The document discusses inflammation and provides details about its introduction, etiology, signs, types (acute and chronic), chemical mediators, inflammatory cells, and morphology. It defines acute inflammation as a rapid response to injury or microbes designed to deliver leukocytes and plasma proteins to the site of injury. Chronic inflammation is defined as inflammation of prolonged duration where active inflammation, tissue injury, and healing proceed simultaneously. It is characterized by infiltration of mononuclear cells and tissue destruction induced by inflammatory cell products, along with repair through angiogenesis and fibrosis.
Introduction
Development of Mast cell
Implication
Properties of Cell
Mediators of Mast cell
Types of Mast cell
Modes of degranulation
Ultra structure of mast cell
Role of mast cell in OLP,OSF, Wound healing, OSCC, pyogenic granuloma, periapical lesion, orofacial granulomatosis
Conclusion
Blood supply,nerve supply and lymphatic drainage of the periodontium finalDr. Neha Pritam
Discussion of the various basic topics required to understand in the subject of periodontics. Periodontium being the tooth supporting tissue ,it is necessary to know the blood supply, nerve supply and the lymphatic drainage of the same in dentistry
ggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans) is a Gram-negative, facultative nonmotile, rod-shaped oral commensal often found in association with localized aggressive periodontitis, a severe infection of the periodontium, although it is also associated with nonoral infections. Its role in periodontitis was first discovered by Danish-born periodontist Jørgen Slots, a professor of dentistry and microbiology at the University of Southern California School of Dentistry.
'Bacterium actinomycetem comitans' was described by Klinger (1912) as coccobacillary bacteria isolated together with Actinomyces from actinomycotic lesions of man. It was reclassified as Actinobacillus actinomycetemcomitans by Topley & Wilson (1929) and as Haemophilus actinomycetemcomitans by Potts et al. (1985). The species has attracted attention because of its association with localized aggressive periodontitis. is explained here by Dr Harshavardhan Patwal
Periodontitis as a manifestation of systemic diseasesDr. vasavi reddy
Describes conditions that show periodontal manifestations inherently and primary cause is the disease itself whereas bacterial plaque acts as a secondary factor.
Inflammation and Immunity in periodontitis pptPerio Files
Local destruction of periodontium occurs mostly by activation of immune and inflammatory response, initiated by plaque. First innate immune response is activated followed by specific immune response.
Useful for BDS and MDS students
Introduction
Development of Mast cell
Implication
Properties of Cell
Mediators of Mast cell
Types of Mast cell
Modes of degranulation
Ultra structure of mast cell
Role of mast cell in OLP,OSF, Wound healing, OSCC, pyogenic granuloma, periapical lesion, orofacial granulomatosis
Conclusion
Blood supply,nerve supply and lymphatic drainage of the periodontium finalDr. Neha Pritam
Discussion of the various basic topics required to understand in the subject of periodontics. Periodontium being the tooth supporting tissue ,it is necessary to know the blood supply, nerve supply and the lymphatic drainage of the same in dentistry
ggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans) is a Gram-negative, facultative nonmotile, rod-shaped oral commensal often found in association with localized aggressive periodontitis, a severe infection of the periodontium, although it is also associated with nonoral infections. Its role in periodontitis was first discovered by Danish-born periodontist Jørgen Slots, a professor of dentistry and microbiology at the University of Southern California School of Dentistry.
'Bacterium actinomycetem comitans' was described by Klinger (1912) as coccobacillary bacteria isolated together with Actinomyces from actinomycotic lesions of man. It was reclassified as Actinobacillus actinomycetemcomitans by Topley & Wilson (1929) and as Haemophilus actinomycetemcomitans by Potts et al. (1985). The species has attracted attention because of its association with localized aggressive periodontitis. is explained here by Dr Harshavardhan Patwal
Periodontitis as a manifestation of systemic diseasesDr. vasavi reddy
Describes conditions that show periodontal manifestations inherently and primary cause is the disease itself whereas bacterial plaque acts as a secondary factor.
Inflammation and Immunity in periodontitis pptPerio Files
Local destruction of periodontium occurs mostly by activation of immune and inflammatory response, initiated by plaque. First innate immune response is activated followed by specific immune response.
Useful for BDS and MDS students
Periodontitis is a chronic infectious inflammatory disease caused by microbes; however the presence of microbes is not enough for the cause of its complex nature of disease. Inflammation is the prime cause of periodontal disease. It commences with the aggregation of pathogenic microbes that induce the host to stimulate a cascade of inflammatory response reactions which in-turn leads to the destruction of the host tissues itself. There is a complex interplay of innate and adaptive immune responses which fights against the pathogens by direct interaction or by release of certain molecules including cytokines.
