Body’s defense reaction to control or limit the spread of the injurious agent.
Distinct from infection.. It is a protective response by the body while the latter is resultant ill-effect by the toxins.
Depending upon the defense capacity of the host and duration of response. Chronic I occurs if the causative agent of acute I persists for longer time or the stimulus is such that it induces chronic I from the beginning.
Changes,, in vascular e there is alteration in the micro vasculature (a, c, v) is the earliest response
Due to changes in the vascular flow
These features thus elicit the classical signs of inflammation-redness, heat, swelling and pain.
Blood monocytes on reaching extravascular space get transformed into macrophages.
Will be discussed in comparison to injury due to sharp object on skin. Loss of collateral circulation ….also another reason why analgesics become ineffective in relieving pain of pulpal origin.
Consists of Vascular changes , infiltration of PMNLs , and exudate accumulation
Inflammation and Healing
PG 1st year
DEPARTMENT OF ORAL
MEDICINE AND RADIOLOGY
CHEMICAL MEDIATORS OF INFLAMMATION
DENTAL ASPECTS OF INFLAMMATION
Inflammation is defined as the local response of living tissues to
injury due to any agent.
The causes of inflammation are many and varied:
Mechanic agents: fractures, foreign corps, sand, etc.
Thermal agents: burns, freezing
Chemical agents: toxic gases, acids, bases
Biological agents: bacteria, viruses, parasites
Circulation disorders: thrombosis, infarction, hemorrhage
Enzymes activation – e.g. acute pancreatitis
Metabolic products – uric acid, urea
CELSUS in 1st century A.D named the famous 4 cardinal signs
of inflammation as:
To these, 5th sign functio laesa, or loss of function was later
added by VIRCHOW
SIGNS OF INFLAMMATION
TYPES OF INFLAMMATION
Fluid accumulation, plasma protein exudation
Lymphocytes, macrophages, plasma cells as inflammatory
1. HAEMODYNAMIC CHANGES:
1. TRANSIENT VASOCONSTRICTION
2. VASODILATATION (arterioles, venules and capillaries)
obvious within half an hour of injury
Increase blood volume in microvascular bed Redness
3. Elevation of HYDROSTATIC PRESSURE
Results in transudation of fluid in the extracellular space
4. Slowing or stasis
Increased vascular permeability
Increased concentration of RBCs
Raised blood viscosity
Slower blood flow
slowing followed by
LEUCOYTE MIGRATION (neutrophils mainly) to the
Leukocytes then move and migrate
through gaps between the endothelial
cells in the extravascular space.
Lewis induced the changes in the skin of the inner aspect of
forearm by firm stroking with a blunt point. The reaction so
elicited is known as
TRIPLE RESPONSE or RED LINE RESPONSE consisting of :
RED LINE- local vasodilatation of capillaries and venules
FLARE - vasodilatation of adjacent arterioles
WHEAL - transudation of fluid into the extravascular space
2. ALTERED VASCULAR PERMEABILITY
In normal circumstances fluid balance is maintained by 2
opposing set of forces:
1. Forces that cause OUTWARD MOVEMENT of fluid from
microcirculation are intravascular hydrostatic pressure and
osmotic pressure of interstitial fluid.
2. Forces that cause INWARD MOVEMENT of interstitial fluid
into circulation are intravascular osmotic pressure and hydrostatic
pressure of interstitial fluid.
Normally whatever little fluid is left in the interstitial compartment
is drained by the lymphatics and thus no oedema results.
In inflamed tissues, the endothelial lining becomes leaky.
Consequently, the intravascular osmotic pressure decreases and
osmotic pressure of the interstitial fluid increases resulting in
excessive outward flow of fluid into the interstitial compartment.
EXUDATIVE INFLAMMATORY OEDEMA
1. Endothelial cell contraction
mediated by histamine, bradykinin, leukotrienes
short duration: 15-30 min.
