Wound healing


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Wound healing

  3. 3. INTRODUCTION • Injury to a tissue may result in cell death and tissue destruction • A wound is a disruption of the anatomic structure and function in any body part. • Healing on the other hand is a cell response to injury in an attempt to restore the normal structure and function .
  4. 4. Involves 2 distinct processes : – Regeneration – Repair At times both the processes take place simultaneously
  5. 5. • Even as cells and tissues are being injured , events that contain that damage and prepare the surviving cells to replicate are set into motion. • Entry of new cells into a tissue population is largely determined by their proliferation rates , while cells can leave the population either by cell death or differentiation into another cell type . • Interestingly regeneration and scar formation are directed by the similar process of cell growth, differentiation and cell matrix formation.
  6. 6. REGENERATION • Is the growth and differentiation of new cells and intercellular substances to form new tissues or parts. Regeneration takes place by growth from the same type of tissue that has been destroyed or from it’s precursor • In order to maintain proper structure of the tissue the parenchymal cells are under the constant regulatory control of their cell cycle which is controlled by Growth factors • Cell cycle : Is defined as the period between two successive cell divisions
  7. 7. Cell cycle and the proliferative capacity of different cells types : Cells are of 3 types depending on their capacity to divide : Labile cells Stable cells Permanent cells
  8. 8.  Regeneration of any type of parenchymal cell involves following two processes :  Proliferation of the original cells from the margin of the injury which migrates so as to cover the gap  Proliferation of the migrated cells with subsequent differentiation and maturation so as to reconstitute the original tissue
  9. 9. Molecular events in cell growth :  Although many chemical mediators affect cell growth POLYPEPTIDE GROWTH FACTORS… are most imp for growth.  GF have a Pleiotropic role :  Cellular proliferation and differentiation : affecting the expression of the genes involved in growth control pathways Tissue remodeling
  10. 10. Major growth factors in wound healing
  11. 11. Molecular events involved in cell division 1. Polypeptide growth factors bind to and activate their receptors , many of which posses intrinsic kinase activity 2.Subsequently they phosphorylate a number of substrates involved in signal transduction and generate 2nd messengers like ras 3. The resultant kinase cascade leads to the activation of nuclear transcription factors , initiates DNA synthesis and ultimately culminates in cell division
  12. 12. 4. Also the process of cell proliferation is directed by a family of proteins called Cyclins which act by controlling the phosphorylation of the proteins involved in mitosis .
  13. 13. Extra cellular matrix and cell matrix interactions  Functions : 1. Turgor to the soft tissue 2. Rigidity to the bone 3. Supplies a substratum for the cell division 4. Regulates growth, movement, and differentiation of the cells living within it.
  14. 14.  ECM consists of 3 components : 1. Collagen 2. Adhesive glycoproteins : fibronectin, integrins , laminin. 3. Proteoglycans.
  15. 15.  To summarize, cell growth and differentiation involves at least two types of signals acting in concert  One derives from the soluble molecules such as polypeptide growth factors and growth inhibitors .  Other involves insoluble elements of ECM interacting with cellular integrins.
  16. 16. REPAIR  Healing of a wound by tissue that does not fully restore the architecture or function of the part (AAP, Glossary of periodontal terms).  Is the replacement of the soft tissue by fibrous tissue . Damage to parenchymal cells leads to a situation where , repair cannot be accomplished by parenchymal regeneration alone.  Thus, these cells begin being replaced by proliferating fibroblasts and vascular endothelial cells within 24 hours .
  17. 17.  By 3 to 5 days there is granulation tissue formation, indicative of healing is well established which then progressively accumulates connective tissue matrix resulting in fibrosis.  Repair involves : 1. Granulation tissue formation. 2.contraction of the wound.
  18. 18.  Granulation tissue formation :it derives its name from the slightly granular and pink appearance of the tissue .  Each granule histologically corresponds to proliferation of new small blood vessels which are slightly lifted on the surface by a thin covering of fibroblasts and young collagen .
