation.
Acute inflammation is the body's initial response to harmful stimuli and involves both vascular and cellular events. The vascular events include increased blood flow, vascular permeability and blood vessel dilation. The cellular events include the recruitment of leukocytes from the bloodstream to the site of injury and their migration into tissues. This is followed by phagocytosis of pathogens and damaged cells by macrophages and neutrophils. Mediators of acute inflammation such as histamine, cytokines and complement proteins are released from cells to promote the inflammatory response. The response and its outcomes can vary depending on factors related to the host and the causative agent.
This document discusses periradicular lesions, which are inflammatory changes that can occur in the tissues surrounding the root apex in response to irritants from infected or inflamed dental pulps. It describes the various irritants that can cause periradicular lesions, including microbes, toxins, mechanical/chemical irritants from root canal procedures. It also discusses the inflammatory process and mediators involved, such as neuropeptides, kinins, cytokines, prostaglandins and leukotrienes. Depending on the nature and extent of the irritants, a variety of tissue changes can result, from transient inflammation to destruction of periradicular tissues.
The document discusses the stages of gingival inflammation. It begins by defining inflammation and providing background on its history. It then discusses 4 stages of gingival inflammation: initial lesion, early lesion, established lesion, and advanced lesion. The initial lesion involves dilation of capillaries and leukocyte recruitment. The early lesion develops within 1 week and may show clinical signs like erythema. The established lesion evolves over months and is characterized by plasma cell predominance. The advanced lesion extends inflammation into alveolar bone, potentially leading to periodontitis in susceptible individuals. Microscopic examination shows features corresponding to the stage of inflammation.
This document discusses sepsis, including definitions, pathophysiology, clinical features, diagnosis, and management. It defines sepsis as a life-threatening condition caused by a dysregulated immune response to infection leading to organ dysfunction. The pathophysiology involves a dysregulated inflammatory response and coagulation system. Signs and symptoms may include altered vital signs and organ dysfunction. Diagnosis involves identifying infection source through cultures and biomarkers. Treatment involves prompt antibiotics, fluid resuscitation, and supportive care based on Surviving Sepsis Campaign guidelines.
The document summarizes key components and mechanisms of the innate immune system in periodontal diseases. The innate immune system provides non-specific defenses and includes intact epithelial barriers, fluids like saliva and GCF, the complement cascade, cell signaling molecules, vasoactive peptides, adhesion molecules, and phagocytic cells like neutrophils and macrophages. These components work together to recognize pathogens, initiate inflammation, and promote pathogen elimination through mechanisms like phagocytosis, helping to maintain periodontal health.
3er Curso Latino Americano de Cicatrización Avanzada en Heridas (I)Karen Pulido
The document discusses various bacterial pathogens commonly found in wounds such as Streptococcus pyogenes, Staphylococcus aureus, and Streptococcus agalactiae. It describes the virulence factors and strategies used by these bacteria to evade the immune system, including the production of biofilms. The summary also outlines approaches to reducing bacterial bioburden in wounds through cleansing, debridement, and judicious use of antibiotics while supporting the host's natural immune response.
Acute inflammation is characterized by five signs: redness, heat, swelling, pain, and loss of function. It involves both vascular and cellular events over a short period of time. The vascular events include increased blood flow and permeability, which leads to fluid leakage. The cellular events involve leukocyte recruitment to the site through adhesion molecules and chemotaxis, followed by activation and phagocytosis of microbes. Acute inflammation can manifest morphologically as serous, fibrinous, purulent or hemorrhagic inflammation. It typically resolves through resolution or repair, but can also lead to suppuration or progress to chronic inflammation.
This document summarizes the stages of gingival inflammation. It begins with initial inflammation seen as vascular changes like dilated capillaries. Early inflammation occurs within 1 week, shown microscopically as PMN infiltration. Established inflammation happens after 2-3 weeks of plaque accumulation and is characterized by B and T lymphocyte accumulation and plasma cell domination. Advanced inflammation involves bone loss and widespread tissue damage. The document provides histological details of the progression from healthy gingiva to advanced periodontitis.
Immunology Lecture day 1 ADDU section DElla Navarro
1. The document provides an overview of immunology and the immune system, including the inflammatory process, anatomy and physiology of the immune system, and different types of immune responses.
2. It discusses the immune system in detail, including the different white blood cells, lymphoid tissues, types of immunity, immune response types, stages of immune response, and immunoglobulins.
3. The document also covers primary and secondary immunodeficiencies like HIV/AIDS, and provides the stages and diagnosis of HIV infection.
This document discusses and classifies acute and subacute osteomyelitis. It begins by defining osteomyelitis as a bone or bone marrow infection. It then classifies osteomyelitis based on timing of onset (acute <2 weeks, subacute 2-6 weeks, chronic >6 weeks) and method of spread (exogenous or hematogenous). Key points include: acute osteomyelitis most commonly spreads hematogenously while staphylococcus aureus is the most common cause; subacute osteomyelitis has an indolent course and is often an incidental finding on imaging. Treatment involves antibiotics, surgery if abscess or lack of response, and immobilization.