Cytokines are cell signalling molecules that aid cell to cell communication in immune responses and stimulate the movement of cells towards sites of inflammation, infection and trauma. Cytokine biology reveals that there are some subsets of cytokines which are pro-inflammatory cytokines which stimulate the inflammatory responses and cause tissue destruction.
A periodontist is expected to have a sound basis of the cytokine profile to understand the pathogenesis of periodontitis and also to discover the new treatment modality of anti-cytokine therapy.
HI,
HERE YOU WILL FIND ALL TYPES OF PPTS OF PERIODONTICS FOR BDS AND MDS
PLS SUBSCRIBE TO MY YOUTUBE CHANNEL FOR MORE UPDATES
https://youtu.be/5zN5MZ-YGP8
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A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
Periodontitis is a chronic infectious inflammatory disease caused by microbes; however the presence of microbes is not enough for the cause of its complex nature of disease. Inflammation is the prime cause of periodontal disease. It commences with the aggregation of pathogenic microbes that induce the host to stimulate a cascade of inflammatory response reactions which in-turn leads to the destruction of the host tissues itself. There is a complex interplay of innate and adaptive immune responses which fights against the pathogens by direct interaction or by release of certain molecules including cytokines.
Cytokines are cell signalling molecules that aid cell to cell communication in immune responses and stimulate the movement of cells towards sites of inflammation, infection and trauma. Cytokine biology reveals that there are some subsets of cytokines which are pro-inflammatory cytokines which stimulate the inflammatory responses and cause tissue destruction.
A periodontist is expected to have a sound basis of the cytokine profile to understand the pathogenesis of periodontitis and also to discover the new treatment modality of anti-cytokine therapy.
HI,
HERE YOU WILL FIND ALL TYPES OF PPTS OF PERIODONTICS FOR BDS AND MDS
PLS SUBSCRIBE TO MY YOUTUBE CHANNEL FOR MORE UPDATES
https://youtu.be/5zN5MZ-YGP8
Thanks for watching bye!!!
A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
Inflammation_ Lecture material for beginners as PPT.pdfBerhanu Mekale
Organized and illustrated lecture material for better understanding of inflammation for undergraduate students. Enjoy reading and let me know if you have any questions or additional information and materials.
The imbalance between free radical production and endogenous antioxidant defence may result in cellular oxidative stress, causing oxidative damage to various cellular components, such as DNA, proteins and membrane lipids. The human system employs the use of endogenous enzymatic and non-enzymatic antioxidant defence systems against the onslaught of free radicals and oxidative stress.
Unsurprisingly, oxidative damage has been implicated in and is believed to be a key factor causing various pathological conditions, such as cardiovascular disease, neurodegenerative disease, diabetes and cancer. Free radicals can be quenched through a number of mechanisms. Antioxidants directly scavenge free radicals (e.g., via hydrogen atom transfer or electron transfer), prevent free radical formation by chelating metal ions and by interrupting the radical chain reactions of lipid peroxidation, thus retarding its progression. Enzymatic antioxidants include superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase. Non-enzymatic antioxidants include vitamins A, C, and E, glutathione, alpha-lipoic acid, carotenoids, and coenzyme Q10. Other antioxidants include polyphenols, minerals (copper, zinc, manganese, and selenium), and cofactors (B-vitamins). Together, antioxidants work synergistically with each other using different mechanisms against different free radicals and stages of oxidative stress.
The benefits associated with antioxidants are numerous and diverse but it can be a minefield when choosing the appropriate antioxidant support for clients. In this hour-long webinar, Dr Nina Bailey discusses the direct and indirect benefits and actions of key antioxidants including (but not limited to) astaxanthin, alpha lipoic acid, polyphenols and co-enzyme Q10, with a focus on:
-Antioxidant sources and benefits
-Mechanisms and actions
-When to combine antioxidants for synergistic effects
-Overcoming bioavailability issues
-Targeted intervention, which antioxidant(s) and why
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
2. contents
Introduction
Etiology
Signs of Inflammation
Types
Acute Inflammation
Chemical Mediators Inflammatory Cells
Factors determining Inflammatory response
Morphology of acute inflammation
Fate of Acute Inflammation
Chronic Inflammation
3. Inflammatory Cells
Factors determining Inflammatory response
Morphology of acute inflammation
Fate of Acute Inflammation
Chronic Inflammation
Features of Chronic Inflammation
Types of chronic inflammation
Systemic effects Inflammatory diseases of the oral cavity
Respective histopathology and therapeutics
Conclusion
References
4. introduction
As per Textbook of Pathology by Harsh Mohan 6th Edition
inflammation is defined as the local response of living mammalian
tissues to injury due to any agent.
