Fracture healing and wound healing


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Fracture healing and wound healing

  1. 1. Fracture healing and wound healing Dr shermil sayd KMCT dental college
  2. 2. Types of Bone • Lamellar Bone • Woven Bone or immature bone (non-lamellar)
  3. 3. Fracture • Fracture is defined as a break in the continuity of bone • Fracture results in loss of its mechanical stability and also partial destruction of blood supply • Healing means to make whole or sound again, to cure, leaving a scar behind. But following fracture a scar is not formed, instead a bone has formed a new at the original fracture site. So rather than bone healing the appropriate nomenclature would be BONE REGENERATION
  4. 4. TYPES OF FRACTURES(7,8,9) • ON BASIS OF ETIOLOGY - Traumatic fracture - pathologic fractures due to some diseases - stress fracture • ON BASIS OF DISPLACEMenT - undisplaced - displaced translation ( shift ) angulation ( tilt ) rotation ( twist )
  5. 5. • ON BASIS OF RELATIONSHIP WITH EXTERNAL ENVIRONMENT - simple / closed fracture - open fracture • ON BASIS OF PATTERN - transverse - oblique - spiral - comminuted - segmental
  6. 6. HEALING AFTER FRACTURE FIXATION • DIRECT/PRIMARY: • Mechanism of bone healing seen when there is no motion at the fracture site (i.e. rigid internal fixation). • Does not involve formation of fracture callus. • Osteoblasts originate from endothelial and perivascular cells.
  7. 7. • INDIRECT/SECONDARY: • Mechanism for healing in fractures that are not rigidly fixed. • Bridging periosteal (soft) callus and medullary (hard) callus re-establish structural continuity. • Callus subsequently undergoes endochondral ossification.
  8. 8. TYPES OF BONE HEALING • PRIMARY 1. CONTACT HEALING: When there is direct contact between the cortical bone ends, lamellar bone forms directly across the fracture line , parallel to long axis of the bone, by direct extension of osteons. 2. GAP HEALING: Osteoblasts differentiate and start depositing osteoids on the exposed surfaces of fragment ends, mostly without a preceding osteoclastic resorption which is later converted into the lamellar bone
  9. 9. • SECONDARY: It is usual type consisting of formation of callus either of cartilaginous or fibrous. This callus is later replaced by lamellar bone. It is comparable to healing of soft tissue by filling of gaps with vascular granulation tissue
  10. 10. MECHANISM OF BONE FORMATION 1. Cutting Cones 2. Intramembranous Bone Formation 3. Endochondral Bone Formation
  11. 11. CUTTING CONES • Primarily a mechanism to remodel bone. • Osteoclasts at the front of the cutting cone remove bone. • Trailing osteoblasts lay down new bone
  12. 12. INTRAMEMBRANOUS BONE FORMATION(PERIOSTEAL) • Mechanism by which a long bone grows in width. • Osteoblasts differentiate directly from pre osteoblasts and lay down seams of osteoid. • Does NOT involve cartilage
  13. 13. ENDOCHONDRAL BONE FORMATION • Mechanism by which a long bone grows in length. • Osteoblasts line a cartilage precursor. • The chondrocytes hypertrophy, degenerate and calcify (area of low oxygen tension). • Vascular invasion of the cartilage occurs followed by ossification (increasing oxygen tension).
  14. 14. STAGES OF FRACTURE HEALING • There are 3 major phases with sub divisions: • A. Reactive Phase: – i. Fracture and inflammatory phase. – ii. Stage of hematoma formation. – iii. Granulation tissue formation. • B. Reparative Phase: – iv. Cartilage Callus formation. – v. Lamellar bone deposition. • C. Remodeling Phase: – vi. Remodeling to original bone contour.
  15. 15. Components of Bone Formation • Cortex • Periosteum • Bone marrow • Soft tissue
  16. 16. A.REACTIVE PHASE • I .Fracture & inflammatory phase : After fracture the first change seen by light and electron microscopy is the presence of blood cells within the tissues which are adjacent to the injury site. Soon after fracture, the blood vessels constrict, stopping any further bleeding
  17. 17. • ii. Stage of Hematoma formation: Within a few hours after fracture, the extravascular blood cells form a blood clot, known as a hematoma. All of the cells within the blood clot degenerate and die. The fracture hematoma immobilizes & splints the fracture. The fracture haematoma provides a fibrin scaffold that facilitates migration of repair cells.
  18. 18. iii. Granulation Tissue Formation: Within this same area, the fibroblasts survive and replicate. They form a loose aggregate of cells, interspersed with small blood vessels, known as granulation tissue which grows forward, outside and inside the bone to bridge the fracture. They are stimulated by vasoactive mediators like serotonin and histamine
  19. 19. B. REPARATIVE PHASE • iv. Cartilage Callus formation : Days after the # the periosteal cells proximal to the fracture gap and fibroblasts develop into chondroblasts which form hyaline cartilage. The periosteal cells distal to the fracture gap develop into osteoblasts which form woven bone. These 2 tissues unite with their counterparts and culminate into new mass of heterogenous tissue called Fracture Callus restoring some of its original strength.
