ACUTE AND

CHRONIC
INFLAMMATION

2015
OVERVIEW OF INFLAMMATION

 Inflamasi adalah suatu respon protektif yang

du tujukan utk menghilangkan penyebab awal
jejas sel serta mebuang sel dan jaringan
nekrotik yang disebabkan olh kerusakan asal.

 Inflamasi
mengencerkan,menghancurkan, atau
menetralkan agen yang berbahaya
(mikroba, toxin)
 Inflamasi berkaitan dengan proses perbaikan yg
mengganti jaringan yang rusak dengan
regenerasi sel parenkim, dan atau dengan
pengisian setiap defek yang tersisa dengan
jaringan parut fibrosa

 walaupun inflamasi membantu membersihkan

infeksi dan bersama-sama proses perbaikan
memungkinkan penyembuhan luka, baik
inflamasi maupun proses perbaikan sangat
potensial menimbulkan bahaya
 ACUTE INFLAMMATION
Rapid in onset and of short duration (a few
minutes - a few days), and is characterized by
fluid and plasma protein exudation and a
predominantly neutrophilic leukocyte.

 CHRONIC INFLAMMATION
Longer duration (days - years), and is typified
by influx of lymphocytes and macrophages
with associated vascular proliferation and
fibrosis (scarring).
 Egyptian Papirus (3000
BC), Celsus Four
cardinal sign:
– Calor
– Rubor
– Tumor
– Dolor
 Virchow:

- Functio laesa
ACUTE INFLAMMATION
ACUTE INFLAMMATION
 Acute inflammation is a rapid response to
injury or microbes and other foreign
substances that is designed to deliver
leukocytes and plasma proteins to sites of
injury.
 Once there, leukocytes clear the invaders and
begin the process of digesting and getting
rid of necrotic tissues.
STIMULI FOR ACUTE INFLAMMATION

 Infections (bacterial, viral, fungal, parasitic)

 Trauma (blunt and penetrating)
 Physical & chemical agents
 Tissue necrosis
 Foreign bodies (splinters, dirt, sutures)
 Immune reactions
ACUTE INFLAMMATION HAS TWO
MAJOR COMPONENTS

 Vascular changes
 Cellular events
A.VASCULAR CHANGES
 Alterations in vessel caliber resulting in
increased blood flow (vasodilation)
 Increased vascular permeability
1.Alterations in vessel caliber resulting in
increased blood flow (vasodilation)
 Vasodilation involves arterioles opening
capillary bed increased blood flow
heat & redness
 Vasodilation is induced by the action of several
mediators Histamine and Nitric oxide on
vascular smooth muscle
 Vasodilation is quick followed by increased
permeability of the microvasculature, with
outpouring protein-rich fluid into the
extravascular tissue

 The loss fluid The red blood cells to

become more concentrated, thereby
increasing blood viscosity and slowing the
circulation.
 These changes are reflected microscopically
called stasis.
As stasis develops, leukocytes (principally
neutrophils) begin to accumulate along the
vascular endothelial surface, a process called
margination. This is the first step in the
journey of the leukocytes through the vascular
wall into the interstitial tissue
 EXUDATE
Inflammatory extravascular fluid that has a
high protein concentrate, cellular debris, and a
specific gravity above 1.020.
 TRANSUDATE
Fluid with low protein component (most of
which is albumin) and a specific gravity of less
than 1.012.
2. Increased vascular permeability in acute
inflammation

 Immediate transient response

 Endothelial cell contraction leading to
intercellular gaps in postcapillary venules is the
most common cause of increased vascular
permeability. It is a reversible process elicited
by histamine, bradykinin, leukotrienes, and
many other chemical mediators.
 Endothelial cell
contraction occurs
rapidlafter binding of
mediators to specific
receptors, is usually
short-lived (15-30
minutes), and is called
the immediate
transient response.

 retraction of endothelial
cells, resulting from
changes in the
 Immediate sustained response
 Endothelial injury vascular leakage by
causing endothelial cell necrosis and
detachment after severe injury (e.g., burns
and some infections).
 In most cases leakage begins immediately
after the injury and persists for several hour (or
days) until the damaged vessels are
thrombosed or repaired.
• This reaction is
known as the
immediate
sustained
response.
• Venules, capillaries,
and arterioles can all
be affected,
depending on the
site of the injury.
 Delayed prolonged leakage
Direct injury to endothelial cells may also
induce a delayed prolonged leakage that
begins after a delay of 2 to 12 hours, lasts for
several hours or even days, and involves
venules and capillaries.
mild to moderate thermal injury,
certain bacterial toxins, and x- or ultraviolet
irradiation (i.e., the sunburn that appears the
evening after a day in the sun).
 Leukocyte-
mediated
endothelial injury
may occur as a
consequence of
leukocyte
accumulation along
the vessel wall.
Activated leukocytes
release many toxic
mediators that may
 Increased transcytosis
 Increased transcytosis of
proteins via an
intracellular vesicular
pathway augments
venular permeability,
especially after exposure
to certain mediators
such as vascular
endothelial growth
factor (VEGF).
 Transcytosis occurs via
channels formed by
 Leakage from new
blood vessels.
 These vessel sprouts
remain leaky until
proliferating endothelial
cells mature sufficiently
to form intercellular
junctions. New
endothelial cells
increased expression of
receptors for vasoactive
mediators, and some of
the factors that induce
angiogenesis (e.g., VEGF)
B.CELLULAR EVENTS
 Leukocyte Recruitment
 Leukocyte Activation
1.Leukocyte Recruitment
 Aktivasi endotel meningkatkan
pengeluaran selektin dan ligan selektin
 Rolling leukosit difasilitasi ol ikatan
selektin pada ligan karbohidrat yang relatif
longgar
 Adhesi kuat difasilitasi ol perubahan
afinitas integrin terhadap ligan endotel yg
diinduksi kemokin
 Transmigrasi antarsel endotel dgn
memanfaatkan interaksi PECAM-1 (CD31)
2.Leukocyte Activation
Proses fagositosis :
 Recognition and attachment

