What Is Inflammation?
Inflammation is a process by which your body's white blood cells and the things they make protect you from infection from outside invaders, such as bacteria and viruses.
But in some diseases, like arthritis, your body's defense system -- your immune system -- triggers inflammation when there are no invaders to fight off. In these autoimmune diseases, your immune system acts as if regular tissues are infected or somehow unusual, causing damage.
Inflammation is the body's response to injury or infection and is characterized by redness, swelling, heat, pain, and loss of function. It involves increased blood flow, exudation of fluid, and emigration of leukocytes. The goals are to remove harmful stimuli, limit tissue damage, and initiate repair. Acute inflammation is short-lived and has beneficial effects like fighting infection, but can also cause harmful tissue swelling and pain.
The document summarizes key aspects of acute and chronic inflammation. Acute inflammation is triggered by various stimuli and involves increased blood flow, vascular permeability, and leukocyte migration. It aims to eliminate injurious agents. Chronic inflammation arises from persistent infections, toxins, or autoimmunity and is characterized by mononuclear cell infiltration and attempts at repair through fibrosis. Nutrition can impact inflammation through deficiencies, essential fatty acids, antioxidants, and factors related to over-nutrition like obesity.
The document summarizes key aspects of acute and chronic inflammation. Acute inflammation is triggered by various stimuli and involves increased blood flow, vascular permeability changes, and leukocyte migration to sites of injury. It aims to eliminate injurious agents and resolve quickly, but can develop into chronic inflammation if the agent persists. Chronic inflammation is prolonged, simultaneously destroys and repairs tissue, and underlies common diseases like arthritis and atherosclerosis.
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 summarizes the key differences between acute and chronic inflammation. Acute inflammation is an initial rapid response to injury or infection that involves increased blood flow and immune cell infiltration. It is typically short-lived and resolves within days. Chronic inflammation is a prolonged response lasting weeks or longer that can cause ongoing tissue damage. It involves different immune cells and may have no obvious symptoms, increasing risk for serious diseases like cancer if left unaddressed.
Inflammation is defined as the local response of tissues to injury or infection. It is characterized by redness, swelling, heat, pain, and loss of function. The inflammatory response involves vascular changes like increased blood flow and permeability, as well as cellular responses. White blood cells like neutrophils and macrophages migrate to the site of injury to remove infectious agents and damaged tissue through phagocytosis. Acute inflammation resolves quickly, while chronic inflammation persists long-term and can cause tissue damage.
Inflammation is the body's protective response to injury or infection. It involves both vascular and cellular events at the site of injury. The basic mechanism of inflammation includes increased blood flow, vascular permeability, exudation of fluid and cells, and changes in other tissues. Chemical mediators like histamine, bradykinin, prostaglandins, leukotrienes, and cytokines are released during inflammation to regulate the inflammatory response. Both acute and chronic inflammation aim to eliminate the initial cause of cell injury, clear out necrotic cells and tissues from the site of injury, and initiate the repair process.
Inflammation is the body's response to injury or infection and is characterized by redness, swelling, heat, pain, and loss of function. It involves increased blood flow, exudation of fluid, and emigration of leukocytes. The goals are to remove harmful stimuli, limit tissue damage, and initiate repair. Acute inflammation is short-lived and has beneficial effects like fighting infection, but can also cause harmful tissue swelling and pain.
The document summarizes key aspects of acute and chronic inflammation. Acute inflammation is triggered by various stimuli and involves increased blood flow, vascular permeability, and leukocyte migration. It aims to eliminate injurious agents. Chronic inflammation arises from persistent infections, toxins, or autoimmunity and is characterized by mononuclear cell infiltration and attempts at repair through fibrosis. Nutrition can impact inflammation through deficiencies, essential fatty acids, antioxidants, and factors related to over-nutrition like obesity.
The document summarizes key aspects of acute and chronic inflammation. Acute inflammation is triggered by various stimuli and involves increased blood flow, vascular permeability changes, and leukocyte migration to sites of injury. It aims to eliminate injurious agents and resolve quickly, but can develop into chronic inflammation if the agent persists. Chronic inflammation is prolonged, simultaneously destroys and repairs tissue, and underlies common diseases like arthritis and atherosclerosis.
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 summarizes the key differences between acute and chronic inflammation. Acute inflammation is an initial rapid response to injury or infection that involves increased blood flow and immune cell infiltration. It is typically short-lived and resolves within days. Chronic inflammation is a prolonged response lasting weeks or longer that can cause ongoing tissue damage. It involves different immune cells and may have no obvious symptoms, increasing risk for serious diseases like cancer if left unaddressed.
Inflammation is defined as the local response of tissues to injury or infection. It is characterized by redness, swelling, heat, pain, and loss of function. The inflammatory response involves vascular changes like increased blood flow and permeability, as well as cellular responses. White blood cells like neutrophils and macrophages migrate to the site of injury to remove infectious agents and damaged tissue through phagocytosis. Acute inflammation resolves quickly, while chronic inflammation persists long-term and can cause tissue damage.