  20. 20. • v. Lamellar bone deposition: Or consolidation ..where hyaline cartilage and woven bone is replaced by lamellar bone. This process is called Endochondral ossification. At this point, the mineralized matrix is penetrated by channels, each containing a microvessel and numerous osteoblasts. This new lamellar bone is in the form of trabecular bone which restores bone’s original strength
  21. 21. C. REMODELLING PHASE • vi. Remodelling to original bone contour: The remodeling process substitutes the trabecular bone with compact bone. The trabecular bone is first resorbed by osteoclasts, creating a shallow resorption pit known as a "Howship's lacuna". Then osteoblasts deposit compact bone within the resorption pit. Eventually, the fracture callus is remodelled
  22. 22. STAGES BASED ON REACTION TO TORSIONAL TESTING • STAGE 1- A healing bone subjected to torsion fails through original # site with a low stiffness pattern. • STAGE 2- The bone still fails through the # site , but the characteristic indicate high stiffness pattern(hard tissue pattern) • STAGE 3 – The bone fails partly through the original # site and partly through the previously intact bone with a high stiffness pattern . • STAGE 4 –Failure does not occur through the # site duplicates the mechanical properties of uninjured tissue
  23. 23. # HEALING IN CANCELLOUS BONE 1.Cancellous bone heals by “CREEPING SUBSTITUTION” New blood vessels can invade the trabeculae of cancellous bone and bone opposition may take place directly on to the surface of trabeculum.
  24. 24. 2.Heals at the point of direct contact: • Cancellous bone certainly can unite very rapidly, but it unites rapidly only at the points of direct contact. 3.No bridging callus : Cancellous bone unites only by contact, not by throwing out callus even when it is cut of due to dense attachment of the periosteum.
  25. 25. 4.No death of osteocytes: Takes place in the cut edges of divided trabeculae in cancellous bone. This must be because of the blood supply is good and large surface area of the trabecular spaces combined with relatively thin trabeculae, keep the osteocytes nourished. 5.Has tendency for late collapse : This lack of callus production by cancellous bone explains the tendency to late collapse which have been distracted. Eg: after reduction of colle’s fracture a hallow cavity is left in the cancellous end of the radius
  26. 26. FRACTURE HEALING IN CHILDREN • Compared with the relatively static mature bone of adult, the changing structure and function, both physiological and biomechanical, of immature bones make them susceptible to different patterns of fracture. • Fracture in children are more common and are more likely to occur after seemingly insignificant trauma. Damage involving specific growth regions such as the physis or epiphyseal ossification center may lead to acute and chronic growth disturbances.
  27. 27. FRACTURE REPAIR IN CHILDREN Fracture healing in children follow same pattern of adults but with some peculiarities : PERIOSTEUM: • In the contrast to adults, the periosteum strips away easily from the underlying bone in children. Allowing fracture haematoma to dissect along the diaphysis and metaphysis and this is evident in the subsequent amount of new bone formation along the shaft. • Dense attachment of the periosteum into the zone of ranvier limit subperiosteal hematoma formation to the metaphysic and diaphysis
  28. 28. REMODELLING IN CHILDREN • The remodelling phase is the longest phase and in children may continue until skeletal maturation. Remodelling is better in children compared to adult, This is in response to constantly changing stress patterns in children during skeletal growth and development
  30. 30. 1.LOCAL FACTORS A. Type of bone: Cancellous (spongy) bone or cortical bone. B. Degree of Trauma: Extensive soft tissue injury and comminuted #‘s V/s Mild contusions C. Vascular Injury: Inadequate blood supply impairs healing. Especially vulnerable areas are the femoral head, talus, and scaphoid bones.
  31. 31. D. Degree of Immobilization: Immobilized for vascular ingrowth and bone healing to occur. Repeated disruptions of repair tissue, especially to areas with marginal blood supply or heavy soft tissue damage, will impair healing. E. Type of Fractures: Intraarticular fractures communicate with synovial fluid, which contains collagenases that retard bone healing Open fractures result in infections Segmental fractures have disrupted blood supply. F.Soft Tissue Interposition: G.others: Bone death caused by radiation, thermal or chemical burns or infection.
  32. 32. 2.CHEMICAL FACTORS 1.MESSENGER SUBSTANCES -Serotonin -Prostaglandins Polypeptides -Histamines -Thromboxane 2.GROWTH 3.PERMEABILITY FACTORS FACTORS -Transforming GF -Proteases -Fibroblast GF - Amines - Platelet derived GF -BMP -Insulin like GF 34
  33. 33. • 1.MESSENGER SUBSTANCE: A.CYTOKINES-IL-1,4,6,11, macrophage and granulocyte/macrophage (GM) (CSFs) & (TNF) stimulate bone resorption. -IL-1 ,6 synthesis is decreased by estrogen B. PROSTAGLANDINS of the E series-Stimulate osteoblastic bone formation and inhibit activity of isolated osteoclasts. C.LEUKOTRINESStimulate osteoblastic bone formation and enhance the capacity of isolated osteoclasts to form resorption pits
  34. 34. 2.GROWTH FACTORS: A. Transforming growth factor(TGF): Superfamily of growth factors (~34 members) Act on serine/threonine kinase cell wall receptors Promotes proliferation and differentiation of osteoblasts, osteoclasts and chondrocytes Stimulates both endochondral and intramembranous bone formation and collagen type 2 synthesis. B.Fibroblast growth factors(FGF): Both acidic (FGF-1) and basic (FGF-2) forms Increase proliferation of chondrocytes and osteoblasts Enhance callus formation & stimulates angiogenesis.
