Total hip arthroplasty (THA) is a successful procedure that has improved patients’ quality of life dramatically.24 However, osteolysis has been recognized as a major limitation to the long-term survival of THA.28,38,56 Revision hip arthroplasty consumes greater healthcare resources at all stages of the process. Preoperatively, patients tend to be more disabled than patients having primary THA and rely on others for help with activities of daily living.47 Intraoperatively, patients having revision THA require a more complex procedure, usually requiring more costly implants and longer anesthesia and operative time. Postoperatively, these patients have a higher rate of complications and a longer rehabilitation time.
The most challenging aspect of revision hip surgery is the treatment of bone loss, which often can be attributed to osteolysis. Osteolysis is defined clinically as the process of progressive destruction of periprosthetic bone, characterized on serial radiographs as progressive radiolucent lines and/or cavitation at the implant-bone or cement-bone interface.9 Without surgical or medical management, osteolysis can progress to aseptic loosening and catastrophic failure of the implant. Medical or surgical treatment of osteolysis and the timing of the treatment are largely unknown.
Etiology
Osteolysis initially was referred to as cement disease because it was thought to be the result of fragmented cement.32 We now know it is an inflammatory response to polyethylene (PE) and metallic wear debris.27 Although many patients with osteolysis may have few or no clinical symptoms, as the process progresses and additional host bone stock is destroyed, implant loosening or periprosthetic fracture can occur. Osteolysis is a multifactorial process we characterize as stemming from host, prosthesis, and surgical factors.
Host Factors
Polyethylene wear and the subsequent development of periprosthetic osteolysis are the major factors limiting the longevity of THAs. Sochart,58 in a retrospective study, concluded that the 20-year survivorship of acetabular components was less than 30% if the wear rate was greater than 0.2 mm per year.
Devane et al14 reported wear rates for 108 consecutive hips and described significantly greater volumetric wear rates in the younger patients, probably because of the higher activity level.
Schmalzried et al53 studied the walking activity of patients after THA by using a pedometer and concluded that individual differences in the activity of the patient can be a substantial source of variability in rates of PE wear. However, there seems to be little association between wear rates and the demographic variables of obesity and gender. There also is little support for the notion that systemic comorbidities such as seropositive arthropathies, diabetes, vascular disease, collagen disease, and immunosuppression are causative of osteolysis after joint arthroplasty.5 However, there is evidence that hypertrophic osteoarthritis may be associated with resistance to osteolysis.34
Evans17 was one of the first researchers to suggest that metal sensitivity may contribute to aseptic loosening. However, this was not reported to be associated with loosening in subsequent studies.6,45
Prosthetic Factors
Various particle generators in THA have been reported including PE, metal debris from the femoral head and neck interface, and cement debris.16 The billions of submicron wear particles that are generated at the material interfaces are the cause of osteolysis. The most common particle in the periprosthetic tissues is PE, which predominantly is generated by Mode 1 wear. There are four modes of wear: (1) Mode 1 wear results from motion occurring between the two primary bearing surfaces, as intended, such as the prosthetic femoral head moving against the PE acetabular bearing surface; (2) Mode 2 refers to the condition of a primary bearing surface moving against a secondary surface which is not intended, for example, when a femoral component penetrates the PE and rubs against the acetabular shell; (3) Mode 3 refers to the situation where the primary surfaces have a third-body particle interposed, such as cement; and (4) Mode 4 refers to two secondary (nonprimary) surfaces rubbing together as occurs in backside wear.49
The remaining particles in the periprosthetic tissues include polymethylmethacrylate (PMMA), Co alloy, and Ti alloy particles. Scanning electron microscopy (SEM) studies of periprosthetic tissues have shown that 70% to 90% of the recovered particles are submicrometer PE particles, with a mean size of approximately 0.5 μm.2
Some implants (such as patch-coated components) have been implicated in aiding the process of osteolysis by allowing the joint fluid carrying submission PE particles to reach the diaphysis. This process leads to distal progressive osteolysis and early implant loosening.18,40,61
Designs with circumferential porous coating provide a more effective seal against distal migration of debris and fluid, provided that ingrowth occurs. However, osteolysis still can occur at the level of the greater and lesser trochanter and metaphyseal area if there is a mismatch (incomplete filling) between the stem and the metaphyseal canal.