As per Robbin’s Basic Pathology 8th edition Inflammation is a
protective response intended to eliminate the initial cause of
injury as well as necrotic cells & tissues resulting from the
original insult
5.
6. YEAR SCIENTIST EVENT
3000 B.C CELCIUS CARDINAL SIGNS OF INFLAMMATION
1793 A.D JOHN HUNTER INFLAMMATION IS A PROTECTIVE
PROCESS
1839-84
A.D
JULIUS COHNHEIN UNDERLYING MECHANISM FOR THE
CARDINAL SIGNS
1882 A.D ELIE METCHINKOFF PHAGOCYTOSIS
1908 A.D PAUL EHLRICH,
METCHKINOFF
CELLULAR & HUMOURAL FACTORS IN
BODY DEFENSE
SIR THOMAS LEWIS CHEMICAL MEDIATORS OF
INFLAMMATION
7. Inflammation is a beneficial host response to foreign invaders &
necrotic tissue , but it is itself capable of causing tissue damage.
5 R’s of inflammation:
Recognition of injurious agent
Recruitment of leukocytes
Removal of agents
Regulation of the response
Resolution
11. SIGNS
cardinal signs
a) Rubor [ redness]
b) Tumor [ swelling]
c) Calor [ heat]
d) Dolor [ pain]
e) Functio Laesa [
loss of function]
12.
13.
14. Acute inflammation
Acute Inflammation as per Robbin’s Basic Pathology 8th edition it is
a rapid response to injury or microbes and other foreign
substances that is designed to deliver leukocytes and plasma
proteins to site of injury .
STIMULI:
19. ALTERED VASCULAR PERMEABILITY:
1.Contraction of endothelial cells- endothelial cells develop
gaps because of vascular leakage [ histamine, bradykinin]
2.Retraction of endothelial cells- structural re-organisation of
endothelial cells that create reversible retraction of intercellular
junction. [ IL 1, TNF α, onset- 4-6hrs, lasts for- 24hrs]
3.Direct injury to endothelial cells- creates necrosis & physical
gap at the site of detached endothelial cells with start of
thrombosis.
4.Endothelial injury mediated by leucocytes- adhesion of leucocytes to
endothelial layer- release of proteolytic enzymes & toxic oxygen
species ( increasing vascular damage).
20.
21.
22.
23. CELLULAR EVENTS:
1. Exudation of leucocytes 2. Phagocytocis
EXUDATION OF LEUCOCYTES:
1. Margination & Pavementing
2. Rolling & Adhesion
3.Emigration
4.Chemotaxis
Across the vessel wall
Along the vessel wall
Outside the vessel wall
26. Chemokine
s bind to
WBC
surface Ca
mobilisation,
cytoskeletal
re-
organisation
occurs
Pseudopod
formed
Integrins
on
pseudopodi
a surface
are
activated
Integrins
bind to
ECM
Cell moves
forward
27. PHAGOCYTOCIS:
1. Recognition & Attachment
2. Engulfment
3. Killing & Degradation-
A. Intracellular mechanism-
1. Oxidative bactericidal mechanism ( oxygen free radicals)
a. MPO Dependent
b. MPO Independent
2. Oxidative bactericidal mechanism ( lysosomal granules)
3. Non oxidative bactericidal mechanism
B. Extracellular mechanism-
1. Degranulation of macrophages & neutrophils
2. Immune mediated lysis of microbes
28. April 19, 2022
• Coating of a particle with a –vely charged
material (OPSONIN) to facilitate
phagocytosis’.Opsonins : C3b, IgG, C4b
Opsonisation
• By receptors on phagocytes
• C31 receptor : for C3b &
• Fc receptor : for IgG
Recognition
• By actin & myosin
Engulfment
• PMN: lysosomal & azurophilic granular
content.MONOCYTES : IL2, 6, TNF,
eicosanoids, O2 metabolites
Degranulation
• O2-NADPH DEPENDANT : by reactive O2
species (peroxidases etc)
• O2- NADPH INDEPENDENT: Granular
Degradation
29.
30.
