Advances in plate fixation of fractures during the past two decades include improved metallurgy, better implant design and manufacturing, new surgical techniques, and enhanced understanding of fracture biology and biomechanics. These changes have resulted in improved results and fewer complications.1 However, fixation failures still occur, and it is imperative that the surgeon scrutinize these failures in an attempt to determine their causes.
The goal of plate fixation is to restore anatomy and impart mechanical limb stability, ultimately allowing uneventful fracture healing,2 thereby promoting early joint mobility and return of function. Impaired fracture healing, prolonged pain, joint stiffness, and physical debilitation are some of the potential consequences of failed fixation.3
Plate fixation constructs have a finite number of load cycles until failure, and the objective of treatment is to achieve union before the construct fails. Fixation failure manifests in many forms, and the surgeon must recognize the different implications when determining the underlying cause. Screws may break or lose stable purchase in bone. Plate breakage or, less commonly, plastic deformation may occur. There are few objective data on the subject, but surgeon error in terms of implant choice and application is a common cause of fixation failure in the early and late postoperative periods. However, even when appropriate implants are correctly applied, nonunion with subsequent hardware failure may occur.4 Recognition of fracture patterns and fixation constructs at higher risk for failure is essential in attempting to prevent this adverse outcome.
The patient who presents with plate fixation failure should first undergo a thorough history and physical examination. Pertinent history factors include time intervals and number of prior surgeries, including review of previous surgical reports. Retained debris, periosteal stripping, or an ongoing infectious process may compromise local biology, delay or preclude union, and lead to fixation failure.
Detailed circumstances of a secondary traumatic event, accurate appraisal of the patient's activity level, and the time course of fracture site pain can assist in determining the problem. Additionally, comorbidities that were ascertained on the initial trauma evaluation should be reappraised. In particular, the patient should be evaluated for obesity, malnutrition, and nicotine use.5 Laboratory tests that quantify nutritional status should be evaluated, even in patients who are obese or appear to be well nourished, and deficiencies should be corrected when possible. Body mass index should be calculated because an elevated value may increase the risk of fixation failure.6
It is important to identify and treat any medical condition that may predispose the patient to peripheral neuropathy, such as diabetes mellitus. Systemic vasculopathic diseases can lead to compromised circulation, potentially inhibiting fracture healing and predisposing the patient to fixation failure.7 Persons with compromised immune function, such as those with chronic renal or hepatic failure, cancer, HIV/AIDS, or connective tissue disease, as well as those receiving corticosteroids or other immune modulators, are susceptible to poor tissue healing, nonunion, and fixation failure. Patients with irradiated bone are also at risk of impaired healing and poor implant purchase.8
Smoking has a dramatic effect on the healing capacity of bone and soft tissues. Cigarette smoke causes direct peripheral vasoconstriction. In one study, digital blood flow decreased by approximately 40% after smoking.9 Significant wound tissue hypoxemia is one outcome of vasoconstriction.10 The effects of smoke on tissues include decreased cell metabolic activity, poor tissue healing, and delayed neoangiogenesis.11 Compared with nonsmokers, smokers with tibial shaft fractures have increased nonunion rates and softtissue complications.12 Smoking can cause osteoporosis, thereby affecting the mechanical properties of bone.13 All of these detrimental effects of smoking may combine to represent a significant underlying cause of nonunion and fixation failure. Consideration should be given to counseling thorough cessation as well as to measuring serum or urinary nicotine concentrations to assess compliance before revision surgery. Nicotine pills, patches, or gum may have many of the same adverse effects as tobacco use on bone healing.
Patient compliance, particularly with regard to adherence to protected weight bearing, may be difficult to manage. Noncompliance as a cause of failure may involve systemic pathology, such as a psychiatric disorder14 or traumatic brain injury, or conditions in which the patient's upper extremity strength is not sufficient to support ambulation restrictions (eg, obesity). However, even when there is a history of noncompliance or a second traumatic event, the surgeon should evaluate the patient for all potential causes of failure before attributing it to noncompliance alone. The patient who is unable or unlikely to comply with weight bearing protection may be restricted to wheelchair use until fracture healing.