  19. 19.  Involves three phases :  Phase of inflammation  Phase of clearance : 1.Combination of Proteolytic enzymes liberated by neutrophils 2. Autolytic enzymes from the dead tissue cells 3. Phagocytic activity of the macrophages . All the above processes leading to clearance of the necrotic tissue , debris and RBCs .
  20. 20.  Phase of ingrowth of granulation tissue : Consists of two main processes  Angiogenesis (neovascularization)  Formation of fibrous tissue(fibrogenesis)
  21. 21. Angiogenesis Is necessary to sustain newly formed granulation tissue . Takes place by proliferation of endothelial cells from the margins of the severed vessels . Relies on the extra cellular matrix in the wound bed
  22. 22. Initially the endothelial cells are solid buds , but within few hours develop a lumen and starts carrying blood . Newly formed blood vessels are leaky accounting for edematous appearance of the new granulation tissue . Soon these blood vessels differentiate into muscular arterioles , thin walled venules and true capillaries
  23. 23. Fibrous tissue formation Newly formed blood vessels are present in an amorphous ground substance or matrix. The new fibroblast originate from fibrocytes as well as the mitotic division of the fibroblasts . As the maturation proceeds : there is an increase in the collagen , and a decrease in the fibroblasts and blood vessels . This leads to the formation of scar know as CICATRISATION
  24. 24.  THUS FIBROSIS OCCURS IN TWO STEPS :  Emigration and proliferation of the fibroblasts at the site of injury  Deposition of these cells which in turn increases collagen synthesis  Above process is directed by growth factors and growth inhibiting factors, sources of which are the macrophages and activated endothelial cells.
  25. 25. Wound contraction and ECM organization  Is a superbly orchestrated interaction of cells, ecm, cytokines  Characterized by the appearance of MYOFIBROBLASTS which is said to correspond to the contraction of the wound  This contraction requires the stimulation by the TGF B1&B2 AND PDGF ,and attachment of fibroblasts to collagen matrix through integrin receptors.  Also metalloproteinases secreted by macrophages play an imp. role in degradation of the collagen which is required for wound contraction.
  26. 26. Healing by first intention Is defined as a wound which has the following characters • Clean and uninfected • Surgically incised • Without much loss of cells and tissues • Edges of the wound are approximated by the surgical sutures
  28. 28.  INITIAL HAEMORRHAGE • Immediately after injury, the space bw the opposing surfaces of the skin becomes filled with blood , due to hemorrhage of the severed vessels . • Clot forms, which seals the incision against dehydration and infection .
  29. 29.  ACUTE INFLAMMATORY RESPONSE : o Ensues within 24 hours . o Margins are infiltrated by neutrophils, monocytes and swollen by fluid exudate. o Autolytic enzymes liberated by dead tissue cells . o Proteolytic enzymes by the neutrophils
  30. 30. o Phagocytic activity by monocytes and tissue macrophages which appear by 3rd day clear away necrotic tissue debris and RBCs . o Ingested Hb gets converted into hemosiderin and hematoidin .
  31. 31.  EPITHELIAL CHANGES : o Basal cells of the epidermis from both the cut margins start proliferating and migrating towards incisional space in the form of epithelial spurs o Well approx. wound is covered by a layer of epithelium in 48 hours. o Migrated epidermal cells separate the underlying viable dermis…. Scab which is cast off o By 5th day multilayer epidermis is formed which differentiates in to superficial and deeper layers.
  32. 32. Organization : o Proceeds in the incisional deficit of the dermis, protected by the overlying new epidermis. o By the 3rd day : capillary buds fibroblasts
  33. 33. • New collagen by the 5th day-dominates till healing is complete. • 4th week Scar tissue with scanty cellular and vascular elements , few inflammatory cells and epithelialised surface is formed.
  34. 34.  RESPONSE TO SUTURES : o Each suture track is a separate wound o Incites the same phenomena as in healing of primary wound o When the sutures are removed around the 7th day much of the epi. suture track is avulsed and remaining epi. tissue in track is absorbed .