31. Factors determining variation in inflammatory response:
a. Type of injury & infection
b. Virulence
c. Dose
d. Portal of entry
e. Product of organisms
Factors involving the host:
a. Systemic diseases
b. Immune status of host
c. Congenital neutrophil defects
d. Leucopenia
Types of Exudation: Serous, fibrinous, purulent, hemorrhagic,
catarrhal
38. AMINES SOURCE STIMULUS FOR PRODUCTION FUNCTIONS
HISTAMI
NE
MAST
CELLS
BASOPHILS
PLATELETS
Physical injury
Anaphylotoxins
(C3a, C5a)
Cytokines
Histamine releasing
factor from WBC
When antibody binds
mast cells
Arteriolar
dilation
Increased
vascular
permeability
of Venules
SEROTO
NIN
PLATELETS
ENTERO
CHROMAFFI
N CELLS
Platelet aggregation Same as
histamine but
less potent
39. Histamine intolerance
Histamine intolerance results from a disequilibrium of accumulated
histamine and the capacity for histamine degradation.
In healthy persons, dietary histamine can be rapidly detoxified by amine
oxidases, whereas persons with low amine oxidase activity are at risk of
histamine toxicity.
Ref- The American Journal of Clinical Nutrition, Volume 85, Issue 5, 1 May
2007, Pages 1185–1196
40.
41. LEUKOTRIENES:
Leukotriene (LT) C4 and its products, LTD4 and LTE4, make up the
biologic mixture previously known as the slow-reacting substance of
anaphylaxis.
Leukotrienes are generated by most cell types that participate in
inflammatory reactions including mast cells, basophils, eosinophils,
neutrophils, and monocytes.
As chemical mediators of inflammation, they have biologic activity
similar to that of histamine.
Studies of the effects of H1- receptor antagonists on leukotriene release
suggest that the mechanism may involve blocking the activity of
receptor-coupled G proteins.
REF- Rihoux JP, Masliah J, Bereziat G, Konig W. G proteins as biological targets
for anti-allergic drugs? Int Arch Allergy Immunol 1997;113:339-41.
42. PROSTAGLANDINS:
Another group of arachidonic acid-derived molecules that mediate
allergic reactions are prostaglandins.
The most abundant cyclooxygenase product generated by the
immunologic activation of human lung mast cells is PGD2.
PGD2 is generated by human mast cells after they are activated through
the IgE receptor or by calcium ionophore.
The biologic effects of prostaglandins generated during mast cell-
dependent reactions in tissues include modulation of smooth muscle
contractility, vascular permeability, sensations of pruritus and pain,
and platelet aggregation and degranulation.
43. Prostaglandins are generated by cyclooxygenase, an enzyme
associated with the endoplasmic reticulum of mast cells.
Similar to 5-lipoxygenase, cyclooxygenase catalyzes the formation of
relatively unstable intermediates PG2 and PGH2
These intermediates may then be converted nonenzymatically or
enzymatically by specific isomerase/peroxidase or synthase enzymes
to yield the primary prostaglandins PGD2, PGE2, and PGFa.
REF- Schwartz LB, Austen KF. Structure and function of the chemical
mediators of mast cells. Prog Allergy 1984;34:271-321
44.
45.
46. Metabolites of ARACHIDONIC ACID ( source: diet/linoleic
acid)
Autocoids or local harmones
Cycloxygenase
Thromboxane
A2
Prostaglandins
Lipoxygenase
leukotrienes
lipoxins
51. PLATELET ACTIVATING FACTOR
[ Acetyl glycerol ether phosphocholine]
Platelet activating factor (PAF) is an ether-linked phospholipid,
designated as such because of its discovery as a basophil-derived
mediator of rabbit platelet activation.
PAF may be produced by several of the cells that participate in the
inflammatory response including mast cells, macrophages,
neutrophils, and eosinophils.
REF- Barnes PJ. Pathophysiology of allergic inflammation. In: Middleton E Jr,
Reed CE, Ellis EF, Adkinson NF Jr, Yunginger JW, Busse WW, editors. Allergy:
principles and practice. 4th ed. Louis(Mo): Mosby; 1993. p. 255-6.
52.