Surgical Factors
Charnley medialized the center of rotation of the prosthetic joint by medializing the acetabular cup, which is theorized to decrease the joint reaction forces and ultimately reduce PE wear rates.27 Wear rates can be improved (decreased) by increasing the femoral offset, thereby increasing the abductor lever arm moment.27 There is evidence that acetabular position also plays an important role in wear debris and loosening. Vertical positioning of the acetabular component can cause peripheral impingement, dislocation, and accelerated third body debris.33 Schmalzried et al52 showed that osteolysis of the ilium was associated with a lateral opening of the acetabular component of 50° or greater in relation to the horizontal.
There is no evidence in the literature to support the association between surgical approaches of the hip and the varying rates of femoral osteolysis. During exposure and closure, the most important factor is to maintain a clean operating field free from third bodies, such as loose bits of bone and cement that will produce wear debris. Thorough irrigation of the field, especially the bearing surface, is essential to prevent third-body wear.27
Pathophysiology
The established paradigm that explains periprosthetic osteolysis is that wear debris particles stimulate the synthesis of proinflammatory factors (cytokines and prostaglandins). These factors initiate a cascade of events that ultimately lead to the final effectors of bone metabolism, receptor activator of nuclear factor kappa B ligand (RANKL) and osteoprotegerin (OPG), which then trigger osteoclastic activity; the osteolytic process then occurs.26 Receptor activator of nuclear factor kappa B ligand is a membrane-bound and soluble cytokine that is expressed by stromal and inflammatory cells in response to resorptive signals, and is required for osteoclast formation and activity. Osteoprotegerin is a soluble decoy receptor that binds to RANKL and prevents it from activating RANK in osteoclast precursors and mature osteoclasts. Therefore, osteolysis occurs as a consequence of increased RANKL production by periprosthetic tissues and decreased OPG production in the bone microenvironment that leads to osteoclastic bone resorption. Another important component of osteolysis is the inhibition of osteoblast function, which is mediated by the wear particles that trigger the proinflammatory cytokines.13 Although they are less important than osteoclasts and osteoblasts, mast cells and macrophages also can produce metalloproteinases (collagenase, gelatinase, and stromelysins) capable of direct bone destruction and, on their death, liberate lysosomal enzymes that have a similar toxic effect on the bone. The net result is progressive bone loss.29
The theory of effective joint space also plays a major role in the development of osteolysis. Effective joint space is defined as the periprosthetic region that is accessible to joint fluid. Wear particles are dispersed along the effective joint space, into bone, and the soft tissues. Joint fluid flow patterns influence the shape and extent of osteolysis. The local concentration of particles is a factor in the local inflammatory reaction and degree of bone resorption in that location. As bone is resorbed and a larger space is produced, encouraging preferential flow of the joint fluid and the wear particles into that location, which fuels additional bone resorption in that area. If the rate of particle production is low, or if the joint fluid is distributed more evenly, the rate of bone resorption is slower and is accompanied by a fibroblastic response, which results in a more linear pattern of bone loss that often follows the contours of the implant.50
After osteolysis occurs, it may cause loosening of implant, which will cause more debris and the vicious cycle then recurs (Fig 1).
;)
Fig 1.:
The wear debris cycle is shown.
Clinical Presentation
Initially, patients may have no clinical symptoms despite radiographic evidence of osteolysis and can remain completely asymptomatic even with substantial bone loss.16 Symptoms usually do not occur until the bone loss has reached the point of implant loosening, implant failure (fracture), or periprosthetic fracture. Patients may present with pain secondary to synovitis secondary to wear debris. In femoral osteolysis, the pain usually is localized to the thigh; pain in the groin or buttocks is associated more often with acetabular disorders. Pain caused by component loosening typically is associated with activity, especially ambulation, and abates with rest. A periprosthetic fracture typically has a sudden onset of pain with activity.
Signs associated with implant loosening and implant fracture may include shortening of the extremity and external rotation. During physical examination, it may be possible to piston the implant in the femoral canal. Sanchez-Sotelo et al48 and Chatoo et al10 reported spontaneous fracture of the pelvis through extensive osteolytic lesions.
