Fracture healing and wound healing

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  • 1.Fracture healing and wound healing Dr shermil sayd KMCT dental college

2. Types of Bone Lamellar Bone Woven Bone or immature bone (non-lamellar) 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. 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. ON BASIS OF RELATIONSHIP WITH EXTERNAL ENVIRONMENT - simple / closed fracture - open fracture ON BASIS OF PATTERN - transverse - oblique - spiral - comminuted - segmental 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. 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 endochondralossification. 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 laterconverted into the lamellar bone 9. SECONDARY: It is usual type consisting of formation of callus either of cartilaginous or fibrous. This callus islater replaced by lamellar bone. It is comparable to healing of soft tissue by filling of gaps withvascular granulation tissue 10. MECHANISM OF BONE FORMATION 1. Cutting Cones 2. Intramembranous Bone Formation 3. Endochondral Bone Formation 11. CUTTING CONES Primarily a mechanismto remodel bone. Osteoclasts at the front of the cutting cone remove bone. Trailing osteoblasts lay down new bone 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. 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. 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. Components of Bone Formation Cortex Periosteum Bone marrow Soft tissue 16. A.REACTIVE PHASE I .Fracture & inflammatoryphase : 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. 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. 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. 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. 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 bones original strength 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. 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. # 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. 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 theperiosteum. 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 colles fracture a hallow cavity is left in the cancellous end of the radius 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. 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. 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 29. FACTORS INFLUENCING BONE HEALING 1. 2. 3. 4. 5. 6.LOCAL FACTORS CHEMICAL FACTORS. VASCULAR FACTORS. SYSTEMIC FACTORS ELECTROMAGNETIC FACTORS TREATMENT FACTORS 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. 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. 2.CHEMICAL FACTORS1.MESSENGER SUBSTANCES -Serotonin -Prostaglandins Polypeptides -Histamines -Thromboxane2.GROWTH 3.PERMEABILITY FACTORS FACTORS -Transforming GF -Proteases -Fibroblast GF - Amines - Platelet derived GF -BMP -Insulin like GF34 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 d