  35. 35. PRIMARY UNION OF SKIN WOUNDS A.The incised wound as well as suture track on either side are filled with blood clot and there is inflammatory response from the margins B.spurs of epidermal cells migrate along the incised margin on either side as well as round the suture track.formation of granulation tissue also begins from below. C.removal of sutures at around 7 th day result in scar tissue at the sites of incision and suture track
  36. 36. Healing by secondary intention  Is defined as-  Wound open with a large tissue defect, at times infected  Extensive loss of cells and tissues  Not approximated by sutures, but is left open
  37. 37. Secondary union consists of the following events :  Initial hemorrhage  Inflammatory process  Epithelial changes  Granulation tissue formation  Wound contraction  Presence of infection
  38. 38. Granulation tissue formation :  Proliferating fibroblasts and neovascularization  Newly formed connective tissue:deep red, granular and very fragile.  With time scar matures :increased collagen decreased vascularity
  39. 39. Wound contraction  Not seen in primary healing  Myofibroblasts are the cells responsible for the contraction of the wound  13rd to 14h its original size
  40. 40. Presence of infection  Bacterial contamination delays healing due to release of bacterial contaminants and provoke necrosis , suppuration , thrombosis.  Surgical removal of the dead tissue ‘debridement’ helps in preventing bacterial infection of the open wounds.
  41. 41. secondary union of wound A. The open wound is filled with blood clot and there is inflammatory response at the junction of viable tissue B. Epithelial spurs from the margins of wound meet in the middle to cover the gap and seperate the underlying viable tissue from necrotic tissue at the surface forming scab C. After contraction of the wound ,a scar smaller than the original wound is left
  42. 42. COMPLICATIONS OF WOUND HEALING • Infection of wound due to entry of bacteria delays the healing • Stich abscess –infection of suture track • Implantation (epidermal) cyst formation may occur due to persistence of epithelial cells in the wound after healing • Pigmentation of healed wounds may at times may have rust like colour due to staining wih haemosiderin • Deficient scar formation due to inadequate formation of granulation tissue • Incisional hernia/wound dehisence a weak scar,especially after laprotomy may be the site of bursting open of a wound
  43. 43. • exuberant granulation/proud flesh Another deviation in wound healing is the formation of excessive amounts of granulation tissue, which protrudes above the level of the surrounding skin and in fact blocks re-epithelialization • Hypertrophied scars and keloid formation at times scar formed is excessive ugly and painful.Excessive formation of collagen in healing may result in keloid (claw like) formation • Excessive contraction exaggeration of wound contractures or cicatrisation • Neoplasia rarely ,scar may be the site for development of carcinoma later eg : squamous cell carcinoma in marjolins ulcer i.e a scar formed following burns on skin
  44. 44. EXTRACELLULAR MATRIX –WOUND STRENGTH • The wound is strengthened by proliferation of fibroblast and myofibroblast which get structural support from the extracellular matrix • In addition ECM can direct cell migration ,attachment , differentiation and organization • ECM has five main components 1)collagen 2)adhesive glycoprotein fibronectin - plasma tissue tenascin or cytotactin thrombospondin 3) basement membrane 4)elastic fibres
  45. 45. • 5)proteoglycans chondroitin sulphate heparin sulphate dermatin sulphate keratin sulphate hyaluronic acid
  46. 46. Factors influencing healing Local factors :  Infection  Poor blood supply  Foreign bodies  Movement  Exposure to ionizing radiation  Exposure to uv light facilitates healing  Type, size and location of the wound-determines whether the wound heals by resolution or organisation
  47. 47.  Systemic factors  Age  Nutrition  Systemic infection  Administration of drugs eg. Glucorticoids  Uncontrolled diabetes  haematological abnormalities.
