HEALING OF ORAL ORA L WOU WOUNDS NDS
DEPARTMEN DEPAR TMENT T OF ORAL O RAL PATHO PATHOLOGY LOGY AND MICRO M ICROBIOLOG BIOLOGY Y.
HEALING Healing is the body¶s 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.
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To ma main inta tain in pr prop oper er st stru ruct cture ure of ti tiss ssue ues, s, th thes esee ce cell llss ar aree un under der constant regulatory control of the cell cycle.
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Cell cycle is defined as the period between two successive cell divisions and divided into 4 unequal phases:
a. b. c. d. e.
M (mitosis) phase G1 (gap 1) phase S (synthesis) phase G2 (gap 2) phase GO (gap 0) phase
REGENERATION AFTER INJURY
REPAIR ´
Repair : Is when healing takes place by proliferation of connective tissue elements resulting in fibrosis and scarring.
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Two processes are involved in repair: Granulation tissue formation Contraction of wound
a. b.
Cells involved in the process of repair; Mesenchymal cells 1. Endothelial cells 2. Macrophages 3. Platelets 4. Parenchymal cells of injured organs 5.
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 in the clot clear off the necrotic tissue, debris and red blood cells.
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PHASE OF IN GROWTH OF GRANULATION TISSUE This phase consists of two main processes ANGIOGENESIS OR NEOVASCULARISATION FIBROGENESIS
a. b.
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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. 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 6 th day. As maturation proceeds, more and more of collagen is formed the number of active fibroblasts and the number of new blood vessels decreases.
CONTRACTION
OF WOUND
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The wound starts contracting after 2-3 days and the process is completed by 14 th day. During this period the wound is reduced by approximately 80% of its original size.
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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
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HEALING BY FIRST PRIMARY UNION.
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HEALING BY SECOND SECONDARY HEALING.
INTENTION
INTENTION
also
called
as
also called as
STEPS AND DURATION OF WOUND HEALING
HEALING BY FIRST INTENTION
Healing of wound with following characteristics: i.
Clean and uninfected
i.
Surgically incised
i.
Without much loss of cells and tissue
i.
Edges of wound are approximated by surgical sutures.
STEPS IN PRIMARY WOUND HEALING
Initial haemorrhage: immediately after injury, the space between the surfaces of incised wound is filled with blood which soon clots. inflammatory response: this occurs within 24 hours of appearance of polymorphs from the margins of incision.
Acute
E pithelial 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 5 th day new collagen fibrils start forming which dominate till healing is completed. Organisation
In 4 weeks a scar tissue with scanty cellular and vascular elements, a few inflammatory cells and epithelialised surface is formed. track s: each suture track is a separate wound and follows the same steps as in healing of primary wound.
S ut ure
When sutures are removed around 7th day, much of the epithelialised suture track is avulsed and the remaining epithelial tissue in the track is absorbed.
PRIMARY HEALING
HEALING BY SECODARY INTENSION This is defined as the healing of a wound with following features. Open with large tissue defects, at times infected i. Having extensive loss of cells and tissues, and ii. The wound is not approximated by sutures but is left open. iii. 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.
SECONDARY WOUND HEALING (VARIOUS CELLS INVOLVED)
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. E pithelial changes:
tissue: the main bulk of secondary healing is by granulations. Granulation tissue is formed by proliferation of fibroblasts and neovascularisation.
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.
G ranulation
W ound contraction:
HEALING BY SECONDARY INTENSION
FACTORS AFFECTING WOUND HEALING LOCAL FACTORS ´
INFECTION: it has been demonstrated that wounds which is completely protected from bacterial irritation heal considerably more slowly than wounds which are exposed to bacteria or other mild physical irritation.
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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.
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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.
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PHYSICAL FACTORS: severe trauma to tissues is obviously a determinant in rapid wound healing.
local temperat ure in the area of wound influences the rate of healing. Thus, in environment hyperthermia, wound healing is accelerated while in hypothermia it is delayed. factors: anemia has been reported to delay wound healing. Similarly dehydration also delays wound healing. cir culatory
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.
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SYSTEMIC INFECTION Delays healing of he wound.
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ADMINISTRATION OF GLUCOCORTICOIDS It has an anti-inflammatory effect thus it delays wound healing.
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UNCONTROLLED DIABETES Diabetics are more prone to develop infections thus delayed wound healing takes place.
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HAEMATOLOGIC ABNORMALITIES There is delayed wound healing
HEALING OF THE BIOPSY WOUND The healing of a biopsy wound of the oral cavity is identical with the healing of a similar wound in any other part of the body and thus may be classified as either primary healing or secondary healing. PRIMARY HEALING OF BIOPSY WOUND
Primary healing or healing by first intension is that type of healing which occurs after the excision of a piece of tissue with the close approximation of the edges of the wound.
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When the edges edges of the wound are brought brought into contact and held in in place by sutures, the blood clots.
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In a ma matt tter er of ho hour urss nu nume mero rous us leucocy leucocyes es are mo mobi bili lize zed d to the area.