53. ‘’ They are polypeptides produced by activated lymphocytes (
LYMPHOKINES) & activated monocytes ( MONOKINES), act on
other cells or the cells that produced them ‘’
MONOKINES : IL-1 , TNF α , IL-8
LYMPHOKINES : TNF ββ, IF γ
CHEMOKINES : IL-8 (monokine) , PF-4
54. IL-1, TNF α & β
• Leukocyte
adhesion
• Thrombogenicity
• Elaboration of
other cytokine
• Fibroblastic
proliferation
IF α
• Activation of
macrophges, PMN
• Synthesis of NO
Chemokines
• IL-8 : for PMNL
• PF-4 : for
PMN,monocytes,
eosinophils
• MCP-1:
monocytes
• EOTAXIN :
eosinophils
62. Kinin System
This system ultimately leads to the formation of BRADYKININ .
Its function are:
Increased vascular permeability
Arteriolar dilation
Smooth muscle contraction
Pain
Kallikrein is an intermediate in this system is a potent activator
of factor 12
68. Complement system
‘’ These are a group of proteins found in plasma & on cell surfaces,
whose primary function is defense against microbes by generating a
pore-like membrane attack complex that ultimately punches holes in
the membranes of microbes’’
•Complement components(numbered C1-C9) are present in plasma as
inactive forms.
•Critical step in the elaboration of the biological functions of
complement is the activation of the 3rd complement, C3.
•C3 cleavage occurs by 2 mechanisms:
•CLASSICAL PATHWAY
•ALTERNATE PATHWAY
69.
70. New mediators of inflammation
Lipoxins -- In addition, two new families of lipid mediators were uncovered,
namely resolvins (resolution phase interaction products)
and protectins, which derive from omega-3 polyunsaturated fatty acid.
They possess potent anti-inflammatory, neuroprotective and pro-resolving
properties.
Ref- Current Opinion in Pharmacology Volume 6, Issue 4, August 2006, Pages
414-420
71.
72. Trans- arachadonic acid- the levels of trans-arachidonic acids in rat
plasma increased following infusion of bacterial endotoxin; therefore, the
isomerization of arachidonic acid is likely to occur in vivo by a mechanism
involving NO2.
Ref-Journal of Physiology and Pharmacology : an Official Journal of the
Polish Physiological Society [01 Dec 2000, 51(4 Pt 1):597-607
73. Chronic inflammation
As per Robbin’s Basic Pathology 8th edition Chronic
inflammation is defined as the inflammation of prolonged
duration ( weeks to years) in which active inflammation, tissue
injury, and healing proceed simulataneously
CHARACTERISTIC FEATURES:
1. Infiltration with mononuclear cells – macrophages, lymphocytes,
plasma cells
2. Tissue destruction – induced by products of inflammatory cells
3. Repair involving new vessel proliferation [ angiogenesis and
fibrosis]
74. ETIOLOGY:
1. Chronic inflammation following acute inflammation
2. Recurrent attacks of acute inflammation
3. Chronic inflammation starting De Novo
TYPES:
1. Chronic Non specific Inflammation: irritant substance – non
specific chronic inflammatory reaction eg chronic osteomyelitis
Variant: chronic suppurative inflammation- infiltration by
polymorphs and abscess formation
2. Chronic granulomatous inflammation : formation of
granuloma eg syphilis, leprosy
75.
76. Chronic inflammatory cells & mediators
1. Macrophages : dominant cells of chronic inflammation.
Collectively known as mononuclear phagocytic system also known
by reticulo endothelial system.
2. Lymphocytes , Plasma cells, eosinophils, mast cells:
Lymphocytes are mobilized into sites of immune stimulus as
well as non immune mediated inflammation.
3. Plasma cells develop from activated B lymphocytes and produce
antibodies [ persistent antigen / altered tissue components]
4. Eosinophils found in inflammatory sites, recruitment driven by
adhesion molecules & mast cells can get involve in both acute &
chronic
77. Blood monocyte
Tissue macrophage (RES)
Migrate into tissue
within 48 hours
after injury
and differentiate
Lymphocyte Plasma cell
78. Ulcers
Fistulas
Granulomatous diseases
Fibrotic diseases (Scaring)
Combinations of the above
79. Major groups of the serum inflammatory markers .
Group Serum inflammatory markers
Acute-phase reactants LBP, CRP, PCT
Mediator activity TNF, IL-1, IL-6, IL-10, IL-18
Cellular activity TNF-RI, TNF-RII, IL-1R, sIL-6-R, mIL-6-,
ICAM-1 Eselectin, CD11b, elastase, HLA-DR class-II antigens,
DNA
CRP, C-reactive protein; HLA, human leukocyte antigen; ICAM, intercellular
adhesion molecule; IL,interleukin; LBP, lipopolysaccharide-binding protein;
PCT, procalcitonin; TNF, tumor necrosis factor.