  35. 35. C.Platelet derived growth factor(PDGF): A dimer, genes PDGF-A and PDGF-B Stimulates bone cell growth Increases type I collagen synthesis by increasing the number of osteoblasts. PDGF-B stimulates bone resorption. D.Insulin like growth factor(ILGF): Two types, IGF1 &IGF2, out of which IGF1 is produced in liver and stimulated by growth hormone. Stimulates bone collagen & matrix synthesis and replicates osteoblasts . It also inhibits collagen degradation.
  36. 36. • E.Bone Morphogenic Proteins (BMP): BMP was discovered by Marshall Urist in 1965. They are Osteoinductive proteins initially isolated from demineralized bone matrix FUNCTIONS: 1. Induce cell differentiation : BMP 3(osteogenin). 2. Promote endochondral ossification: BMP 2 & 7. 3. Regulate extracellular matrix production :BMP1. 4.Increase fusion rates in Spinal fusions): BMP 2 5.Non unions: BMP 7 as good as bone grafting These are included in the TGF-β family except BMP 1. Must be applied locally because of rapid systemic clearance .
  37. 37. 3.PERMEABILITY FACTORS: -Protease – Plasmin , Kalikrein, Globulin permeability factor. -Polypeptides –leucotaxime, Bradykinin, Kallidin -Amines – Adrenalin, nor-adrenalin, Histamine These factors work in ways that : – – – – – – – Increase capillary permeability Alteration in diffusion mechanism in intracellular matrix Cellular migration Proliferation & differentiation New blood vessel formation Matrix synthesis Growth & development
  38. 38. 3.VASCULAR FACTORS A. Metalloproteinases Degrade cartilage and bones to allow invasion of vessels B. Angiogenic factors: Vascular-endothelial growth factors mediate neoangiogenesis & endothelial-cell specific mitogens C. Angiopoietin (І & ІІ) Regulate formation of larger vessels and branches.
  39. 39. 4.SYSTEMIC FACTORS A.Age: Young patients heal rapidly and have a remarkable ability to remodel V/S old . B.Nutrition: An adequate metabolic stage with sufficient carbohydrates and protein is necessary. C.Systemic Diseases: And those causing an immunocompromised state will likely delay healing. Illnesses like Marfan’s syndrome and Ehlers-Danlos syndrome cause abnormal musculoskeletal healing
  40. 40. D.HORMONES: • Estrogen Stimulates fracture healing through receptor mediated mechanism. • Thyroid hormones Thyroxine and triiodothyronine stimulate osteoclastic bone resorption. • Glucocorticoids Inhibit calcium absorption from the gut causing increased PTH and therefore increased osteoclastic bone resorption. • Parathyroid Hormone • Growth Hormone: Mediated through IGF-1 (Somatomedin-C) Increases callus formation and fracture strength
  41. 41. 5.ELECTROMAGNETIC FACTORS In vitro bone deformation produces piezoelectric currents and streaming potentials. Electromagnetic (EM) devices are based on Wolff’s Law that bone responds to mechanical stress: Exogenous EM fields may simulate mechanical loading and stimulate bone growth and repair
  43. 43. RECENT ADVANCES • GROWTH FACTOR THERAPY(3) Due to their ability to stimulate proliferation and differentiation of mesenchymal and osteoprogenitor cells they have shown great promise for their ability to promote fracture repair . • APPLICATION OF PLATELET RICH PLASMA(4) Injecting platelet rich plasma at fracture site helps in fracture healing . • TISSUE ENGINEERING, STEM CELLS AND GENE THERAPIES(5) In past decade tissue culture and stem cells have been implicated in enhancing fracture healing and articular cartilage regeneration.
  44. 44. • Nanotechnology(1) based on understanding cell-implant interactions. Cells do not interact directly with an implant but instead interact through a layer of proteins that absorb almost instantaneously to the implant after insertion. Scientists have improved numerous implant materials, including titanium and titanium alloys, porous polymers, bone cements and hydroxyapatite, by placing nanoscale features on their surfaces. The bulk materials' properties remain unchanged, maintaining their desirable mechanical properties, but the surface changes enhance the interactions with proteins. This causes bone-forming cells to adhere to the implant and activates them to grow more bone.
