Chronic inflammation /orthodontic courses by Indian dental academy

CHRONIC
INFLAMMATION
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

 Learning Objectives
 The student should be able to :
 Define Inflammation.
 What are the causes of inflammation?
 Describe the signs and symptoms of Inflammation?
 Describe the types of Inflammation
 Describe the causes of acute inflammation.
 Describe the causes of chronic inflammation.
 What are the morphological features of Chronic
Inflammation?
 What is granulomatous Inflammation?

 Inflammation is part of the complex biological response
of vascular tissues to harmful stimuli such as pathogens,
damaged cells or irritants.
 It is a complex reaction in tissues that consists mainly of
responses of blood vessels and leukocytes.
 The body’s principal defenders against foreign invaders are
plasma proteins and circulating leukocytes(WBC),as well as
tissue phagocytes that are derived from circulating cells.

 The presence of proteins and leukocytes in the blood gives
them the ability to home to any site where they may be
needed.
 Because invaders such as microbes and necrotic cells are
typically present in tissues, outside the circulation it follows
that the circulating cells and proteins have to be rapidly
recruited to the extravascular sites.
 The inflammatory response coordinates the reaction s of
plasma proteins to achieve this goal.

 Causes of Inflammation
 Burns
 Chemical irritants
 Toxins
 Infection by pathogens
 Physical injury, blunt or penetrating

 Immune reactions due to hypersensitivity
 Ionizing radiation
 Foreign bodies, including splinters, dirt and debris
 Stress
 Trauma
 Alcohol

 Signs of Inflammation
 Dolor (pain)
 Calor (heat)
 Rubor (redness)
 Tumor (swelling)
 Functio laesa (loss of function)

 Symptoms of Inflammation
 Pain
 Redness
 Bruising
 Swollen area that is warm to the touch
 Tender muscle points

 Fever
 Chills
 Stuffy nose and head
 Breathing problems (asthma)
 Fluid retention
 Blood clots

Types of Inflammation
1.Acute Inflammation
2.Chronic Inflammation

 Acute Inflammation
 Rapid in onset(typically minutes)
 Short duration,lasting for hours or a few days
 Main Characteristics;
 Exudation of fluid and plasma proteins(edema)
 Emigration of leukocytes predominantly neutrophils(also
called polymorphonuclear leukocytes.

 When acute inflammation is successful in eliminating the
offenders the reaction subsides,but if the response fails to
clear the invaders it can progress to a chronic phase.

Chronic inflammation is considered to be inflammation of
prolonged duration(weeks to months to years) in which
active inflammation,tissue injury,and healing proceed
simultaneously.

 Chronic inflammation may progress from acute inflammation.
 This transition occurs when the acute response cannot be
resolved,either because of the persistence of the injurious
agent or because of the interference in the normal process of
healing.

 Chronic inflammation arises in the following;
1.Persistent infections
• Bacteria.
 Viruses.
 Fungi.
 Parasites

2.Prolonged exposure to potentially toxic agents
• Endogenous, (atherosclerosis).
• Exogenous,(by particulate silica-Silicosis).
3.Autoimmune diseases
 Rheumatoid arthritis.
 Lupus erythematosus.

Morphological Features of Chronic Inflammation
 These are characterized by:
 I - Infiltration by mononuclear cells.
 II - Tissue destruction.
 III - Removal of damaged tissue, (healing).

 I - Infiltration by mononuclear cells:
 The mononuclear cells become predominant after 48
hours.These include;
 Macrophages.
 Lymphocytes.
 Plasma cells.
 Eosinophils.
 Mast cells.

 Macrophages
 Macrophages are one component of the mononuclear
phagocyte system.
 The mononuclear phagocyte system (sometimes called
reticuloendothelial system) consists of closely related cells of
bone marrow origin, including blood monocytes and tissue
macrophages.

 The tissue macrophages are diffusely scattered in the
connective tissue or located in organs such as
 the liver (Kupffer cells),
 spleen and lymph nodes (sinus histiocytes),
 lungs (alveolar macrophages),
 and central nervous system (microglia)

 Mononuclear phagocytes arise from a common precursor
in the bone marrow, which gives rise to blood monocytes.
 From the blood, monocytes migrate into various tissues
and differentiate into macrophages.

 The half-life of blood monocytes is about 1 day,
whereas the life span of tissue macrophages is
several months or years.
 The journey from bone marrow stem cell to tissue
macrophage is regulated by a variety of growth and
differentiation factors, cytokines, adhesion
molecules, and cellular interactions.




 Monocytes begin to emigrate into extravascular tissues quite
early in acute inflammation, and within 48 hours they may
constitute the predominant cell type called macrophages.
 Macrophages may be activated by a variety of stimuli,
including microbial products that engage TLRs and other
cellular receptors, cytokines (e.g., IFN-γ) secreted by
sensitized T lymphocytes and by natural killer cells, and other
chemical mediators.

 The roles of activated macrophages in chronic inflammation

 The products of activated macrophages serve to eliminate
injurious agents such as microbes and to initiate the process
of repair, and are responsible for much of the tissue injury in
chronic inflammation.
 Activation of macrophages results in increased levels of
lysosomal enzymes and reactive oxygen and nitrogen species,
and production of cytokines, growth factors, and other
mediators of inflammation.

 Some of these products are toxic to microbes and host
cells(e.g., reactive oxygen and nitrogen species) or to
extracellular matrix (proteases); some cause influx of other
cell types (e.g., cytokines, chemotactic factors).
 The others cause fibroblast proliferation, collagen deposition,
and angiogenesis(e.g., growth factors).

