Fracture Healing

Fracture Healing

Introduction Pathology & Stages Local Factors influencing Osteogenesis Differences in healing of fractured bone treated byconservative & operative methods

Introduction Fracture is a break in the structural continuityof bone. The healing of fracture is in many wayssimiliar to the healing in soft tissue woundsexcept that the end result is mineralisedmesenchymal tissue i.e. BONE. Fracture healing starts as soon as bonebreaks and continues modelling for manyyears

Bone is unique in its ability to repair itself.,it cancompletely reconstitute itself by reactivatingprocesses. Bone repair is a highly regulated process that can beseperated into overlapping histologic,bio-chemical &bio-mechanical stages. The completion of each stage initiates the next stageand this is accomplished by a series of interactionsand communications among various cells andproteins located in healing zone.

Pathology & Staging The events in the process of fracture healing can bedivided into 3 phases. 1.Inflammation Phase 2.Reparative Phase 3.Remodelling Phase

Inflammation beginsimmediately afterinjury and is followedrapidly by repair. After repair hasreplaced the lost anddamaged cells andmatrix,a prolongedremodelling phasebegins.

Inflammation Phase An injury that fractures bones damages not only thecells,blood vessels and bone matrix,but also thesurrounding soft tissue including the periosteumand blood vessels. Immediately after fracture,rupture of blood vesselsresults in hematoma which fills the fracture gap andalso the surrounding area. The clotted blood provides a fibrin mesh which helpsseal off fracture site and allows the influx ofinflammatory cells and ingrowth of fibroblasts &new capillary vessels.

Initial events following fractureof a long bone diaphysis

The degranulated platelets and migrating inflammatorycells release PDGF, TGF-BETA, FGF and othercytokines,which activates the osteoprogenitor cells in theperiosteum,medullary cavity,and surrounding softtissues and stimulate the production of osteoclastic andosteoblastic activity. Thus by the end of first week,the hematoma isorganizing,the adjacent soft tissue is being modulated forfuture matrix production. This fusiform & predominantly uncalcified tissue calledsoft tissue callus or procallus provides some anchorgebetween ends of fractured bones but offers no structuralrigidity for weight bearing.

Reparative Phase The inflammatory cells releases the cytokines thatstimulate angiogenesis. As the inflammatory response subsides,necrotictissue and exudate are reabsorbed and fibroblastsand chondrocytes appear and start producing a newmatrix,the fracture callus . Electronegativity found in the region of freshfracture may also simulate the osteogenesis.

Early repair of a diaphysealfracture of a long bone

The activated osteoprogenitor cells deposit sub-periosteal trabeculae of woven bone orientedperpendicular to cortical axis and within themedullary cavity. In some cases the activated mesenchymal cells in softtissue and bone surrounding the fracture line alsodifferentiate into chondroblasts that makefibrocartilge and hyaline cartilage. The newly formed cartilage undergoes enchondralossification forming a network of bone In this fashion,the fractured ends are bridged by abony callus and as it mineralizes,the stiffness andstrength of callus increase to point where controlledweight bearing can be tolerated.

Remodelling Phase As the callus matures and transmits weight-bearingforces,the portions that are not physically stressedare reabsorbed,and in this manner the callus isreduced in size until the shape and outline offractured bone has been reestablished. The medullary cavity is also restored.

Progressive fracture healing byfracture callus

Healing

Factors influencingosteogenesis 1.2.3.4.Injury variablesPatient variablesTissue variablesTreatment variables

1.Injury varibles I).OPEN FRACTURES: Severe open fractures cause soft tissue disruption,fracture displacement, and, in some instances,significant bone loss. Extensive tearing or crushing of the soft tissuedisrupts the blood supply to the fracture site, leavingnecrotic bone and soft tissue, impeding orpreventing formation of a fracture hematoma, anddelaying formation of repair tissue

II).SEVERITY OF INJURY: They may be associated with large soft tissuewounds, loss of soft tissue, displacement andcomminution of the bone fragments, loss of bone,and decreased blood supply to the fracture site. Comminution of bone fragments usually indicatesthat there is also extensive soft tissue injury.

Displacement of the fracture fragments and severetrauma to the soft tissues retard fracture healing,probably because the extensive tissue damageincreases the volume of necrotic tissue, impedes themigration of mesenchymal cells and vascularinvasion, decreases the number of viablemesenchymal cells, and disrupts the local bloodsupply.

Open fracture

III).INTRA-ARTICULAR FRACTURES : Because they extend into joint surfaces and jointmotion or loading may cause movement of thefracture fragments, intra-articular fractures canpresent with challenging problems. Most intraarticular fractures heal, but if thealignment and congruity of the joint surface is notrestored, the joint may be unstable, and,in someinstances, especially if the fracture is not rigidlystabilized, healing may be delayed or nonunion mayoccur.

IV).SEGMENTAL FRACTURES : A segmental fracture of a long bone impairs or disruptsthe intramedullary blood supply to the middle fragment. If there is severe soft tissue trauma, the periosteal bloodsupply to the middle fragment may also becompromised.,possibly because of this, the probability ofdelayed union or nonunion, proximally or distally, maybe increased. These problems occur most frequently in segmentalfractures of the tibia, especially at the distal fracture site.