  46. 46. MAL UNION • A MALUNITED Fracture is one that has healed with the fragments in a non anatomical position • CAUSES 1 INACCURATE REDUCTION 2 INEFFECTIVE IMMOBILIZATION
  49. 49. Correction • Operative treatment for most malunited fracture should not be considered until 6 to 12 months but in INTRA ARTICULAR fracture early operative treatment is needed. • Surgeon should look for before surgery- OSTEOPOROSIS  SOFT TISSUE  HOW MUCH FUNCTION CAN BE GAINED
  50. 50. ILIZAROV TECHNIQUE is BEST Simultaneous restoration of ALIGNMENT  ROTATION LENGTH
  51. 51. Delayed Union • The exact time when a given fracture should be united cannot be defined • Union is delayed when healing has not advanced at the average rate for the location and type of fracture (Btn 3-6 mths) • Treatment usually is by an efficient cast that allows as much function as possible can be continued for 4 to 12 additional weeks
  52. 52. • If still nonunited a decision should be made to treat the fracture as nonunion • External ultrasound or electrical stimulation may be considered • Surgical treatment should be carried out to remove interposed soft tissues and to oppose widely separated fragments • Iliac grafts should be used if plates and screws are placed but grafts are not usually needed when using intramedullary nailing, unless reduction is done open
  53. 53. Nonunion • FDA defined nonunion as “established when a minimum of 9 months has elapsed since fracture with no visible progressive signs of healing for 3 months” • Every fracture has its own timetable (ie long bone shaft fracture 6 months, femoral neck fracture 3 months)
  54. 54. Delayed/Nonunion Factors contributing to development: • Systemic • Local
  55. 55. Systemic factors: • Metabolic • Nutritional status • General health • Activity level • Tobacco and alcohol use
  56. 56. Local factors • Open • Infected • Segmental (impaired blood supply) • Comminuted • Insecurely fixed • Immobilized for an insufficient time • Treated by ill-advised open reduction • Distracted by (traction/plate and screws) • Irradiated bone • Delayed weight-bearing > 6 weeks • Soft tissue injury > method of initial treatment
  57. 57. Nonunited fractures form two types of pseudoarthrosis: • Hypervascular or hypertrophic • Avascular or atrophic
  58. 58. Hypervascular or Hypertrophic: 1. Elephant foot (hypertophic, rich in callus) 2. Horse foot (mildly hypertophic, poor in callus) 3. Oligotrophic (not hypertrophic, no callus) Hypervascular nonunions. A, "Elephant foot" nonunion. B, "Horse hoof" nonunion. C, Oligotrophic nonunion (see text). (Redrawn from Weber BG, Cech O, eds: Pseudarthrosis, Bern, Switzerland, 1976, Hans Huber.)
  59. 59. Vascular or Atrophic • Torsion wedge (intermediate fragment) • Comminuted (necrotic intermediate fragment) • Defect (loss of fragment of the diathesis) • Atrophic (scar tissue with no estrogenic potential is Avascular nonunions. A, Torsion wedge nonunion. B, Comminuted nonunion. C, Defect replacing the missing nonunion. D, Atrophic nonunion (see text). fragment) (Redrawn from Weber BG, Cech O, eds: Pseudarthrosis, Bern, Switzerland, 1976, Hans Huber.)
  60. 60. Classification (Paley et al) • Type A<2cm of bone loss A1 (Mobile deformity) A2 (fixed deformity) A2-1 stiff w/o deformity A2-2 stiff w/ fixed deformity • Type B>2cm of bone loss B1 with bony defect B2 loss of bone length B3 both A, Type A nonunions (less than 1 cm of bone loss): A1, lax (mobile); A2, stiff (nonmobile) (not shown); A2-1, no deformity; A2-2, fixed deformity. B, Type B nonunions (more than 1 cm of bone loss): B1, bony defect, no shortening; B2, shortening, no bony defect; B3, bony defect and shortening.