  48. 48. HEALING IN SPECIALIZED TISSUES FRACTURE HEALING: However, basic events in healing of any type of fracture are similar and resemble healing of skin wound to some extent. The process of fracture healing can occur in two ways: - Direct or primary bone healing occurs without callus formation. - Indirect or secondary bone healing occurs with a callus precursor stage
  49. 49. • Primary union of fractures involves a direct attempt by the cortex to re-establish itself after interruption. • Bone on one side of the cortex must unite with bone on the other side of the cortex to re-establish mechanical continuity. • This process seems to occur only when anatomic restoration of the fracture fragments takes place, • by rigid internal fixation, • and when the stability of fracture reduction is ensured by a substantial decrease in interfragmentary strain.
  50. 50. • Under these conditions, bone-resorbing cells on one side of the fracture show a tunnelling resorptive response, whereby they re-establish new haversian systems by providing pathways for the penetration of blood vessels . • Secondary union is the more common process of fracture healing it is described under three headings i) Procallus formation ii) Osseous callus formation iii) Remodelling
  51. 51. PROCALLUS FORMATION:Steps involved in the formation of procallus are as follows • Haematoma forms due to bleeding from torn blood vessels, filling the area surrounding the fracture. Loose meshwork is formed by blood and fibrin clot which acts as framework for subsequent granulation tissue formation • Local inflammatory response occurs at the site of injury with exudation of fibrin, polymorphs and macrophages. The macrophages clear away the fibrin, red blood cells, inflammatory exudate and debris. Fragments of necrosed bone are scavenged by macrophages and osteoclasts.
  52. 52. • Ingrowth of granulation tissue begins with neovascularisation and proliferation of mesenchymal cells from periosteum and endosteum. A soft tissue callus is thus formed which joins the ends of fractured bone without much strength. • Callus composed of woven bone and cartilage starts within the first few days. The cells of inner layer of the periosteum have osteogenic potential and lay down collagen as well as osteoid matrix in the granulation tissue.The osteoid undergoes calcification and is called woven bone callus
  53. 53. • In poorly immobilised fractures (e.g. fracture ribs), the subperiosteal osteoblasts may form cartilage at the fracture site. At times, callus is composed of woven bone as well as cartilage, temporarily immobilising the bone ends. This stage is called provisional callus or procallus formation and is divided into • external procallus • intermediate procallus • Internal procallus.
  54. 54. OSSEOUS CALLUS FORMATION procallus acts as scaffolding on which osseous callus composed of lamellar bone is formed. The woven bone is cleared away by incoming osteoclasts and the calcified cartilage disintegrates. In their place, newly-formed blood vessels and osteoblasts invade, laying down osteoid which is calcified and lamellar bone is formed by developing Haversian system concentrically around the blood vessels.
  55. 55. REMODELLING During the formation of lamellar bone, osteoblastic laying and osteoclastic removal are taking place remodelling the united bone ends, which after sometime, is indistinguishable from normal bone. The external callus is cleared away, compact bone (cortex) is formed in place of intermediate callus and the bone marrow cavity develops in internal callus
  56. 56. FRACTURE HEALING A.Haematoma formation and local inflammatory response at the fracture site B.Ingrowth of granulation tissue with formation of soft tissue callus C.Formation of procallus composed of woven bone and cartilage with its charecteristic fusiform appearance and having three arbitrary componenets-external ,intermediate and internal callus. D.Formation of osseous callus composed of lamellar bone following clearance of woven bone and cartilage E.Remodelling bone ends the external callus cleared away,intermediate callus converted in to lamellar bone and internal callus in to developing bone marrow cavity
  57. 57. • Complication of fracture healing fibrous union -a false joint (pseudoarthrosis). non - union -soft tissue is interposed delayed union - delayed wound healing
  58. 58. Healing of Nervous Tissue CENTRAL NERVOUS SYSTEM  The nerve cells of the brain, spinal cord and ganglia once destroyed are not replaced.  Axons of CNS also do not show any significant regeneration.  The damaged neuroglial cells, however, may show proliferation of astrocytes called gliosis.
