FRACTURE HEALING

FRACTURE HEALING

It is useful to review fracture healing, as it relates to treatment and outcome. Following a fracture, bone can heal in two di ff er - ent ways: direct (primary) bone healing or indirect (secondary) bone healing. One can conceptualise direct bone healing as being akin to a wound that is stitched together whereas indirect bone healing is similar to forming a scab that over time turns ): to nor mal tissue. Through intervention, the clinician is able - to influence the healing response of the tissue: direct bone healing being more likely if the two bone ends are squeezed together (compression), and indirect healing should there be - movement (termed strain) at the fracture site. If there is too much movement, i.e. the fracture is too unstable, healing of the fracture may not occur. /uni25CF Direct bone healing , as the name implies, heals directly with bone and without callus formation. It happens in an - environment of cortical apposition and absolute stability with no movement or gap between the fracture fragments. - directed across the fracture interface. Osteoclastic cutting cones cut across the fracture line, with following osteoblasts laying down lamellar bone across the fracture. This is sim ilar to the normal remodelling process that occurs in bone all the time as part of skeletal homeostasis. /uni25CF Indirect bone healing involves a transition from one tissue to another with callus formation. It is the most common form of bone healing. Following the injury , haematoma fills the gap at the fracture site. In response to a varying strain and under the influence of bone- stimulating factors, the tissue undergoes di ff erentiation, from haematoma to fibrous tissue and then to soft callus, followed by mineralisation and formation of mature bone. The amount of strain determines the nature of tissue it di ff erentiates into: under 100% leads to fibrous tissue, under 10% soft callus, less than 2% hard callus and progressive mineralisation (Perren’s theory of bone healing). Hence a little movement is good, too much movement is bad. Bone healing requires not only an advantageous mechan ical environment but also an advantageous biological envi ronment. Principally this can be described in terms of blood supply and the preservation of blood supply from the sur rounding soft tissues, the periosteum and the nutrient arterial supply to bone. Should the inflow be a ff ected through trauma or peripheral vascular disease, or should there be an extensive soft-tissue injur y causing poor bone perfusion, bone healing can be a ff ected. Similarly , microscopic inflow issues at the tis sue perfusion level, e.g. as a result of diabetes, may also lead to poor bone healing. Infection may also create a biological insult to bone healing; therefore, open fractures with their extensive soft-tissue injury and increased probability of infection are prone to impair ed bone healing. FRACTURE HEALING

It is useful to review fracture healing, as it relates to treatment and outcome. Following a fracture, bone can heal in two di ff er - ent ways: direct (primary) bone healing or indirect (secondary) bone healing. One can conceptualise direct bone healing as being akin to a wound that is stitched together whereas indirect bone healing is similar to forming a scab that over time turns ): to nor mal tissue. Through intervention, the clinician is able - to influence the healing response of the tissue: direct bone healing being more likely if the two bone ends are squeezed together (compression), and indirect healing should there be - movement (termed strain) at the fracture site. If there is too much movement, i.e. the fracture is too unstable, healing of the fracture may not occur. /uni25CF Direct bone healing , as the name implies, heals directly with bone and without callus formation. It happens in an - environment of cortical apposition and absolute stability with no movement or gap between the fracture fragments. - directed across the fracture interface. Osteoclastic cutting cones cut across the fracture line, with following osteoblasts laying down lamellar bone across the fracture. This is sim ilar to the normal remodelling process that occurs in bone all the time as part of skeletal homeostasis. /uni25CF Indirect bone healing involves a transition from one tissue to another with callus formation. It is the most common form of bone healing. Following the injury , haematoma fills the gap at the fracture site. In response to a varying strain and under the influence of bone- stimulating factors, the tissue undergoes di ff erentiation, from haematoma to fibrous tissue and then to soft callus, followed by mineralisation and formation of mature bone. The amount of strain determines the nature of tissue it di ff erentiates into: under 100% leads to fibrous tissue, under 10% soft callus, less than 2% hard callus and progressive mineralisation (Perren’s theory of bone healing). Hence a little movement is good, too much movement is bad. Bone healing requires not only an advantageous mechan ical environment but also an advantageous biological envi ronment. Principally this can be described in terms of blood supply and the preservation of blood supply from the sur rounding soft tissues, the periosteum and the nutrient arterial supply to bone. Should the inflow be a ff ected through trauma or peripheral vascular disease, or should there be an extensive soft-tissue injur y causing poor bone perfusion, bone healing can be a ff ected. Similarly , microscopic inflow issues at the tis sue perfusion level, e.g. as a result of diabetes, may also lead to poor bone healing. Infection may also create a biological insult to bone healing; therefore, open fractures with their extensive soft-tissue injury and increased probability of infection are prone to impair ed bone healing. FRACTURE HEALING

It is useful to review fracture healing, as it relates to treatment and outcome. Following a fracture, bone can heal in two di ff er - ent ways: direct (primary) bone healing or indirect (secondary) bone healing. One can conceptualise direct bone healing as being akin to a wound that is stitched together whereas indirect bone healing is similar to forming a scab that over time turns ): to nor mal tissue. Through intervention, the clinician is able - to influence the healing response of the tissue: direct bone healing being more likely if the two bone ends are squeezed together (compression), and indirect healing should there be - movement (termed strain) at the fracture site. If there is too much movement, i.e. the fracture is too unstable, healing of the fracture may not occur. /uni25CF Direct bone healing , as the name implies, heals directly with bone and without callus formation. It happens in an - environment of cortical apposition and absolute stability with no movement or gap between the fracture fragments. - directed across the fracture interface. Osteoclastic cutting cones cut across the fracture line, with following osteoblasts laying down lamellar bone across the fracture. This is sim ilar to the normal remodelling process that occurs in bone all the time as part of skeletal homeostasis. /uni25CF Indirect bone healing involves a transition from one tissue to another with callus formation. It is the most common form of bone healing. Following the injury , haematoma fills the gap at the fracture site. In response to a varying strain and under the influence of bone- stimulating factors, the tissue undergoes di ff erentiation, from haematoma to fibrous tissue and then to soft callus, followed by mineralisation and formation of mature bone. The amount of strain determines the nature of tissue it di ff erentiates into: under 100% leads to fibrous tissue, under 10% soft callus, less than 2% hard callus and progressive mineralisation (Perren’s theory of bone healing). Hence a little movement is good, too much movement is bad. Bone healing requires not only an advantageous mechan ical environment but also an advantageous biological envi ronment. Principally this can be described in terms of blood supply and the preservation of blood supply from the sur rounding soft tissues, the periosteum and the nutrient arterial supply to bone. Should the inflow be a ff ected through trauma or peripheral vascular disease, or should there be an extensive soft-tissue injur y causing poor bone perfusion, bone healing can be a ff ected. Similarly , microscopic inflow issues at the tis sue perfusion level, e.g. as a result of diabetes, may also lead to poor bone healing. Infection may also create a biological insult to bone healing; therefore, open fractures with their extensive soft-tissue injury and increased probability of infection are prone to impair ed bone healing.