Radiographic Evaluation
Cemented Femoral Component
The development of either focal or linear osteolysis depends primarily on the access of particulate debris and joint fluid to the periprosthetic environment.9 Early cementing techniques (first generation) were associated with circumferential osteolysis. A cementing technique that produces a homogeneous mantle effectively seals the implant from access of fluid and particulate debris generated. Figure 2 shows osteolysis at the cement-bone interface in a cemented femoral component.
Fig 2.:
Definite signs of loosening of the cemented stem are evident by a radiolucent line at the cement-bone interface.
Radiographic signs of loosening are divided into three categories: (1) definite loosening, evidenced by migration of the component or cement column, including subsidence of the component or cement-component complex; other findings include progressive varus positioning, fracture or fragmentation of the cement, and, occasionally, fracture or deformation of the femoral component; (2) probable loosening, which entails a complete radiolucent zone around the cement-bone interface seen on at least one radiograph; and (3) possible loosening, which describes a radiolucent zone occupying more than 50% but less than 100% of the cement-bone interface.9
Uncemented Femoral Component
Design of the implant seems to play a significant role in the radiologic appearance of osteolysis. Implants with patch porous coating provide low-resistance pathways for debris and fluid to travel, resulting in middle to distal focal osteolysis. Designs with circumferential porous coating provide an effective seal against distal migration of debris and fluid, provided that ingrowth occurs.
Stability can be gauged by formation of new bone between the porous coating and the endosteal surface (osteointegration). The major signs of osteointegration include the absence of motion-induced reactive lines around the porous coating, the absence of pedestal formation at the tip of the implant, and the presence of spot-welds. Stress shielding is an absolute indicator of osseous integration. Proximally coated implants are designed for proximal fixation; however, if ingrowth fails to occur, debris and fluid can gain access to the diaphysis through the noningrowth regions. Figure 3 shows osteolysis at the metaphyseal area in a circumferential proximally coated stem. When circumferential bone ingrowth does not occur, fibrous ingrowth stabilization may result, with reactive lines adjacent to the implant. The fibrous tissue may provide a partial barrier to the fluid and debris in the effective joint space. If osteolysis occurs, it tends to be linear, producing an expanding linear line around the component with progressive loss of diaphyseal bone.
Fig 3.:
Focal osteolysis is evident at the metaphyseal area (greater and lesser trochanter) in an uncemented proximally coated femoral stem.
Cemented Acetabular Component
Osteolysis in cemented acetabular components most often is the linear type at the cement-bone interface, therefore acetabular components usually loosen at the cement-bone interface and rarely loosen at the implant-cement interface. The fibrous layer that forms between the cement and bone in cemented acetabular components may limit the migration of wear particles, resulting in a more linear pattern of pelvic osteolysis. Signs of a loose cemented acetabular component include: a radiolucent zone surrounding the entire component perimeter, superomedial migration of the cup and cement (socket break-in), fracture of the acetabular bone stock, and changes in the degree of inclination or version of the component seen on serial radiographs (socket break-out). Figure 4 shows severe osteolysis of the cemented cup with migration of the cup.
Fig 4.:
The radiograph shows migration of cemented cup.
Uncemented Acetabular Component
Pelvic osteolysis associated with uncemented cups is more localized and expansive than that associated with cemented components. Polyethylene backside wear and the existence of screw holes may contribute to pelvic osteolysis. Figure 5 shows osteolysis in an uncemented cup. A loose uncemented acetabular component commonly is associated with socket migration, screw breakage, defoliation of the porous surface, and fracture of the metal shell.
Fig 5.:
Osteolysis (expansile type) can be seen around an uncemented acetabular component.
Fig 6.:
The treatment algorithm we use for acetabular osteolysis is shown.
Medical Treatment of Osteolysis
Based on the etiology of osteolysis, extensive research has been done to find a therapeutic intervention for this condition. This work has been focused in two directions: inhibition of proinflammatory signals and antiosteoclast activity. The initial quest to identify a drug to prevent or retard progression of osteolysis led to investigation of PG, which was the first proinflammatory mediator identified to be highly expressed in periprosthetic membranes.19 Early animal studies that used nonselective NSAIDs (naproxen),20,21 and a more recent study that used selective cyclooxygenase (COX) inhibitors and mice genetically deficient in COX-1 and COX-2,65 clearly defined the COX-2, PGE2 pathway as critical to wear debris-induced osteolysis. Unfortunately, the value of COX-2 inhibition for its antiresorptive effects is counterbalanced by its inhibitory effects on osteoblasts and bone formation.66 These adverse effects were foreshadowed in part by the successful use of NSAIDs after total joint replacement to prevent heterotopic bone formation.