2. Retraction of EC
TNF and IL-1
onset of response takes 4-6 hrs after injury and lasts for 2-4
hours or more
3. Endothelial injury
immediate sustained response,
lasts for several hours or days
4. Leukocyte-mediated endothelial injury
activation of leucocytes release proteolytic enzymes and toxic
under the influence of VASCULAR ENDOTHELIAL GROWTH
FACTOR during the process of repair are leaky
Venules Delayed 24
hrs or more
IL-1, TNF In vitro only
All Any type VEGF tumours
1. EXUDATION OF LEUCOCYTES
Most important feature of inflammatory response.
The escape of leucocytes from lumen of microvasculature to the
In acute inflammation, polymorphonuclear neutrophils comprise
the first line of defense, followed later by the monocytes and
CHANGES LEADING TO MIGRATION
1. CHANGES IN THE FORMED ELEMENTS OF BLOOD
subsequently, SLOWING of BLOOD STREAM
The central stream of cells widens and peripheral plasma zone
becomes narrower because of loss of plasma by exudation.
The neutrophils of the central column come close to the vessel
2. ROLLING AND ADHESION:
Peripherally marginated and pavemented neutrophils slowly roll
over the endothelial cells lining the vessel wall.
Transient bond between the leucocytes and the endothelial cells
E-selectin (cytokine-activated Endothelial cells)
P-selectin (Preformed and stored in endothelial cells)
L-selectin (expressed on surface of Lymphocytes and
Activated during the process of loose and transient adhesions
between the endothelial cells and leucocytes.
IMMUNOGLOBULIN SUPER FAMILY ADHESION
Neutrophils move till a suitable site is reached
Subsequently, crosses the basement membrane by damaging it
locally with secreted collagenases and escape out into the
Simultaneously escape of RBCs takes place through the gaps
between the endothelial cells.
Diapedesis gives Hemorrhagic appearance to the inflammatory
The chemotactic factor mediated transmigration of leucocytes
after crossing several barriers to reach the interstitial tissues is
Well illustrated by BOYDEN’S CHAMBER EXPERIMENT.
In this, a millipore filter separates the suspension of leucocytes
from the test solution in tissue culture chamber.
If the test solution contains chemotactic agent, the leucocytes
migrate through the pores of filter towards the chemotactic agent.
AGENTS ACTING AS CHEMOTACTIC SUBSTANCES
EXOGENOUS SUBSTANCES ENDOGENOUS SUBSTANCES
a) Peptides – N –
c) Components of
d) Cytokine :
IL – 1, 5 , 6
f) Chemotactic factor for
g) Eotaxin chemotactic
factor for eosinophils
ENGULFMENT of solid particulate material by the cells (cell
The cells performing this function are PHAGOCYTES.
There are two main types of cells:
1. PMNs which appear early in acute inflammatory response and
are called as MICROPHAGES.
2. Circulating monocytes and fixed tissue mononuclear
phagocytes called as MACROPHAGES.
The process of phagocytosis is same for both polymorphs and
macrophages and involves 4 steps:
RECOGNITION AND ATTACHMENT OF
ENGULFMENT WITH FORMATION OF
KILLING & DEGRADATION STAGE
Opsonins are naturally occuring factors in the serum.
1. IgG opsonin: Fc fragment of immunoglobulin G. It is naturally
occuring antibody in the serum that coats the bacteria while PMNs
possess receptors for the same.
2. C3b opsonin: fragment of complement. It is generated by the
activation of complement pathway.
3. Lectins: carbohydrate binding proteins in the plasma which bind
to the bacterial cell wall.
The opsonised particle is ready to be engulfed.
formation of cytoplasmic pseudopods around the particle
enveloping in the phagocytic vacuole
Eventually, the plasma membrane breaks from the cell surface and
the lysosomes of the cell fuse with the phagocytic vacuole
PHAGOLYSOSOME or PHAGOSOME
Preformed granule stored products of PMNs are released
Mononuclear phagocyte also secrete enzymes eg
• IL-2 and 6,, TNF
• Arachidonic acid metabolites (Prostaglandins ,
leukotrienes , platelet activating factor)
• Oxygen metabolites (superoxide oxygen, hydrogen
peroxide, hypochlorous acid)
KILLING OR DEGRADATION STAGE
The micro-organisms after being killed are degraded by hydrolytic
The antimicrobial agents act by 2 mechanisms:
OXYGEN - DEPENDENT BACTERICIDAL MECHANISM
OXYGEN - INDEPENDENT MECHANISM
OXYGEN DEPENDENT BACTERICIDAL
An important mechanism of microbicidal killing is by production of
(O2, H2O2, HOCl, HOI, HOBr)
This type of activity is carried out either through enzyme
MYELOPEROXIDASE (MPO) present in the granules of
neutrophils and monocytes, or independent of enzyme MPO.