Inflammation is the body's protective response to injury or infection that involves increased blood flow, swelling, heat, pain, and loss of function. The document outlines the general considerations of inflammation including its definition, causes, and cardinal signs. It then discusses the major events of acute inflammation including vascular changes, exudation of fluid, and recruitment and activation of leukocytes. Finally, it classifies inflammation into acute and chronic types and further classifies acute inflammation based on the type of exudate produced (serous, fibrinous, suppurative, hemorrhagic).
The document summarizes the stages of gingivitis:
1) The initial lesion involves vascular changes like dilated capillaries. Microscopically there are acute inflammatory changes beneath the junctional epithelium.
2) The early lesion evolves within 1 week, appearing as early gingivitis. Microscopically there is leukocyte infiltration and rete pegs develop in the junctional epithelium.
3) The established lesion involves predominance of plasma cells and B lymphocytes. Microscopically there is widening of intercellular spaces and degradation of collagen around inflammatory cells.
4) The advanced lesion extends into alveolar bone. Microscopically there is widespread tissue damage and
Acute inflammation is characterized by five signs: redness, heat, swelling, pain, and loss of function. The main events of acute inflammation are vascular events like vasodilation and increased permeability, and cellular events involving leukocyte recruitment and activation. This results in an inflammatory cell-rich exudate. Acute inflammation can resolve, repair through regeneration or fibrosis, lead to suppuration or pus formation, or progress to chronic inflammation. Examples include acute appendicitis, meningitis, and pneumonia.
Acute inflammation in pathologic basis of diseasesoyovwipedro2
Acute inflammation is characterized by five signs: redness, heat, swelling, pain, and loss of function. The main events of acute inflammation are vascular events like vasodilation and increased permeability, and cellular events involving leukocyte recruitment and activation. This results in an inflammatory cell-rich exudate. Acute inflammation can resolve, repair through regeneration or fibrosis, lead to suppuration or pus formation, or progress to chronic inflammation. Examples include acute appendicitis, meningitis, and pneumonia.
This document summarizes inflammation and the cellular responses involved. It describes inflammation as the body's protective response to injury that is interwoven with the repair process. The cardinal signs of acute inflammation are described as heat, redness, swelling, pain, and loss of function. Both acute and chronic inflammation involve vascular changes, leukocyte migration, and chemical mediators like histamine, cytokines, and arachidonic acid metabolites. Phagocytosis, granulomatous inflammation, healing, and extracellular matrix remodeling are also summarized.
Similar to Gingival inflammation - Dr Priya Jose.pptx (20)
The thyroid gland is the largest endocrine gland located in the neck. It produces thyroid hormones such as T4 and T3 that regulate metabolism. The thyroid follicles contain colloid made of thyroglobulin, which iodine is attached to in order to produce the hormones. The hormones are then released into circulation and have widespread effects increasing the basal metabolic rate and promoting growth and development. Thyroid hormone production is regulated by TSH from the pituitary gland in a negative feedback loop. Disorders can result from too much or too little thyroid hormone production and affect many body systems.
The document provides an overview of the anatomy and physiology of the visual system. It discusses the major parts of the eye including the sclera, cornea, iris, retina, rods and cones. It describes how light is focused on the retina through the lens system and how visual signals are transmitted via the optic nerve and pathways to the visual cortex. It also covers topics like color vision, accommodation, dark adaptation and various eye movements.
This document summarizes the transport and exchange of respiratory gases in the body. It discusses the diffusion of oxygen and carbon dioxide across membranes, factors that affect diffusion, and the roles of hemoglobin and bicarbonate ions in transporting oxygen and carbon dioxide in the blood and tissues. The oxygen-hemoglobin dissociation curve and factors that can shift it are also described.
Spermatogenesis is the process by which male germ cells develop into mature sperm cells. It begins at puberty and continues throughout a man's life. The process occurs in the testes and epididymis. In the testes, spermatogonia undergo mitosis and meiosis to form haploid spermatids. Spermatids then undergo spermiogenesis to form mature sperm, acquiring motility and other structures. Hormones like FSH, LH and testosterone regulate spermatogenesis, which produces several hundred million sperm daily.
Alveolar bone forms the sockets that hold teeth in place and is a component of the periodontium. It develops during tooth formation and is resorbed when teeth are lost. Alveolar bone consists of alveolar bone proper that lines tooth sockets and supporting alveolar bone made of cortical plates and spongy bone. It undergoes remodeling to accommodate tooth movement and is sensitive to pressure and functional demands, making it important for orthodontics and adapting to tooth loss.
Dentin is the hard tissue that forms the bulk of the tooth beneath enamel. It consists of a bone-like matrix with dentinal tubules that contain odontoblast processes and nerves. Dentin is less mineralized than enamel but provides strength and protects the pulp. The three main theories of dentin hypersensitivity are direct neural stimulation, transduction, and the most accepted hydrodynamic theory, which proposes that fluid movement in the dentinal tubules causes mechanical stimulation of intratubular nerves when exposed dentin is subjected to stimuli.