Inflammation is the body's protective response to injury or infection. It involves both vascular and cellular events at the site of injury. The basic mechanism of inflammation includes increased blood flow, vascular permeability, exudation of fluid and cells, and changes in other tissues. Chemical mediators like histamine, bradykinin, prostaglandins, leukotrienes, and cytokines are released during inflammation to regulate the inflammatory response. Both acute and chronic inflammation aim to eliminate the initial cause of cell injury, clear out necrotic cells and tissues from the site of injury, and initiate the repair process.
Inflammation is the body's response to injury or infection that involves vascular and cellular events. The cardinal signs of inflammation are redness, swelling, heat, pain, and loss of function. Inflammation can be either acute (minutes to days) or chronic (weeks to months). Chemical mediators like histamine, prostaglandins, and leukotrienes are released during inflammation and cause changes like increased vascular permeability and leukocyte migration. Repair after inflammation occurs through regeneration of tissues like skin, or through healing by scar formation. Healing involves granulation tissue formation, angiogenesis, fibroblast proliferation and extracellular matrix deposition.
This document discusses inflammation. It defines inflammation as the body's local response to injury or infection aimed at eliminating the cause of injury and initiating repair. The cardinal signs of inflammation are redness, swelling, heat, pain, and loss of function. The early response involves vasodilation and increased permeability, causing swelling. The late response involves neutrophils in acute inflammation and macrophages in chronic cases, which work to destroy pathogens and initiate healing. Understanding inflammation is important for diagnosing conditions like appendicitis and treating diseases.
Inflammation is the protective response of tissues to injury. The key events of acute inflammation are vasodilation, increased vascular permeability, and leukocyte emigration. Increased permeability allows plasma proteins and cells to exit vessels and accumulate at sites of injury. This leads to edema, which can be an exudate or transudate depending on protein content. Exudates have high protein levels from significant vessel changes, while transudates have low protein from hydrostatic/osmotic imbalance without major vessel changes. The mechanisms driving permeability involve histamine and other mediators causing both immediate and delayed responses from the endothelium.
Inflammation is the protective response of tissues to injury. The key events of acute inflammation are vasodilation, increased vascular permeability, and leukocyte emigration. Increased permeability allows plasma proteins and cells to exit vessels and accumulate at sites of injury. This leads to edema, which can be an exudate or transudate depending on protein content. Exudates have high protein levels from significant vessel changes, while transudates have low protein from hydrostatic/osmotic imbalance without major vessel changes. The mechanisms driving permeability involve histamine and other mediators causing both immediate and delayed responses from the endothelium.
The document discusses inflammation and necrosis. It begins by introducing inflammation as the body's defense response to eliminate injurious agents and remove necrotic tissue. It then provides a brief history of observations and descriptions of inflammation dating back to ancient Egypt. The document defines inflammation and describes the types as acute or chronic. It discusses the vascular changes that occur during inflammation including increased blood flow, vascular permeability, and cellular events such as exudation of leukocytes and phagocytosis.
Inflammation is the body's response to infection, injury, or irritation. It is characterized by redness, swelling, heat, and pain at the site of injury or infection. When tissue is damaged, chemicals are released that cause blood vessels to become leaky and allow immune cells like neutrophils and macrophages to migrate to the injured site. These cells destroy and remove pathogens, limit their spread, and initiate tissue repair. Acute inflammation resolves quickly, while chronic inflammation persists long-term and can damage tissue over years.
The document provides information about inflammation including its causes, classification, and mechanisms. It discusses how inflammation is the body's response to harmful stimuli and can be either acute or chronic. Acute inflammation develops rapidly in response to injury and involves innate immune responses, while chronic inflammation can last months to years and involves adaptive immunity. The key events of acute inflammation are increased blood flow, vascular permeability, and migration of immune cells to the site of injury.
Inflammation (Acute and Chronic) Prof Mulazim Hussain BukhariMulazim Bukhari
This document discusses acute inflammation. It defines inflammation, outlines the causes and molecular events of inflammation including vasodilation, vascular leakage, and leukocyte recruitment. It describes the cardinal signs of inflammation and summarizes the mechanisms of increased vascular permeability and leukocyte extravasation through selectin-mediated rolling, integrin-mediated adhesion, and transmigration across endothelial cells.
This document summarizes a seminar presentation on inflammation given by Manu S J to the Department of Pharmacology at PES College of Pharmacy. It defines inflammation, describes the classic signs of acute inflammation and the pathophysiology involving increased blood flow, vascular permeability, and cellular infiltration. It also discusses causes of inflammation including infection and injury, and the roles of chemical mediators like histamine, cytokines, and complement proteins in propagating the inflammatory response. Chronic inflammation is characterized by prolonged duration and tissue proliferation or destruction. Granulomatous inflammation involves macrophage aggregation forming granulomas.
Inflammation is the protective response to eliminate the cause of cell injury and damaged tissue. It is characterized by redness, heat, swelling, pain, and loss of function. The signs are caused by increased blood flow and vascular permeability. Inflammation can be acute, lasting minutes to days, or chronic, lasting weeks or months. Acute inflammation involves recruitment of leukocytes from the bloodstream to fight infection at the site of injury. Chronic inflammation is prolonged and involves tissue destruction by mononuclear cells and attempts at healing through fibrosis. Mediators like cytokines prolong the inflammatory response.