Few agents released from the granules of phagocytic cells do not
require oxygen. These include:
Permeability increasing factors
OXYGEN INDEPENDENT BACTERICIDAL
CHEMICAL MEDIATORS OF
Also called as PERMEABILITY factors or ENDOGENOUS
The substances acting as chemical mediators of inflammation
may be released from the cells, the plasma, or damaged tissue
Classified into 2 groups:
Mediators released by CELLS
Mediators originating from PLASMA
SOURCE : 1) Mast cells in C.T adjacent
to blood vessels
2) Blood basophils
STIMULI : Injury
Fragments of complement -
C3a , C5a
Neuropeptides such as
Cytokines IL – 1 , 8
SOURCE : 1) Platelets
2) Enterochromaffin cells
3) nervous tissue
4) mast cells
STIMULI : Platelet aggregation after
contact with collagen ,
Action: vasodilatation, increased vascular permeability, itching
A fatty acid with 2 main sources :
Directly through diet
Through conversion of essential fatty acid, linoleic acid to
ARACHIDONIC ACID ARACHIDONIC
ACID METABOLITESLipo-oxygenase Pathway
CYCLO – OXY- GENASE
Prostaglandin - PGD2 , E2 ,
LIPO – OXY – GENASE
5 – HETE
ARACHIDONIC ACID METABOLITES
GRANULES OF NEUTROPHILS:
GRANULES OF MONOCYTES AND TISSUE MACROPHAGES:
produced mainly by: activated lymphocytes & macrophages ,
also from endothelium, epithelium & connective tissue cells.
TNF and IL-1
• major cytokines that mediate inflammation.
Produced mainly by activated macrophages
• Immune reactions,
• physical injury & variety of inflammatory stimuli.
• endotoxins & other microbial products
1. Release of histamine from mast cells and basophils
2. Increased vascular permeability causing odema in
4. Chemotactic agent
FATE OF ACUTE INFLAMMATION
It is a prolonged process in which tissue destruction and
inflammation occurs at the same time.
> 48 hours (weeks, months, years)
Mononuclear cells (Macrophages, Lymphocytes, Plasma cells)
Can be caused by 1 of the following 3 ways:
1. Chronic inflammation following acute inflammation
2. Recurrent attacks of acute inflammation
3. Chronic inflammation starting de novo
FEATURES OF CHRONIC INFLAMMATION
Infiltration with mononuclear
cells – macrophages,
lymphocytes & plasma cells
Healing by Proliferation &
connective tissue replacement of
• Incr. lysosomal enzymes
• Greater ability to
ACTIVATION OF MACROPHAGE
IFN - ɤ
Persistent macrophage accumulation by
following mechanisms :
1. )Recruitment from circulation –
Chemotactic stimuli include :
b) Platelet derived growth factor
c) Transforming growth factor
2.) Local proliferation of macrophages
3.) Immobilization of macrophages
Resulting in the formation of granulation tissue
REACTIONS OF PULP TO BACTERIAL INVASION
ᶲ Vascular changes take place
inside blood vessels.
ᶲ PMNLs reach the area of
ANATOMICAL FEATURES OF PULP THAT TEND TO
ALTER THE RESPONSE
Enclosure of pulp in rigid calcified walls - PREVENTS EXCESSIVE
SWELLING.. Thus more painful.
Pressure leads to decrease Blood supply and Ischaemia – does not get
corrected since collateral circulation cannot develop through tiny apical
HISTOLOGIC FEATURES OF PULPITIS
PREDOMINATE - chiefly
plasma cells &
Fibroblastic activity is
collagen fibres seen in
• Continued vascular
• Accumulation of oedemal
fluid in connective tissue
• Pavementing of PMNLs
along endothelial wall
• Inflammation of periodontal ligament around root apex..