Physical examination also should include assessment of local erythema, elevated temperature, and skin changes, all of which may be indicative of infection. Gross motion at the fracture site provides insight into the relative stiffness of a nonunion. Limb deformity should be measured clinically in all planes. Tenderness at the fracture site may be present in the case of implant failure. The status of the soft tissues in the fracture region, including previous traumatic wounds and surgical incisions, will directly affect future reconstruction options. Adjacent joint range of motion also will determine whether arthrolysis is necessary at the time of revision fixation. Joint stiffness can place a significant amount of stress across implants used in the setting of metaphyseal nonunions.15
Laboratory tests are necessary to evaluate for metabolic diseases and infection. Primary and secondary osteoporosis affect the mechanical properties of bone and impair stable implant purchase.16 Other metabolic abnormalities (eg, vitamin D deficiency) can lead to osteomalacia, with similar effects on bone quality.4 Patient infection status (ie, never infected, previously infected, currently infected) is a critical factor in treatment planning. The serum C-reactive protein level can be useful in the diagnosis of osteomyelitis.17 Other studies, such as a tagged white blood cell scan, fracture aspiration, and intraoperative frozen sections may be helpful, but few data are available proving their efficacy.
Following these evaluations, a complete set of radiographs should be obtained, including orthogonal views incorporating the joint above and below the lesion. Stress radiographs or CT scans, with or without a scanogram, may be useful. Although most cases are obvious on presentation, the diagnosis of fixation failure is not always straightforward in the early stages. Construct instability is indicated by often subtle radiographic signs, including slight loss of fracture reduction, cavitation halos around screw shafts (ie, windshield wiper effect), and screw backout (Figure 1). Change in screw position in the bone and bending of a plate are suggestive of fixation instability. Broken screws with minimal displacement may be an early sign of fixation failure. However, this may be difficult to visualize radiographically because of implant overlap. Although a significant shift in fracture fragment position is the sine qua non of fixation failure, it is often optimistically considered “settling” into a stable position. One should be wary of this interpretation.
The surgeon should assess for a callus response that is appropriate relative to the construct type. In rigidly stabilized fractures, callus formation suggests motion at the fracture site; this may not warrant immediate treatment. Conversely, lack of callus formation in a flexible construct, such as with spanning of a comminuted metadiaphyseal fracture, may denote a failure of biology or an overly rigid construct. A proactive approach should be taken with early signs of failure. The first step is often a reduction in weight bearing. Secondary surgeries are best performed prior to catastrophic construct failure and substantial patient debilitation.
Determination of Specific Causes
A thorough patient workup may reveal potential underlying causes of failure, including systemic comorbidities, immunosuppressive medications, psychiatric issues, and local fracture variables, such as infection or osteoporosis. All failed fixation cases should be scrutinized for technical adequacy. The first determination should be whether rigid, absolute stability or flexible, relative stability was attempted. Each type of fixation technique leads to a unique healing environment, and different fixation features are required with each to achieve the best results. Newer hybrid fixation methods may offer benefits of both fixation modes.18
Absolute Versus Relative Stability
Rigid fixation is required to achieve absolute fracture stability. Anatomic reduction and compression fixation is required in articular fractures,19 and this is usually the preferred technique when plating transverse, short oblique, or simple diaphyseal and metaphyseal fractures. Insufficient construct stiffness may allow local strains to exceed the tissue tolerance for bone formation, thereby impeding healing.2 The placement of more screws per fracture fragment increases construct stiffness to a point, particularly in torsion.20 However, there are negative consequences with greater screw density. Each screw creates an additional stress riser when the implant is removed, and each drill pass through the intramedullary canal, opposite cortex, and periosteum causes additional vascular insult.2 Thus, balance needs to be struck between obtaining adequate stiffness and stability and minimizing the detrimental effects of filling every screw hole.21 Not every screw hole in a plate needs to be filled.
