WOUND HEALING AND ENDODONTICS

 Introduction
 History of wound healing
 Classification of wound
 Healing
 Regeneration
 Repair

 Types of wound healing
 Factors affecting wound healing
 Healing of fracture
 Healing after non surgical root canal therapy
 Healing of excisional dento alveolar wound
 Healing after replantation
 Complication of healing
 Conclusion
 references

WOUND:
“A cut or break in the continuity of any tissue,
caused by injury or operation”
(Baillière’s 23rd Ed)
HEALING:
Healing is the body’s response to injury in an attempt to
restore normal structure and function.

 2000B.C. by Sumerians
 – Spiritual method: Incantation.
 – Physical method: Poultice-like materials.
 • Egyptians:
 – Infected & disease wound VS Noninfected wound.
 • 1650B.C.Edwin Smith Surgical Papyrus:
 – Describes at least 48 different types of wounds.
 • 1550B.C.Ebers Papyrus:
 – Anti Biotic properties: Honey.
 – Absorbent properties: Lint
 – Barrier: Grease

 The Greeks : Acute or chronic wound.
 • Galan(120-201A.D.):
 Maintaining moist ,ensure adequate healing.
 • Ignaz Philipp Semmelweis: (1818-1865)
 Decrease incidences of puerperal fever when wash hand with soap &
hypochlorite.
 • Louis Pasteur(1822-1895):
 Dispelling Theory of germ.
 • Joseph Lister(1865):
 Using of phenol for soaking instruments & spraying ,reduce mortality
rate from 50 to 15%.

Wounds can be classified according to their nature:
 Abrasion
 Contusion
 Incision
 Laceration
 Open
 Penetrating
 Puncture
 Septic etc……………

Depending on contamination:
 Clean - (non traumatic)
 Clean contaminated
 Contaminated
 Dirty
Wounds may be classified according to the
number of skin layers involved:
 Superficial
 Involves only the epidermis
 Partial Thickness
 Involves the epidermis and the dermis
 Full Thickness
 Involves the epidermis, dermis, fat, fascia and exposes bone

The process of healing involves 2 distinct
processes:
A. REGENERATION
B. REPAIR

 REGENERATION: Is when healing takes place by proliferation
of parenchymal cells and usually results in complete restoration of the
original tissues.
 To maintain proper structure of tissues, these cells are under constant
regulatory control of the cell cycle.
 Cell cycle is defined as the period between two successive cell divisions and
divided into 4 unequal phases:
 A. M (mitosis) phase
 B. G1 (gap 1) phase
 C. S (synthesis) phase
 D. G2 (gap 2) phase
 E. GO (gap 0) phase

 REPAIR : 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
3. Macrophages
4. Platelets
5. Parenchymal cells of injured organs

 Phases in the formation of granulation tissue:
 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 in the
clot clear off the necrotic tissue, debris and red
blood cells.

 PHASE OF INGROWTH OF
GRANULATION TISSUE:
 This phase consists of two main processes
A. ANGIOGENESIS OR NEOVASCULARISATION
B. FIBROGENESIS

 Formation of new blood vessels at the site of injury
takes place by proliferation of endothelial cells from the
margins of severed blood vessels.
 The newly formed blood vessels are more leaky
accounting for the more edematous appearance of new
granulation tissue.

FIBROGNESIS:
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.
Collagen fibrils appear by about 6thday.
As maturation proceeds
more and more of collagen is formed the number of
active fibroblasts and the number of new blood vessels
decreases.

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:
 Factors responsible for wound contraction:
1.Dehydration due to removal of fluids by drying.
2.Contraction of collagen
3.Discovery of myofibroblasts.

HEALING BY FIRST INTENTION
also called as
PRIMARY UNION.
HEALING BY SECOND INTENTION
also called as
SECONDARY HEALING.

 Healing of wound with following characteristics:
i. Clean and uninfected
ii. Surgically incised
iii. Without much loss of cells and tissue
iv. Edges of wound are approximated by surgical sutures.

Initial hemorrhage:
 immediately after injury, the space between the surfaces of
incised wound is filled with blood which soon clots.
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 start
proliferating and migrating towards incisional space in the
form of epithelial spurs.

 By 3rd day, fibroblasts also invade 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
is formed.
Suture tracks:
 Each suture track is a separate wound and follows the same
steps as in healing of primary wound.
 When sutures are removed around 7thday, much of the
epithelialised suture track is avulsed and the remaining
epithelial tissue in the track is absorbed.

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 till they meet in the middle and re-
epithelialise the gap completely.

 Granulation tissue:
 The main bulk of secondary healing is by granulation tissue.
 Granulation tissue is formed by proliferation of fibroblasts
and neovascularisation.
 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.

 Immobilisation:
If the wound is an area which is subjected to constant movement
so that formation of new connective tissue is continuously disrupted
(e.g.: corner of the mouth), it will result in delayed wound healing.
 PHYSICAL FACTORS:
 severe trauma: to tissues is obviously a determinant in rapid
wound healing.
 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.
FACTROS AFFECTINGWOUND HEALING

 SYSTEMIC FACTORS:
 NUTRITIONAL FACTORS:
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.

 SYSTEMIC INFECTION :
Delays healing of he wound.
 ADMINISTRATION OF
GLUCOCORTICOIDS
It has an anti-inflammatory effect thus it delays wound
healing.
 UNCONTROLLED DIABETES
Diabetics are more prone to develop infections thus
delayed wound healing takes place.
 HAEMATOLOGIC ABNORMALITIES
There is delayed wound healing

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.

 When the blood vessels rupture the osteocytes or the bone
cells of the haversian system supplied by this vessel die.
 Concomitant with this , there is death of the bone marrow
adjacent to the fracture line.