This document provides an overview of inflammation. It defines inflammation and divides it into acute and chronic types. The components of inflammation include vascular reactions and cellular reactions. Acute inflammation is characterized by neutrophil accumulation and lasts for a short period, while chronic inflammation involves lymphocytes and macrophages and lasts longer. The document further describes the stimuli, vascular changes, and cellular events involved in acute inflammation, including leukocyte margination, rolling, adhesion, transmigration, and phagocytosis. It also discusses the chemical mediators and outcomes of acute inflammation.
Inflammation is the body's protective response to eliminate the initial cause of cell injury and promote tissue repair. The classical signs of acute inflammation are heat, redness, swelling, pain, and loss of function. Acute inflammation is short-lived and involves increased blood flow, vascular permeability, and recruitment of immune cells like neutrophils to the injured site. Chronic inflammation lasts longer and is characterized by lymphocytes, plasma cells and macrophages, tissue destruction, and fibrosis. The outcome of acute inflammation is typically resolution and healing of the damaged tissues.
Acute inflammation is the early response of tissues to injury and involves vascular and cellular events. The vascular events include vasodilation, increased vascular permeability allowing plasma proteins to leave circulation, and accumulation of leukocytes from the blood vessels into tissues. The principal leukocytes in acute inflammation are neutrophils. The cellular events in acute inflammation help destroy, dilute or isolate injurious agents. Mediators of acute inflammation include histamine, prostaglandins, nitric oxide, complement factors and cytokines. Acute inflammation is rapid in onset, relatively short in duration and aims to return tissues to normal function.
This document discusses inflammation and its causes, types, and vascular events. It defines inflammation as the body's protective response to eliminate injurious stimuli and damaged tissue. Inflammation can be acute or chronic depending on the severity and duration of the stimulus. The key vascular events of acute inflammation include increased blood flow causing redness and heat, increased vascular permeability allowing fluid proteins to leave blood vessels and cause swelling, and leukocyte emigration to sites of injury. This leads to the five cardinal signs of inflammation. The document explores the mechanisms behind these vascular changes in detail.
This document provides an overview of inflammation and healing. It defines inflammation as the body's response to injury, discussing the causes, signs, and types (acute and chronic) of inflammation. Acute inflammation involves vascular changes like increased blood flow and permeability, as well as cellular events like leukocyte migration and phagocytosis. Chemical mediators released from cells and plasma regulate these inflammatory responses. Healing is defined as the process of tissue regeneration and repair after injury or inflammation.
Inflammation and Healing (wound healing)Rajat Nanda
This document provides information on inflammation and healing in 3 sections. The first section defines inflammation, describes the causes and signs of inflammation, and outlines the types, features, and chemical mediators involved in acute and chronic inflammation. The second section defines healing and describes the processes of regeneration, repair, and wound healing. The third section focuses specifically on chronic inflammation, defining it, outlining its causes and general features including mononuclear cell infiltration, tissue destruction by activated macrophages, and proliferative changes involved in the healing process.
8 OUT COMES OF ACUTE INFLAMMATION.8 OUT COMES OF ACUTE INFLAMMATION.ssuser12303b
8 OUT COMES OF ACUTE INFLAMMATION.ppt8 OUT COMES OF ACUTE INFLAMMATION.ppt8 OUT COMES OF ACUTE INFLAMMATION.ppt8 OUT COMES OF ACUTE INFLAMMATION.ppt8 OUT COMES OF ACUTE INFLAMMATION.ppt
Inflammation is the body's immune response to injury or infection. It involves vascular changes like increased blood flow and permeability, as well as cellular events like leukocyte migration and phagocytosis. The classic signs are redness, swelling, heat, pain, and loss of function. Acute inflammation follows two main phases - vascular events that alter blood vessels, and cellular events where leukocytes migrate to the site and phagocytose pathogens. This process aims to destroy infectious agents and initiate healing.
This document provides an overview of inflammation. It defines inflammation and discusses the causes, classification, and processes involved in acute and chronic inflammation. For acute inflammation, it describes the vascular and cellular responses, including migration of leukocytes, chemotaxis, and phagocytosis. It outlines the five cardinal signs of acute inflammation and different morphological types. Chronic inflammation is defined and its causes, cells involved, and classifications are explained. Granulomatous inflammation and its pathogenesis are also covered.
Inflammation is the body's response to injury or infection that involves vascular and cellular events. The cardinal signs of inflammation are redness, swelling, heat, pain, and loss of function. Inflammation can be either acute (minutes to days) or chronic (weeks to months). Chemical mediators like histamine, prostaglandins, and leukotrienes are released during inflammation and cause changes like increased vascular permeability and leukocyte migration. Repair after inflammation occurs through regeneration of tissues like skin, or through healing by scar formation. Healing involves granulation tissue formation, angiogenesis, fibroblast proliferation and extracellular matrix deposition.
