Tornetta Rockwood Adults 9781975137298 FINAL VERSION

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SECTION ONE • General Principles

the defect diameter grows from 10% to 20%. Increasing the defect further results in a linear decrease in strength until 60%, at which point the defect is the same diameter as the intramed- ullary canal (Fig. 1-11). 41,79,113

100

BIOMECHANICAL ASPECTS OF BONE HEALING

INTERPLAY BETWEEN BIOLOGY AND MECHANICS Fracture healing is a complex biologic and mechanical process. Although the interaction between the biologic processes and the mechanics is not fully understood, 13,46 it is clear that the mechanical environment at the fracture site largely determines the mode of fracture healing. 167 A fracture treated nonsurgi- cally or with an implant designed to allow controlled fracture motion results in “natural” bone healing with fracture callus. In the case of rigid internal fixation with directly opposed fracture ends and interfragmentary compression to prevent fracture site motion, fractures are expected to heal by “direct” bone healing. A nonunion can result either from excessive interfragmentary motion or from deficient interfragmentary motion in the pres- ence of a residual fracture gap. 48 NATURAL BONE HEALING Many mechanical factors—including the fracture geometry; the fracture type; and the direction, magnitude, and history of interfragmentary motion—affect the progression of natural bone healing. 13 A bone healing environment that allows controlled interfragmentary motion is often termed “relatively stable.” A rel- atively stable environment exists after nonsurgical stabilization with casts and fracture braces or after surgical fixation using intra- medullary nails, external fixators, or flexible plate constructs. In these situations, fracture healing progresses through well-estab- lished biologic and biomechanical stages that gradually increase the stability of the fracture by depositing tissue with progressively increasing structural qualities at the fracture site (Fig. 1-12). 126 Each biologic stage of natural bone healing includes specific

% original ultimate torque

0 10

% defect diameter/outer bone diameter

concentration at the end of the plate and placing the stress risers generated by the screw holes at different levels in the bone. Dual plate fixation is commonly used in distal humerus and proximal tibia fractures. These constructs are especially at risk for peri-implant fractures given the increased stress gradi- ent from instrumented bone to normal bone. Placing the end screws of both plates at the same level results in a higher risk of fracture than placing the screws at different levels. 105 Bone Defect and Fracture Risk Removal of plates and screws after fracture healing is rarely required. When a plate and screws are removed, the residual holes from the screws present a risk for refracture secondary to the resulting defect in bone. 112,120 These fractures may occur as a result of bending or torsion and are related to a combination of cortical stress shielding and the presence of stress risers caused by empty screw holes. 181 The reduction in torsional strength around a circular defect is related to the size of the defect. Benchtop studies suggest that holes less than 10% of the outer bone diameter cause no change in torsional strength. A large (34%) drop in strength occurs as Figure 1-11. The decrease in torsional strength with increasing corti- cal defect diameter. Defects up to 10% of the bone diameter show no decrease in ultimate strength There is a large decrease between 10% and 20%, with a linear decrease for larger defect sizes. 79

Figure 1-12. Qualitative temporal represen- tation of the tissue deposited during natural bone healing. As more mature tissue forms, the resistance to refracture increases.

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