80. Overview of Environmental Stimuli Into Biochemical
Inflammation Environmental Stimuli (triggers):
Activation of NF-kB
Increased expression of pro-inflammatory genes
Production of cytokines Pro-inflammatory enzymes (iNOS-inducible nitric
oxide synthase, Cox-2 –cylcooxygenase-2, Lipox- lipoxygenase) Adhesion
molecules
(IL-6 stimulates production of CRP) (Cyclooxygenase-2 transforms
arachidonic acid into thromboxanes and prostaglandins-E2) (IL-1 induces
the production of collagenase/matrix metalloproteinases both of which
destroy connective tissue) (Lipooxygenase acts on arachidonic acid to
produce leukotrienes) (inducible nitric oxide synthase→ nitric oxide)
(Tumor necrosis factor-α) (Adhesion molecules)
Autoimmune disease, cardiovascular disease, insulin resistance,
neurodegenerative disease, cancer, chronic inflammation
81. Molecular display of the microvascular environment theory .
Source: Adapted with permission from Giannoudis PV,Hildebrand F, Pape HC.
Inflammatory serum markers in patients with multiple trauma—can they
predict outcome? J Bone Joint Surgery (Bri) 2004;86-B(3):31323.
82. Granulomatous inflammation
a) Distinctive pattern of chronic inflammation
b) Characterized by aggregates of activated macrophages –
epitheloid pattern
c) Granulomas form in setting of persistent T cell response to
microbe. Eg- M tuberculi, T pallidum, etc
d) Granuloma may also develop in response to relatively inert
foreign bodies
e) Formation of a granuloma effectively walls off the
offending agent- useful as defense mechanism
f) Granulomatous inflammation with subsequent fibrosis-
organ dysfunction
83. Specific infections (immune granuloma):
Mycobacteria (tuberculosis, leprosy)
syphilis, brucellosis
Foreign bodies:
Endogenous
( keratin, necrotic bone or adipose tissue
uric acid crystals)
Exogenous
(wood, silica, asbestos, silicone…)
Specific chemicals:
Beryllium
Drugs
Allupurinol, phenylbutazone,
sulphonamides (in liver)
Unknown origin
Sarcoidosis
Hypersensitivity pneumonitis
Tuberculosis
Foreign body aspiration
Berrylliosis
85. Age-associated chronic inflammation
A network of inflammatory sensors, including the Nlrp3 inflammasome,
recognizes the endogenous damage signals and initiates immune reactions
that are necessary for physiological repair.
Release of harmful products from the normal microbial constituents of the
human body such as oral and gut microbiomes.
Chronic low-grade inflammation in the elderly is to some extent directly
related to cellular senescence.
Increased inflammation in the elderly may derive from enhanced activation
of the coagulation system with age.
Inflammaging in the elderly is probably related to age-related immune changes
or immunosenescence
86. Molecular diagnosis and treatment of chronic inflammatory
diseases
Emerging approach to investigate patients with complex inflammatory
diseases using whole exome sequencing or whole-genome sequencing (WGS)
next-generation technologies.
WGS was tested in systemic autoimmune disorders & > 50% patients didn’t
show mutations.
This study selected 10 genes (MEFV, MVK, TNFRSF1A, NLRP3, NLRP12,
NOD2,PSTPIP1, IL1RN, LPIN2, and PSMB8) and undertook the molecular
diagnosis and genotype interpretation of SAIDs in 50 patients.
The study concludes that the molecular diagnosis of SAIDs is possible using
the multigene NGS technology.
88. Citation of Inflammatory lesions of oral cavity
Aphthous stomatitis (canker sores)
Traumatic ulcer
Geographic tongue (benign migratory glossitis) /
erythema migrans)
Lichen planus
Inflammatory papillary hyperplasia
Epulis fissuratum (inflammatory fibrous hyperplasia)
Contact stomatitis from cinnamon/medication burn
Dentifrice Related Sloughing
Carcinomas
REF: Marjorie Woods 2014, “Benign Inflammatory Lesions/Conditions of
Oral Mucous Membranes”, Diagnosis and management of oral lesions and
conditions- Aresource handbook for the clinician”, DOI: 10.5772/57597
89. Aphthous stomatitis (canker sores)
Patients with mild or intermittent lesions may not require any
treatment or may use over-the-counter anesthetic or protective
bioadhesive products.
90. Traumatic ulcer:
Traumatic ulcers are frequently observed in the oral cavity and
can be of such varying size and shape that they are difficult to
characterize.
