INFLAMMATION, HEALING AND REPAIR
GUIDED BY: DR. AMIT GOEL PRESENTED BY : DR. DIVYA THAKUR
PROFESSOR PG 1ST YEAR
DEPARTMENT OF PERIODONTICS DEPARTMENT OF
PERIODONTICS
CONTENTS
• INTRODUCTION
• DEFINITIONS
• HISTORICAL BACKGROUND
• CLASSIFICATION OF INFLAMMATION
• EVENTS OF INFLAMMATION
• INFLAMMATORY CONDITIONS IN ORAL CAVITY
• WOUND HEALING
• REPAIR
• CONCLUSION
• REFERENCES
1/55
INTRODUCTION
Inflammation is the body's response to injury. It works to heal wounds, but it
can also play a role in some chronic diseases. It is the body's way of
signalling the immune system to heal and repair damaged tissue, as well as
defend itself against foreign invaders, such as virus, bacteria etc.
2/55
DEFINITIONS
3/55
HISTORY
4/55
SIGNS OF INFLAMMATION
FUNCTIO-
CALOR RUBOR TUMOR DOLOR LAESA 5/55
6/55
ATION
CLASSIFICATION OF INFLAMMATION CLASSIFIC
Depending, upon the
intensity of injury,
duration of the response,
& defense capacity of the
host :
7/55
ACUTE INFLAMMATION
INFECTIONS IMMUNE REACTIONS
STIMULI
TISSUE
NECROSIS FOREIGN BODIES
TRAUMA – PHYSICAL
& CHEMICAL AGENTS 8/55
EVENTS IN INFLAMMATION
-Hemodynamic changes -Exudation of leucocytes
- Increased vascular permeability - Phagocytosis
9/55
VASCULAR EVENTS
HAEMODYNAMIC CHANGES
Transient vasoconstriction
ProlongedVasodilatation Histamine Increased vascular
permeability
Arterioles
Fluid in extra
Increased blood flow HEAT/ vascular space
REDNESS
SWELLING
10/55
Slow blood flow, increased Engorgement of small vessels
concentration of RBCs, increased
viscosity
STASIS OF BLOOD
LEUCOCYTIC MIGRATION
EMIGRATION 11/55
LEWIS EXPERIMENT
• Lewis induced the changes in the skin of inner aspect of forearm by firm
stroking with a blunt point, the reaction is known as triple response or red line
response consisting of the following:
12/55
INCREASED VASCULAR PERMEABILITY HALLMARK
• There is escape of fluid, blood cells and proteins from the blood vessels into the
interstitial tissues through the endothelial wall of peripheral vascular bed-
Accumulation of oedema fluid.
• Transudate- filtrate of plasma formed in the earliest phase of inflammation due to
increased hydrostatic pressure without alteration in the vascular permeability.
• Subsequently, the characteristic inflammatory oedema, appears by increased vascular
permeability of microcirculation – exudate.
13/55
MECHANISM OF THE INCREASED VASCULAR
PERMEABILTY
1. Contraction of endothelial cells
2. Direct injury to endothelial cells
3. Endothelial injury mediated by leucocytes
4. Leakiness in Neovascularisation
CELLULAR EVENTS
15/55
PHAGOCYTOSIS
• First reported by Elie Metchnikoff
• The process of engulfment of solid particulate material by the cells.
17/55
KILLING AND DEGRADATION
Mechanism of microbial killing:
2O’2+ 2 H+ H2O2
Superoxide will subsequently converted into H2O2 which has
bactericidal effect. 19/55
CHEMICAL MEDIATORS OF INFLAMMATION
CELL DERIVED MEDIATORS
20/55
LIPOOXYGENASE PATHWAY
CYCLOOXYGENSE PATHWAY
21/55
22/55
PLASMA- DERIVED FACTOR XII
MEDIATORS KININ SYSTEM
contact
FACTOR XII A
CLOTTING
FIBRINOLYTIC SYSTEM
SYSTEM KININ SYSTEM
PLASMINOGEN
ACTIVATOR
PLASMINOGEN FIBRINOGEN
BRADYKININ
THROMBIN
PLASMIN
FIBRINOPEPTIDES FIBRIN
Permeability factors
COMPLEMENT SYSTEM ( C3a, C5a)
MAC(C5b- C9)
23/55
COMPLEMENT SYSTEM
Activation of complement system can occur either:
Action of anaphylatoxin:
. i) Release of histamine
ii) Increase vascular permeability
iii) C3b augment phagocytosis
iv) C5a chemotactic for leucocytes
v) MAC is a lipid dissolving agent
and causes holes in the
phospholipid membrane of the
cell.