  59. 59. PERIPHERAL NERVOUS SYSTEM • In contrast to the cells of CNS, the peripheral nerves show regeneration, mainly from proliferation of Schwann cells and fibrils from distal end. Briefly, it consists of the following: • Myelin sheath and axon of the intact distal nerve undergo Wallerian degeneration up to the next node of Ranvier towards the proximal end. • Degenerated debris are cleared away by macrophages. Regeneration in the form of sprouting of fibrils takes place from the viable end of axon.
  60. 60. • These fibrils grow along the track of degenerated nerve so that in about 6-7 weeks, the peripheral stump consists of tube filled with elongated Schwann cells. • One of the fibrils from the proximal stump enters the old neural tube and develops into new functional axon
  61. 61. Healing of Muscle All three types of muscle fibres have limited capacity to regenerate SKELETAL MUSCLE • On injury, the cut ends of muscle fibres retract but are held together by stromal connective tissue. • The injured site is filled with fibrinous material, polymorphs and macrophages. • After clearance of damaged fibres by macrophages, one of the following two types of regeneration of muscle fibres can occur
  62. 62. • If the muscle sheath is intact, sarcolemmal tubes containing histiocytes appear along the endomysial tube which, in about 3 months time, restores properly oriented muscle fibres e.g. in Zenker’s degeneration of muscle in typhoid fever. • If the muscle sheath is damaged, it forms a disorganised multinucleate mass and scar composed of fibrovascular tissue e.g. in Volkmann’s ischaemic contracture.
  63. 63. SMOOTH MUSCLE • Non-striated muscle has limited regenerative capacity e.g. appearance of smooth muscle in the arterioles in granulation tissue. • However, in large destructive lesions, the smooth muscle is replaced by permanent scar tissue.
  64. 64. CARDIAC MUSCLE • Destruction of heart muscle is replaced by fibrous tissue. • However, in situations where the endomysium of individual cardiac fibre is intact (e.g. in diphtheria and coxsackie virus infections), regeneration of cardiac fibres may occur in young patients.
  65. 65. Healing of Mucosal Surfaces • The cells of mucosal surfaces have very good regeneration and are normally being lost and replaced continuously e.g. mucosa of alimentary tract, respiratory tract, urinary tract,uterine endometrium etc. • This occurs by proliferation from margins, migration, multilayering and differentiation of epithelial cells in the same way as in the epidermal cells in healing of skin wounds.
  66. 66. Healing of Solid Epithelial Organs • Following gross tissue damage to organs like the kidney, liver and thyroid, the replacement is by fibrous scar e.g. in chronic pyelonephritis and cirrhosis of liver. • However, in parenchymal cell damage with intact basement membrane or intact supporting stromal tissue, regeneration may occur. For example: • In tubular necrosis of kidney with intact basement membrane, proliferation and slow migration of tubular epithelial cells may occur to form renal tubules. • In viral hepatitis, if part of the liver lobule is damaged with intact stromal network, proliferation of hepatocytes may result in restoration of liver lobule
  67. 67. Healing of oral wounds • Oral wounds heals faster and with less scarring than extra oral wounds • It is mainly due to : factors in saliva specific microflora of the oral cavity resemblance of fetal fibroblast with gingival fibroblast
  68. 68. Factor Mechanism saliva Moisture ,ionic strength, Growth factors(EGF,TGFβ,FGF,IGF…)& unknown factors bacteria Stimulation of macrophage influx, Direct stimulative action on keratinocyte and fibroblast Phenotype of cells Fetal like fibroblasts with unique response , Specialised epithelium & Connective tissue
  69. 69. Role of saliva & gingival crevicular fluid in oral wound healing • Animals instintly lick their wounds which appear to result in faster wound healing • People with xerostomia/sialadenectomised animals show dealyed healing of oral wounds • Physico-chemical factors favouring healing are appropriate PH ionic strength calcium and magnisium ions • Saliva has an efficient capacity to reduce redox activity caused by transitional metal ions and inhibit the production of free radicals that may be beneficial for the healing process
  70. 70. Lubrication of oral mucosa is beneficial for wound healing  Advantages of moist environment prevention of tissue dehydration and cell death accelerated angiogenesis incremental breakdown of fibrin and tissue debris  Presence of growth factors - growth factors are produced by salivary glands or derived from plasma through gingival crevice Epidermal growth factor Transforming growth factorβ Fibroblast growth factor Insulin growth factor