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Con onne nect ctiv ivee tis issu suee ce cell llss in th thee im imm med ediiat atee vi vici cini nity ty un unde derrgo transformation into fibroblasts , which in turn undergo mitotic division, and the new fibroblasts begin to migrate into the line of incision. These cells form thin collagen fibrils which coalesce in general direction parallel to the surface of the wound.
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Endothelial cells of the capillaries begin to proliferate, and small capillary buds grow out and across the wound which eventually forms new capillaries filled with blood.
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When there is close appro approximat ximation ion of the edges of the wound, the surface epithelium proliferates rapidly across the line of incision and re-establishes the integrity of the surface. su rface.
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In due cou ourrse of time the col olllagen fibrils coal ales escce an and d cont co ntra ract ctss so that the biops biopsy y wound wound ap appe pear arss as a li line near ar scar which can be depressed below the surface.
PRIMARY HEALING OF BIOPSY WOUND
Pictures 1-6 shows the biopsy of the labial mucosa and the wound is approximated with the sutures. In this case the healing occurs by primary intension.
SECONDARY HEALING OF BIOPSY WOUND
Healing by second intention or the healing of the open wound occurs when there is loss of tissue and the edges of the wound cannot be approximated. In this type of healing process the wound µgranulates in¶ since the material, which fills the defect is the granulation tissue. E.g.: removal of a lesion from the palate or large lesion of alveolar ridge heals by secondary intension since the edges of the wound cannot be coapted.
S teps
in secondary healing of biopsy wound
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After the removal of the lesion the blood clot fills the defect and the healing process begins.
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Cellular proliferation begins around the periphery of the wound.
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The fibroblasts and the endothelial cells grow into the clot along the fibrin strands.
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Polymorphonuclear leucocytes, and later lymphocytes , and mononuclear phagocytes migrate into the granulation tissue from the adjacent vessels and tissues.
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Large number of leucocytes also accumulate on the surface of the wound.
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As the granulation tissue matures, it becomes more fibrous through condensation of collagen bundles, and the surface of the granulation tissue becomes epithelised.
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The collagen fibrils coalesce and the lesion becomes somewhat less vascular and eventually the evidence of the wound may be a small depressed area of the mucosa.
SECONDARY WOUND HEALING IN A BIOPSY SITE ON THE PALATE
HEALING OF GINGIVECTOMY WOUND EARLY HEALING PHASE
Healing of the gingivectomy wound takes place rapidly regardless of whether the postoperative pack is used . Healing of gingivectomy wound is basically similar to healing of wound elsewhere in the body, but is somewhat modified by special anatomy of the involved region.
STEPS IN
H E AL IN G OF G IN G IV ECTOMY WOU ND
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Two days after the gingivectomy the surface of the tissue is covered by a grayish blood clot, and beneath this clot is histologic evidence of delicate connective tissue proliferation.
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Four days after the operation, the deeper portion of the blood clot demonstrates considerable organization, while the superficial portion exhibits dense numbers of polymorphonuclear leucocytes entrapped in fibrinous network.
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There is proliferation of young capillaries and young connective tissue cells into the base of the blood vessels.
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Infiltration of polymorphonuclear leucocytes in the deeper connective tissue is present in varying degrees.
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The epithelium has extended over a portion of the wound below the necrotic surface layer of the clot, but above the proliferating and organising connective tissue.
LATE HEALING PHASE ´
Continuation of the healing process is manifested by condensation of the young connective tissue with nearly complete organization of the clot after 8-10 days.
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Clinically, the wound is red, granular in appearance and bleeds rapidly.
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Epithilization is usually complete within 10-14 days after gingivectomy.
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The epithilium remains thin and begins to mature and form rete pegs only after two week interval. Healing of the interproximal tissue appears to lag behind that adjacent to the labial or buccal surfaces this is because the epithelium must grow in front from the labial and the lingual areas, a relatively greater distance.
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, and the ends of the torn blood vessels in the periodontal ligament becomes scaled off.
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Within the first 24-48 hours after extraction there are alterations in the vascular bed.
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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.
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The surface of the crest of the alveolar bone which is the neck of the socket exhibits the beginning of osteoclastic activity.
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During this stage the blood clot begins to undergo organization by the ingrowth around the periphery of fibroblasts and occasional small capillaries from the residual periodontal ligament. The edge of the wound exhibits continued epithelial proliferation.
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Blood cot is filled with thick layer of fibrin, but at this early period visible reactivity on the part of the body I the form of layering of leucocytes is not prominent.
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.
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This clot forms the scaffold on which the cells associated with healing process may migrate. It is the temporary structure.
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The epithelium at the periphery of the wound exhibits evidence of proliferation in the form of mild mitotic activity.
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The crest of the alveolar bone which is the neck of the socket exhibits the beginning of osteoclastic activity.
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During this stage the blood clot begins to undergo organization by the ingrowth around the periphery of fibroblasts and occasional small capillaries from the residual periodontal ligament. The edge of the wound exhibits continued epithelial proliferation.
SECOND WEEK WOUND
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During the second week, the blood clot becomes organized by fibroblasts growing into the clot on the fibrinous meshwork.