 In short-lived inflammation, if the irritant is eliminated,
macrophages eventually disappear (either dying off or making
their way into the lymphatics and lymph nodes).
 In chronic inflammation, macrophage accumulation persists,
as a result of continuous recruitment from the circulation and
local proliferation at the site of inflammation.

 LYMPHOCYTES
 Lymphocytes are mobilized in the setting of any specific
immune stimulus(i.e., infections)as well as in non-immune-
mediated inflammation (e.g., due to infarction or tissue
trauma).
 T lymphocytes have a reciprocal relationship to macrophages
in chronic inflammation.

 They are initially activated by interaction with
macrophages presenting processed antigen fragments
on the cell surface.
 The activated lymphocytes then produce a variety of
mediators, including IFN-Gamma,major stimulating
cytokine for activating monocytes and macrophages

• Activated macrophages in turn release cytokines, including
IL-1 and TNF,that further activate lymphocytes as well as
other cell types.
 The end result is an inflammatory focus where macrophages
and T cells can persistently stimulate one another until the
triggering antigen is removed.

 PLASMA CELLS
 They are the terminally differentiated end product of B-cell
activation.
 They can produce antibodies directed against antigens in the
inflammatory site or against altered tissue components.

 Eosinophils

 They are abundant in immune reactions mediated by IgE and
in parasitic infections.
 A chemokine that is especially important for eosinophil
recruitment is eotaxin.
 Eosinophils have granules that contain major basic protein, a
highly cationic protein that is toxic to parasites but also causes
lysis of mammalian epithelial cells.

A focus of inflammation showing numerous eosinophils

 Mast cells
 They are sentinel cells widely distributed in connective tissues
throughout the body.
 They can participate in both acute and chronic inflammatory
responses.
 Mast cells express on their surface the receptor (FcεRI) that
binds the Fc portion of IgE antibody.

 In immediate hypersensitivity reactions, IgE antibodies bound
to the cells' Fc receptors specifically recognize antigen, and
the cells degranulate and release mediators, such as histamine
and prostaglandins.
 This type of response occurs during allergic reactions to
foods, insect venom, or drugs, sometimes with catastrophic
results (e.g. anaphylactic shock).

 II - Tissue destruction:
 Occur due to:
 Inflammatory cells.
 Persistent infecting material.

 III - Removal of damaged tissue, (healing):
 Occur by proliferation of small blood vessels, (angiogenesis).
 Proliferation of fibroblast, (fibrosis-repair).

 GRANULOMATOUS INFLAMMATION
 Granulomatous inflammation is a distinctive pattern of
chronic inflammation that is encountered in a limited number
of infectious and some non-infectious conditions.
 Immune reactions are usually involved in the development of
granulomas.

 A granuloma is a focus of chronic inflammation consisting of
a microscopic aggregation of macrophages that are
transformed into epithelium-like cells, surrounded by a collar
of mononuclear leukocytes, principally lymphocytes and
occasionally plasma cells.

 In the usual hematoxylin and eosin–stained tissue sections, the
epithelioid cells have a pale pink granular cytoplasm with
indistinct cell boundaries, often appearing to merge into one
another.
 The nucleus is less dense than that of a lymphocyte, is oval or
elongate, and may show folding of the nuclear membrane.
 Older granulomas develop an enclosing rim of fibroblasts and
connective tissue.

 Epithelioid cells fuse to form giant cells in the periphery or
sometimes in the center of granulomas.
 These giant cells may attain diameters of 40 to 50 μm.
 They have a large mass of cytoplasm containing 20 or more
small nuclei arranged either peripherally (Langhans-type giant
cell) or haphazardly (foreign body–type giant cell).

 Examples of Granulomatous Inflammation
 Bacterial
 Tuberculosis
 Leprosy
 Syphilitic gumma
 Cat-Scratch disease
 Parasitic
 Schistosomiasis

 Fungal
 Histoplasma Capsulatum
 Blastomycosis
 Cryptococcus neoformans
 Coccidioides immitis
 Inorganic Metals or Dusts
 Silicosis
 Berylliosis

 Foreign Body
 Suture
 Breast Prosthesis
 Vascular graft
 Unknown
 Sarcoidosis

Disease Cause TissueReaction
Tuberculosis Mycobacterium tuberculosis Caseating granuloma (tubercle):
focus of activated macrophages
(epithelioid cells), rimmed by
fibroblasts, lymphocytes,
histiocytes, occasional Langhans
giant cells; central necrosis with
amorphous granular debris; acid-
fast bacilli
Leprosy Mycobacterium leprae Acid-fast bacilli in macrophages;
noncaseating granulomas
Syphilis Treponema pallidum Gumma: microscopic to grossly
visible lesion, enclosing wall of
histiocytes; plasma cell infiltrate;
central cells necrotic without loss
of cellular outline

Disease Cause Tissue Reaction
Sarcoidosis Unknown etiology Non caseating
granulomas with
abundant activated
macrophages
Cat-scratch disease Gram-negative bacillus Rounded or stellate
granuloma containing
central granular debris
and recognizable
neutrophils; giant cells
uncommon
Crohn disease
(inflammatory
bowel disease)
Immune reaction against
intestinal bacteria, self-
antigens
Occasional noncaseating
granulomas in the wall of
the intestine, with dense
chronic inflammatory
infiltrate

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Chronic inflammation /orthodontic courses by Indian dental academy

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