This document summarizes the specialized mucosa and papillae found on the dorsal surface of the tongue. It describes the four main types of papillae - filliform, fungiform, circumvallate, and foliate papillae. It details their locations, histological features, and functions. The document also discusses taste buds and their role in gustation. Finally, it covers the clinical significance of some variations in tongue morphology and the differences seen in other species.
The document provides information on the structure and functions of the dental pulp. It begins with definitions and general anatomy, describing the pulp as a soft connective tissue enclosed within dentin. It then discusses the zones and structural features of the pulp in more detail. This includes the odontoblastic zone containing odontoblasts and nerve endings, the cell-free zone with capillaries and nerves, and the cell-rich zone with fibroblasts and blood vessels. Key cell types like odontoblasts, fibroblasts, and immune cells are also described. The functions of the pulp in dentin formation, nutrition, and defense are highlighted.
This document discusses the various sequelae that can result from pulpitis, including both acute and chronic forms of pulpitis, apical periodontitis, periapical abscess, osteomyelitis, and periapical cysts. It provides details on the etiology, clinical features, and treatment for each condition. Pulpitis can lead to further inflammation of the surrounding tissues like the apical periodontium and bone. Without proper treatment, pulpitis risks developing into more serious conditions such as apical abscesses or osteomyelitis that require surgical intervention.
This document provides an overview of forensic odontology and the role of dental evidence in various contexts. It discusses personal identification using dental records, identification in mass disasters, extracting dental DNA for identification, analyzing bite marks, and the duties of forensic odontologists, such as documenting evidence, comparing records, and testifying as expert witnesses. The key applications of forensic odontology include identifying unknown remains, assisting in mass disasters, and analyzing bite marks and other dental evidence in legal cases.
1. Amelogenesis involves the life cycle of ameloblasts from the pre-secretory to post-secretory phases as they form enamel.
2. In the secretory phase, ameloblasts deposit enamel matrix proteins and undergo partial mineralization, developing Tome's process which is responsible for enamel rod and interrod formation.
3. Enamel maturation then occurs, fully mineralizing the enamel from the dentin-enamel junction outward in a gradual process modulated by alternating ameloblast types.
The document discusses the periodontal ligament. It describes the periodontal ligament as the connective tissue that surrounds the root and connects it to the alveolar bone. It is made up of principal fibers, cells, ground substance, blood vessels and nerves. The principal fibers are organized into groups like the alveolar crest fibers, horizontal fibers, oblique fibers, and apical fibers that provide support and resist various forces on the teeth. The periodontal ligament also contains cells like fibroblasts, cementoblasts and osteoblasts that allow for remodeling of the tissues. It carries out functions like shock absorption and sensation in addition to attachment of teeth to bone.
Odontogenic tumors arise from tooth-forming tissues and can be divided into three categories: tumors of odontogenic epithelium without mesenchyme, tumors with both epithelium and mesenchyme, and tumors of mesenchyme alone. Ameloblastoma is the most common odontogenic tumor, representing 1% of jaw tumors. It typically presents as a multilocular radiolucency in the mandible and is classified as solid/multicystic, unicystic, or peripheral. Histologically it demonstrates islands of epithelial cells resembling dental lamina. Treatment involves wide local excision due to its persistence and recurrence.
Dental caries is caused by acids produced by bacteria in the mouth that metabolize sugars. It is a chemoparasitic process involving tooth demineralization in two stages. Key factors are the "cariogenic" bacteria Streptococcus mutans and Lactobacillus, along with frequent sugar consumption. Early theories attributed caries to worms, humoral imbalances, or chemical/parasitic causes. Current understanding involves the interplay of host tooth/plaque, carbohydrate substrates, and cariogenic microbes. Nursing bottle caries occurs when babies sleep with bottles containing sugars.
This document discusses ethics in research. It defines research ethics as applying ethical standards to all stages of research, from planning to evaluation. Key principles discussed include honesty, objectivity, integrity, care for participants, openness, respect for intellectual property, confidentiality, non-discrimination, and social responsibility. The document also covers issues like authorship, plagiarism, peer review, research with animals and humans, and addressing misconduct. Overall, it emphasizes that ethical research promotes values like trust, accountability and protecting participants.
This document discusses dental ethics and ethical principles that dental professionals should follow. It notes that dentistry, as a profession, is bound by an ethical code of conduct that seeks to determine what actions professionals should and should not take. The document outlines basic ethical principles like autonomy, justice, and confidentiality. It also provides examples of ethical and unethical behaviors. Additionally, it discusses professional codes of ethics, reasons for having codes, and how to resolve ethical dilemmas.
The document discusses stainless steel crowns, including their definition as prefabricated crown forms adapted to individual teeth and cemented. It covers the history, classifications, indications and contraindications for stainless steel crowns in both primary and permanent teeth. The clinical procedure section describes tooth preparation, crown selection and adaptation, and cementation."
This document defines and classifies oral habits such as thumb sucking and tongue thrusting. It discusses the etiology, diagnosis, and treatment of these habits. Specifically, it notes that oral habits can lead to dentofacial deformities if they persist for long periods. Diagnosis involves examining the patient's swallowing pattern and looking for signs like an open bite. Treatment may involve counseling, reminder appliances to interrupt the habit, or myofunctional exercises to train correct tongue and swallowing posture. The goal is to intercept oral habits before they cause dental or skeletal issues.