This document discusses inflammation. It defines inflammation as the body's local response to injury or infection aimed at eliminating the cause of injury and initiating repair. The cardinal signs of inflammation are redness, swelling, heat, pain, and loss of function. The early response involves vasodilation and increased permeability, causing swelling. The late response involves neutrophils in acute inflammation and macrophages in chronic cases, which work to destroy pathogens and initiate healing. Understanding inflammation is important for diagnosing conditions like appendicitis and treating diseases.
Inflammation is the protective response of tissues to injury. The key events of acute inflammation are vasodilation, increased vascular permeability, and leukocyte emigration. Increased permeability allows plasma proteins and cells to exit vessels and accumulate at sites of injury. This leads to edema, which can be an exudate or transudate depending on protein content. Exudates have high protein levels from significant vessel changes, while transudates have low protein from hydrostatic/osmotic imbalance without major vessel changes. The mechanisms driving permeability involve histamine and other mediators causing both immediate and delayed responses from the endothelium.
Inflammation is the protective response of tissues to injury. The key events of acute inflammation are vasodilation, increased vascular permeability, and leukocyte emigration. Increased permeability allows plasma proteins and cells to exit vessels and accumulate at sites of injury. This leads to edema, which can be an exudate or transudate depending on protein content. Exudates have high protein levels from significant vessel changes, while transudates have low protein from hydrostatic/osmotic imbalance without major vessel changes. The mechanisms driving permeability involve histamine and other mediators causing both immediate and delayed responses from the endothelium.
The document discusses inflammation and necrosis. It begins by introducing inflammation as the body's defense response to eliminate injurious agents and remove necrotic tissue. It then provides a brief history of observations and descriptions of inflammation dating back to ancient Egypt. The document defines inflammation and describes the types as acute or chronic. It discusses the vascular changes that occur during inflammation including increased blood flow, vascular permeability, and cellular events such as exudation of leukocytes and phagocytosis.
Inflammation is the body's response to infection, injury, or irritation. It is characterized by redness, swelling, heat, and pain at the site of injury or infection. When tissue is damaged, chemicals are released that cause blood vessels to become leaky and allow immune cells like neutrophils and macrophages to migrate to the injured site. These cells destroy and remove pathogens, limit their spread, and initiate tissue repair. Acute inflammation resolves quickly, while chronic inflammation persists long-term and can damage tissue over years.
The document provides information about inflammation including its causes, classification, and mechanisms. It discusses how inflammation is the body's response to harmful stimuli and can be either acute or chronic. Acute inflammation develops rapidly in response to injury and involves innate immune responses, while chronic inflammation can last months to years and involves adaptive immunity. The key events of acute inflammation are increased blood flow, vascular permeability, and migration of immune cells to the site of injury.
Inflammation (Acute and Chronic) Prof Mulazim Hussain BukhariMulazim Bukhari
This document discusses acute inflammation. It defines inflammation, outlines the causes and molecular events of inflammation including vasodilation, vascular leakage, and leukocyte recruitment. It describes the cardinal signs of inflammation and summarizes the mechanisms of increased vascular permeability and leukocyte extravasation through selectin-mediated rolling, integrin-mediated adhesion, and transmigration across endothelial cells.
This document summarizes a seminar presentation on inflammation given by Manu S J to the Department of Pharmacology at PES College of Pharmacy. It defines inflammation, describes the classic signs of acute inflammation and the pathophysiology involving increased blood flow, vascular permeability, and cellular infiltration. It also discusses causes of inflammation including infection and injury, and the roles of chemical mediators like histamine, cytokines, and complement proteins in propagating the inflammatory response. Chronic inflammation is characterized by prolonged duration and tissue proliferation or destruction. Granulomatous inflammation involves macrophage aggregation forming granulomas.
Inflammation is the protective response to eliminate the cause of cell injury and damaged tissue. It is characterized by redness, heat, swelling, pain, and loss of function. The signs are caused by increased blood flow and vascular permeability. Inflammation can be acute, lasting minutes to days, or chronic, lasting weeks or months. Acute inflammation involves recruitment of leukocytes from the bloodstream to fight infection at the site of injury. Chronic inflammation is prolonged and involves tissue destruction by mononuclear cells and attempts at healing through fibrosis. Mediators like cytokines prolong the inflammatory response.
This document provides an overview of inflammation. It defines inflammation and divides it into acute and chronic types. The components of inflammation include vascular reactions and cellular reactions. Acute inflammation is characterized by neutrophil accumulation and lasts for a short period, while chronic inflammation involves lymphocytes and macrophages and lasts longer. The document further describes the stimuli, vascular changes, and cellular events involved in acute inflammation, including leukocyte margination, rolling, adhesion, transmigration, and phagocytosis. It also discusses the chemical mediators and outcomes of acute inflammation.
Inflammation is the body's protective response to eliminate the initial cause of cell injury and promote tissue repair. The classical signs of acute inflammation are heat, redness, swelling, pain, and loss of function. Acute inflammation is short-lived and involves increased blood flow, vascular permeability, and recruitment of immune cells like neutrophils to the injured site. Chronic inflammation lasts longer and is characterized by lymphocytes, plasma cells and macrophages, tissue destruction, and fibrosis. The outcome of acute inflammation is typically resolution and healing of the damaged tissues.