The length of the implant around the area of fracture that is unsupported by screws is known as the working length. This length is a major determinant of construct stiffness. With compression plating technique for simple fractures, plate stress is minimized by placing screws with maximum spacing near the fracture and at the ends of the plate (ie, near-near, far-far).21,22 In a failed construct in which absolute stability was attempted, a plate that is too short, too small, or too flexible, with associated callus formation, can signal technical shortcomings that may have contributed to the failure.21
Until recently, bridge plating techniques using more flexible plate fixation constructs were not widely employed.23,24 Several studies have clarified that minimizing soft-tissue dissection by use of indirect reduction techniques, and bridging fractures with stable, somewhat flexible fixation, may be preferable in managing many comminuted extraarticular fractures.23-25 To maintain implant stability until healing occurs, a plate of adequate length (usually as long as is anatomically reasonable) should be chosen for distribution of stresses.26 It is equally important to achieve an appropriate amount of sustained micromotion to permit callus formation. Construct stiffness should be considered when analyzing an instance of failed fixation.
Construct Stiffness and Plate Length
Construct stiffness can be controlled by many variables, including the implant material, offset from the bone, plate length, and working length. Despite the assumptions of many biomechanical studies, more rigid fixation is not always advantageous to healing.27 To allow for uneventful healing when a plate is used in a bridging application, the construct stiffness must be neither too low nor too high (Figure 2). It is possible to create a construct that is too stiff and thus allows too little fracture micromotion to lead to callus formation27 (Figure 3).
Little empiric evidence exists that is helpful in guiding construct creation with the ideal stiffness. In both locking and nonlocking constructs, at least two or three empty plate holes at the fracture site are typically necessary to allow adequate construct flexibility when bridging a fracture; two or three holes also are needed to avoid stress concentration on the plate that could lead to early plate failure.28 The constraints of the fracture pattern dictate many aspects of the fixation. The ideal number and spacing of screws to allow for successful bridge plating has yet to be fully delineated in a biologic model, and additional research is necessary before definitive recommendations can be made.
Regardless of the surgical technique used, the selected implant must have inherent strength that is adequate for the anatomic region in which the fracture is located. Prior to any revision procedure, the surgeon should determine whether the appropriate implant was used in the initial surgery. For example, although reconstruction plates allow for easy contouring, they are relatively flexible and generally should be avoided for diaphyseal bones, even smaller bones such as the humerus and those of the forearm.28
Plate length is extremely important; this is another parameter that should be closely analyzed in a failed construct. A relatively long plate can effectively disperse forces, thereby transferring less stress to the end screws, resulting in increased overall construct strength.20,21 When a longer plate is used as a neutralization plate in a construct requiring absolute stability, fewer screws are necessary to achieve greater strength, as long as they are widely spaced.21,22,26 Similarly, in fracture bridge plating, a longer plate leads to a stronger construct with regard to overall maintenance of implant purchase.26 The fracture site stiffness depends in part on the number of screws, either locking or nonlocking, and the working length.20,22,29 Local anatomy and potentially increased soft-tissue dissection also must be taken into account when deciding on plate length.
Plate breakage at the fracture site may be caused by an excessively long working length, leading to insufficient stiffness and thereby resulting in large plate deviations and early fatigue failure. Biologic failure must also be considered in this setting. Conversely, screws placed very close on either side of the fracture, particularly in the setting of far cortex comminution, may concentrate stress on the plate and cause failure at the level of an empty plate hole. Many cases of screw pullout or catastrophic failure are caused by placement of an implant of inadequate length that did not effectively absorb and transfer force to the end screws.
Stiffness mismatch between implant and bone may cause secondary fracture at the end of the plate. When an overly stiff implant is applied, as when too many screws are used, the stress at the level of transition may lead to failure30 (Figure 4). Because locking screws can increase the construct stiffness,18 stress concentration may be exaggerated. Alternatively, too many screws and a significant stiffness mismatch between the plate and bone can impair callus formation.31 Both of these scenarios occur frequently in osteoporotic bone because the pathophysiology changes the mechanical properties of the bone, which includes decreasing its stiffness.32 The surgeon must be aware that although increasing the number of screws can increase the total surface area of implant purchase,2 this also leads to a potentially detrimental increase in overall construct stiffness.