Changes localised around root
apex…..since richly vascular.
Vascular changes , infiltration of
PMNLs , and exudate
Resorption of bone –
REGENERATION AND REPAIR
HEALING BY PRIMARY AND SECONDARY
FACTORS AFFECTING HEALING
HEALING IN ORAL TISSUES
A circumscribed injury which is caused by external force
and it can involve any tissue and organ.
It can be classified based on:
Origin of the wound.
Contamination of the wound.
Depth of the wound.
BASED ON ORIGIN
1. Abraded wound
2. Punctured wound
3. Incised wound
4. Cut wound
5. Crushed wound
6. Torn wound
7. Bite wound
8. Shot wound
Acid & base
Burning & freezing
Toxins & venoms
BASED ON CONTAMINATION
1. Clean wound
2. Clean & contaminated wound
3. Contaminated wound
BASED ON THE DEPTH
1. Superficial wound = only epidermis.
2. Partial thickness wound = epidermis + dermis.
3. Full thickness wound= epidermis + dermis +
4. Deep wound = epidermis + dermis +
subcutaneous fats + exposed muscles, bone connective
tissue, organs etc.
Healing is the body’s response to injury in an
attempt to restore normal structure and
The process of healing involves 2 distinct processes:
Regeneration : Is when healing takes place by
proliferation of parenchymal cells and usually
results in complete restoration of the original
To maintain proper structure of tissues, these cells
are under constant regulatory control of the cell
Is when healing takes place by proliferation of connective
tissue elements resulting in fibrosis and scarring.
Two processes are involved in repair:
a. Granulation tissue formation
b. Contraction of wound
Cells involved in the process of repair;
1. Mesenchymal cells
2. Endothelial cells
5. Parenchymal cells of injured organs
PHASE OF INFLAMMATION
Following injury blood clots at the site of injury.There is acute
inflammatory response with exudation of plasma, neutrophils,
and some monocytes within 24 hours.
PHASE OF CLEARANCE
Proteolytic enzymes liberated from neutophils, autolytic enzymes
from dead tissue and phagocytic activity of macrophages, clear
off the necrotic tissue, debris and red blood cells.
PHASE OF GROWTH OF GRANULATION TISSUE
This phase consists of two main processes
a. ANGIOGENESIS OR NEOVASCULARISATION
ANGIOGENESIS ( NEOVASCULARISATION)
Formation of new blood vessels at the site of injury takes place
by proliferation of endothelial cells from the margins of severed
The newly formed blood vessels are more leaky accounting for
the more edematous appearance of new granulation tissue.
Soon these blood vessels differentiate into muscular arterioles,
thin-walled venules and true capillaries.
Angiogenesis takes place under the influence of :
1. Vascular endothelial growth factor
2. Platelet derived growth factor
3. Transforming growth factor- β
4. Fibroblast growth factor
The newly formed blood vessels are present in an
amorphous ground substance. The new fibroblasts
originate from the fibrocytes as well as by mitotic
division of fibroblasts.
Some of these fibroblast has functional and structural
similarities to smooth muscles cell called as
Collagen fibrils appear by about 6th day. As maturation
proceeds, more and more of collagen is formed the
number of active fibroblasts and the number of new
blood vessels decreases.
This result in the formation of inactive looking scar
known as cicatrisation.
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 responsible for wound contraction:
1. Dehydration due to removal of fluids by drying.
2. Contraction of collagen
3. Discovery of myofibroblasts.
TYPES OF WOUND HEALING
HEALING BY FIRST INTENTION also called as
HEALING BY SECOND INTENTION also called as
HEALING BY FIRST INTENTION
Healing of wound with following characteristics:
Clean and uninfected
Without much loss of cells and tissue
Edges of wound are approximated by surgical sutures.
STEPS IN PRIMARY WOUND HEALING
INITIAL HEMORRHAGE: Immediately after injury, the space
between the surfaces of incised wound is filled with blood which
soon clots, and prevent further infection.
ACUTE INFLAMMATORY RESPONSE: This occurs within 24
hours of appearance of polymorphs from the margins of incision.