Acute inflammation is the early response of tissues to injury and involves vascular and cellular events. The vascular events include vasodilation, increased vascular permeability allowing plasma proteins to leave circulation, and accumulation of leukocytes from the blood vessels into tissues. The principal leukocytes in acute inflammation are neutrophils. The cellular events in acute inflammation help destroy, dilute or isolate injurious agents. Mediators of acute inflammation include histamine, prostaglandins, nitric oxide, complement factors and cytokines. Acute inflammation is rapid in onset, relatively short in duration and aims to return tissues to normal function.
This document discusses inflammation and its causes, types, and vascular events. It defines inflammation as the body's protective response to eliminate injurious stimuli and damaged tissue. Inflammation can be acute or chronic depending on the severity and duration of the stimulus. The key vascular events of acute inflammation include increased blood flow causing redness and heat, increased vascular permeability allowing fluid proteins to leave blood vessels and cause swelling, and leukocyte emigration to sites of injury. This leads to the five cardinal signs of inflammation. The document explores the mechanisms behind these vascular changes in detail.
This document provides an overview of inflammation and healing. It defines inflammation as the body's response to injury, discussing the causes, signs, and types (acute and chronic) of inflammation. Acute inflammation involves vascular changes like increased blood flow and permeability, as well as cellular events like leukocyte migration and phagocytosis. Chemical mediators released from cells and plasma regulate these inflammatory responses. Healing is defined as the process of tissue regeneration and repair after injury or inflammation.
Inflammation and Healing (wound healing)Rajat Nanda
This document provides information on inflammation and healing in 3 sections. The first section defines inflammation, describes the causes and signs of inflammation, and outlines the types, features, and chemical mediators involved in acute and chronic inflammation. The second section defines healing and describes the processes of regeneration, repair, and wound healing. The third section focuses specifically on chronic inflammation, defining it, outlining its causes and general features including mononuclear cell infiltration, tissue destruction by activated macrophages, and proliferative changes involved in the healing process.
8 OUT COMES OF ACUTE INFLAMMATION.8 OUT COMES OF ACUTE INFLAMMATION.ssuser12303b
8 OUT COMES OF ACUTE INFLAMMATION.ppt8 OUT COMES OF ACUTE INFLAMMATION.ppt8 OUT COMES OF ACUTE INFLAMMATION.ppt8 OUT COMES OF ACUTE INFLAMMATION.ppt8 OUT COMES OF ACUTE INFLAMMATION.ppt
Inflammation is the body's immune response to injury or infection. It involves vascular changes like increased blood flow and permeability, as well as cellular events like leukocyte migration and phagocytosis. The classic signs are redness, swelling, heat, pain, and loss of function. Acute inflammation follows two main phases - vascular events that alter blood vessels, and cellular events where leukocytes migrate to the site and phagocytose pathogens. This process aims to destroy infectious agents and initiate healing.
This document provides an overview of inflammation. It defines inflammation and discusses the causes, classification, and processes involved in acute and chronic inflammation. For acute inflammation, it describes the vascular and cellular responses, including migration of leukocytes, chemotaxis, and phagocytosis. It outlines the five cardinal signs of acute inflammation and different morphological types. Chronic inflammation is defined and its causes, cells involved, and classifications are explained. Granulomatous inflammation and its pathogenesis are also covered.
Similar to 11. INFLAMMATION DENTISTRY IN SIMPLER TERMS.ppt (20)
LECT 4 DENTAL CALCULUS INCLUDING FORMATION AND CAUSES.pptxSamkeloKhumalo2
Effects of Dental Calculus on Oral Health:
Gingivitis and Periodontal Disease:
Dental calculus provides a rough surface that facilitates plaque accumulation and retention. This can contribute to gingival inflammation (gingivitis) and the development and progression of periodontal disease by harboring bacteria and bacterial toxins that damage the periodontal tissues.
Dental Esthetics:
Supragingival calculus deposits can cause discoloration and staining of the teeth, affecting dental esthetics.
Halitosis (Bad Breath):
Dental calculus can contribute to halitosis by providing a reservoir for odor-producing bacteria and bacterial by-products.
Prevention and Management:
Regular Dental Cleanings: Professional dental cleanings (scaling and root planing) are essential for removing calculus deposits and maintaining optimal oral health.
Good Oral Hygiene: Effective oral hygiene practices, including regular brushing and flossing, are crucial for preventing plaque accumulation and calculus formation.
Antimicrobial Agents: Mouth rinses containing antimicrobial agents, such as chlorhexidine or essential oils, may be used as adjuncts to mechanical plaque removal to help reduce bacterial load and calculus formation.
In summary, dental calculus is a hard, calcified deposit that forms on the teeth due to the mineralization of dental plaque. It can contribute to gingivitis, periodontal disease, dental esthetic problems, and halitosis. Effective prevention and management strategies, including regular dental cleanings and good oral hygiene practices, are essential for maintaining optimal oral health and preventing the adverse effects of dental calculus.
