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Inflamation &

Wound Healing
DR. YUDI PURNOMO
INTRODUCTION
 Inflammation : is the complex biological response
of vascular tissues to harmful stimuli, such as
pathogens, damaged cells, or irritants.

 It is a protective attempt by the organism to


remove the injurious stimuli as well as initiate the
healing process for the tissue.

 In the absence of inflammation, wounds and


infections would never heal and progressive
destruction of the tissue would compromise the
survival of the organism.
Efek Terhadap Jaringan Tergantung :
- lama jejas - jumlah dan jenis sel
- sifat agen - kemampuan regenerasi sel

Kerusakan Struktur dan Komponen Fungsional Sel


tergantung sifat dan jenis agen (sel dengan fungsi spesifik
rentan terhadap agen tertentu )

Kematian Sel Melalui :


1. disrupsi mekanikal
2. disintegrasi fungsi membr
3. tertutupnya jalur metabolik
4. DNA rusak
5. defisiensi metabolit yang penting
ETIOLOGI
 Burns
 Chemical irritants
 Frostbite
 Toxins
 Infection by pathogens
 Necrosis
 Physical injury, blunt or penetrating
 Immune reactions due to hypersensitivity
 Ionizing radiation
 Foreign bodies, including splinters and dirt
ETIOLOGI
GOAL
 The inflammatory response is closely intertwined with the
process of repair

 Inflammation serves :

 to destroy, dilute, or wall off the injurious


agent,

 but in turn, set into motion a series of


events that, as far possible, heal and
reconstitute the damage tissue.
TIPE INFLAMASI
Acute Chronic

Persistent acute inflammation due to non-


Causative Pathogens, injured
degradable pathogens, persistent foreign
agent tissues
bodies, or autoimmune reactions

Mononuclear cells (monocytes,


Major cells
Neutrophils macrophages, lymphocytes, plasma
involved cells), fibroblasts
IFN-γ and other cytokines, growth factors,
Primary Vasoactive amines,
reactive oxygen species, hydrolytic
mediators eicosanoids
enzymes
Onset Immediate Delayed

Duration Few days Up to many months, or years

Healing, abscess
Outcomes formation, chronic Tissue destruction, fibrosis
inflammation
MECHANISM OF INFLAMMATION

 The process of acute inflammation is initiated


by the blood vessels local to the injured
tissue, which alter to allow the exudation of
plasma proteins and leukocytes into the
surrounding tissue.

 The increased flow of fluid into the tissue


causes the characteristic swelling associated
with inflammation, and the increased blood
flow to the area causes the reddened colour
and increased heat.
MECHANISM OF INFLAMMATION
 The blood vessels also alter to permit the extravasation of
leukocytes through the endothelium and basement membrane
constituting the blood vessel.

 Once in the tissue, the cells migrate along a chemotactic


gradient to reach the site of injury, where they can attempt to
remove the stimulus and repair the tissue

 Inflammation is terminated when the injurious stimulus is


removed and the major features Of chronic inflammation.
MECHANISM OF
INFLAMMATION
MECHANISM OF
INFLAMMATION
SIGN & SYMPTOMS
INFLAMMATION
The classic signs and symptoms of acute inflammation:

English Latin

Redness Rubor

Heat Calor

Swelling Edema

Pain Dolor

Loss of function Functio laesa


INFLAMMATION MEDIATOR
CELL DERIVED MEDIATOR PLASMA DERIVED MEDIATOR

HISTAMIN BRADIKININ

LEUKOTRIENE PLASMIN

IFN- GAMMA THROMBIN

TNF- ALFA COMPLEMENT

PROSTAGLANDIN FACTOR XII

NO MEMBRANE ATTACK COMPLEX

INTERLEUKIN (IL)
LEUCOCYTES
EXTRAVASATION
 Leukocyte localisation and recruitment to the
endothelium local to the site of inflammation –
involving margination and adhesion to the endothelial
cells.

 Migration across the endothelium, known as


transmigration, via the process of diapedesis

 Movement of leukocytes within the tissue via


chemotaxis:
MECHANISM OF
INFLAMMATION
TYPE OF INFLAMMATION
Acute Chronic
Persistent acute
inflammation due to non-
Causative agent Pathogens, injured tissues degradable pathogens,
persistent foreign bodies, or
autoimmune reactions
Mononuclear cells
Major cells (monocytes, macrophages,
Neutrophils
involved lymphocytes, plasma cells),
fibroblasts
IFN-γ and other cytokines,
growth factors, reactive
Primary mediators Vasoactive amines, eicosanoids
oxygen species, hydrolytic
enzymes
Onset Immediate Delayed
Up to many months, or
Duration Few days
years
Healing, abscess formation, chronic
Outcomes Tissue destruction, fibrosis
inflammation
ROLE OF INFLAMMATION
(+)
 It is a protective attempt by the
organism to remove the injurious stimuli
as well as initiate the healing process
for the tissue.
 In the absence of inflammation,
wounds and infections would never
heal and progressive destruction of the
tissue would compromise the survival
of the organism
INFLAMMATION & WOUND HEALING
ROLE OF INFLAMMATION (-
)
 However, inflammation which runs
unchecked can also lead to a host of
diseases, such as hay fever,
atherosclerosis, and rheumatoid
arthritis.

 It
is for this reason that inflammation is
normally tightly regulated by the body
Essential Points
21
1. Inflammation is fundamentally a protective response
the ultimate goal of which is to rid the organism of
both the initial cause of cell injury (e.g., microbes,
toxins) and the consequences of such injury (e.g.,
necrotic cells, and tissues).
2. Without inflammation, Infection would go unchecked,
wound would never heal, and injured organs might
remain permanent festering sores.
3. The inflammatory response is closely intertwined
with the process of repair. Inflammation serves
to destroy, dilute, or wall off the injurious agent,
but in turn, set into motion a series of events that,
as far possible, heal and reconstitute the damage
tissue.
4. Inflammation and repair may be potentially harmful,
however. 22
5. The inflammatory response occurs in the vascularized
connective tissue. The circulating cells include
neutrophils, monocytes, eosinophils, lymphocytes,
basophiles, and platelets. The connective tissue cells
are the mast cells (peri vascular), fibroblast, and
residence macrophage and lymphocytes.
6. Inflammation is divided into acute and chronic
patterns.
• Acute :short duration; minutes, hours, or few days.
Its main caracteristics; exudation of liquid and plasma
Proteins (edema), emigration of leukocytes predominantly
neutrophils.
• Chronic inflammation; longer duration, associated with the
present of macrophage, lymphocytes, the proliferation
of blood vessels, fibrosis, and tissue necrosis.
7. The vascular and cellular response of acute and
chronic inflammation are mediated by chemical 23
factors derived from plasma or cells and trigerred
by the inflammatory stimulus.
8. Inflammation is terminated when the injurious
stimulus is removed and the major features of
chronic inflammation.
9. Five cardinal signs of inflammation ;
• Rubor (redness)
• Tumor (swelling)
• Calor (heat)
• Dolor (pain)
• Loss of function (functio laesa)
wound healing

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