This document discusses space management and space maintainers. It begins by defining space management and explaining that premature loss of primary teeth is a common cause of malocclusion. It then discusses the objectives and indications of space maintenance, as well as causes of space loss. The document provides details on different types of space maintainers, including removable, fixed, band and loop, and lingual arch space maintainers. It discusses factors to consider for space maintenance such as the amount of space closure, eruption timing of permanent successors, and oral musculature. Overall, the document provides a comprehensive overview of space management and different approaches to space maintenance.
This document provides information on managing medically compromised patients in dentistry. It discusses various conditions including heart diseases, leukemia, diabetes mellitus, and cystic fibrosis. For each condition, it describes clinical manifestations, oral manifestations, and important considerations for dental treatment. Key points discussed include the need for medical consultations, antibiotic prophylaxis if needed, and modifying treatment for patients with low platelet counts or susceptibility to infections.
The biomechanics of running involves the study of the mechanical principles underlying running movements. It includes the analysis of the running gait cycle, which consists of the stance phase (foot contact to push-off) and the swing phase (foot lift-off to next contact). Key aspects include kinematics (joint angles and movements, stride length and frequency) and kinetics (forces involved in running, including ground reaction and muscle forces). Understanding these factors helps in improving running performance, optimizing technique, and preventing injuries.
Travel Clinic Cardiff: Health Advice for International TravelersNX Healthcare
Travel Clinic Cardiff offers comprehensive travel health services, including vaccinations, travel advice, and preventive care for international travelers. Our expert team ensures you are well-prepared and protected for your journey, providing personalized consultations tailored to your destination. Conveniently located in Cardiff, we help you travel with confidence and peace of mind. Visit us: www.nxhealthcare.co.uk
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14...Donc Test
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition (Hinkle, 2017) Verified Chapter's 1 - 73 Complete.pdf
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition (Hinkle, 2017) Verified Chapter's 1 - 73 Complete.pdf
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition (Hinkle, 2017) Verified Chapter's 1 - 73 Complete.pdf
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7shruti jagirdar
Unit 4: MRA 103T Regulatory affairs
This guideline is directed principally toward new Molecular Entities that are
likely to have significant use in the elderly, either because the disease intended
to be treated is characteristically a disease of aging ( e.g., Alzheimer's disease) or
because the population to be treated is known to include substantial numbers of
geriatric patients (e.g., hypertension).
Congestive Heart failure is caused by low cardiac output and high sympathetic discharge. Diuretics reduce preload, ACE inhibitors lower afterload, beta blockers reduce sympathetic activity, and digitalis has inotropic effects. Newer medications target vasodilation and myosin activation to improve heart efficiency while lowering energy requirements. Combination therapy, following an assessment of cardiac function and volume status, is the most effective strategy to heart failure care.
Giloy in Ayurveda - Classical Categorization and SynonymsPlanet Ayurveda
Giloy, also known as Guduchi or Amrita in classical Ayurvedic texts, is a revered herb renowned for its myriad health benefits. It is categorized as a Rasayana, meaning it has rejuvenating properties that enhance vitality and longevity. Giloy is celebrated for its ability to boost the immune system, detoxify the body, and promote overall wellness. Its anti-inflammatory, antipyretic, and antioxidant properties make it a staple in managing conditions like fever, diabetes, and stress. The versatility and efficacy of Giloy in supporting health naturally highlight its importance in Ayurveda. At Planet Ayurveda, we provide a comprehensive range of health services and 100% herbal supplements that harness the power of natural ingredients like Giloy. Our products are globally available and affordable, ensuring that everyone can benefit from the ancient wisdom of Ayurveda. If you or your loved ones are dealing with health issues, contact Planet Ayurveda at 01725214040 to book an online video consultation with our professional doctors. Let us help you achieve optimal health and wellness naturally.
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
Pictorial and detailed description of patellar instability with sign and symptoms and how to diagnose , what investigations you should go with and how to approach with treatment options . I have presented this slide in my 2nd year junior residency in orthopedics at LLRM medical college Meerut and got good reviews for it
After getting it read you will definitely understand the topic.
PGx Analysis in VarSeq: A User’s PerspectiveGolden Helix
Since our release of the PGx capabilities in VarSeq, we’ve had a few months to gather some insights from various use cases. Some users approach PGx workflows by means of array genotyping or what seems to be a growing trend of adding the star allele calling to the existing NGS pipeline for whole genome data. Luckily, both approaches are supported with the VarSeq software platform. The genotyping method being used will also dictate what the scope of the tertiary analysis will be. For example, are your PGx reports a standalone pipeline or would your lab’s goal be to handle a dual-purpose workflow and report on PGx + Diagnostic findings.
The purpose of this webcast is to:
Discuss and demonstrate the approaches with array and NGS genotyping methods for star allele calling to prep for downstream analysis.
Following genotyping, explore alternative tertiary workflow concepts in VarSeq to handle PGx reporting.
Moreover, we will include insights users will need to consider when validating their PGx workflow for all possible star alleles and options you have for automating your PGx analysis for large number of samples. Please join us for a session dedicated to the application of star allele genotyping and subsequent PGx workflows in our VarSeq software.