Relieving an obvious source of irritation or toxic agent should
result in resolution of an ulcer.
91. Geographic tongue (benign migratory glossitis) / erythema migrans
It is an inflammatory disorder characterized by multiple
erythematous areas representing loss of filiform papillae
surrounded by a yellow-white irregular border.
No treatment is required .If a patient complains of burning or
sensitivity that affects daily life, topical corticosteroids such as
betamethasone.
92. Lichen planus
Relatively common chronic, inflammatory, mucocutaneous disease .
Cutaneous lesions appear as multiple pruritic, purplish, polygonal
papules.
Usually asymptomatic and treatment is not necessary.For
symptomatic OLP, topical steroids, such astriamcinolone
mouthwash or mixed with orabase, clobetasol or fluocinonide are
used first in treatment.
93. Inflammatory papillary hyperplasia
Inflammatory papillary hyperplasia (IPH) is a reactive tissue
response that is usually found in the hard palate underneath an
ill-fitting dental prosthesis/exhibits parafunctional habits.
It is usually asymptomatic and the mucosa is erythematous, with
a pebbly appearance.
.
94. Epulis fissuratum (inflammatory fibrous hyperplasia)
Lesion consists of folds of hyperplastic tissue into which the flange
of a complete or partial denture rest, most often in the maxillary
anterior vestibule, although sometimes it can be seen lingual to the
mandibular ridge.
95. Contact stomatitis from cinnamon/medication burn
Diffuse gingival involvement with enlargement, edema and
erythema. Sloughing of superficial epithelium is common.
96. Dentifrice Related Sloughing
Dentifrice related sloughing of the oral mucosa is an increasingly
common finding and may be caused by a variety of additives found
in many dentifrices.
97. Carcinoma of the oral cavity
As per Yujuan Sun & Nan Liu 2016 Oral squamous cell
carcinoma (OSCC) is an aggressive, invasive malignancy of
epithelial origin.
The progression from premalignant lesions—oral leukoplakia
(OLK) and oral lichen planus (OLP)—to OSCC involves complex
inflammatory processes that have not been elucidated.
Immunohistochemical staining of CD4, FOXP3, CD68, TGF-𝛽1,
IL-10, IL-4, IFN-𝛾, and MCP-1 showed - Tregs and TAMs in
parallel with disease progression in OLK and OSCC. IL-10
gradually increased during the early stages of OLK and in OSCC
98.
99. Cytokines are a group of small proteins involved in the regulation
of infection, immune responses and inflammation.
Altered cytokine responsiveness has been linked to Oral Squamous
Cell Carcinoma (OSCC), research to date indicates the possibility of
using salivary pro- and anti-inflammatory proteins for screening of
oral disorders.
The goal of the innovative salivary diagnostics is the identification
of a single or multiple biomarkers that will serve as a clinical test
facilitating the diagnosis of patients predisposed to develop OSCC
REF: Valentina R. Dikova et al “Salivary inflammatory proteins in patients
with oral potentially malignantdisorders” J Clin Exp Dent. 2019;11(7):e659-
64
Molecular biology
100. As per Shitalkumar Sagori et al 2016 Oral lichen planus (OLP) is a
chronic inflammatory mucosal disease that is usually detected in
0.5–2.2% of the human population.
Desmocollin-1 expression increased the risk of dysplasia and
cancer.
It was the only independent predictor of the substitute endpoint
of oral cancer emerging from OLP while E-cadherin loss may
play roles in different aspects of the pathogenesis of OLP
including apoptosis of basal keratinocytes and migration of T-cells
into the epithelial compartment
REF: Shitalkumari Sagari et al 2016 , “Molecular markers in oral lichen planus:
A systematic review” , Jpurnal of oral and maxillofacial pathology, 2016 Jan-Apr;
20(1): 115–121. doi: 10.4103/0973-029X.180964
101. 1. Chronic inflammatory illnesses such as diabetes, arthritis, and
heart disease are now seen as problems that might have an
impact on the periodontium.
2. Macrophages are key cells for the inflammatory processes as
regulators directing inflammation to chronic pathological
changes or resolution with no damage or scar tissue formation.
3. Macrophages are involved in a remarkably diverse array of
homeostatic processes of vital importance to the host. With their
critical role in immunity, macrophages are also widely
recognized as ubiquitous mediators of cellular turnover and
maintenance of extracellular matrix homeostasis.