Locked plating represents a novel biomechanical approach for fracture fixation and has clear advantages in certain situations.2,18,29,33 A key principle in the use of locking plates is to follow the correct temporal sequence; reduction must be obtained before locking screws are placed.31 However, maintaining focus on the order of the technical steps and implant application should not overshadow the most critical technical aspect—reduction accuracy. The angular stability obtained between the screw and plate can function as a surrogate cortex; however, this feature should not be relied on to overcome an imperfect fracture reduction.
As with standard plates, locking plates can fatigue and fail when the bone is unable to assume timely load transmission. In particular, fractures with associated medial comminution have a tendency to fail in varus, such as in the proximal humerus, proximal femur, and proximal tibia.34,35 Laterally based locking plates offer a potential solution for the stabilization of difficult metadiaphyseal fractures.1
Aside from these specific indications, locking plates should be used judiciously. The necessity of a fixedangle device should be carefully considered and their use well thought out. These devices should not be used by default. Clinical scenarios such as osteoporosis and comminuted metaphyseal fractures with short end segments may benefit from fixed-angle stabilization. Additionally, open fractures may be at risk for prolonged union time, and locked plating may be indicated. The increased cost of locking plates may be justified by their ability to offer more stable and durable fixation in these situations.36 Locking plates are generally not necessary in patients younger than age 50 years who have healthy bone. Additionally, in simple fractures and partial articular fractures (ie, AO/OTA type B), locking plates are unnecessary and may be detrimental (Figure 5).
Stoffel et al29 provided several recommendations for the use of locking plates in bridging mode in the femur or tibia. One such recommendation involves using three screws on either side of the fracture, with two screws as near as possible to the fracture. In the humerus and forearm, where torsional forces are more prominent, three or four screws should be used on each side.29 However, these experiments were performed in a surrogate healthy bone model, with titanium plates and unicortical screws. Thus, these recommendations may not be universally applicable to the use of stainless steel bicortical screws in osteoporotic bone. Other authors recommended that three or four screw holes be left open over the bridged fracture segment to minimize focal plate stresses.36 Unicortical screws alone should not be used for diaphyseal fixation37 (Figure 6).
Failed locking constructs should be analyzed specifically for plate span width, working length, and screw density.31 Plate span width (plate length divided by fracture length) should be >2 to 3 in comminuted fractures36 and >8 to 10 when a locked plate is used for neutralization of a simple fracture pattern (Figure 7). When long plates are used for neutralization of simple fracture patterns, transverse or short oblique fractures must be adequately compressed to avoid excessive fracture site and plate strain. Ideally, the screw density (the number of screws divided by the number of plate holes) should be <0.4 to 0.5.38 Deviations from these principles can lead to fixation failure of locking plates.
Treatment of Failed Fixation
Surgical management of failed fixation can be especially arduous, and early recognition and treatment of the construct at risk is essential. The risk of catastrophic fixation failure can be minimized by adhering to sound biologic and mechanical principles at the index procedure, or with timely intervention when detected early in the postoperative period. Surgery to correct fixation failure must be meticulously planned and executed, and several biologic and mechanical factors must be considered.
The most important prerequisite for obtaining sound fracture union following fixation failure is adequate fracture site vascularity. Frequently, the local biology is compromised by traumatic softtissue injury, one or more previous surgical approaches, infection, or patient systemic disease. In planning for a revision procedure, a general assessment should be made of the biologic impairment. Poor fracture site vascularity may be indicated by atrophic-appearing fracture radiographs. The proposed intervention should take these factors into consideration. Timing, surgical approaches, fracture visualization, and reduction techniques should be planned such that any remaining vascularity is maintained and disruption of the periosteal cortical perfusion is minimized.
For a fracture site that appears to be atrophic, one or several methods of biologic augmentation should be applied, either at the time of implant revision or during a separate stage. Historically, autogenous bone grafting has been the preferred option.39 The iliac crest is the most popular donor site because of the high volume of progenitor cells as well as the availability of cancellous and cortical bone. However, the patient should be counseled on the potential risk of significant morbidity, including protracted pain, iatrogenic fracture, and nerve injury.40 Other available donor sites include the distal femur, proximal tibia, and calcaneal tuberosity. More recently, the Reamer/Irrigator/Aspirator (RIA; Synthes, West Chester, PA) was developed to harvest intramedullary bone graft. Early results are encouraging.41 Other forms of biologic enhancement, such as bone marrow aspirate, demineralized bone matrix, platelet-rich plasma, and bone morphogenetic proteins, may be used alone or in combination.42
Bone grafting may be required in the setting of segmental defect following reconstruction. Determining the optimal timing for bone grafting can be difficult. History of infection, physical examination, C-reactive protein concentration, peripheral erythrocyte sedimentation rate, and intraoperative Gram stain or frozen section are factors to consider when deciding whether bone grafting at the time of the initial revision is advisable.
