wound healing and endodontics
TRANSCRIPT
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Wound healing
Presented byDr. Jagadeesh k
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Contents
Introduction History of wound healing Classification of wound Healing Regeneration Repair
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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
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introduction
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.
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IMPORTANCE !!!
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History of wound healing
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
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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%.
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Classification of wound
Wounds can be classified according to their nature:
Abrasion Contusion Incision Laceration Open Penetrating Puncture Septic etc……………
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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
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Healing
The process of healing involves 2 distinct processes:
A. REGENERATIONB. REPAIR
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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.
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
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Regeneration after injury
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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 formationB. Contraction of wound
Cells involved in the process of repair: 1. Mesenchymal cells2. Endothelial cells3. Macrophages4. Platelets5. Parenchymal cells of injured organs
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Repair of wound
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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.
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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 INGROWTH OF GRANULATION TISSUE:
This phase consists of two main processes
A. ANGIOGENESIS OR NEOVASCULARISATIONB. FIBROGENESIS
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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.
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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.
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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:
Factors responsible for wound contraction:
1.Dehydration due to removal of fluids by drying.2.Contraction of collagen3.Discovery of myofibroblasts.
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Types of wound healing
HEALING BY FIRST INTENTIONalso called as
PRIMARY UNION.
HEALING BY SECOND INTENTIONalso called as
SECONDARY HEALING.
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Healing by first intention Healing of wound with following characteristics:
i. Clean and uninfectedii. Surgically incisediii. Without much loss of cells and tissueiv. Edges of wound are approximated by surgical sutures.
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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.
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.
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Organization
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.
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Primary healing
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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.
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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.
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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.
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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 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 AFFECTING WOUND HEALING
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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.
ADMINISTRATION OF GLUCOCORTICOIDS
It has an anti-inflammatory effect thus it delays wound healing.
UNCONTROLLED DIABETESDiabetics are more prone to develop infections thus
delayed wound healing takes place.
HAEMATOLOGIC ABNORMALITIESThere is delayed wound healing
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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.
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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.
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Callus formation
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.
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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.
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.
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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.
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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.
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Remodeling of the callus
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.
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Stages in healing of fracture
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Complications of fracture healing 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.
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Periapical Wound Healing After NonsurgicalRoot Canal Therapy
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
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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.
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EXCISIONAL DENTOALVEOLAR WOUND
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.
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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.
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Cementoblasts: Cementogenesis
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.
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Can Radicular Cysts in Apical Periodontitis Lesions Regress After Nonsurgical Endodontic Therapy?
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.
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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.
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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.
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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.
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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.
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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.
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Osseointegration of implant
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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.
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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.
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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.
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Conclusion
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.
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References
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 and Wounds (http:/ / www. ncbi. nlm. nih. gov/ pmc/ journals/ 211/ )
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PATHWAYS OF PULP – KENNETH M .HARGREAVES
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THANK U !!!!!