24/55
CHRONIC INFLAMMATION
• It is defined as a prolonged process in which tissue destruction and
inflammation occurs at the same time.
•TIME- > 48
hours (weeks,
months, years) CAUSES
•Mononuclear
cells
(Macrophages,
Lymphocytes,
Plasma cells
25/55
GENERAL FEATURES
TISSUE
DESTRUCTION
OR NECROSIS
26/55
TYPES OF CHRONIC INFLAMMATION
Chronic Non-specific Chronic granulomatous
inflammation inflammation
27/55
OUTCOME OF ACUTE AND CHRONIC
INFLAMMATION
28/55
VARIOUS INFLAMMATORY CONDITIONS OF
ORAL CAVITY
Gingivitis due to
Gingivitis Eruption Gingivitis
orthodontic appliance
29/55
DENTURE
PERICORONITIS
STOMATITIS
30/55
INFLAMMATORY CONDITIONS ASSOCIATED WITH PULP
According to Grossman
Inflammatory Pulp Pulp necrosis
diseases of pulp degeneration
Reversible pulpitis
Irreversible pulpitis
Symptomatic Asymptomatic
Acute Chronic
(acute) (chronic)
31/55
Abnormally Abnormally Symptomatic
Hyperplastic Internal
responsive to responsive to with pulp
pulpitis resorption
cold heat exposure
33/55
WOUND HEALING
WOUND A cut or break in the continuity of the tissue caused by
any injury or after surgery.
HEALING is the body’s response to injury in an attempt to restore
the normal structure & function.
34/55
REGENERATION
•Healing takes place by proliferation of parenchymal cells and usually results in
complete restoration of original tissues.
•The factors which control healing & repair are complex & they include the
production of variety of growth factors:
FACTOR
S
35/55
REPAIR
PHASES
ANGIOGENESIS FIBROGENESIS
36/55
CONTRACTION OF WOUND
• The wound starts contracting after 2-3 days and the process is completed by 14th
day. During this period the wound is reduced by approximately 80% of its original
size.
• Contraction of wound helps in rapid healing. FACTORS
1. Dehydration due to removal of
fluids by drying.
2. Contraction of collagen
3. Discovery of myofibroblasts.
37/55
TYPES OF WOUND HEALING
38/55
HEALING BY PRIMARY
INTENTION
CONDITIONS
•Clean and uninfected
wounds
• Surgically incised
• Edges are
approximated by
surgical sutures
• Without much loss of
tissue & cells
39/55
HEALING BY
SECONDARY
INTENTION
CONDITIONS
•Open wound with a
large tissue defect
•Having extensive
loss of cells and
tissue
•Wound is not
approximated by
sutures
40/55
FACTORS AFFECTING WOUND HEALING
LOCAL SYSTEMIC
• Mechanical injury
• Age
• Nutrition
• Infection
• Trauma
• Edema • Metabolic diseases
• Ischemia/necrotic tissue • Immuno suppression
• Low oxygen tension • Connective tissue disorders
• Foreign bodies • Smoking
42/55
COMPLICATIONS OF WOUND HEALING
Infection Keloid & hypertrophic PIGMENTARY CHANGES
scar
Infections of the wound •Excessive formation
delay the healing of collagen in healing In oral cavity
process. Systemic may result in keloid. hypopigmented scars are
conditions such as • Hypertrophic scar less common but some
diabetes mellitus, occur in lesions leave
immunosuppressive wounds where hyperpigmentation while
state etc. make the healing is delayed. healing e.g. lichenplanus,
individual prone to These scars are more lichenoid reactions.
infection. cellular and vascular.