Nutritional deficiency Disorder are problems in india.
It is very important to learn about Indian child's nutritional parameters as well the Disease related to alteration in their Nutrition.
- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Discover the benefits of homeopathic medicine for irregular periods with our guide on 5 common remedies. Learn how these natural treatments can help regulate menstrual cycles and improve overall menstrual health.
Visit Us: https://drdeepikashomeopathy.com/service/irregular-periods-treatment/
2. INDEX
General aspects of inflammation
Steps
Cells involved
Factors influencing
Definition of gingival inflammation
Studies involved
Initiation of gingival inflammation
Steps in gingival inflammation
Cells involved
Conclusion
Reference
3. DEFINITION
Inflammation is a non specific, localized immune reaction of
the organism, which tries to localized the pathogen agent.
Many consider the syndrome a self-defense mechanism.
It consist in vascular, metabolic, cellular changes, triggered by
the entering of pathogen agent in healthy tissues of the body.
4. ETIOLOGY
The causes of inflammation are many and varied:
Exogenous causes:
Physical agents
Mechanic agents: fractures, foreign corps, sand, etc.
Thermal agents: burns, freezing
Chemical agents: toxic gases, acids, bases
Biological agents: bacteria, viruses, parasites
Endogenous causes:
Circulation disorders: thrombosis, infarction,
hemorrhage
Enzymes activation – e.g. acute pancreatitis
Metabolic products deposals – uric acid, urea
5. CARDINAL SIGNS
Celsus described the local reaction of injury in terms that have
come to be known as the cardinal signs of inflammation.
These signs are:
rubor (redness)
tumor (swelling)
calor (heat)
dolor (pain)
functio laesa, or loss of function
(In the second century AD, the Greek physician Galen
added this fifth cardinal sign)
6. GENERAL ASPECTS OF INFLAMMATION
Changes in acute inflammation
Vascular events
Haemodynamic changes
Altered vascular permeability
Endothelial cell contraction
Endothelial cell retraction
Direct endothelial cell injury
Leucocyte mediated endothelial injury
Cellular events
Exudation of leucocytes
Changes in the formed elements of blood
Adhesion or rolling
Emigration
Chemostasis
Phagocytosis
Attachment stage (opsonization)
Engulfment stage
Secretion(degranulation stage)
Killing or degradation stage
17. DEFINITION
Gingivitis is defined as an inflammation confined to the tissues of
the marginal gingiva.
AAP
Current concept- result of epidemiological studies, analysis of
autopsy and biopsy material , clinical trials and animal experimentation.
18. SOME STUDIES
Extent of periodontal disease increases with age &
with inadequate oral hygiene.
Few subjects in each age group suffer from
advanced periodontal destruction.(Loe et al 1986)
Socransky et al 1984 – periodontitis progresses in
episodes of exacerbation & remission- burst
hypothesis.
Progression is a continous than episodic &
detaction of burst due to an inadequate resolution
of clinical measurement (Jeffcoat & Reddy 1991)
19. INITIATION OF PERIODONTAL DISEASE
Micro organism quickly start to colonize clean tooth
surface once an individual abstains from
mechanical tooth cleaning.(Loe et al, 1965).
Removal of subgingival deposit help in successfully
treating periodontal disease.(Ramfjord et al 1968)
Long term observation in Beagle dogs concluded
that inflammation occur in animals that accumulate
plaque(Saxa et al 1967)
20. Some imbalance of host –microbe relationship is
occuring in the destructive lesions, which may be unique
to that site and to periodontally susceptible individuals
generally.
21. SOME TERMINOLOGY
Pristine gingiva-
State of super health
Normal gingiva that is free from “ significant “ accumulation of
inflammatory cells histologically .
Healthy gingiva –
Clinically similar to pristine gingiva
Histologically features of inflammatory infiltrate with predominantly
neutrophils associated with junctional epithelium and lymphocytes in
the subjacent connective tisssue.
22. FEATURES OF CLINICALLY HEALTHY GINGIVA
Infiltrate of inflammatory cells(PMN) in JE &
lymphocyte in CT.
Very early stage collagen depletion is noted.
Exudative & transudative fluid & plasma protein
arrive –GCF
Infiltrate 5 % of CT
Recruitment of PMN by chemoattractant action ( IL-
8,C5a, leukotriene B4, LPS, formyl methionyl leucyl
phenylalanine)
Later leukocytes arrive( Attstrom 1971)
Cytokines & adhesion molecules
23. DEFENSIVE FACTOR
Regular shedding of epithelial cells into the oral
cavity.
Intact epithelial barrier.
Positive fluid flow of gingival crevice
Antimicribial effect of antibody
Phagocytic function of neutrophil & macrophage
Detrimental effect of complement
24. Weakening host factors seen during
Hormones –puberty & pregnancy
Drugs-cyclosporin
Systemic infection
Neutrophil depletion or dysfunction
33. CELLS INVOLVED
Antigen presenting cell
TCR
T cell mediated process
B cell mediated process
34.
35.
36.
37.
38.
39.