Management of dead space with antibiotic-impregnated cement or calcium sulfate beads has been shown to be extremely effective in conjunction with a staged approach.43 Alternatively, an antibiotic cement rod can be used in the diaphysis and may provide a limited amount of fracture stabilization.44 Masquelet pioneered the use of a cement spacer in bone defects to induce the development of a pseudosynovial membrane around the spacer.45 The membrane that forms is rich in osteoinductive and other growth factors. This technique may be an excellent option for segmental defect reconstruction in appropriately selected cases.
Restoration of the mechanical limb axis is a top priority in reconstruction. This may require osteotomy, with direct or indirect reduction techniques. The femoral distractor is a powerful tool that provides a significant mechanical advantage and makes it possible to achieve correction in multiple planes simultaneously. Well-contoured compression plates and, in some cases, fixed-angle plates, can be used for indirect reduction provided that adequate preoperative planning has been performed. Intraoperative plain radiographs are invaluable in accurately assessing limb alignment.
After malalignment correction is addressed, an appropriate method of stabilization should be selected. The specific features of the failed construct should be taken into account with the proposed revision construct. Hardware removal, re-reduction, and plate fixation with a longer or stouter implant is often appropriate for management of acute failure of a plate construct.
Particular attention should be paid to failure of laterally based plates in the presence of medial comminution. For example, comminuted distal femoral fractures and bicondylar tibial plateau fractures have historically had a high rate of late varus deformity when stabilized with laterally applied standard plates.35 Failed plate fixation associated with opposite-side comminution may occur in other anatomic areas, as well. Although lateral locking plates may provide adequate fixation in these fracture patterns, supplemental medial fixation may be required, such as placement of an additional medial plate in the distal femur35 (Figure 8). Also, an oblique screw can be angled toward the medial femoral condyle to function as a more vertical strut.46 In proximal humeral fractures with medial metaphyseal comminution, use of a lateral locking plate alone has led to a high rate of loss of reduction.3,34 Focused reconstruction of the medial column with inferomedially placed calcar screws or fibular allograft may improve stabilization34,47 (Figure 9). Other general techniques for reconstruction in the setting of failed plate fixation with medial comminution include structural bone grafting and endosteal plating (Figure 10).
Morphologic changes in osteoporotic bone include thinned cortices, decreased trabecular density, and decreased stiffness.32 Because these changes alter the structural and mechanical properties of bone, associated fractures can be considered to be pathologic.16 Affected patients are usually elderly and may have concomitant impaired balance, vision, and cognition, all of which affect the ability to comply with weightbearing restrictions. These factors have direct implications in planning fracture fixation techniques. Little is known about the direct effects of osteoporosis on fracture healing; however, experimental models have shown a disturbance in the development of callus strength.48
To avoid fixation failure in osteoporotic bone, the surgeon should focus on minimizing implant strain and improving screw holding power.16 Rigid metal implants are not adapted to the altered biomechanical properties of osteoporotic bone; thus, more flexible fixation methods, such as tension band constructs, antiglide plating, and intramedullary nails, are recommended to minimize the bone-implant interface stresses.