  61. 61. Treatment: 1. Electrical 2. Electromagnetic 3. Ultrasound 4. External fixation (ie deformity, infection, bone loss) 5. Surgical • • • Hypertrophic: stable fixation of fragments Atrophic: decortications and bone grafting According to classification: type A : restoration of alignment, compression type B : cortical osteotomy, bone transport or lengthening
  62. 62. Surgical guidelines: • Good reduction • Bone grafting • Firm stabilization
  63. 63. Reduction of the fragments: • Extensive dissection is undesirable, leaving periosteum, callus, and fibrous tissue, to preserve vascularity and stability, resecting only the scar tissue and the rounded ends of the bones • External fixator, Intramedullary nailing, Ilizarov frame
  64. 64. Bone Grafting origins: • Autogenous “the golden standard” • Allograft • Synthetic substitute
  65. 65. Bone grafting techniques: • Onlay • Dual onlay • Cancellous insert • Massive sliding graft • Whole fibular transplant • Vascularized free fibular graft • Intramedullary fibular graft
  67. 67. Stabilization of bone fragments: • Internal fixation (hypertrophic #): intramedullary, or plates and screws • External fixation(defects associated#): ie Ilizarov
  68. 68. Factors complicating nonunion • Infection • Poor tissue quality • Short periarticular fragments • Significant deformity
  69. 69. Mandible Fractures
  70. 70. Healing Primary Healing • In rigid fixation techniques • Lag screws, compression plates, Recon plate, external fixation, Wire fixation, Miniplate fixation • No callus formation • Question of bone resorption
  71. 71. Secondary bone healing • Callus formation • Remodeling and strengthening • MMF, Wire fixation, Miniplate fixation
  72. 72. Closed Reduction • Favorable, non-displaced fractures • Grossly comminuted fractures when adequate stabilization unlikely • Severely atrophic edentulous mandible • Children with developing dentition
  73. 73. • Length of MMF – De Amaratuga – 75% of children under 15 healed by 2 weeks, 75% young adults 4 wks – Juniper and Awty – 82% had healed at 4 wks – Longer period for edentulous fractures 610wks
  74. 74. Open Reduction • Displaced unfavorable fractures • Mandible fractures with associated midface fractures • When MMF contraindicated or not possible • Patient comfort • Facilitate return to work
  75. 75. Intraosseous wiring • Semirigid fixation • Cheap • Technically difficult • Primary and Secondary bone healing
  76. 76. Lag Screws • Rigid fixation (Compression) • Good for anterior mandible fractures, Oblique body fractures, mandible angle fractures • Cheap • Technically difficult • Injury to inferior alveolar neurovascular bundle
  77. 77. Lag Screw Technique
  78. 78. Compression plates • Rigid fixation • Allow primary bone healing • Difficult to bend • Operator dependent • No need for MMF
  79. 79. • Miniplates – Semi Semi-rigid fixation – Allows primary and secondary bone healing – Easily bendable – More forgiving – Short period MMF Recommended
  80. 80. Reconstruction Plates • Good for comminuted fractures • Bulky, palpable • Difficult to bend
  81. 81. External Fixation • Alternative form of rigid fixation • Grossly comminuted fractures, contaminated fractures, non-union • Often used when all else fails
  82. 82. MAXILLARY FRACTURES • Fractures of the maxilla occur less frequently than those of the mandible or nose due to the strong structural support of this bone • Reestablishing continuity of these buttresses is the foundation on which maxillary fracture treatment is based.
  83. 83. LeFort classification of midfacial fractures.
  84. 84. • The Lefort I fracture, or transverse fracture,extends through the base of the maxillary sinuses above the teeth apices essentially separating the alveolar processes, palate, and pterygoid processes from the facial structures above. This transverse fracture across the entire lower maxilla separates the alveolus as a mobile unit from the rest of the midface. Fracture dislocations of segments of the alveolus may be associated with this fracture.
  85. 85. • A pyramidal fracture of the maxilla is synonymous with a LeFort II fracture. This fracture pattern begins laterally, similar to a LeFort I, but medially diverges in a superior direction to include part of the medial orbit as well as the nose. • The fracture extends diagonally from the pterygoid plates through the maxilla to the inferior orbital rim and up the medial wall of the orbit to the nose. This separates the maxillary alveolus, medial wall of the orbit and nose as a separate piece
  86. 86. • A LeFort III fracture or craniofacial dysjunction denotes a complete separation of the midface or facial bones from the cranium. This fracture transverses the zygomaticofrontal suture, continues through the floor of the orbit, and finally through the nasofrontal suture. The bones of the orbit are separated through the lateral wall, floor, and medial wall.
  87. 87. Treatment • by reduction and immobilization • Establishment of preinjury occlusion and midface buttress alignment • reestablish normal height and projection of the face • To accomplish this, the structural buttress of the maxilla must be aligned and stabilized to provide the necessary support and contour to the midface. • The proper occlusal relationship between the dental arches is established with intermaxillary fixation (IMF), or more appropriately termed maxillomandibular fixation
  88. 88. Wound healing
  89. 89. Wound Healing • Wound- Discontinuity of the skin, mucous membrane or tissue caused by physical, chemical or biological insult • Wound healing is a complex and dynamic process of restoring cellular structures and tissue layers • There are 3 distinct phases • There are various categories of wound healing  the ultimate outcome of any healing process is repair of a tissue defect
  90. 90. • The types of wound healing: o 1° healing o Delayed 1° healing o 2° healing o (Epithelialisation) Even though different categories exist, the interactions of cellular and extracellular constituents are similar.