40.
41. STAGE IN THE PATHOGENESIS OF GINGVAL
INFLAMMATION
Page & Schroeder -1976- depending according to clinical & histo
pathological evidence.
Stage I- initial lesion
Stage II- Early lesion
Stage III-Established lesion
Stage IV- Advanced lesion
-STATE OF PROGRESSION OF GINGIVITIS TO PERIODONTITIS
42. Mostly non-human experiment.-( animal biopsy &
some young adolescent)
A new classification is outlined.
43.
44. Within 10-20 days of plaque accumulation , clinical
signs of gingivitis are established.
45. INITIAL LESION
Clinical Within 24 hours
Subclinical gingivitis – not apparent
Histological Changes in microvascular plexus-dialation of arteriole,
capillary & venules of dentogingival plexus.
Hydrostatic pressure inc ,intercellular gap formed, fluid
& protein exuded.
GCF inc( washing)-plasma proteins defense action
PMN cell migration –adhesion molecules
Leukocyte migrate up cytokineretained longer help of
CD 44 receptor- diapedesis.
Perivasular connective tissue matrix –exudation &
deposition of fibrin
Cellular response is well established. Help of cytokine
46.
47. STAGE II –EARLY LESION
Clinical After 1 week
Detected clinically- second week
Subgingivally located biofilm is formed
Gingiva becomes erythematous –proliferation of
capillary
No clear cut dividing line
GCF flow reach maximum in 6 -12 days after clinical
gingivitis
Histology Vessels remain dialated,number increase
Lymphocytes ( 75
5 % T cells & PMN are predominant two to three fold
.Few plasma cells are seen
15% volume
Fibroblast degenerate –more infiltration
Collagen destruction occur(70%).
Main fiber affected are circular & dento gingival fibers
Basal cells of JE & SE proliferated
Epithelial rete pegs invading coronal portion of lesion.
48.
49. STAGE III- ESTABLISHED LESION
Clinically More edematous swelling
Chronic gingivitis 2 – 3weeks after plaque –
Anoxemia, blood flow stasis, slightly bluish in color
Extravasation of erythrocytes
histologically Increased fluid exudation & leukocyte migration into tissue
Dominated by plasma cells- situated primarly in coronal CT &
vessels
Predominant Ig is Ig G 1 & Ig G 3
Collagen loss both lateral & apical loss-leukocytic inflitration
JE proliferate & rete pegs extend deeper-epithelial integreity &
barrier
JE is changed – not closely attached
Pocket epithelium- heavy leukocyte infiltrate
Basal lamina may be destroyed
JE more permeable- underlying CT –necrosis
Elevated levels of acid & alkaline phosphatase, beta –
glucuronidase, beta glucosidase, cytochrome oxidase,esterase
Neutral mucopoltsaccharide are dec
50. Two types
One remains stable-not progessing for months or years
Second –Active –progressive & destructive advanced
lesion.
51. Proportion of T cell decrease,B cell increase
Change in microbial flora or infectiopn of gingival
tissues.
52.
53. STAGE IV – ADVANCED LESION
Clinical Phase of periodontal breakdown.
Formation of periodontal pocket, suppuration,
mobility, migration & tooth exfoliation
Histological As pocket deepens –apically migration of JE
Destructive episode
Flourishes anaerobic niche
Infiltrate extend laterally & apically
Features of established
Except- alveolar bone loss, fiber damage
extensive,JE migrate apically, wide spread
manifestation of inflammatory & immuno
pathological tissur damage.
No longer localized .
Plasma cell domination
Areas of temporary ulceration.
54. GINGIVAL INFLAMMATION ASSESSMENT:
IMAGE ANALYSIS
non-index method to measure gingival condition.
the quantitative analysis of gingival swelling and
color characteristics of gingiva by digital images
before and after treatment of individual patients.
Image analysis using using Serif photo pluse-6
software.
(MATLAB software) would give more precise
readings
Journal of Indian Society of Periodontology - Vol 16, Issue 2, Apr-Jun 2012
55. CONCLUSION
Gingival inflammation has two components- Acute
& chronic .
Each gingival region can have varying amounts of
acute & chronic component.
Those with acute inflammatory changes – there is
dramatic change in treament.
The more inflamed a gingival unit appear clinically,
the better the chances of therapeutic measures
resulting in a return to normal gingivak health.
56. REFERENCES
Carranza’s Textbook of Periodontology-10th &11th edition
Clinical periodontology and implant dentistry –Jan
Linde-5 th edition
Textbook of Periodontology and Oral implantology-
Nayak-First edition
Loe H, Theilade E, Jensen SB (1965) Experimental
Gingivitis in Man.J Periodontol 36: 177–187
Eberhard J, Reimers N, Dommisch H, Hacker J, Freitag
S, et al. (2005) The effect of the topical administration of
bioactive glass on inflammatory markers of human
experimental gingivitis. Biomaterials 26: 1545–155
Li Y, Lee S, Hujoel P, Su M, Zhang W, et al. (2010)
Prevalence and severity of gingivitis in American adults.