Fractures resulting from osteoporosis frequently involve metaphyseal areas of bone.16 These areas are affected by clinically significant osteopenia earlier than cortical bone because of the greater trabecular surface area, which undergoes more rapid bone turnover. Achieving direct cortical contact during reduction is important in minimizing the stresses borne by the implants. To obtain such contact, it may be preferable to impact the fracture into a stable position and accept a slight limb-length discrepancy rather than maintain anatomic length and bridge the associated comminution, particularly in the upper extremity. Plate fixation involving cortical contact results in threefold less construct strain than does fracture-spanning fixation.22 It is especially helpful when cortical contact is achieved opposite the plate.49 Far cortical contact allows the plate to act as a tension band rather than a pure bridge. In plating osteoporotic fractures, it is particularly important to use a long implant with screws both near to and far from the fracture to minimize stress concentration. Long plates also afford some protection from future fragility fracture along the diaphysis, in a manner similar to that provided by a full-length intramedullary device.
Resistance to screw pullout, or holding power, is related to the quality of bone, length of thread purchase, and thread diameter.50 Thinned cortices in osteoporotic bone directly reduce screw holding power by diminishing the length of thread purchase.16 The effect of varying thread diameter is lost when the mineral density of the bone is <0.4 gm/cm2.51 When possible, the surgeon should place the screws so that they engage cortical bone rather than rely on tenuous fixation in the thinned trabecular bone found in the metaphysis. Novel approaches include use of fibular allograft, filling the intramedullary canal with Kirschner wires to gain an interference fit, and use of endosteal plates to recreate the opposite cortex to decrease the likelihood of implant failure.
In contrast to “normal” bone, in which the length of the screw protruding beyond the far cortex has little effect on screw holding power, fixation of self-tapping screws in osteoporotic bone is maximal when the screw protrudes ≥2 mm beyond the far cortex.52 Although obtaining maximal pullout resistance should be the goal, placement of “proud” screws may cause local problems unrelated to fracture healing, such as painful hardware prominence in areas with little muscular protection. Locked plating also provides a potential advantage in osteoporotic fractures, provided the reduction is optimized.36
Several techniques have been developed to improve screw purchase and pullout strength in osteoporotic bone. Augmentation with polymethylmethacrylate or calcium phosphate cement, using the interstitial mechanical intrusion of the cement into the cancellous architecture, creates a strong composite, which is especially helpful when fixation is reliant on purchase in cancellous bone.53 This technique can add complexity to revision procedures should failure occur. Caution must be exercised when placing the cement to avoid extrusion into the fracture gap itself.
Reasons for fixation failure vary widely and may be multifactorial. In planning subsequent treatment, it is imperative that the surgeon attempt to discern the cause of failure. Contributors to implant failure may include systemic patient comorbidities, local pathology at the fracture site, surgeon technical error, and patient postoperative noncompliance. Patients frequently have several variables predisposing them to failure. Early and appropriate recognition of fractures and fracture fixation constructs at risk, analysis of the root cause of failure, greater awareness of common causes of failure, and a thorough workup will allow the surgeon to maximize the chance of successful treatment. Structural and biologic alterations in osteoporotic bone demand adherence to specific principles of plate fixation, including the use of full-length implants, locking constructs, bicortical screws, possible cement augmentation, and stable and accurate fracture reduction.
Evidence-based Medicine: Levels of evidence are listed in the table of contents. In this article, no level I studies are cited. Level II studies include references 8-13, 18-22, 27, 29, 30, 33, 37, 41, 42, 45, 48, and 50-53. Level IV studies include references 1, 3, 4, 6, 14, 15, 24, 26, 28, 34, 35, 39, 40, 43, 44, 46, and 47. References 2, 5, 7, 16, 17, 25, 31, 32, 36, 38, and 49 are level V studies.
Citation numbers printed in bold type indicate references published within the past 5 years.