  71. 71. ROLE OF BACTERIA IN WOUND HEALING • oral cavity harbours more than 500 bacterial species • Wound colonize by pathoogic bacteria have delayed wound healing • In 1921 carrel reported that wounds of dogs treated with certain concentrations of staphylococcus aureus healed faster than untreated wounds • Inflammatory reaction that is prerequisite for tissue repair is accentuated by bacterial contamination • Bacteria present in wound will attract macrophages in to the area and induce their cytokine secretion
  72. 72. • As a consequence blood supply and granulation tissue formation are accentuated in wound healing • Proliferation of mesenchymal cells is increased and synthesis rate of connective tissue component is stimulated leading to greater tensile strength of the contaminated wounds in the course of healing • Depending on the type and concentration of bacteria either accelerate or delay wound healing
  73. 73. Periodontal wound healing HEALING FOLLOWING SCALING & ROOT PLANING • Immediately after Scaling of Teeth the epithelial attachment will be severed, junctional & crevicular epithelium partially removed • Numerous polymorphonuclear leucocytes can be seen between residual epithelial cells & crevicular surface in about 2 hrs • There is dilation of blood vessels, oedema & necrosis in the lateral wall of the pocket • The remaining epithelial cells show very little pre-mitotic activity at that time. 24 hrs after scaling a widespread &intense labeling of the cells have been observed, in all areas of the remaining epithelium& in 2 days the entire pocket is epithlialized.
  74. 74. • In 4-5 days a new epithelial attachment may appear at bottom of sulcus. Depending on the severity of inflammation & the depth of the gingival crevice, complete epithelial healing occurs in 1-2 weeks • Immature collagen fibers occur within 21days. Following scaling, root planning & curettage procedure healing occurs with the formation of a long thin junctional epithelium with no connective tissue attachment.
  75. 75. HEALING FOLLOWING CURETTAGE • A blood clot forms between the root surface & the lateral wall of the pocket, soon after the curettage • Large number of polymorphonuclear leucocytes appear in the area shortly after the procedure • This is followed by rapid proliferation of granulation tissue. • Epithelial cells proliferate along the sulcus.
  76. 76. • Epitheliasation of the inner surface of the lateral wall is completed in 2-7 days • The junctional epithelium is also formed in about 5 days • Healing results in the formation of a long junctional epithelium adherent to the root surface.
  77. 77. Healing after surgical gingivectomy • Initial response after gingivetomy is the formation of a protective surface clot • Underlying tissue becomes acutely inflamed with some necrosis • Clot is then replaced by granulation tissue • By 24 hours there is an increase in new connective tissue cells, mainly angioblasts just beneath the surface layer of inflammation and necrosis
  78. 78. • By the 3rd day numerous young fibroblast are located In the area • The highly vascular granulation tissue grows coronally,creating a new free gingival margin and sulcus • Capillaries derived from the blood vessels of the periodontal ligament migrate in to the granulation tissue and within 2 weeks they connect with gingiva vessels
  79. 79. • After 12 to 24 hours ,epithelial cells at the margins of the wound start to migrate over the granulation tissue,seperating it from the contaminated surface layer of the clot • Epithelial activity at the margins reaches peak in 24 to 33 hours • The new epithelial cells arise from the basal and deeper spinous layers of the wound edge epithelium and migrate over the wound over a fibrin layer that is later resorbed and replaced by a connective tissue bed • The epithelial cells advances by tumbling action,with cell becoming fixed to the substrate by heidesmosomes and a new basement lamina
  80. 80. • After 5 to 14 days, surface epithelization is generally completed • During the first 4 weeks after gingivectomy ,keratinization is less than it was before surgery • Complete epithelial repair takes about one month • Vasodilation and vascularity begin to decrease after fourth day of healing and appear to be almost normal by the sixteenth day
  81. 81. • Complete repair of the connective tissue takes about 7 weeks • The flow of gingival fluid in humans is initially increased after gingivectomy and diminishes as healing progresses • Maximal flow is reached after 1week,coinciding with the time of maximal inflammation • In patients with physiologic gingival melanosis the pigmentation is diminished in the healed gingiva
  82. 82. HEALING FOLLOWING ELECTROSURGICAL GINGIVECTOMY There appears to be little difference in the results obtained after shallow gingival resection with electrosurgery and that with periodontal knives. However, when used for deep resection close to bone, electrosurgery can produce gingival recession, bone necrosis and sequestration, loss of bone height, furcation exposure, and tooth mobility, which do not occur with the use of periodontal knives.