LECT 3 DENTAL PLAQUE DEFINITION AND AETIOLOGY .pptxSamkeloKhumalo2
Dental plaque is a soft, sticky, colorless or pale yellow biofilm that forms on the teeth and along the gumline. It is composed of a complex microbial community embedded in a matrix of polymers, salivary proteins, and bacterial by-products. Dental plaque is a primary etiological factor in the development of various oral health conditions, including dental caries (tooth decay) and periodontal disease (gum disease). Here's an overview of dental plaque:
Composition of Dental Plaque:
Microbial Components:
Bacteria: Dental plaque contains a diverse array of bacteria, with over 700 different species identified in the oral cavity. Some of the most common bacteria associated with plaque include Streptococcus mutans, Streptococcus sobrinus, Lactobacillus spp., and various species of Actinomyces, Prevotella, and Fusobacterium.
Fungi and Yeasts: In addition to bacteria, dental plaque may also contain fungi and yeasts, such as Candida species.
Matrix and Salivary Components:
Polymers: Dental plaque is held together by polymers produced by bacteria, primarily extracellular polysaccharides (EPS) and glucans.
Salivary Proteins: Salivary proteins, such as mucins and glycoproteins, contribute to the formation and structure of dental plaque.
Bacterial By-Products:
Acids: Bacteria in dental plaque metabolize sugars and carbohydrates from food, producing acids as by-products. These acids can demineralize the tooth enamel, leading to the development of dental caries.
Toxins and Enzymes: Some bacteria in dental plaque produce toxins and enzymes that can damage the tooth structure and contribute to periodontal disease.
Periodontal disease, also known as gum disease, is a common and serious oral health condition that affects the supporting structures of the teeth, including the gums, periodontal ligament, and alveolar bone. The etiology of periodontal disease is multifactorial, involving a combination of bacterial infection, host response, and various risk factors. Here's an overview of the etiology of periodontal disease:
Dental Plaque and Bacterial Infection:
The primary etiological factor of periodontal disease is dental plaque, a biofilm that forms on the teeth and gum line.
Specific bacteria within dental plaque, such as Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola (often referred to as the "red complex"), are particularly pathogenic and play a key role in the initiation and progression of periodontal disease.
When plaque is not adequately removed through oral hygiene practices, these bacteria can proliferate and produce toxins that induce inflammation and damage to the periodontal tissues.
Host Response:
The body's immune response to the bacterial infection is a crucial component in the development and progression of periodontal disease.
In susceptible individuals, an exaggerated immune response can lead to chronic inflammation and tissue destruction.
Genetic factors may influence an individual's susceptibility to periodontal disease by affecting the immune response and inflammatory pathways.
Risk Factors:
Poor Oral Hygiene: Inadequate brushing and flossing allow plaque to accumulate, increasing the risk of periodontal disease.
Smoking and Tobacco Use: Tobacco use is a significant risk factor for periodontal disease and can impair the body's immune response to bacterial infection.
Age: The risk of periodontal disease increases with age, partly due to cumulative exposure to risk factors and changes in the oral microbiome.
Systemic Conditions: Certain systemic conditions, such as diabetes, cardiovascular disease, and immunocompromised states, can increase susceptibility to periodontal disease.
Hormonal Changes: Hormonal fluctuations during puberty, pregnancy, and menopause can affect gum health and increase the risk of periodontal disease.
Local Factors:
Anatomy of Teeth: Misaligned or crowded teeth can create areas that are difficult to clean, increasing the risk of plaque accumulation and periodontal disease.
Dental Restorations: Poorly fitting dental restorations or orthodontic appliances can contribute to plaque retention and periodontal inflammation.
Environmental and Behavioral Factors:
Diet: Consumption of a diet high in sugars and carbohydrates can promote bacterial growth and plaque formation.
Stress: Chronic stress may impair the immune response and increase susceptibility to periodontal disease.
Stages of Periodontal Disease:
Gingivitis: The earliest stage of periodontal disease, characterized by inflammation of the gums (gingiva) without loss of supporting bone.
BIOLOGICAL EFFECTS OF Radiation IN DENTISTRY. ppt.pdfSamkeloKhumalo2
Radiation damage to tissue and/or organs depends on the dose of radiation received, or the absorbed dose which is expressed in a unit called the gray (Gy). The potential damage from an absorbed dose depends on the type of radiation and the sensitivity of the different tissues and organs.
1.THE EPILEPTIC Patient And How To Manage Them In Dentistry.pptxSamkeloKhumalo2
Epilepsy is a chronic neurological disorder characterized by recurrent seizures. Epilepsy generally begins in childhood, potentially impeding education, employment, social relationships, and the development of a sense of self-worth. The number of decayed and missing teeth, the degree of abrasion, and periodontal indices are significantly worse in patients with epilepsy. Epileptic patients require special care during dental treatment.
LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UPRAHUL
This Dissertation explores the particular circumstances of Mirzapur, a region located in the
core of India. Mirzapur, with its varied terrains and abundant biodiversity, offers an optimal
environment for investigating the changes in vegetation cover dynamics. Our study utilizes
advanced technologies such as GIS (Geographic Information Systems) and Remote sensing to
analyze the transformations that have taken place over the course of a decade.
The complex relationship between human activities and the environment has been the focus
of extensive research and worry. As the global community grapples with swift urbanization,
population expansion, and economic progress, the effects on natural ecosystems are becoming
more evident. A crucial element of this impact is the alteration of vegetation cover, which plays a
significant role in maintaining the ecological equilibrium of our planet.Land serves as the foundation for all human activities and provides the necessary materials for
these activities. As the most crucial natural resource, its utilization by humans results in different
'Land uses,' which are determined by both human activities and the physical characteristics of the
land.
The utilization of land is impacted by human needs and environmental factors. In countries
like India, rapid population growth and the emphasis on extensive resource exploitation can lead
to significant land degradation, adversely affecting the region's land cover.
Therefore, human intervention has significantly influenced land use patterns over many
centuries, evolving its structure over time and space. In the present era, these changes have
accelerated due to factors such as agriculture and urbanization. Information regarding land use and
cover is essential for various planning and management tasks related to the Earth's surface,
providing crucial environmental data for scientific, resource management, policy purposes, and
diverse human activities.
Accurate understanding of land use and cover is imperative for the development planning
of any area. Consequently, a wide range of professionals, including earth system scientists, land
and water managers, and urban planners, are interested in obtaining data on land use and cover
changes, conversion trends, and other related patterns. The spatial dimensions of land use and
cover support policymakers and scientists in making well-informed decisions, as alterations in
these patterns indicate shifts in economic and social conditions. Monitoring such changes with the
help of Advanced technologies like Remote Sensing and Geographic Information Systems is
crucial for coordinated efforts across different administrative levels. Advanced technologies like
Remote Sensing and Geographic Information Systems
9
Changes in vegetation cover refer to variations in the distribution, composition, and overall
structure of plant communities across different temporal and spatial scales. These changes can
occur natural.
How to Build a Module in Odoo 17 Using the Scaffold MethodCeline George
Odoo provides an option for creating a module by using a single line command. By using this command the user can make a whole structure of a module. It is very easy for a beginner to make a module. There is no need to make each file manually. This slide will show how to create a module using the scaffold method.
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
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4. MICROSCOPIC FEATURES
OF INFLAMMATION
In order:
Arteriolar dilatation: sometimes preced by transient vasoconstriction
Increased in blood flow: through arterioles, capillaries and vessels
Increased permeability: of microvessels allows for the
Exudation: of fluid through permeable vessels
Concentration or packing of red cells in vessels due to fluid loss. This
results in increased viscosity of the blood
Slowing or complete cessation of blood flow
Peripheral margination or pavementing of white cells which stick to the
endothelium in microvessels. Adhesion takes place by virtue of cells
adhesion molecules (CAM)
Emigration of white cells by active passage through vessel wall into the
inflammatory focus, first polymorphonuclear leucocytes, then monocytes
together with passive escape of red blood cells forced out with them by
process known as Diapedesis
(see diagram at lecture)
5. White cells find their way to site of injury by
process of chemotaxis
Chemotatic agents are bacterial products,
components of complement system(C5a,
components of the lipoxygenase pathway
of arachordonic acid metabolism especially
leukotriene B4
Polymorphonuclearcytes are characteristic
histological finding in acute inflammation
6. THESE CHANGES CAN BE
SUMMED UP AS:
Vascular: active hyperaemia
Exudative: fluid or cellular exudate.