EPITHELIAL CHANGES: The basal cells of epidermis from
both cut margins starts proliferating and migrating towards
incisional space in the form of epithelial spurs.
A well approximated wound is covered by a layer of epithelial cell
in 48 hrs. The migrated epithelial cell separates the necrotic cells
and clot forming a scab which cast off. The basal cells continues to
divide. By 5th day new epidermis is formed.
ORGANISATION : by 3rd day, fibroblasts also invades the
wound area. By 5th day new collagen fibrils start forming
which dominate till healing is completed.
In 4 weeks a scar tissue with scanty cellular and vascular
elements, a few inflammatory cells and epithelialised surface
HEALING BY SECONDARY INTENTION
This is defined as the healing of a wound with following features.
i. Open with large tissue defects, at times infected
ii. Having extensive loss of cells and tissues, and
iii. The wound is not approximated by sutures but is left open.
STEPS IN HEALING OF SECONDARY WOUND:
Initial haemorrhage: as a result of injury the wound space is
filled with blood and fibrin clot which dries.
Inflammatory phase: there is initial acute inflammatory
response followed by appearance of macrophages which clear
off the debris.
EPITHELIAL CHANGES: The epidermal cells from both the
margins proliferate and migrate into the wound in the form of spurs
till they meet in the middle and re-epithelialise the gap completely.
However, the proliferating epithelial cells do not cover the wound
completely until the granulation tissue from the base has started fill
the wound space.
GRANULATION TISSUE: The main bulk of secondary healing is
by granulation. Granulation tissue is formed by proliferation of
fibroblasts and neovascularisation. The newly formed granulation
tissue is deep red, granular and very fragile. With time, it becomes
pale white due to increased in collagen and decreased blood supply.
WOUND CONTRACTION: This phase is not seen in primary
healing. Due to the action of myofibroblasts present in granulation
tissue, the wound contracts to one-third of its original size. It occurs
during the formation of active granulation tissue.
DIFFERENCE BETWEEN 1˚ & 2˚ UNION OF WOUND
FEATURES PRIMARY SECONDARY
CLEANLINESS CLEAN NOT CLEAN
INFECTION NOT INFECTED INFECTED
MARGINS SURGICALLY CLEAN IRREGULAR
SUTURES USED NOT USED
HEALING SMALL GRANULATION
OUT COME LINEAR SCAR IRREGULAR WOUND
COMPLICATION NOT FRQUENT FREQUENT
FACTORS AFFECTING WOUND HEALING
Local factors Systemic factors
INFECTION NUTRITIONAL FACTORS
LOCATION OF THE WOUND AGE OF THE PATIENT
IMMOBILISATION SYSTEMIC INFECTION
PHYSICAL FACTORS ADMINISTRATION OF
FACTORS AFFECTING WOUND
It has been demonstrated that wounds which is completely
protected from bacterial irritation heal considerably more rapidly
than wounds which are exposed to bacteria or other mild
LOCATION OF THE WOUND:
wounds in the area in which there is a good vascular bed heal
considerably more rapidly than the area in which is relatively
If the wound is in an area which is subjected to constant
movement so that formation of new connective tissue is
continuously distrupted (e.g.: corner of the mouth), it will result
in delayed wound healing.
severe trauma to tissues is obviously a determinant in rapid
local temperature in the area of wound influences the rate of
healing. Thus, in environment hyperthermia, wound healing is
accelerated while in hypothermia it is delayed.
circulatory factors: anemia has been reported to delay wound
healing. Similarly dehydration also delays wound healing.
Delay in the healing of wounds may occur in a person who is
deficient in variety of essential foods such as proteins, vitamins,
especially vitamin A, D and B complex.
AGE OF THE PATIENT:
Wounds in younger persons heals more rapidly than wounds In
elderly persons and the rate of wound healing appears to be in
inverse proportion to the age of the patient.
Delays healing of the wound.
ADMINISTRATION OF GLUCOCORTICOIDS
It has an anti-inflammatory effect thus it delays wound healing.
Diabetics are more prone to develop infections thus delayed
wound healing takes place.