  83. 83. HEALING FOLLOWING DEPIGMENTATION OF GINGIVA: Healing after surgical depigmentation: • After surgery it was found necessary to cover the exposed lamina propria with periodontal packs for 7 to 10 days. The wound healed uneventfully. After 6 weeks the attached gingiva regenerated by only a delicate scar present. The newly formed gingiva was clinically non-pigmented. Healing following cryosurgical depigmentation: • At 2nd to 3rd day: superficial necrosis becomes apparent and a whitish slough could be separated from the underlying tissue, leaving a clean pink surface. • In 1-2 weeks: normal gingiva • In 3-4 weeks: keratinization completed. • No postoperative pain, hemorrhage, infection or scarring seen in patients.
  84. 84. Healing following depigmentation by laser: • During lasing gingiva gets covered with a yellowish layer, that could be easily removed by a wet gauze. • After 1-2 weeks: completion of re-epithelization. • At 4th week: gingiva is similar to normal untreated gingiva i.e., lacking melanin pigmentation completely
  85. 85. HEALING FOLLOWING FLAPSURGERY • Immediately after suturing of the flap against tooth surface a clot forms between the 2 tissues • The clot consists of fibrin reticulum with many polymorphonuclear leukocytes, erythrocytes & remnents of injured clots • At edge of flap numerous capillaries are seen • 1-3days after surgery space between flap & tooth surface & bone appears reduced & the epithelial cells along border of the flap start migrating By 1 week after surgery • epithelial cells have migrated &established an attachment to root surface by means of hemidesmosomes
  86. 86. • The blood clot is replaced by granulation tissue proliferating from the gingival connective tissue, alveolar bone and periodontal ligament • By 2nd week collagen fibers begins to appear. Collagen fibers gets arranged parallel to root surface rather than at right angles. The attachment between soft tissue & tooth surface is weak • By end of one month following surgery the epithelial attachment is well formed & the gingival crevice is also well epithealised • There is beginning functional arrangement of supracrestal fibres.
  87. 87. In cases where MUCOPERIOSTEAL FLAP • has been reflected, superficial bone necrosis have been observed during first 3 days • Osteoclastic Resorption occurs in that area which reaches its peak at 4-6 days • Osteoblastic Remodelling occurs subsequently • Loss of alveolar bone height by about 1 mm may be expected after healing.
  88. 88. HEALING FOLLOWING OSSEOUS RES ECTION • Osseous surgery initiates a inflammatory response • Elevation of Mucoperiosteal Flap results in temporary loss of nutrient supply to the bone • In additition surgical resection of bone also contributes to inflammatory changes. Necrosis of the alveolar crest & osteoclastic resorption of the bone takes place initially • The osteoclastic resorption is followed by bone deposition & remodeling.