Oedema, space occupied by fluid
separating fibres and cells
Fibrin precipitation
Accumulation of white cells,
especially PMN in and on vessel
walls and in tissues
7. VASCULAR
PERMEABILITY
3 types of this response can be described
1.) Immediate Transient
Response which comes immediately after injury
Lasts for 15-30 minutes
Brought about by histamine and other chemical mediators
Leakage occurs from gaps in small venules
2.) Immediate Sustained
More severe injury to all small vessels (arterioles, venules and capillaries)
E.g. severe burn
Necrosis of endothelial cells occur and leakage for several days until damage vessels are thrombosed e.g. repaired
3.) Delayed Prolonged
Leakage may take some hours to develop and lasts for hours or days
Affects capillaries and venules
E.g. sunburn, moderate heat xray
Other causes will be bacterial toxins and delayed hypersensitivity reactions
Increased hydrostatic pressure leads to fluids leaving permeable vessels either by pinocytosis, gaps in intercellular
junctions of endothelial cells which are opened up by the chemical mediators of inflammation
Fluid part of exudates = to plasma in composition
Fluid/ exudates acts by:
Diluting toxins
Transporting antibiotics, drugs to site of inflammation
Precipitating fibrin to wall off the area ant to aid phagocytosis
10. Lymphatics dilate and drain oedema fluid
and waste products from
the inflamed area
An immune response maybe evoked by
transport of macrophages containing
antigenic material to the lymph nodes
Drainage lymph nodes maybe enlargened
and tender
11. CLINICAL CARDINAL
SIGNS OF INFLAMMATION
Can Be Related To Vascular Changes:
1.) Redness And Heart
Increased blood supply with vascular dilation
2.) Swelling
Due to oedema caused by the exudation of fluid from vessels
into the tissues
3.) Pain
Maybe due to oedema causing increased tissue tension and
pressure on nerve endings. Release chemical mediators of
inflammation (such as bradykinin) may also, cause pain
4.) Loss
Of function may occur following the swelling and the pain or
following inflammatory destruction of tissue
13. CHEMICAL MEDIATORS
OF INFLAMMATION
1.) Vasoactive Amines
E.g. histamine and 5- hydroxy tryptamine
Released by mast cells in tissue and basophils in blood and platelets
following certain stimuli e.g. trauma, IgE hypersensitivity, release of
fragments of complement (C3a and C5a)
2.) The Complement System
System activate by antigen- antibody complexes (classic pathway) or variety
of substances such as bacterial toxins (alternate globulins)
C3a and C5a increase vascular permeability
C5a exert chemotatic influence
Acts as opsonins (C3b) and lyse the membranes of cells and organisms
3.) The Kinin System, The Coagulation System And Fibrinolytic System
Related systems maybe activated together by contact activation factor
(factor x11)
Contact Activation
14. CHEMICAL MEDIATORS
OF INFLAMMATION
Bradykinin
Increase in vascular permeability
Is a vasodilator
Causes pain
Plasmin
Activates C3to C3a, which is permeability
Spilt fibrin and increases vascular permeability
Lyses and fibrin formed
Conversion Of Fibrinogen To Fibrin
Increases vascular permeability
Has chemotatic effect
18. IMPORTANT CELLS TO
REVISE IS:
1.) Polymorphonulear Leucocytes
Neutrophils
Esonophils
Basophils
2.) Mononuclear Phagocytes
3.) Lymphocytes
4.) Plasma Cells
19. INFLAMMATION
Inflammation can be classified according to the nature of the inflammatory
exudates:
One such type is Suppurative Inflammation
This inflammation is accompanied by pus
Localized collection of pus is known as an abscess
Abscess forms when the destructive inflammatory process is walled off, at
first by fibrin and inflammatory cells, and later by newly formed connective
tissue
If pus formation, continues after being walled off then it can be very painful
Whilst pus remains in situ, healing cannot easily take place
Pus must be removed and this can happen naturally because with increasing
tension the pus will tend to track between tissue planes to surface
Therefore, abscess must be incised and drained to minimize tissue damage
and relieve pain, as well as, reducing the chances of spread of infection due
to the tracking or pointing of the abscess
21. CHRONIC INFLAMMATION
Is a prolonged process in which destruction
and inflammation are proceeding at the
same time as attempt at healing
Acute inflammation can be assumed to be
entering a chronic phase after it has
persisted for a week or two
Chronic inflammation although some
polymorphs are present, macrophages,
lymphocytes and plasma cells are the main
cells present
23. HISTOLOGICAL FEATURES
OF CHRONIC
INFLAMMATION
1.) Exudation
Persistence of acute inflammatory changes
Continued tissue destruction
2.) Macrophage Accumulation
Macrophages presents in very large numbers
3.) Repair
Reparative granulation tissue can be formed
Granulation Tissue Consist of:
Newly formed capillaries and budding endothelial cells
Proliferating fibroblasts and collagen
Lymphocytes, plasma cells and other inflammatory cells
So called because when seen at bottom of healing wound granulation
tissue 6.)
has a red granular appeerance
May progress or nature to form proper fibrous tissue which will form a
scar
24. CLASSIFICATION OF
CHRONIC INFLAMMATION
1.) Non-Specific Chronic inflammation
Due to organisms of various sort or in response to foreign material
E.g. chronic ostemyelitis
Occurs in long bones of children or young adults
Follow acute inflammation in the bone
Increased tissue tension due to exudates is exerted against unyielding bone and there is
compression of blood vessels leading to ischaemia and necrosis of the actual bone
Pus is formed which tracks under the periosteum, further interfering with blood supply
Pus maybe discharges from the surface penetrating muscles and skin with formation of
sinuses
Dead bone acts as a foreign body in which organisms can continue to grow
At the same time, it prevents adequate draining of pus and delays healing
In chronic osteomyelitis, dead bone is known as Sequestrum
New bone formation can further prevent proper healing as it blocks drainage
End result is chronic supparative inflammation of bone or chronic osteomyelitis
This can cause death due to persistence of infection
Fortunately, due to antibiotics at an early stage and surgical treatment to bring about
drainage, the disease is no longer the danger it used to be
28. EFFECTS OF CHRONIC
INFLAMMATION
1.) Systemic effects from chronic inflammation
similar to those in acute inflammation
Fever manifests as night sweats rather than
shivering and chills
Leucoytosis more likely to involved mononuclear
cells than polymorphs
Increased protein synthesis
Loss of appetite and weight loss
Tiredness, headaches and general feeling of being
are difficult to explain