  91. 91. Primary wound healing • Also known as “healing by primary intention” • Think of a typical surgical wound: the wound edges are approximated • Minimal number of cellular constituents die • Results in a small line of scar tissue • Minimizes the need for granulation tissue so scarring is minimized
  92. 92. The importance factors for good wound healing • • • • • • • Technique Choice of suture Choice of needle Training Instruments Antibiotics Aftercare
  93. 93. Delayed Primary healing • Occurs if wound egdes are not approximated immediately • May be desired in contaminated wounds • By day 4: phagocytosis of contaminated tissues has occurred Usually wound is closed surgically at this stage If contamination is present still : chronic inflammation ensues leading to prominent scar eventually
  94. 94. Secondary Healing • Also called healing by secondary intention • A full thickness wound is allowed to heal by itself: there is no approximation of wound edges • Large amounts of granulation tissue formed • Wound eventually very contracted • Takes much longer to heal
  95. 95. Fungal sinusitis
  96. 96. Post op
  97. 97. 2 weeks post op – healing by 2 intention
  98. 98. Epithelialization • Epithelization is the process by which epithelial cells migrate and replicate via mitosis and traverse the wound • Common in the healing of ulcers and erosions • Occurs by one of 2 mechanisms
  99. 99. Epithelialization: Mechanisms • Mechanism 1 If basement membrane is intact ie some dermis or dermal appendages remain Epithelialization occurs by epithelial cells migrating upwards
  100. 100. • Mechanism 2 Occurs in a deeper wound A single layer of epithelial cells advance from the wound edges to cover the wound They then stratify so wound cover is complete
  101. 101. Normal Wound Healing • I. II. III. There are 3 phases Inflammatory phase: Days 0-4 Proliferative phase : Days 5-21 Remodelling phase: Days 22-60
  102. 102. • I. II. III. IV. It can also be classified in 4 stages: Haemostasis Inflammation Granulation Remodelling
  103. 103. Haemostasis • • o o o Injury causes local bleeding Vasoconstriction is mediated by : Adrenaline Thrombaxane A2 Prostaglandin 2α
  104. 104. • Platelets then adhere to damaged endothelium and discharge ADP o Which promotes thrombocyte clumping and “dams” the wound • Inflammation is initiated by cytokine release from platelets
  105. 105. • α-granules from platelets release: Platelet Derived Growth Factor (PDGF) Platelet factor IV Transforming Growth Factor β • Thrombocyte dense bodies release: Histamine Serotonin
  106. 106. • PDGF attracts fibroblasts chemotactically Leading to collagen deposition in later stages of wound healing • Fibrinogen → Fibrin Thus providing the structural support for the cellular components of inflammation
  107. 107. Inflammatory Phase • Capillary dilatation occurs due to: Histamine Bradykinin Prostaglandins • This dilatation allows inflammatory cells to reach the wound site
  108. 108. • These PMNs or leukocytes have several functions: • Scavenge for debris • Debride the wound • Help to kill bacteria by: -oxidative burst mechanisms -opsonisation
  109. 109. • Opsonin “factor which enhances the efficiency of phagocytosis because it is recognized by receptors on leucocytes 2 major opsonins are: fragment of IgG A product of complement, C3b
  110. 110. • Monocytes now enter the wound and become macrophages • They have numerous functions -Secretion of numerous enzymes and cytokines  Collagenases and elastases -To break down injured tissues  PDGF, TGFβ, IL, TNF -To stimulate proliferation of fibroblasts, endothelial and smooth muscle cells
  111. 111. • Angiogenesis The formation of new blood vessels Formed by endothelial cells becoming new capillaries within the wound bed Angiogenesis stimulated by TNFα
  112. 112. Proliferative Phase • Collagen deposition Type III collagen is laid down by fibroblasts Fibroblasts are attracted by TGFβ and PDGF Total collagen content increases until day 21 • Granulation Tissue Is the combination of collagen deposition and angiogenesis
  113. 113. Granulation Tissue • Definition: Newly formed connective tissue, often found at the edge or base of ulcers and wounds made up of : capillaries, fibroblasts, myofibroblasts, and inflammatory cells embedded in a mucin rich ground substance during healing
  114. 114. Occasionally overgranulation can occur (as above following a flexor tendon repair) Treatment is steroid topical cream (1% hydrocortisone cream)
  115. 115. • Re-epithelialization occurs next: By upward migration of epithelial cells if BM is intact Or from wound edges
  116. 116. Remodelling Phase • Fibroblasts become myofibroblasts And wound begins to contract Can contract 0.75mm per day Can over contract however Contraction allows wound to become smaller A large wound can contract by up to 40-80%
  117. 117. • Type III collagen is degraded  And replaced with Type I • Water is removed from the scar, allowing collagen to cross-link • Wound vascularity decreases • Collagen cross linkage allows:  Increased scar strength  Scar contracture  Decreased scar thickness
  118. 118. Wound Strength • During phase 1 and 2 (inflammatory and proliferative phases) Wounds have very little strength • During remodelling: Wounds rapidly gain strength o @ 6 weeks: wound is 50% of final strength o @12 months: wound is maximal strength: but this is only 75% of pre-injury tissue strength
  119. 119. Healing complications
  120. 120. Abnormal Scars • Hypertrophic Scars • Keloid Scars
  121. 121. Hypertrophic Scars • • • • • • Raised, red and thickened Limited to boundaries of scar Occurs shortly after injury Common on anterior chest and deltoids Regresses over time Related to wound tension and prolonged inflammatory phase of healing
  122. 122. Hypertrophic Scars
  123. 123. • Treatment: Surgical excision Intralesional Triamcenelone acetate injection
  124. 124. Keloid Scars • • • • • • • • • Raised, red and thickened scar Extends beyond original scar boundary Occurs months after injury Does not regress Commoner in darker skinned people Familial tendency Autoimmune phenomenon Worsened by surgery and in pregnancy Regresses post menopause
  125. 125. Keloid Scars