Am J Dent 23: 9–13
62. Interleukin-1 Intrabony defects
Influence of IL-1 gene polymorphism on clinical and
radiographic healing outcomes of GTR therapy did not
reveal any statistically significant differences between IL-
1 + and IL-1 – patients.
Interleukin -4 Evaluation of IL-4 gene polymorphisms in the intron 2 and
in the promoter
region (PP +and IP+) showed no association with
periodontal disease
susceptibility.
Interleukin-2 It is established that – 330 (T→G) polymorphism in IL-2
gene is associated with
severity and active role in pathogenesis of periodontal
disease
Tumor necrosis factor -α Research to investigate 4 polymorphisms in TNF- α gene
which were all transitions from G to A, 3 in the promoter
positions: – 376, – 308, – 238 and at position + 489, could
not be identified as susceptibility or severity factors in
periodontitis.
63. Interleuin-10 Three single-nucleotide polymorphisms (SNPs) in the
IL10 gene at positions – 1087, a G to A substitution, –
819, a C to T substitution and – 592, a C to A substitution
have been associated with altered synthesis of IL10
HLA Genetics The MHC genes are the most polymorphic genes present
in the genome of every species.
Studies suggested that patients with HLA-DRB1*1501-
DQB1*0602 genotype may have accelerated T cell
response and increased susceptibility to periodontitis
FcγReceptor polymorphisms, When one or several of FcγR-mediated leukocyte
functions are less or over
efficient due to polymorphisms, it is conceivable that
susceptibility for or severity of periodontitis is seen.
Vitamin D receptor (VDR)
polymorphisms
Studies demonstrated vitamin D receptor (VDR) gene is
localized in chromosome 12 with a cluster of
polymorphisms: BsmI, ApaI and TaqI and relationship
between TaqI VDR gene polymorphisms and periodontitis
Matrix
metalloproteinases(MMP)
polymorphisms
A single nucleotide polymorphism in the promoter region
of - 1607 bp of MMP-1 gene a, 5’-GGA-3’, instead of 5’-
GAT-3’ has been found to be associated
66. The “red-complex organisms” – Porphyromonas
gingivalis, Tannerella forsythia, and Treponema
denticola
Inhibition of the chemokine IL-8
Modulation of signalling in “lipid rafts” - between TLR2
and CXC-chemokine receptor 4 (CXCR4) after they are
recruited to a lipid raft inresponse to P. gingivalis fimbriae.
Directly antagonizing TLR4 through production of Lipid
A
67. DIAGNOSTIC METHOD TO ASSESS
INFLAMMATION
Genetic analysis
Clinical method
Bleeding on probing
Probes
Gingival temperature
Biochemical analysis
Microbiological analysis
Image Analysis
68. PROTEOLYTIC HYDROLYTIC
Collagenase
Elastase
Cathepsin – G
Cathepsin – B
Cathepsin – D
Dipeptidylpeptidases
Tryptase
Aryl Sulphatase
-Glucuronidase
Alkaline Phosphatase
Acid Phosphotase
Myeloperoxidase
Lysozyme
Lactoferrin
69. FACTORS THAT MAY MODIFY THE INFLAMMATORY
RESPONSE
Mechanical
Calculus
Caries
Restorations *overhangs will increase plaque
Prosthesis
Tooth Anatomic Factors
Systemic
Uncontrolled diabetes *most common cause of perio disease – if you have diabetes
you are more prone to periodontal disease. Glucose control and periodontal disease
are linked.
Obesity = more prone to perio disease; overweight means you hae more fat and fat
cells produce cytokines, these produce inflammatory mediators. More cytokines
than normal more risk of perio problems.
PMN defects
Hematological
Pregnancy
Puberty
Immune disturbances
HIV/AIDS *a person can have this from birth, we don’t have a lot of statistics on this
topic.
Medications
Nutritional deficiencies
70. Genetic
Agranulocytosis
Cyclic neutropenia *lack of PMN’s – no first responders to the
inflammation.
Other neutropenias
Lazy leukocyte syndrome
Leukoctye adhesion deficiency (LAD)
Down’s syndrome
Papillon-Lefevre syndrome
Hypophosphatasia *prepubertal patients tend to have these problems.
Chediak-Higashi syndrome
Ehlers-Danlos syndrome
Habits: smoking,
Systemic disorders: HIV and Diabetes
71. Innate and Adaptive Immunity
Immune Cells
*the vast majority of the immune cells are neutrophils –
these are the first responders
*they have a 48 hour lifespan in the blood with migration to
sites for phagocytosis.
Monocytes are on the scene – in the tissue these become
macrophages.
Cytokines
Definition: soluble, locally active polypepties: regulate cell
growth, differentiation, function
Produced by cells of the immune system
Specific cytokines may have different biologic properties
depending on their concentration, the cells producing
them, the cells being acted upon, and the extracellular
matrix.
72. October 30–November 2, 1999, the International Workshop for a Classification of Periodontal Diseases and Conditions
73. TOLL LIKE RECEPTOR
First identified as fruit flies-Drosophila spp.-Christiane
Nüsslein-Volhard -1985
The first reported human TLR was described by
Nomura et al. in 1994 , and mapped to a chromosome
by Taguchi et al. in 1996
TLR cause APC to upregulate the co-stimulatory B7
molecules.