Pengenalan dan perlekatan partikel pada

leukosit yang menelan
 Engulfment Penelanan dengan
pembentukan vakuola fagositik
 Killing and degradation Pembunuhan
dan degradasi material yang ditelan
OUTCOMES OF ACUTE
INFLAMMATION
 Complete resolution
 Healing by connective tissue replacement (fibrosis)
 Progression to chronic inflammation
Morfologic Pattern of Acute
Inflammation

1. SEROUS INFLAMMATION
2. FIBRINOUS INFLAMMATION
3. SUPPURATIVE OR PURULENT INFLAMMATION
4. ULCER
1. Serous
Inflammation
 Ditandai melubernya

cairan relatif
mengandung kadar
protein yg rendah.
Dibentuk dari serum
atau hasil sekresi
mesothel rongga
tubuh (misal:
peritoneum, ruang
2. Fibrinous
Inflammation
 Jejas yang lebih
berat permeabilitas
vaskuler
lebih besar
molekul lebih besar
misal Fibrinogen
dapat melintasi
barier
pembuluhdarah
fibrin berada di
3. Suppurative or
Purulent
Inflammation
 Ditandai dengan

produksi nanah
(pus) dalam jumlah
banyak
neutrophil, sel-sel
nekrotik, cairan
edema.
 Misal: Infekfi bacteri
 4. Ulcer
 Defek lokal, atau
exkavasi, permukaan
organ atau jaringan
yang diproduksi
oleh sloughing
(shedding) jaringan
keradangan nekrotik
 Misal: mukosa
rongga mulut,
permukaan saluran
CHEMICAL MEDIATORS OF
INFLAMMATION

Mediators may be produced:

 Locally by cells at the site of inflammation

Leukocytes that are recruited to the site from

the blood , tissue macrophages, mast cells,
 endothelial cells at the site of inflammation

 Circulating in the plasma (typically synthesized

by the liver)
CHRONIC INFLAMMATION
 Chronic inflammation is inflammation of
prolonged duration (weeks to months to years)
in which active inflammation, tissue injury, and
healing proceed simultaneously.
 Infiltration with mononuclear cells: including
macrophages, lymphocytes, and plasma cells
 Tissue destruction: largely induced by the
products of the inflammatory cells
 Repair: Involving new vessel proliferation
(angiogenesis) and fibrosis
Inflamasi kronik dapat terjadi pada:
 INFEKSI VIRUS

Infeksi intrasel, perlu limfosit (dan makrofag)

untuk mengidentifikasi serta eradikasi

 INFEKSI MIKROBA PERSISTEN

Misal: TBC, Treponema pallidum
Mengakibatkan patogenitas langsung yg
lemah, menimbulkan respos imun
hypersensitifitas lambat, menghasilkan radang
granulomatosa
 PAPARAN INFLAMASI YANG LAMA TERHADAP
AGEN YANG BERPOTENSI TOKSIK
Misal: paparan material eksogen yang tak
dapat didegradasi, misal partikel silika
terinhalasi.

 PENYAKIT AUTOIMUN
Misal: Artritis Rheumatoid
Chronic Inflammatory Cells
 Macrophages, the
dominant cells of
chronic
inflammation, are
tissue cells derived
from circulating
blood monocytes
after their
emigration from the
bloodstream.
 Lymhocyte
Both T and B lymphocytes migrate into
inflammatory sites using some of the same
adhesion molecule pairs and chemokines that
recruit other leukocytes.
 Plasma calls
 Eosinophils : parasitic infections or as part of
immune reactions mediated by IgE, typically
associated with allergies.
 Mast cells
Granulomatous Inflammation
 Merupakan proses radang kronik yang khas
terdiri dari sel-sel macrophage yang teraktifasi
menyerupai sel epithel (disebut epithelioid)
 Misal: Tuberculosis, Lepra, Syphilis, Cat-scratch
disease
Two types of granulomas:
 Foreign body granuloma

talc, suture, fiber

 Immune granuloma

Disebabkan insoluble particle, khususnya

mikroba yang dapat menginduksi respon
immun. Macrophage mencaplok partikel
yang tak dapat dihancurkan tsb
mengaktifkan T lymphosit Epithelioid dan
multinucleated giant cell
EFEK SISTEMIK INFLAMASI
 Demam, malaise, anoreksi,

 Laju endap darah yang meningkat (kadar

fibrinogen meningkat mudah beraglutinasi)

 Leukositosis

 Other manifestation (increased pulse,decrease

sweating, chills, anorexia, malaise,somnolence)

 Severe bacterial infection (sepsis)
TERIMA KASIH