There is delayed wound healing
HEALING OF EXTRACTION WOUND
IMMEDIATE REACTION FOLLOWING EXTRACTION
After the extraction, the blood which fills the socket coagulates,
red blood cells being entrapped in the fibrin meshwork.
The resultant fibrin meshwork containing entrapped red blood
cells seals off the torn blood vessels and reduces the size of the
extraction of wound.
Within the first 24-48 hours after extraction there are alterations
in the vascular bed.
There is vasodilation and engorgement of blood vessels in the
remnants of the periodontal ligament and the mobilization of
leucocytes to the immediate area around the wound.
FIRST WEEK WOUND
Within the first week after tooth extraction, proliferation of
fibroblasts from connective tissue cells in the remnants of the
periodontal ligament is evident, and these fibroblasts have
begun to grow into the clot around the entire periphery.
This clot forms the scaffold on which the cells associated with
healing process may migrate. It is the temporary structure.
The epithelium at the periphery of the wound grow over the
surface of the organizing clot.
Osteoclasts accumulate along the alveolar bone crest setting the
stage for active crestal resorption.
Angiogenesis proceeds in the remnants of the periodontal
SECOND WEEK WOUND
During the second week, the blood clot continues to get
organized through fibroplasia and new blood vessels that
penetrate towards the center of the clot.
Trabeculae of the osteoid slowly extend into the clot from the
alveolus, and osteoclastic resoption of the cortical margin of the
alveolar socket is more distinct.
The remnants of the periodontal ligament gradually undergo
degeneration and are no longer recognizable.
THIRD WEEK WOUND
As healing continues into the third week , the original clot
appear completely organized by mature granulation tissue and
poorly calcified bone at the wound perimeter.
The surface of the wound is re-epithelised with minimum or no
Very young trabeculae of osteoid bone forms around the entire
periphery of the wound from the socket wall.
The original cortical bone of the alveolar socket undergoes
remodeling so that it is no longer consist of such a dense layer.
The crest of the alveolar bone is rounded off by osteoclastic
FOURTH WEEK WOUND
During the fourth week the wound begins the final stage of
healing, in which there is continued deposition and remodeling
resorption of the bone filling the alveolar socket.
Much of this early bone is poorly calcified, as is evident from
its general radiolucency on the radiograph.
Radiographic evidence of bone formation does not become
prominent until the sixth or eighth week after tooth extraction.
HEALING AFTER EXTRACTION OF
1- immediate reaction after extraction
2-second week after extraction
3-third week after extraction
4-six to eight weeks after extraction (complete
COMPLICATION OF HEALING OF
The most common and painful complication in the healing
of human extraction wound is alveolar osteitis or dry
It is basically a focal, in which the blood clot has
disintegrated or been lost.
The condition is extremely painful without suppuration and
the presence of foul odor.
The condition derives its name from the fact that after the
clot is lost the socket has a dry appearance because of the
It is more commonly associated with difficult and traumatic
extractions like the removal of impacted third molars.
Destruction of the clot is caused by the proteolytic enzymes
produced by bacteria or local fibrinolytic activity.
FIBROUS HEALING OF EXTRACTION WOUND
It occurs more frequently when the extraction is accompanied
by the loss of both the buccal and the lingual cortical plates of
bone and the loss of periosteum as well.
On a radiograph the lesion appears as a well circumscribed
radiolucent area in the site of a previous extraction wound .
There is no certain way of differentiating fibrous healing from
the residual infection like residual cyst or granuloma.
The areas of fibrous healing consists of dense bundles of
collagen fibrils with occasional fibrocytes and few blood
vessels. The lesion is a fibrous scar tissue with little or no
evidence of ossification.
HEALING OF FRACTURE
IMMEDIATE EFFECTS OF FRACTURE
When fracture of a bone occurs, the haversian vessels of the
bone are torn at the fracture site along with the vessels of the
periosteum and the marrow cavity. This evokes acute
inflammation in the soft tissue adjacent to the fracture line.
Because of the disruption of the vessels, there is considerable
amount of blood in this general area and at the same time there
is loss of circulation and blood supply.