Kregor PJ, Stannard JA, Zlowodzki M, Cole PA: Treatment of distal femur fractures using the less invasive stabilization system: Surgical experience and early clinical results in 103 fractures. J Orthop Trauma
2. Perren SM: Evolution of the internal fixation of long bone fractures: The scientific basis of biological internal fixation. Choosing a new balance between stability and biology. J Bone Joint Surg Br
Owsley KC, Gorczyca JT: Fracture displacement and screw cutout after open reduction and locked plate fixation of proximal humeral fractures [corrected]. J Bone Joint Surg Am
Brinker MR, O'Connor DP, Monla YT, Earthman TP: Metabolic and endocrine abnormalities in patients with nonunions. J Orthop Trauma
Lynch JR, Taitsman LA, Barei DP, Nork SE: Femoral nonunion: Risk factors and treatment options. J Am Acad Orthop Surg
6. Böstman OM: Body-weight related to loss of reduction of fractures of the distal tibia and ankle. J Bone Joint Surg Br
Wukich DK, Kline AJ: The management of ankle fractures in patients with diabetes. J Bone Joint Surg Am
8. Widmann RF, Pelker RR, Friedlaender GE, Panjabi MM, Peschel RE: Effects of prefracture irradiation on the biomechanical parameters of fracture healing. J Orthop Res
9. Akishima S, Matsushita S, Sato F, et al: Cigarette-smoke-induced vasoconstriction of peripheral arteries: Evaluation by synchrotron radiation microangiography. Circ J
10. Jensen JA, Goodson WH, Hopf HW, Hunt TK: Cigarette smoking decreases tissue oxygen. Arch Surg
Gullihorn L, Karpman R, Lippiello L: Differential effects of nicotine and smoke condensate on bone cell metabolic activity. J Orthop Trauma
Castillo RC, Bosse MJ, MacKenzie EJ, Patterson BM, LEAP Study Group: Impact of smoking on fracture healing and risk of complications in limbthreatening open tibia fractures. J Orthop Trauma
13. Cornuz J, Feskanich D, Willett WC, Colditz GA: Smoking, smoking cessation, and risk of hip fracture in women. Am J Med
Crichlow RJ, Andres PL, Morrison SM, Haley SM, Vrahas MS: Depression in orthopaedic trauma patients: Prevalence and severity. J Bone Joint Surg Am
Gardner MJ, Toro-Arbelaez JB, Harrison M, Hierholzer C, Lorich DG, Helfet DL: Open reduction and internal fixation of distal femoral nonunions: Long-term functional outcomes following a treatment protocol. J Trauma
16. Cornell CN: Internal fracture fixation in patients with osteoporosis. J Am Acad Orthop Surg
Patzakis MJ, Zalavras CG: Chronic posttraumatic osteomyelitis and infected nonunion of the tibia: Current management concepts. J Am Acad Orthop Surg
Gardner MJ, Griffith MH, Demetrakopoulos D, et al: Hybrid locked plating of osteoporotic fractures of the humerus. J Bone Joint Surg Am
19. Brown TD, Anderson DD, Nepola JV, Singerman RJ, Pedersen DR, Brand RA: Contact stress aberrations following imprecise reduction of simple tibial plateau fractures. J Orthop Res
20. Törnkvist H, Hearn TC, Schatzker J: The strength of plate fixation in relation to the number and spacing of bone screws. J Orthop Trauma
21. Sanders R, Haidukewych GJ, Milne T, Dennis J, Latta LL: Minimal versus maximal plate fixation techniques of the ulna: The biomechanical effect of number of screws and plate length. J Orthop Trauma
22. Ellis T, Bourgeault CA, Kyle RF: Screw position affects dynamic compression plate strain in an in vitro fracture model. J Orthop Trauma
23. Mast JW, Jakob R, Ganz R: Planning and Reduction Technique in Fracture Surg
ery. Berlin, Germany, Springer, 1989.
24. Kinast C, Bolhofner BR, Mast JW, Ganz R: Subtrochanteric fractures of the femur: Results of treatment with the 95 degrees condylar blade-plate. Clin Orthop Relat Res
25. Gerber C, Mast JW, Ganz R: Biological internal fixation of fractures. Arch Orthop Trauma Surg
26. Rozbruch SR, Müller U, Gautier E, Ganz R: The evolution of femoral shaft plating technique. Clin Orthop Relat Res
Epari DR, Kassi JP, Schell H, Duda GN: Timely fracture-healing requires optimization of axial fixation stability. J Bone Joint Surg Am
Sommer C, Babst R, Müller M, Hanson B: Locking compression plate loosening and plate breakage: A report of four cases. J Orthop Trauma
29. Stoffel K, Dieter U, Stachowiak G, Gächter A, Kuster MS: Biomechanical testing of the LCP: How can stability in locked internal fixators be controlled? Injury
30. Gautier E, Perren SM, Cordey J: Strain distribution in plated and unplated sheep tibia an in vivo experiment. Injury
2000; 31(suppl 3):C37-C44.