Another approach toward identifying drug targets for aseptic loosening has been elucidation of the signal transduction pathways that become activated in inflammatory cells after particle stimulation. One of these pathways involves the activation of protein kinase A via cyclic AMP, which leads to tumor necrosis factor-alpha (TNF-α) production.4 Pollice et al43 studied the effect of pentoxifylline on the treatment of osteolysis. Pentoxifylline (Trental; Aventis, Bridgewater, NJ) is a methylxanthine-derived drug that has been used for more than 20 years for treatment of peripheral vascular disease. Pentoxifylline also is a potent inhibitor of TNF-α secretion, in vitro and in vivo, and has shown efficacy in the treatment of certain animal and human inflammatory diseases.5,15 Pentoxifylline has a potential therapeutic role in the treatment of aseptic loosening of total joint replacement components because it inhibits TNF-α secretion by particle-stimulated human peripheral blood monocytes. In the study by Pollice et al,43 the purpose was to determine whether the particle-stimulated secretion of TNF-α by peripheral blood monocytes was inhibited in volunteers who had received pentoxifylline orally.
They concluded that their study was the first to show the ability of an oral drug to decrease the release of TNF-α from human peripheral blood monocytes exposed ex vivo to particle debris.43 The ability to suppress the release of TNF-α in patients with a total joint replacement may help control osteolysis and reduce development of aseptic loosening. This effect could increase implant longevity and decrease the need for revision arthroplasty.
The revolution in molecular biology that occurred in the last decade provided researchers with critical tools to elucidate the role of a particular gene in a disease process. With this technology, the dominant role of TNF-α was elucidated. Tumor necrosis factor blockade with a genetically engineered receptor antagonist etanercept (Enbrel, Immunex, Seattle, WA) and a monoclonal antibody infliximab (Remicade, Centocor, Malvern, PA) has transformed the treatment and prognosis of patients with rheumatoid arthritis (RA), ankylosing spondylitis, Crohn’s disease, and psoriasis. The prominent role of TNF in inflammatory bone loss and the evidence that antiTNF therapy prevents radiographic progression of erosions in RA are particularly important in aseptic loosening.36
Childs et al11 reported the efficacy of etanercept for wear debris-induced osteolysis. In vitro, they showed that etanercept can inhibit osteoclastic bone resorption in a bone wafer pit assay and cytokine production from Ti-stimulated macrophages. Using a quantitative in vivo model of wear debris-induced osteolysis, they showed that etanercept prevents bone resorption and osteoclastogenesis. In mice treated with etanercept at the time of osteolysis induction, bone resorption and osteoclast numbers were reduced to background levels in normal and human TNF-α transgenic mice. To evaluate its effect on established osteolysis, etanercept was administered 5 days after Ti implantation, and they observed that additional osteolysis was prevented. These studies were extended to show that similar efficacy could be achieved via gene therapy.11 These data support the concept that TNF-α is involved critically in osteoclastogenesis and bone resorption during periprosthetic osteolysis and suggest that soluble TNF-α inhibitors may be useful as therapeutic agents for the treatment of prosthetic loosening in humans.
An obvious therapeutic intervention for osteolysis is the use of bisphosphonates that have been proven to be safe and effective in the treatment of osteoporosis and other metabolic bone diseases. Millett et al42 studied the effect of alendronate on the treatment of osteolysis in the rat model. They concluded that the intraarticular injection of PE particles caused substantial bone loss around a loaded implant. Alendronate effectively prevented and treated the particle-induced periprosthetic bone loss in a rat model. A similar conclusion was derived by Shanbhag et al55 from studies with the canine model. Unfortunately, there is no clinical evidence that bisphosphonates can prevent periprosthetic osteolysis.
