DR. GAURAV S . SALUNKHE

PG-STUDENT

ORAL & MAXILLOFACIAL PATHOLOGY

DR. D Y. PATIL DENTAL COLLEGE & HOSPITAL

WOUND HEALING

WHAT IS WOUND ?

It is a circumscribed injury which is caused by external force and it can involved any tissue and organ.

Margins of wound

Wound edge

Wound cornerSurface of wound

Base of wound

Cross section of the wound

Wound edgeWound depthSurface of woundBase of the wound

It can be classified based on

1) Origin of the wound.2) Contamination of the wound.3) Depth of the wound.

Based on origin

Mechanical1. Abraded wound 2. Punctured wound 3. Incised wound 4. Cut wound 5. Crushed wound6. Torn wound7. Bite wound8. Shot wound Chemical Acid & baseRadiation Thermal Burning & freezing Special Toxins & venoms

Abrasions. They occur when the skin is rubbed away by friction against another rough surface (e.g. rope burns and skinned knees).

Avulsions. Occur when an entire structure or part of it is forcibly pulled away, such as the loss of a permanent tooth or an ear lobe. Explosions, gunshots, and animal bites may cause avulsions.

Contusions. Also called bruises, these are the result of a forceful trauma that injures an internal structure without breaking the skin. Blows to the chest, abdomen, or head with a blunt instrument (e.g. a football or a fist) can cause contusions.

Crush wounds. Occur when a heavy object falls onto a person, splitting the skin and shattering or tearing underlying structures.

Cuts. Slicing wounds made with a sharp instrument, leaving even edges. They may be as minimal as a paper cut or as significant as a surgical incision.

Lacerations. Also called tears, these are separating wounds that produce ragged edges. They are produced by a tremendous force against the body, either from an internal source as in childbirth, or from an external source like a punch.

Missile wounds. Also called velocity wounds, they are caused by an object entering the body at a high speed, typically a bullet.

Punctures. Deep, narrow wounds produced by sharp objects such as nails, knives, and broken glass.

Contusions

Crushed wound

Punctures

Avulsions

Burns

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

+ subcutaneous fats

4. Deep wound = epidermis + dermis + subcutaneous fats + exposed muscles, bone connective tissue, organs etc.

Superficial

Partial thickness

Full thickness

Deep wound

HEALING Healing is the body’s response to injury in an

attempt to restore normal structure and function.

The process of healing involves 2 distinct processes:

a. REGENERATION

b. REPAIR

REGENERATION

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.

REPAIR

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

REPAIR OF WOUND

GRANULATION TISSUE

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 from neutophils, autolytic enzymes from dead tissue and phagocytic activity of macrophages, clear off the necrotic tissue, debris and red blood cells.

PHASE OF IN GROWTH OF GRANULATION TISSUE

This phase consists of two main processes

a. ANGIOGENESIS OR NEOVASCULARISATION

b. FIBROGENESIS

ANGIOGENESIS ( NEOVASCULARISATION) 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.

Soon these blood vessels differentiate into muscular arterioles,thin-walled venules and true capillaries.

Angiogenesis takes place under the influence of :

1. Vascular endotheial growth factor

2. Platelet derived growth factor

3. Transforming growth factor- β

4. Fibroblast growth factor

Vascular endothelial growth factor: elaborated by mesenchymal cells as the receptors are present on endothelial cells only.

Platelet derived growth factor, transforming growth factor- β, fibroblast growth factor are all associated with cellular proliferation.

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.

Some of these fibroblast has functional and structural similarities to smooth muscles cell called as myofibroblast.

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 scare known as cicatrisation.

Granulation tissue

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 PRIMARY UNION.

HEALING BY SECOND INTENTION also called as SECONDARY HEALING.

HEALING BY FIRST INTENTION

Healing of wound with following characteristics:

Clean and uninfected

Surgically incised

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 is cast off. The basal cells countinues 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 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 7th day, much of the epithelialised suture track is avulsed.

PRIMARY HEALING

HEALING BY SECODARY INTENSION

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. In this way the pre-existing viable connective tissue is separated from the necrotic material and clot on the surface forming the scab, which is cast off.

Granulation tissue: The main bulk of secondary healing is by granulations. 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.

SECONDARY WOUND HEALING(various cells involved)

Click icon to add picture

Difference between 1˚ & 2˚ union of wound

FEATURES PRIMARY SECONDARY

CLEANLINESS CLAEN NOT CLEAN

INFECTION NOT INFECTED INFECTED

MARGINS SURGICALLY CLEAN IRREGULAR

SUTURES USEAD NOT USED

HEALING SMALL GRANULATION TISSUE

LARGE GRANULATION TISSUE

OUT COME LINEAR SCAR IRREGULAR WOUND

COMPICATION 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 GLUCOCORTICOIDS

UNCONTROLLED DIABETES

FACTORS AFFECTING WOUND HEALING

LOCAL FACTORS

INFECTION:

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 physical irritation.

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 avascular.

IMMOBILISATION:

If the wound is 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.

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.

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

HEALING OF EXTACTION 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 resoption.

Angiogenesis proceeds in the remnants of the periodontal ligaments.

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 scar formation.

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 resoption.

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 he 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 TOOTH

1- immediate reaction after extraction

2-second week after extraction

3-third week after extraction

4-six to eight weeks after extraction( complete healing)

COMPLICATION OF HEALING OF EXTRACTON WOUND

DRY SOCKETFIBROUS UNION

DRY SOCKETThe most common and painful complication in the healing of

human extraction wound is alveolar osteitis or dry socket.

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 exposed bone.

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.

DRY SOCKET

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 formation2) Reparative phase: -callus formation -lamellar bone deposition3) Remodelling phase:

Reactive phase

Soon after fracture the blood vessels constrict, stopping any further bleeding.

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 Granulation tissue.

Reparative phase

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 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.

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.

Remodelling phase

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.

STAGES IN HEALING OF FRACTURE

COMPLICATIONS OF FRACTURE HEALING

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.

FIBROUS UNION

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 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 OF IMPLANTS

Osseointegration is a direct structural and functional 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.

OSSEOINTEGRATION OF IMPLANT

COMPLICATIONS OF WOUND HEALING

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 hypertropic 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 hyperpigmented and hypopigmeted areas.

In oral cavity hypopigmented scars are less common but some lesions leave hyperigmentation while healing e.g. lichenplanus, lichenoid reactions.

CICATRIZATION

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.

IMPLANTATION CYSTS

Epithelial cysts may slide and get entrapped in the wound and later may proliferate to form implantation cysts.

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