  89. 89. • The initial loss in bone height is compensated to some extent by the repair and remodeling. • Thus final loss in bone height is clinically insignificant • Osteoblastic activity is even seen after 1 yr. post-operatively • As mucoperiosteum is sutured back on to alveolar process the osteoclastic activity doesn’t lost for long
  90. 90. Healing after implant placement • The interface area consists of bone, marrow tissue, and a hematoma mixed with bone fragments from the drilling process. • In the early phase of healing, woven bone is formed by osteoblasts at the surfaces of trabecular and endosteal cortical bone surrounding the implant. • The newly formed bone approaching the implant surface leads to bone condensation into both, the implant threads and towards the implant surface. • Consequently, the amount of bone in the threads and the degree of bone-implant contact increase with time. • In the late phases of healing, lamellar bone replaces woven bone in a process of creeping substitution.
  91. 91. STAGES OF HEALING OF IMPLANTS a. Woven Bone Formation: When bone matrix is exposed to extra-cellular fluid, non-collagenous proteins & growth factors are set free & initiate repair. • Woven bone is first formed & bridge a gap within a few days. • Woven bone formation dominates the first4-6 weeks b. Lamellar Bone Formation : From 2nd month post-operatively the microscopic structure of bone changes to lamellar or parallel fibered bone c. Bone Remodelling : It begins around 3rd month post- operatively.Initially rapid remodeling occurs which slows down & continuos for rest of the life Thus complete healing probably takes longer than 3 to 6 months.
  92. 92. LASERS IN WOUND HEALING • Lasers employing low-level radiant energy have been claimed to produce a positive effect on the biological and bio-chemical processes of wound re-constitution. • It has been reported that low level radiant energy of lasers has accelerated wound healing, reduced pain and enhanced neural regeneration. • Dermatologic investigations have demonstrated more rapid epithelialization, enhanced neovascularization, and increased production of collagen by fibroblasts in vivo by the application of radiation from argon or helium neon lasers.
  93. 93. • Reports have also shown increased synthesis of collagen and enhanced phagocytic activity of leukocytes after use of low- level laser irradiance of tissues in vitro. • At present, majority of laser wound healing literature has focused on the proliferative phase of wound healing, the period of 10 to 14 days after wounding that is characterized by populations of proliferating fibroblasts and the initiation of the synthesis of collagen.
  94. 94. summary The healing wound, as a prototype of tissue repair, is a dynamic and changing process .The early phase is one of inflammation, followed by a stage of fibroplasia, followed by tissue remodelling and scarring. Different mechanisms occurring at different times trigger the release of chemical signals that modulate the orderly migration, proliferation, and differentiation of cells and the synthesis and degradation of ECM proteins. These proteins, in turn, directly affect cellular events and modulate cell responsiveness to soluble growth factors. The magic behind the seemingly precise orchestration of these events under normal conditions remains beyond our grasp but almost certainly lies in the regulation of specific soluble mediators and their receptors on particular cells, cell-matrix interactions and a controlling effect of physical factors,including forces generated by changes
  95. 95. To conclude with, the ideal healing in periodontics should lead to the adequate function and acceptable aesthetics. Thorough knowledge regarding the nature and relationship of various periodontal tissues is necessary to achieve adequate healing.
  96. 96. References • Anderson’ s - basic pathology • Harshmohan - essential pathology for dentral students • Jan lindhe - clinical periodontology & implant dentistry • Carranza - clinical periodontology • Perio 2000 - vol 1 :periodontal regenaration (basic consideration in periodontal wound healing to achieve regeneration) vol 24:connective tissue of periodontium (cell biology of wound healing) • Journel of dental rsearch 2010 march ,89(3),219-229 (factors affecting wound healing)  Lars Sennerby : Implant Integration and Stability. In : Partick Palacci, Esthetic implant dentistry, soft and hard tissue management. Germany: Quintessence Publishing Company, 2001.  Guy A. Catone, Edward Halusic. Photobiology of lasers in oral and maxillofacial surgery. In: Guy A. Catone, Charles C. Alling. Lasers applications in oral and maxillofacial surgery. USA: W.B. Saunders company, 1997.