Bone Healing in Fracture

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    INTRODU

    Fracture healing can occur in two way :

    1) Primary bone healing

    2) Secondary bone healing

    1. Primary bone healing also known as Haversian remodelling

    occurs with absolute stability constructs

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    2. Secondary bone healing

    A. Involves responses in the periosteum and external soft tissues. There are two types :Enchondral healing ;

    occurs with non-rigid fixation, as fracture braces, external fixation, bridge plintramedullary nailing, etc

    Intramembranous healing ;occurs with semi-rigid fixation, such as locked plating (in a non-absolute staconstruct)

    B. Secondary bone healing can occur as either enchondral or intramembranous alone, combination of the two.

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    Most fractures are splinted, not to ensure union but to:

    (1) alleviate pain

    (2) ensure that union takes place in good position

    (3) permit early movement of the limb and a return of function.

    The process of fracture repair varies according to the type of bone involved and the

    amount of movement at the fracture site.

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    This is the natural form of healing in tubular bones, in the absence of rigid fixation, i

    proceeds in 5 stages:

    Tissue destruction and haematoma formation

    Inflammation and cellular proliferation

    Callus formation

    Consolidation

    Remodelling

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    TISSUE DESTRUCTIOHAEMATOMA FORMA

    A disruption of the endosteal and periosteal blood

    supply following an injury causes haematoma formation

    in the vicinity of the fracture.

    This haematoma may occur as a localized collection of

    blood bounded by aperiosteal envelope.

    Provides source of hemopoieitic cells capable of

    secreting growth factors.

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    INFLAMMATION AND CELPROLIFER

    Within 8 hours of the fracture acute inflammatory reaction

    migration of inflammatory cells (cytokines and various growth factors)

    initiation of proliferation and differentiation of mesenchymal stem cells

    periosteum, the breached medullary canal and the surrounding muscle.

    The clotted haematoma is slowly absorbed and fine new capillaries grow into the

    area.

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    CALLUS FORM The differentiating stem cells provide chrondrogenic and osteogenic cell

    populations

    the local biological and biomechanical environment start forming bone

    also includes osteoclasts mop up dead bone.

    The thick cellular mass, with its islands of immature bone and cartilage, forms the

    callus or splint on the periosteal and endosteal surfaces.

    the immature fibre bone (or woven bone) becomes more densely mine

    movement at the fracture site decreases progressively and at about

    injury the fracture unites .

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    The formation of new bone is facilitated by avariety of osteoinductive factors;

    platelet-derived growth factor ( PDGF )

    transforming growth factor ( TGF )

    insulin-like growth factor ( IGF)

    basic fibroblast growth factor ( BFGF)

    bone morphogenetic protein ( BMP).

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    CONSOLIDA

    Continuing osteoclastic and osteoblastic activity the woven bone lam

    The system is now rigid enough to allow osteoclasts to burrow through the debris at

    the fracture line, and close behind them.

    Osteoblasts fill in the remaining gaps between the fragments with new bone.

    This is a slow process and it may be several months before the bone is strong

    to carry normal loads

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    REMODE

    The fracture has been bridged by a cuff of solid bone.

    Over a period of months, or even years , this crude weld is resh

    continuous process of alternating bone resorption and formation.

    Eventually, and especially in children, the bone reassumes something like its normal

    shape.

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    VARIABLES THAT INFFRACTURE H

    1. Internal variables blood supply (most important)

    head injury may increase osteogenic response

    2. External variables

    Nicotine Diet

    Low intensity pulsed ultrasound (LIPUS)

    Bone stimulators

    COX-2

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    Non-union

    Sometimes the normal process of fracture repair is thwarted and the bone fails to

    unite. Causes of non-union are:

    (1) distraction and separation of the fragments, sometimes the result of interposition of

    soft tissues between the fragments(2) excessive movement at the fracture line

    (3) a severe injury that renders the local tissues nonviable or nearly so

    (4) a poor local blood supply

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    Hypertrophic nonunion

    caused by inadequate immobilization with adequate blood supply

    typically heal once mechanical stability is improved

    Atrophic non-union

    caused by inadequate immobilization and inadequate blood supply

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    THANK Y