31. Wagner M: General principles for the clinical use of the LCP. Injury
2003; 34(suppl 2):B31-B42.
Chao EY, Inoue N, Koo TK, Kim YH: Biomechanical considerations of fracture treatment and bone quality maintenance in elderly patients and patients with osteoporosis. Clin Orthop Relat Res
Gardner MJ, Brophy RH, Campbell D, et al: The mechanical behavior of locking compression plates compared with dynamic compression plates in a cadaver radius model. J Orthop Trauma
Gardner MJ, Weil Y, Barker JU, Kelly BT, Helfet DL, Lorich DG: The importance of medial support in locked plating of proximal humerus fractures. J Orthop Trauma
35. Sanders R, Swiontkowski M, Rosen H, Helfet D: Double-plating of comminuted, unstable fractures of the distal part of the femur. J Bone Joint Surg Am
Smith WR, Ziran BH, Anglen JO, Stahel PF: Locking plates: Tips and tricks. J Bone Joint Surg Am
Fulkerson E, Egol KA, Kubiak EN, Liporace F, Kummer FJ, Koval KJ: Fixation of diaphyseal fractures with a segmental defect: A biomechanical comparison of locked and conventional plating techniques. J Trauma
38. Gautier E, Sommer C: Guidelines for the clinical application of the LCP. Injury
39. Borrelli J Jr, Prickett WD, Ricci WM: Treatment of nonunions and osseous defects with bone graft and calcium sulfate. Clin Orthop Relat Res
40. Goulet JA, Senunas LE, DeSilva GL, Greenfield ML: Autogenous iliac crest bone graft: Complications and functional assessment. Clin Orthop Relat Res
Hammer TO, Wieling R, Green JM, Südkamp NP, Schneider E, Müller CA: Effect of re-implanted particles from intramedullary reaming on mechanical properties and callus formation: A laboratory study. J Bone Joint Surg Br
De Long WG Jr, Einhorn TA, Koval K, et al: Bone grafts and bone graft substitutes in orthopaedic trauma surgery: A critical analysis. J Bone Joint Surg Am
43. Ueng SW, Wei FC, Shih CH: Management of femoral diaphyseal infected nonunion with antibiotic beads local therapy, external skeletal fixation, and staged bone grafting. J Trauma
44. Paley D, Herzenberg JE: Intramedullary infections treated with antibiotic cement rods: Preliminary results in nine cases. J Orthop Trauma
Pelissier P, Masquelet AC, Bareille R, Pelissier SM, Amedee J: Induced membranes secrete growth factors including vascular and osteoinductive factors and could stimulate bone regeneration. J Orthop Res
46. Simonian PT, Thompson GJ, Emley W, Harrington RM, Benirschke SK, Swiontkowski MF: Angulated screw placement in the lateral condylar buttress plate for supracondylar femoral fractures. Injury
Gardner MJ, Boraiah S, Helfet DL, Lorich DG: Indirect medial reduction and strut support of proximal humerus fractures using an endosteal implant. J Orthop Trauma
McCann RM, Colleary G, Geddis C, et al: Effect of osteoporosis on bone mineral density and fracture repair in a rat femoral fracture model. J Orthop Res
49. Schatzker J: Fractures of the distal femur revisited. Clin Orthop Relat Res
Seebeck J, Goldhahn J, Morlock MM, Schneider E: Mechanical behavior of screws in normal and osteoporotic bone. Osteoporos Int
51. Turner IG, Rice GN: Comparison of bone screw holding strength in healthy bovine and osteoporotic human cancellous bone. Clin Mater
Battula S, Schoenfeld A, Vrabec G, Njus GO: Experimental evaluation of the holding power/stiffness of the selftapping bone screws in normal and osteoporotic bone material. Clin Biomech (Bristol, Avon)
Collinge C, Merk B, Lautenschlager EP: Mechanical evaluation of fracture fixation augmented with tricalcium phosphate bone cement in a porous osteoporotic cancellous bone model. J Orthop Trauma