  126. 126. • Treatment: Surgical excision : caveat- recurrence = 65% Compression treatment CO2 lasers Cryotherapy
  127. 127. Factors influencing scarring • These can be broken down into: i. Patient factors ii. Surgical factors
  128. 128. Patient Factors • Age Elderly scar well • Skin type Celtics : hypertrophic scar tendency Dark skinned: keloid scars
  129. 129. • Anatomic region Midline Deltoid region Sternotomy • Patient morbidity Nutritional state Diabetes Wound infections
  130. 130. • Local tissue Oedema Previous radiotherapy Vascular insufficiency
  131. 131. Surgical factors • Atraumatic skin handling • Eversion of wound edges Inversion places keratinised epidermis between the healing surfaces = delayed healing • Tension free closure • Clean and healthy wound edges
  132. 132. Everted Edges
  133. 133. Inverted Edges
  134. 134. • Scar orientation Parallel to lines of relaxed skin tension Langers lines • Suture tension Over-tight: pressure necrosis Under-tight: wound gaping and widened scar
  135. 135. Langers Lines
  136. 136. Acute Inflammation • o o o Definition The cellular and vascular response to injury Short in duration Has cellular and chemical components
  137. 137. Acute Inflammation: Causes • Injury by: o Pathogens  Bacteria, viruses, parasites o Chemical agents  Acids, alkalis o Physical agents  Heat, trauma (surgery), radiation o Tissue death  Infarction
  138. 138. Stages of Acute Inflammation • Dilatation of local capillaries •  endothelial permeability • Leakage of protein-rich fluid into interstitial space – including fibrinogen • Fibrinogen → fibrin • Margination of leukocytes to peripheries of capillaries Mostly neutrophils
  139. 139. Stages of Acute Inflammation • Acute Inflammation is mediated by: Chemicals: interleukins and histamine Proteins: complement cascade
  140. 140. Complement Cascade • •  I. II.  Component of innate immune system Cascade of proteins Resulting in formation of MembraneAttack-Complex (MAC) which can Destroy invading bacteria Recruit other cells ie neutrophils Can also act as opsonins: enhancing phagocytosis
  141. 141. Complement Cascade • I. II. 2 main activating arms of CC: Classic pathway: consists of antigenantibody complexes Alternative pathway: activated directly by contact with micro-organisms
  142. 142. Chronic Inflammation • o o o Definition Tissue response to persistent injury Long in duration Cellular components differ from acute inflammation
  143. 143. Chronic Inflammation • Causes Foreign bodies: ie sutures Bacteria: ie TB Chronic abscess: ie osteomyelitis Transplant: ie chronic rejection IBD Progression from AI
  144. 144. Chronic Inflammation • Key points Histological pattern not as predictable as acute inflammation There may be areas of acute inflammation occurring simultaneously Granulation tissue and fibrosis may both be present: indicating the tissues attempts at repair
  145. 145. Chronic Inflammation Lymphocytes predominate Macrophages present too • In granulomatous inflammation they fuse forming multinucleate Langhans giant cells Plasma cells are also present
  146. 146. Chronic Inflammation • Macrophages Derived from monocytes Phagocytosis and killing of pathogens by lysosomes Langhans giant cell formation
  147. 147. Chronic Inflammation: Effects • • • • Secondary infection ie chronic epithelial injury Scarring Resolution: restoration of normality Local lymphadenopathy
  148. 148. The Surgical Wound • It is often said that it is “controlled trauma” Carried out in a sterile environment Under aseptic conditions
  149. 149. • Many protocols are put in place to prevent infections in surgical wounds o Hand washing o Gowns and gloves o Painting and draping o Drains o Antibiotics o Laminar flow theatres o Sterile instruments o Sterile dressings
  150. 150. Surgery • But wound infections can occur despite these measures causing: • Death • Morbidity • Longer hospital stays • Cosmetically displeasing wounds
  151. 151. Healthy Wound
  152. 152. Wound Infection
  153. 153. Wound Dehiscence
  154. 154. Operation Types • The risk of a wound infection depends on the operation • For that reason, operations are classified into distinct types o Clean o Clean-Contaminated o Contaminated o Dirty
  155. 155. Class I :Clean wounds • • • • Elective operations (non emergency) Non traumatic injury Good surgical technique Respiratory, gastrointestinal, biliary and genitourinary tracts not breached • Risk of infection < 2% • Eg: mastectomy, hernia repair
  156. 156. Class II: Clean - Contaminated • Urgent or emergency case that is otherwise clean • GI, GU or respiratory tracts entered electively, no spillage or unusual contamination • Minor break in sterile technique occurred • Endogenous flora involved • Risk of infection: <10 % • Eg: appendicectomy, bowel resection
  157. 157. Class III: Contaminated • Non-purulent inflammation • Gross spillage from GIT, entry into GU or biliary tract in the presence of infected bile/urine. • Major break in technique • Penetrating trauma < 4hrs old • Chronic open wounds • Risk of infection: 20% • Eg: GSW, rectal surgery
  158. 158. Class IV : Dirty • Purulent inflammation (abscess) • Pre-operative perforation of GI, GU, biliary or respiratory tract • Penetrating trauma > 4 hrs • Existing acute bacterial infection or a perforated viscera is encountered (clean tissue is transected to gain access to pus). • Risk of infection: 40%
  159. 159. Signs of Infection • The cardinal points of acute inflammation I. Calor II. Rubor III. Dolor IV. Tumour V. Functio Laesa
  160. 160. Signs of Infection • Patient may be systemically unwell ↑ Temp Tachycardic Hypotension Wound breakdown Wound discharge Warm peripheries Septic shock
  161. 161. Prevention • • • • • • • Aseptic technique Good technique Prophylactic antibiotics where appropriate Microbiology input Clean operating theatre Elective surgery Good post op care
  162. 162. Conclusion • Fracture and wound healing is influenced by many variables including mechanical stability, electrical environment, biochemical factors and blood flow etc… • Our ability to enhance fracture and wound healing will increase as we better understand the interaction between these variables.