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New delicate capillaries penetrate to the centre of the clot.
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The remnants of the periodontal ligament gradually undergo degeneration and are no longer recognizable.
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The wall of the bony socket now appears lightly frayed, in some cases the trabeculae of osteoid can be seen extending outward from the wall of the alveolus.
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Epithelial proliferation over the surface of the wound is extensive, although the wound is usually not covered.
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The margin of the alveolar socket exhibits prominent osteoclastic resorption.
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Fragments of the necrotic bone, which may have been fractured from the rim of the socket during the extraction are seen in the process of resorption of sequestration.
THIRD WEEK WOUND ´
As healing continues into the third week , the original clot appear completely organized by mature granulation tissue.
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Very young trabeculae of osteoid or uncalcified bone form around the entire periphery of the wound from the socket wall.
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This early bone formed by osteoblasts derived from the pluripotent cells of the original periodontal ligament which assumes an osteogenic function.
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The original cortical bone of the alveolar socket undergoes remodeling so that it no longer consists of such a dense layer.
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The crest of the alveolar bone is rounded off by osteoclastic resorption .
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By this time the surface of the wound may have become completely epithelized.
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.
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Much of this early bone is poorly calcified, as is evident from its general radiolucency on the radiograph.
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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)
HEALING OF EXTRACTION WOUND
COMPLICATION
OF HEALING OF EXTRACTON WOUND ´ ´
DRY SOCKET FIBROUS UNION
DRY SOCKET ´ The most common and painful complication in the healing of human extraction wound is alveolar osteitis or dry socket. ´
It is basically a focal osteomyelitis in which the blood clot has disintegrated or been lost.
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The condition is extremely painful without suppuration and the presence of foul odor.
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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.
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It is more commonly associated with difficult and traumatic extractions like the removal of impacted third molars.
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Destruction of the clot is caused by the proteolytic enzymes produced by bacteria or local fibrinolytic activity.
Clot lysis occurs by two mechanisms: a. b.
Plasminogen dependent pathway Plasminogen independent pathway
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Plasminogen is hepatically synthesized and released into the circulation. It transforms into plasmin, which in turn acts on the fibrinogen and fibrin, causing clot dissolution.
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This condition starts by the second or third postoperative day and lasts for about 7-10 days and is extremely painful.
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.
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On a radiograph the lesion appears as a well circumscribed radiolucent area in the site of a previous extraction wound .
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There is no certain way of differentiating fibrous healing from the residual infection like residual cyst or granuloma.
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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.
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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.
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When the blood vessels rupture the osteocytes or the bone cells of the haversian system supplied by this vessel die.
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Concomitant with this , there is death of the bone marrow adjacent to the fracture line.
CALLUS
FORMATION
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Callus in Latin means overgrowth of hard skin.
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Callus unites the fractured ends of bone, and it is composed varied amounts of fibrous tissue, cartilage and bone.
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The external callus consists of the new issue which forms around the outside of two fragments of bone.
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The internal callus is the new tissue arising from the marrow cavity.
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Periosteum is important in callus formation. The cells of periosteum immediately adjacent to the periosteum torn at the fracture line usually die.
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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.
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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.
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The continued proliferation of these osteogenic cells forms a collar of callus around or over the surface of the fracture.
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The new bone which begins to form in the external callus usually consists of irregular trabeculae of bone at right angles to the surface.
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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 lay down cartilage.
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This cartilage fuses with the bone without any sharp line of demarcation.
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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.
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The internal callus forms from the endosteum of the haversian canal and the undifferentiated cells of bone marrow.
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The new bone formed at the end of each fragment gradually unites and establishes continuity of bone.
REMODELLING OF THE CALLUS ´
The external and the internal calluses, which unite the two fragments of bone, must be remodelled because there is always an abundance of new bone produced.
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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.
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The external callus should be remodelled excess bone is removed.
so that in time
STAGES IN HEALING OF FRACTURE
COMPLICATIONS
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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
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Following replantation the clot forms between the root surface and ruptured periodontal ligament.
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Proliferation of the fibroblasts and the endothelial cells occurs in the periodontal ligament remnants on the side of the alveolar bone.
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The reconnection of the periodontal ligament is evident by the extension of collagen fibers from the cementum to the alveolar bone.
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The epithelium is reattached to the tooth at the end of the first week.
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Complete regeneration of the periodontal ligament takes place between two to four weeks.
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In the course of time, a number of teeth results in resorption or ankylosis.
HEALING AFTER REPLANTATION
OSSEOINTEGRATION OF IMPLANTS
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Osseointegration is a direct structural and functional connection between ordered living bone and the surface of the load carrying implant.
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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.
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After the implant insertion, a period of 10-12 weeks of healing is required.
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During healing, compact and cancellous bone forms around the implant together with variable amount of fibrous marrow.
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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.
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The implant and the mucosal interface serve the similar functions as the dentogingival.
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The connective tissue of the mucosa forms the intimate contact with the implant.
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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
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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. K eloid
and hypertropi c scars are not seen in the wo unds of the oral cavity.
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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.
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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.