Leads to T-cell proliferation.
74. These germline-encoded receptors, collectively
known as pattern-recognition receptors (PRRs),
can detect and respond to conserved and generally
distinct microbial structures that are shared by
related groups of microorganisms (1).
These microbial structures are referred to as
pathogen-associated molecular patterns (PAMPs),
and include bacterial lipopolysaccharides,
peptidoglycan, lipoproteins, bacterial DNA, and
double-stranded RNA.
Upon interaction with these PAMPs, TLRs activate
the innate immune cells through intracellular
signaling pathways.
75. With IL 1 - “Interleukin-1 Receptor/Toll-Like
Receptor Superfamily”
Three subgroups of TIR domains exist
Subgroup 1 TIR domains are receptors for interleukins
and all have extracellular immunoglobulin (Ig) domains.
Subgroup 2 TIR domains are classical TLRs, and bind
directly or indirectly to molecules of microbial origin.
A third subgroup -consists of adaptor proteins that are
exclusively cytosolic and mediate signaling from
proteins of subgroups 1 and 2
76. STRUCTURE
TLRs are transmembrane glycoproteins possessing
varying numbers of extracellular N-terminal leucine-rich
repeat (LRR) domain, followed by a cysteine-rich region,
a transmembrane domain and a C-terminal cytoplasmic
Toll/IL-1R (TIR) domain .
The LRR domain is important for ligand binding and
associated signaling, and is a common feature of PRRs.
The TIR domain is important in protein- protein
interaction and is typically associated with innate
immunity.
77.
78.
79. Toll-like receptors (TLRs 1, 2, 4, 5 and 6) that
recognize extracellular microbial structures are
expressed on the host cell surface.
Toll-like receptors (TLRs 3, 7, 8 and 9) specifically
detecting viral or bacterial nucleic acids are
expressed intracellularly on endocytic vesicles
84. Continuous model (1900-1950’s)
Continuous through life at the same rate of loss (i.e.,
everyone gets periodontal disease)
Progressive model (1940-1960-2)
Progressive loss over time of some sites
No destruction in others.
Time of onset and extent vary among sites.
(e.g., Periodontal disease affects mainly the posterior
teeth)
85. Random burst model (1970-2000’s)
Activity occurs at random at any site
Some sites show no activity
Some sites have one or more burst of activitiy
Cumulative extent of destruction varies among sites
i.e., periodontitis is different in various sites in the same
individual and it is difficult to predict attachment loss
Asynchronous Burst
Asynchronous multiple burst model (1970s-
2000s)
Several sites have one or more burst of activity
during one period of life
Prolonged period of inactivity; remission.
This is similar to random burst but it takes into
account the risk factors of overhangs, smoking,
diabetes, etc.
86. OBESITY & PERIODONTAL DISEASE
In 1977, Perlstein et al. observed histopathologic changes
in the periodontium in hereditary obese Zucker rats.
In 1998, Saito et al. analyzed 241 healthy Japanese
individuals and showed, for the first time, an association
between obesity and periodontal disease in humans.
Genco et al. analyzed National Health and Nutrition
Examination Survey (NHANES III) data and demonstrated
that BMI was positively correlated ; they found that this
relationship is modulated by Insulin resistance.
87. Suggesting that periodontitis might impact diabetes with topical
antibiotics improves HbA1c by reducing hs-CRP, which may
relate to amelioration of insulin resistancein type 2 diabetic
patients with periodontal disease.
It has been suggested that the secretion of TNF-α by adipose
tissue triggered by LPS from periodontal gram-negative
bacteria promotes hepatic dyslipidemia and decreases insulin.
Type 2 diabetes and decreased insulin sensitivity are
associated with the production of advanced glycation end
products (AGE), which trigger inflammatory cytokine production,
thus predisposing to inflammatory diseases such as
periodontitis.
88. Adipose-Tissue-Derived Hormones and Cytokines
(Adipokines) Inflammatory Markers
Adipose tissue secretes proinflammatory cytokines such as tumor
necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6).
Leptin-
pleiotropic cytokine, secreted by adipocytes
“lipostat” –regulate adipose tissue mass
Decreased leptin levels –increasing pocket pocketing depth.
Adiponectin, Resistin and other Adipose- Tissue-Derived
Cytokines
Apidonectin- reduced levels in obesity, insulin resistance or type 2
diabetes
Resistin
Visfatin- insulin like effects
Serum – retinol- binding protein4 (RBP4)
subgroup 1 TIR domains are receptors for interleukins that are produced by macrophages, monocytes and dendritic cells, and all have extracellular immunoglobulin (Ig) domains.
subgroup 2 TIR domains are classical TLRs, and bind directly or indirectly to molecules of microbial origin.
A third subgroup of proteins containing TIR domains consists of adaptor proteins that are exclusively cytosolic and mediate signaling from proteins of subgroups 1 and 2
Insulin sensitivity-adiponectin levels –insulin sensitivity , antiatherogenic , anti inflammatory .
Resistin like molecules(RELM) – insulin sensitivity, more closely related to inflammatory processes than to insulin resistance.