Based on our current knowledge, the drugs with the greatest potential for treatment of osteolysis are the RANK antagonists OPG, RANK:Fc, and antiRANKL.54 It has been shown that RANK signaling is required for wear debris-induced osteolysis in vivo.12 Ulrich-Vinther et al62 investigated whether gene therapy using a recombinant adeno-associated viral (rAAV) vector that expresses OPG can inhibit wear debris-induced osteolysis. The rAAV vector coexpressing OPG (rAAV-OPG-IRES-EGFP) was generated. The experiment was done in vitro and in vivo using mouse calvarial and Ti particles. They concluded that one intramuscular injection of the rAAV-OPG-IRES-EGFP vector can efficiently transduce myocytes to produce high levels of OPG. Osteoprotegerin effectively inhibits wear debris-induced osteoclastogenesis and osteolysis.
There is no approved drug therapy to prevent or inhibit periprosthetic osteolysis. Although preclinical studies have identified potential drug therapies, there is no evidence that these drugs can effectively treat aseptic loosening in patients. Although additional research is warranted, it is evident that the greatest obstacle to therapeutic intervention is absence of a reliable outcome measure with which drug efficacy could be evaluated critically in a multicenter, Phase III clinical trial. Therefore, investigators are developing algorithms that will permit the use of volumetric three-dimensional computed tomography (3-D CT) to quantify the size and location of periprosthetic osteolysis and evaluate its progression with time.37,44 After this technology is validated, it will be useful for drug trials and for understanding the natural history of osteolysis.
Femoral Osteolysis
Host factors such as symptoms, patient age, activity level, and medical status, and radiographic findings such as lesion location, size, and likelihood of its progression, must be considered before selecting the appropriate treatment. Two principles must be considered in the treatment of femoral osteolysis. First, the source of the particles must be identified and removed. Second, removal of loose or burnished components and grafting of the bony defect often are required.
In extensively porous-coated ingrown stems, osteolytic lesions occur primarily in Gruen Zones 1 and 7 (greater and lesser trochanter) and do not necessarily result in component loosening. This is in contradistinction to the patch-coated femoral components that allow the joint fluid to reach the diaphysis and result in structural bone loss more distally.6,16,61
The threshold to revise patch-coated stems should be lower than the extensively porous-coated ingrown stems. In the asymptomatic patient with a well-fixed stem, curettage and grafting of the lesions, retention of the stem, and exchange of the femoral head and acetabular liner may be sufficient. We prefer that cavitary lesions at and distal to the stem be revised because of the increased risk of periprosthetic fracture even though the stem still may be well fixed distally. In elderly patients who are asymptomatic, patients who are sedentary, or patients who are medically unfit, simple observation of these lesions every 3 to 4 months may be reasonable.
Pelvic Osteolysis
Uncemented cups were classified by Rubash et al46 into three groups based on the stability of the acetabular shell and the exchangeability of the PE liner: focal osteolysis with well-fixed shell and PE liner is exchangeable (Type 1); focal osteolysis with well-fixed shell but PE liner is unexchangable (Type 2); and osteolysis with obvious loosening of the cup (Type 3). Evaluation of pelvic osteolytic lesions must include patient symptoms, location, likelihood of progression, the amount of bone loss, and component stability.
If surgery is deemed necessary, then we recommend that the procedure address not only the osteolytic lesion, but the particle generators. This would include removal of the granulomatous material, filling the defects with a graft material, and possible exchange of the components, depending on component stability and potential for additional debris generation.