 Callus in Latin means overgrowth of hard
skin.
 Callus unites the fractured ends of bone, and it
is composed varied amounts of fibrous tissue,
cartilage and bone.
 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 cavity.

 Periosteum is important in callus formation. The
cells of periosteum immediately adjacent to the
periosteum torn at the fracture line usually die.
 The outer layer of the periosteum is relatively
inert and is actually lifted away from the surface
of the bone by proliferation of the cells in the
inner layer.
 These cells assume the features of the osteoblasts,
and within few days after fracture, begin
formation of the new bone at some distance from
the fracture site.

 The continued proliferation of these osteogenic
cells forms a collar of callus around or over the
surface of the fracture.
 The new bone which begins to form in the
external callus usually consists of irregular
trabeculae of bone at right angles to the surface.
 Away from the fracture line in the rapidly
growing area of the collar, varying
number of cells of the osteogenic layer
differentiate into chondroblasts rather than
osteoblasts and laydown cartilage.

 This cartilage fuses with the bone without any
sharp line of demarcation.
 As callus formation progresses, the cartilage cells
begin to mature, and the cartilage begins to calcify
in a fashion similar to normal endochondral bone
formation.
 The internal callus forms from the endosteum of
the haversian canal and the undifferentiated cells of
bone marrow.
 The new bone formed at the end of each fragment
gradually unites and establishes continuity of bone.

 The external and the internal calluses, which
unite the two fragments of bone, must be
remodeled because there is always an
abundance of new bone produced.
 The new bone is usually joined to the
fragments of the dead bone. These fragments
are slowly resorbed and replaced by mature
type of bone.
 The external callus should be remodeled so
that in time excess bone is removed.

 DELAYED UNION OR NONUNION
 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.
 FIBROUSUNION
 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.

 Follows the general principle of wound
healing
 largely accomplished by regeneration and to
some degree by fibrosis.
 The process of periapical wound healing after
nonsurgical root canal therapy may be similar
to wound healing following guided tissue
regeneration in periodontal therapy

 Root resorption that involves cementum or
both cementum and dentin can only be
repaired by cementoid tissue, because
multipotent stem cells of the periodontal
ligament are incapable of differentiating into
odontoblasts that produce dentin.

 The maturation phase of hard-tissue healing differs
markedly from that for soft tissues.
 Osteoblasts: Osteogenesis
 Granulation tissue begins to proliferate from the severed
periodontal ligament by 2 to 4 days after root-end
resection.
 This tissue rapidly encapsulates the root end.
Simultaneously, endosteal proliferation into the coagulum
occurs from the deep surface of the bony wound edge.
 The coagulum in the bony crypt is quickly converted into a
mass of granulation tissue.

 several different cell types migrate into the
coagulum, including osteoprogenitor cells,
preosteoblasts, and osteoblasts.
 These cells begin the formation of woven
bone within the mass of granulation tissue.
 New bone formation is apparent about 6 days
after surgery.

 During regeneration of the periradicular
tissues, cementum forms over the surface of
surgically resected root ends
 Cementogenesis begins 10 to 12 days after
root-end resection.
 Cementoblasts develop at the root periphery
and proceed centrally toward the root canal.

 pocket cysts in apical periodontitis lesions
might regress after nonsurgical root canal
therapy by the mechanism of apoptosis or
programmed cell death.
 apical true cysts may be less likely to heal
after nonsurgical root canal therapy because
of their self-sustaining nature.

 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 first week.
 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.

 Osseointegration is a direct structural and functio
nal connection between ordered living bone and
the surface of the load carrying implant.
 Factors that determine the outcome of the implant
treatment depend on the biocompatibility of the
implants, status of the host tissue, surgical
technique, and the loading condition.
 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.
 Implants do not have a direct contact with the
bone and a certain amount of bone marrow and
soft tissue are interposed between the bone and
the implant.
 The implant and the mucosal interface serve
the similar functions as the dentogingival.

 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.

 INFECTION
 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 complications. hypertrophic scar occur in
wounds where healing is delayed. These scars are more
cellular and vascular.

 Keloid and hyper tropic scars are not seen in the
wounds of the oral cavity.
 PIGMENTARY CHANGES
 These are common in healing of wounds on skin
and may appear and may appear as hyper
pigmented and hypopigmeted areas. In oral cavity
hypopigmented scars are less common but some
lesions leave hyperpigmentation while healing
e.g. lichen planus, lichenoid reactions.

 CICATRIZATION
 Cicatrization refers to late reduction in the size
of the scar in contrast to immediate wound
contraction. Its a complication due to burns on
the skin.
 IMPLANTATION CYSTS
 Epithelial cells may slide and get entrapped in
the wound and later may proliferate to form
implantation cysts.

 Wound care is becoming more complex as the
range of wounds increases Correction of the
underlying causative factors is essential Key
principles must be adhered to with regard to
basic patient and wound assessment.

 Robbins and Cotran. Pathologic Basis of Disease. 7th
ed. Philadelphia, Elsevier Saunders; 2007: 61-78.
 Harsh Mohan. Essential pathology for dental
students. 2nd ed. New Delhi, Jaypee; 2002: 126-134.
 Das. Concise textbook of surgery. 3rd ed. Calcutta,
Dr.S.Das publishers; 2002: 1-7.
 Newman MG,Takei HH, Klokkevold PR, Carranza FA.
Clinical Periodontology. 10th ed. Missouri: Saunders;
2009: 912, 914-915, 935-936, 960, 1010-1011.
 Journal of Burns andWounds (http:/ / www. ncbi. nlm.
nih. gov/ pmc/ journals/ 211/ )

 PATHWAYS OF PULP – KENNETH M
.HARGREAVES

WOUND HEALING AND ENDODONTICS

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