43/55
IMPLANTATION
CICATRISATION
CYSTS
Cicatrisation refers to
late reduction in the size Epithelial cysts may
of the scar in contrast to slide and get entrapped
immediate wound in the wound and later
contraction. It is a may proliferate to form
complication due to implantation cysts.
burns on the skin.
44/55
HEALING OF EXTRACTION SOCKETS
45/55
HEALING OF REIMPLANTED TOOTH
46/55
HEALING FOLLOWING SCALING & ROOT
PLANING
2 hours:
•Numerous polymorphonuclear leucocytes can be seen b/w residual epithelial cells
& crevicular surface.
•Dilation of blood vessels, oedema & necrosis in the lateral wall of the pocket
24 hrs: widespread infiltration of inflammatory cells and migration of keratinocytes
have been observed, in all areas of the remaining epithelium
2 days: Entire pocket is epithelialized
47/55
HEALING FOLLOWING FLAP
HEALING FOLLOWING
SURGERY
CURETTAGE
In 4-5 days , new epithelial
Clot attachment appear at the
formation
bottom of the sulcus
Soon after curettage, blood clot forms b/w root surface & pocket wall
1-3 days, migration of epithelial cells
Depending on the severity of
Migration ofthe inflammation & the
PMN’s
by 1 week, depth
epithelial
of the attachment by complete
gingival crevice, means ofepithelial
hemidesmosomes
healing occurs in 1-2 weeks.
Granulation tissue Proliferation
granulation tissue replaces clot
Epithelization
Connective tissue repair completed
by immaturein 2-7 days
collagen fibers occurs
by 2nd week, collagen fibres appear & arranged
within 21 days
parallel to root surface
Healing occurs with
Junctional the formation
epithelium formed of long ,thin junctional
in about 5 days ep .
by end of 1 month,Withwellnoformed epithelial attachment
C.T attachment.
48/55
HEALING IN SPECIALISED TISSUES
Fracture Healing
Healing of fracture by callus formation depends on:
Traumatic or pathological
Complete or incomplete like green-stick fracture
Simple, comminuted or compound
49/55
FRACTURE HEALING
Complications of fracture healing –
•Delayed union and non union
•Fibrous union
•Lack of calcification
50/55
PERIRADICULAR WOUND HEALING
• Follows the general principles of wound healing .
• In nonsurgical cases when root canal has been treated reservoir of bacteria or
noxious products gets eliminated; after cleaning and obturation, periradicular
tissue undergoes repair.
• Principle cells of repair are fibroblasts which lay down cellular fibrous tissue. In
some cases collagen fibers which lays down acellular dense tissue.
• In surgical cases, healing by first intention occurs within 5 days but if sutures tear,
healing occur through formation of granulation tissue in 4- 6 weeks, completed
usually in a year . 51/55
OSSEOINTEGRATION OF IMPLANTS
• Osseointegration is a direct structural and functional connection between ordered
living bone and the surface of the load carrying implant.
• After the implant insertion, a period of 10-12 weeks of healing is required.
• During healing, compact and cancellous bone forms around the implant together
with variable amount of fibrous marrow.
• The connective tissue of the mucosa forms the intimate contact with the implant.
• The collagen fibers of the connective tissue runs parallel to the long axis of the
implant, and the epithelium is attached to the implant by means of basal lamina and
hemidesmosomes. 52/55
CONCLUSION
Inflammatory response is closely interwined with the process of repair.
Inflammation serves to destroy, dilute or wall off injurious agents and leads to
healing of damaged tissue.
Thus, inflammation and repair describes remarkable capacity of human body to
restore its form and function.
53/55
REFERENCES
1) Cotran, Kumar, Robbins. 5th edition. Saunders: Pathological Basis of Disease;
International edition.
2) Harshmohan. 4th edition. Jaypee: Essential pathology for Dental Students;2012.
3) Newman, Takei,Klokkevold,Carranza. 11th edition. Saunders: Clinical
Periodontology;2011
4) Pathology in dentistry-Shefield
5) Text book of oral pathology – Shafers
6 )Oral medicine – Tyldessly & Field 4th edition
7).Essentials of Oral pathology & Oral Medicine- R.A.Cawson
54/55
S