Intraoperative assessment is the definitive method to assess loosening of the components. If possible, the surgeon should assess all areas of ingrowth, surface ongrowth, and the presence of macroscopic soft tissue at the interface. Firm pressure should be placed on the cup first through its central axis, then through its periphery, looking for interface motion or expression of fluid. Either of these findings implies that the component is not well-fixed and should be exchanged. Grasping the cup with a clamp through screw holes and twisting is another method that has been described to assess stability.3
In cemented cups, linear or focal osteolysis in two or three acetabular zones has been associated with 71% and 94% incidences of loosening of the component, respectively.25 A loose cemented component must be revised, preferably with an ingrowth cup. Bone stock deficiencies must be treated with the appropriate graft. If the pelvic bed has been irradiated previously, a PE liner may need to be reimplanted with cemented fixation.30,41
If the cup is not loose, then the degree of wear should be evaluated. Worn cups with eccentricity of the femoral head should be replaced. Thirty-two-millimeter heads, which have been shown to have the highest degree of volumetric wear, and 22-mm heads, which have been associated with the highest degree of linear wear, should be replaced by an intermediate head size such as 26- or 28-mm heads and associated liners. We prefer to approach pelvic osteolytic lesions through a rectangular trapdoor created in the ilium that allows direct access to the lesion. The bony lesion then is grafted with allograft and the rectangular bony fragment is turned 90° to stop outflow of the graft material. Satisfactory results have been reported for bone grafting with autogenous bone, allograft bone, demineralized bone matrix, calcium sulfate, or combinations of these, and other materials.51
For Type I uncemented cups, the cup is stable but is associated with a discrete focal osteolytic lesion, usually located in Zones 1 or 3 or both and occasionally adjacent to the screws. The component usually can be retained. Particulate bone graft can be packed into the readily accessible osteolytic cavities either through the holes in the cup or through an iliac trapdoor. In addition, the PE liner in modular cups can be replaced as long as the locking mechanism is intact.57
Type II components also are stable, but function of the cup is compromised. For example, the locking mechanism of a modular cup may be damaged, there may be extensive wear of the shell, or the shell may be malpositioned. In these cases, the entire component should be removed, defects should be filled with the appropriate graft material, and a new cup should be reimplanted.57
Type III cups are unstable and have migrated into the osteolytic lesion, necessitating revision of the components.57 Assessment of the bone deficiency is critical. Particulate bone graft, bulk allograft, and structural allograft may be necessary to fill the defect.22,23,64Figure 5 shows our preferred treatment algorithm for acetabular osteolysis.
Maloney et al39 reported treatment of 68 well-fixed acetabular cups with pelvic osteolysis. Forty hips were classified as Type I and 28 hips were classified as Type II. In 40 patients (40 hips) (Type I), the PE liner was exchanged and the osteolytic lesions were debrided. Allograft chips were packed into the lytic defect in 29 patients. The remaining 11 patients were treated by debridement without grafting. At followup, all of the cups were stable radiographically. Approximately ⅓ of the lesions had resolved completely regardless of whether they were grafted. The remaining ⅔ had decreased in size. In 28 hips (Type II), the socket was revised. Amstutz et al1 reported that 71% of the revised cups had circumferential radiolucencies after 2 years, with 9% requiring repeat revision. Callaghan et al7 reported that radiolucencies occurred after 2 to 5 years adjacent to 75% of revised cups that had been inserted with cement, and 34% progressed to become circumferential.
DISCUSSION
Radiographs provide limited information regarding the location and the amount of osteolysis after THA.8,31,60,63 A recent case series using CT found silent osteolysis, (defined as a sharply demarcated area adjacent to the implant devoid of trabeculae) in 48% of 80 patients followed up for 6 to 11 years after THA. Only ½ of these lesions were identified on simultaneous conventional radiographs.59 Looney et al37 also found plain radiographs are a poor measure of the extent of osteolysis compared with CT. It is evident from these and other studies that plain radiography lacks the sensitivity to identify early osteolytic changes after THA.59 Puri et al,44 Stulberg et al,59 and Looney et al37 proposed using helical CT, special CT, and 3-D CT to identify osteolytic lesions. Even though 3-D CT is precise and able to measure the lesion in three dimensions, it is costly and exposes the patient to high levels of radiation, making it impractical for serial measures.
Sanchez-Sotelo et al48 and Chatoo et al10 reported spontaneous fracture of the pelvis through extensive osteolytic lesions. The cost of implants and operative time for revision THA are significantly higher than those for primary THA.35 Maloney et al39 and Schmalzried et al51 recommended surgery for the silent lesions to prevent loosening and revision surgery. Surgical treatment has been shown to be beneficial for patients with clinical and radiographic progression of disease.51 Retention or revision procedure depends on stability of the components, the remaining bone stock, and modularity of the components. However, the principles of the treatment are to identify and replace the potential particle generators, to eliminate the granulation tissue or periprosthetic membrane, and to fill the defect with bone or bone substitute. Currently, there is no approved drug therapy to prevent or inhibit periprosthetic osteolysis. Although preclinical studies have identified potential drug therapies, there is no evidence that these drugs can effectively treat established osteolysis.
Detection and monitoring osteolysis at an earlier stage are needed to prevent loosening and fracture. Currently, 3-D CT seems to be the gold standard for detection of osteolysis but it is costly and cannot be done at community centers. Recent advances in molecular biology may help identify a novel drug or agent that can retard or inhibit periprosthetic osteolysis.
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