REF: Hatice Hastark et al 2012, “ oral inflammatory diseases and systemic
inflammation: role of macrophage”, frontiers in immunology, vol 3, article 118,
pg 1-17
102. conclusion
Inflammation is the immune system’s response to harmful stimuli,
such as pathogens, damaged cells, toxic compounds, or
irradiation and acts by removing injurious stimuli and initiating
the healing process.
It is therefore a defense mechanism that is vital to health .
Usually, during acute inflammatory responses, cellular and
molecular events and interactions efficiently minimize impending
injury or infection. This mitigation process contributes to
restoration of tissue homeostasis and resolution of the acute
inflammation.
However, uncontrolled acute inflammation may become chronic,
contributing to a variety of chronic inflammatory diseases.
103. bibliography
1. Text book of Pathology by Harsh Mohan 6th edition
2. Robbin’s Basic Pathology 8th edition
3. Yujuan Sun & Nan Liu et al 2016, Immunosuppression Induced by
Chronic Inflammation and the Progression to Oral Squamous Cell
Carcinoma” , Mediators of Inflammation Volume 2016, Article ID 5715719,
12 pages http://dx.doi.org/10.1155/2016/5715719
4. Valentina R. Dikova et al “Salivary inflammatory proteins in patients with
oral potentially malignantdisorders” J Clin Exp Dent. 2019;11(7):e659-64
5. Shitalkumari Sagari et al 2016 , “Molecular markers in oral lichen planus:
A systematic review” , Jpurnal of oral and maxillofacial pathology, 2016
Jan-Apr; 20(1): 115–121. doi: 10.4103/0973-029X.180964
104. 6.Marjorie Woods 2014, “Benign Inflammatory Lesions/Conditions of Oral
Mucous Membranes”, Diagnosis and management of oral lesions and
conditions- Aresource handbook for the clinician”, DOI: 10.5772/57597
7. Dhavendra kumar 2020, “Molecular biology of acute and chronic
inflammation”, Clinical Molecular Medicine.DOI:
https://doi.org/10.1016/B978-0-12-809356-6.00022-8
Editor's Notes
Difference in etiology of acute & chronic inflammation
THIS IS THE SUMMARY OF THE ENTIRE PROCESS OF ACUTE INFLAMMATION, WHICH I WILL BE COVERING ONE BY ONE
Now coming to Vascular events first. The 1st step is the hemodynamic change wherein there is….
2. Erythema [ characteristic feature of acute inflammation
3. With increase of vascular permeability protein rich fluid moves into extra vascular spaces increasing the blood viscocity & slowing of circulation. Depicted microscopically by numerous dilated blood vessels packed with RBC’S and slow flowing blood called stasis.
Now as stasis develops neutrophils begin to accumulate along the vascular endothelial surface called margination which is considered to be the 1st step in the journey of leukocytes through the vascular wall into the interstitial tissue.
These are the pathological outcomes of the alterations that take place in the endothelial lining which contributes to the increased vascular permeability in the phase of acute inflammation.
Transudate: increase in hydrostatic pressure, decrease in osmotic pressure , permeability is normal, low specific gravity, ultrafiltrate of blood plasma.
Exudate: increase in hydrostatic pressure, decrease in osmotic pressure, increased in permeability , high specific gravity, rich in plasma proteins.
Both are known as edema
The 2nd phase of acute inflammation is cellular events
Margination is re-distribution of wbc along the endothelial lining because of stasis in microcirculation.
Rolling is when the leucocytes keeps getting rolled over the endothelial membrane by transiently binding with the endothelial membrane and then again detaching. E & P selectins are found in activated[ mediated by TNF] endothelial cells, L selectin are found in leucocytes. Corresponding ligands for these selectins is Sialyted Oligosaccharides for eg Sialyl Lewis [ found on leucocytes & endothelial cells] . Not in normal endothelial cells. V CAM- VASCULAR CELL ADHESION MOLECULE, ICAM- INTRACELLULAR CELL ADHESION MOLECULE act under IL1 . PECAM- Platelet endothelial cell adhesion molecule mediate diapedesis which is a member of immunoglobulin family CD 31. break basement membrane by secreting collagenase. Chemotaxis is migration of leucocytes to chemotactic gradient.
Chemoattractants bind to specific receptors onto the leucocytes that lead to polymerization of actin and localization of myosin in leucocytes, leucocytes extend filopodia which pulls the cells in the direction of the extension, results in forward movement of leucocytes, towards direction of the source of chemoattractants.
Macrophages are diffusely scattered in most connective tissue and are also found in liver ( kuffer cells) spleen and lymph nodes ( sinus histiocytes) .