Three major phase occurs:
1) Reactive phase:
-fracture and inflammation
-granulation tissue formation
2) Reparative phase:
-lamellar bone deposition
3) Remodelling phase:
Soon after fracture the blood vessels constrict, stopping any
Within a few hours after fracture, the extravascular blood cells
forms a blood clot called as Hematoma.
All of the cells within the blood clot degenerate and die.
Some of the cells adjacent to the fracture site also die, but
fibroblast survive and replicate forming a loose aggregates of
cells interspersed with small blood vessels known as
Days after fracture, the cells of the periosteum replicates.
The Periosteal cells proximal (close) to the fracture gap
develops into chondroblasts which forms hyaline cartilage.
Periosteal cells distal (far away ) from the fracture gap develops
into osteoblasts which forms woven bone.
The fibroblast with in the granulation tissue develops in to
chondroblasts which also forms hyaline cartilage.
The two new tissue grow in size until they meet their counter part
from other part of fracture.
This process is called as Callus formation.
Callus in Latin means overgrowth of hard skin.
Composed of varied amounts of fibrous tissue, cartilage and
The external callus consists of the new tissue which forms
around the outside of two fragments of bone.
The internal callus is the new tissue arising from the marrow
The next step is deposition of lamellar bone by replacing hyaline
cartilage and woven bone.
The replacement process is called endochondral ossification.
The lamellar bone begins forming soon after the collagen
matrix of either tissue becomes mineralized.
The new bone is formed in the form of trabecular bone.
In this, the trabecular bone is replaced by compact bone.
It takes 3-5 yrs depending on factors like type of fracture,
age of patient, or general condition of patients.
COMPLICATIONS OF FRACTURE
DELAYED UNION OR NON UNION
This results when the calluses of the osteogenic tissue over
each of the two fragments fail to meet and fuse or when
endosteal formation of bone is inadequate.
The Fractured ends of fragments are united by fibrous tissue,
but there is failure of ossification.
LACK OF CALCIFICATION
This may occur in unusual circumstances of dietary deficiency
or mineral imbalance which is seldom seen clinically.
HEALING AFTER REPLANTATION
Following replantation the clot forms between the root
surface and ruptured periodontal ligament.
Proliferation of the fibroblasts and the endothelial cells
occurs in the periodontal ligament remnants on the side
of the alveolar bone.
The reconnection of the periodontal ligament is evident
by the extension of collagen fibers from the cementum to
the alveolar bone.
The epithelium is reattached to the tooth at the end of the
Complete regeneration of the periodontal ligament takes
place between two to four weeks.
In the course of time, a number of teeth results in
resorption or ankylosis.
COMPLICATIONS OF WOUND HEALING
Wounds may provide a portal of entry to microorganisms.
Infections of the wound delay the healing process. Systemic
conditions such as diabetes mellitus, immunosuppressive state
etc. make the individual prone to infection.
KELOID AND HYPERTROPIC SCAR
Keloids are overgrown scar tissues with no tendency for
resolution. They occur in wound, which heal without any
Hypertrophic scar occur in wounds where healing is delayed.
These scars are more cellular and vascular.
Keloid and hypertropic scars are not seen in the wounds of
the oral cavity.
These are common in healing of wounds on skin and may
appear and may appear as hyperpigmented and hypopigmeted
In oral cavity hypopigmented scars are less common but some
lesions leave hyperigmentation while healing e.g. lichenplanus,
Cicatrization refers to late reduction in the size of the scar
in contrast to immediate wound contraction. It a
complication due to burns on the skin.
Epithelial cysts may slide and get entrapped in the wound
and later may proliferate to form implantation cysts.
Healing – NEW CONCEPTS
Healing of chronic wound can be enhanced by one of the following methods
1. Topical application of growth factors.
2. Hyperbaric oxygen therapy.
3. Electrical stimulation for wound healing
Low frequency pulsed current (LFPC)
High voltage pulsed current (HVPC)
4. Topical application of cultured keratinocytes.
5. Vacuum assisted closure of the wound.
1) Robbin’s & Cotron Pathological basis of diseases
2) Essential pathology for dental students - Harsh mohan
3) Text book of oral pathology - Shafers