V).SOFT TISSUE INTERPOSITION : Interposition of soft tissue, including muscle, fascia,tendon, and occasionally nerves and vessels, betweenfracture fragments compromises fracture healing. Soft tissue interposition should be suspected when thebone fragments cannot be brought into apposition oralignment during attempted closed reduction. If this occurs, an open reduction may be necessary toextricate the interposed tissue and achieve an acceptableposition of the fracture.

VI).DAMAGE TO BLOOD SUPPLY : Lack of an adequate vascular supply can significantlydelay or prevent fracture healing. Insufficient blood supply for fracture healing may resultfrom a severe soft tissue and bone injury or from thenormally limited blood supply to some bones or boneregions. For example, the vulnerable blood supplies of the femoralhead,scaphoid, and talus may predispose these bones todelayed union or nonunion, even in the absence of severesoft tissue damage or fracture displacement.

2.Patient Variables I)AGE: Infants have the most rapid rate of fracture healing. The rate of healing declines with increasing age up toskeletal maturity, but after completion of skeletalgrowth the rate of fracture healing does not appearto decline significantly with increasing age, nor doesthe risk of non-unions significantly increase. The rapid bone remodelling that accompaniesgrowth allows correction of a greater degree ofdeformity in children.

II)NUTRITION:- The cell migration and proliferation and matrix synthesisnecessary to heal a fracture require substantial energy. Furthermore, to synthesize large volumes ofcollagens, proteoglycans, and other matrixmacromolecules, the cells need a steady supply ofproteins and carbohydrates, the components of thesemolecules. As a result, the metabolic state of the patient can alter theoutcome of injury, and in severely malnourishedpatients, injuries that would heal rapidly in wellnourished people may fail to heal.

III).SYSTEMIC HORMONES: A variety of hormones can influence fracture healing. Corticosteroids may compromise fracture healingpossibly by inhibiting differentiation of osteoblasts frommesenchymal cells and by decreasing synthesis of boneorganic matrix components necessary for repair. Prolonged corticosteroid administration may alsodecrease bone density and compromise the surgeon'sability to achieve stable internal fixation, leading tononunion.

The role of growth hormone in fracture healingremains uncertain. Thyroid hormone, calcitonin, insulin, and anabolicsteroids have been reported in experimentalsituations to enhance the rate of fracture healing. Diabetes, hypervitaminosis D, and rickets have beenshown to retard fracture healing in experimentalsituations. Nicotine and nicotine products(cigarette smoking)inhibits fracture healing.

3.Tissue Variables I)FORM OF BONE(CORTICAL ORCANCELLOUS): Healing of cancellous and cortical fractures differsprobably because of the differences in surfacearea, cellularity and vascularity. Opposed cancellous bone surfaces usually uniterapidly., possibly because the large surface area ofcancellous bone per unit volume creates many pointsof bone contact rich in cells and blood supply andbecause osteoblasts form new bone directly onexisting trabeculae.

In contrast, cortical bone has a much smaller surfacearea per unit volume and usually a less extensiveinternal blood supply, and regions of necroticcortical bone must be removed before new bone canform.

II)BONE NECROSIS: Normally, healing proceeds from both sides of afracture,but if one fracture fragment has lost itsblood supply, healing depends entirely on ingrowthof capillaries from the living side or surrounding softtissues. If a fracture fragment is avascular the fracture canheal, but the rate is slower and the incidence ofhealing is lower than if both fragments have anormal blood supply.

If both fragments are avascular, the chances forunion decrease further. Traumatic or surgical disruption of blood vessels,infection, prolonged use of corticosteroids, andradiation treatment can cause bone necrosis.

Bone necrosis after a severe opentibia fracture with failure of softtissue coverage

III)BONE DISEASE: Fractures through bone involved with primary orsecondary malignancies usually do not heal if theneoplasm is not treated. Subperiosteal new bone and fracture callus mayform,but the mass of malignant cells impairs orprevents fracture healing,particularly if themalignant cells continue to destroy bone.

Fractures through infected bone present a similarproblem. Thus, healing of fractures through malignancies orinfections usually requires treatment of theunderlying local disease or removal of the involvedbone. Depending on the extent of bone involvement andthe aggressiveness of the lesion, fractures throughbones with nonmalignant conditions like simplebone cysts and Paget's disease will heal.

The most prevalent bone disease, osteoporosis, doesnot impair fracture healing, but where there isdiminished surface contact of opposing cortical orcancellous bone surfaces because of decreased bonemass, the time required to restore normal bonemechanical strength may be increased.

IV)INFECTION:- Infection can slow or prevent healing. For fracture healing to proceed at the maximum rate, thelocal cells must be devoted primarily to healing thefracture. If infection occurs after fracture or if the fracture occurs asa result of the infection, many cells must be diverted toattempt to wall off and eliminate the infection and energyconsumption increases. Furthermore, infection may cause necrosis of normaltissue, edema, and thrombosis of blood vessels, therebyretarding or preventing healing.

4.Treatment Variables Apposition of fracture fragments,decreasing thefracture gap decreases the volume of repair tissueneeded to heal a fracture. Restoring fracture fragment apposition is especiallyimportant. Fracture stabilization by traction, castimmobilization, external fixation, or internal fixationcan facilitate fracture healing by preventing repeateddisruption of repair tissue.