BASICS OF INFLAMMATION FOR GENERAL AND MAXILLOFACIAL PATHOLOGY RESIDENTS

1. Dr Pushpanjali Das Mds
Part I
inflammation

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

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

8. etiology
Infective agent: Bacteria, Viruses, Fungi, Parasite
Immunological agents: Cell mediated and Antigen Antibody
reactions.
Physical agents: Heat ,Cold, Radiation, Mechanical Trauma
Chemical agents: Organic & Inorganic poisons

11. SIGNS
cardinal signs
a) Rubor [ redness]
b) Tumor [ swelling]
c) Calor [ heat]
d) Dolor [ pain]
e) Functio Laesa [
loss of function]

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:

16. VASCULAR
Transient
vasoconstriction
Persistent, progressive
vasodilatation
Increased
permeability
Stasis of blood
Leukocytic
margination
CELLULA
R
Rolling
Adhesion
Emigration
Chemotaxis
Phagocytosis

17. MAJOR COMPONENTS:
VASCULAR EVENTS-
1. Haemodynamic changes. 2. Vascular permeability
HAEMODYNAMIC CHANGE:
1. Immediate transient vasoconstriction of arterioles lasting for
5mins.
2. Followed by persistent progressive vasodilators [ erythema]
3. Elevation of local hydrostatic pressure shifting fluid into
intracellular space [ Arteriolar vasodilatation & blood flow]
4. Stasis of microcirculation
5. Emigration & Margination of leucocytes.

18. HAEMODYNAMIC CHANGES

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).

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

24. TNF α , IL 1
INTEGRIN
LIGANDS

25. Chemoattractants:
Soluble bacterial products Exogenous
Complement components (C5a)
Cytokines (chemokine family,IL-8)
LTB4 (AA metabolite)
Endogenous

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

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

32. Morphology of Acute Inflammation:
 Pseudomembranous inflammation
 Ulcer
 Suppuration
 Cellulitis
 Bacterial infection of the blood- bacteremia, pyemia,
septicaemia
Systemic effects of acute inflammation:
Fever , leukocytosis, lymphangitis , shock, DIC, bleeding & death.
FATE: 1. Resolution 2. Healing 3. Suppuration 4. Chronic
Inflammation

33. MORPHOLOGY PATTERNS

34. Ulcerative inflammation

35. •Complete resolution
•Healing by connective tissue
replacement (fibrosis/scar formation)
•Progression to chronic inflammation

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

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

46.  Metabolites of ARACHIDONIC ACID ( source: diet/linoleic
acid)
 Autocoids or local harmones
Cycloxygenase
Thromboxane
A2
Prostaglandins
Lipoxygenase
leukotrienes
lipoxins

47. MEDIATOR TX A2 PG I 2 PG E2, D2, F2
SOURCE Platelets Endothelium Mast cells
FUNCTION
 vaso
constriction
Platelet
aggregation
Vasodilator
Platelet
aggregation
inhibitor
Vasodilation
Edema

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.

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

55. CYTOKINES IN INFLAMMATION

56. SUBSTANCE SOURCE FUNCTION
NITRIC OXIDE Endothelium, activated
macrophage
 vasodilation
Microbicidal
Anti-platelet
activation
OXYGEN
METABOLITES
Metabolic reactions Endothelial cell
damage
Increased vascular
permeability
Activation of protease
Inactivation of anti
protease causing tissue
damage

60. Plasma Derived Mediators:

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

66. Fibrinolytic System
•Fibrin degradation products
- increased vascular permeability.
•Plasmin
-cleaves the complement C3 to C3a
-Activates 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

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

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

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

84. Molecular pathology of chronic inflammation

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.

87. Systemic effects
1. Fever
2. Anemia
3. Leukocytosis
4. Elevated ESR
5. Amyloidosis

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

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