  163. 163. References 1. Opportunities for nanotechnology-enabled bioactive bone implants Phong A. Tran, Love Sarin, Robert H. Hurt and Thomas J. Webster, J. Mater. Chem., 2009, 19, 2653 2. Bone morphogenetic protein (BMP) for fracture healing in adults, Cochrane Database Syst Rev. 2010 Jun 16;(6):CD006950. doi: 10.1002/14651858.CD006950.pub2 3. Growth factors for skeletal reconstruction and fracture repair. Curr Opin Investig Drugs. 2004 Apr;5(4):419-23 4. Role of platelet-rich plasma in acceleration of bone fracture healing,Ann Plast Surg. 2008 Sep;61(3):337-44. doi: 10.1097/SAP.0b013e318157a185 5. In vitro and in vivo induction of bone formation based on ex vivo gene therapy using rat adipose derived adult stem cells expressing BMP-7,M Yang1, Cytotherapy (2005) Vol. 7, No. 3, 273/281 6. Pathologic bone fractures: definition and classification Langenbecks Arch Chir Suppl II Verh Dtsch Ges Chir. 1989:479-86 7. Buitrago-Tellez CH, Schilli W, Bohnert M, et al (2002) A comprehensive classification of craniofacial fractures: postmortem and clinical studies with twoand three-dimensional computed tomography. Injury; 33(8):651–668 8. Spiessl B (1989) AO Classification of Mandibular Fractures. Spiessl B (ed), Internal Fixation of the Mandible: A Manual of AO/ASIF Principles with a Contribution by B. Rahn. 1st ed. Berlin, Heidelberg, New York: Springer-Verlag
  164. 164. 9.Müller ME, Nazarian S, Koch P, et al (1990) The Comprehensive Classification of Fractures of Long Bones. 1st ed. Berlin, Heidelberg, New York: Springer-Verlag 10. CAMPBELL TEXTBOOK OF ORTHOPAEDICS 11TH EDITION 11. FUNDAMENTAL OF PEDIATRIC ORTHOPAEDICS By Lynn T. Stahel 12. Buckwalter, Einhorn, Simon (ed.) Orthopaedic Basic Science 2nd ed. AAOS, 1999 13. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism 4th ed. Lippincott Williams and Wilkins, 1999. 14. Weber BG, Cech O, eds: Pseudarthrosis, Bern, Switzerland, 1976, Hans Huber.) 15. Treatment of Mandible Fractures using Bioabsorbable plates”, Plastic and Reconstructive Surgery, vol110, july2002, 25-31 16. Ellis, E. “Treatment Methods for Fractures of the Mandibular Angle." Journal of CraniomaxillofacialTrauma, vol. 28. 1999: 243-252 17. Ellis, E., et. al. “Lag Screw Fixation of Mandibular Angle Fractures.” Journal of Oral Maxillofacial Surgery, vol. 49. 1991: 234-243. 18. Kaplan et al. "Immediate Mobilization Following Fixation of Mandible Fractures, A Prospective Randomized Study." Laryngoscope, vol. 111(9). Sept 2001: 1520-1524Spinaand 19. Fonder MA, Lazarus GS, Cowan DA, Aronson-Cook B, Kohli AR, Mamelak AJ. Treating the chronic wound: A practical approach to the care of nonhealing wounds and wound care dressings. J Am Acad Dermatol. 2008 Feb;58(2):185-20
  165. 165. 20. Oral and maxillofacial surgery, daniel m laskin 21. Contemporary oral and maxillofacial surgery, peterson 22. Oral pathology, shafers 23. General pathology, harshvardhan 24. Textbook of orthopaedics, weslers