Cysts: Osteolysis and Stress Shielding; More Than Just
Filling a VoidSunil Dhar, MBBS, MS, MCh Orth, FRCS Ed Orth
Dakshinamurthy Sunderamoorthy, MBBS, MRCS Ed, FRCS Ed (Tr & Orth)
Haroon Majeed, MBBS, MRCS
IntroductionTotal ankle arthroplasty (TAA) is being used increasing-ly for the treatment of end-stage arthritis of the ankle joint.1-16 With better understanding of the mechanics of the ankle and related soft tissues and joints of the foot, combined with considerable improvement in the design of prostheses, the medium-term outcomes following this procedure have become more predictable and sat-isfactory.7,8 However, a substantial failure rate remains, and one of the main reasons for this is prosthetic loos-ening and subsidence resulting from aseptic bone loss. This will likely have a major effect on the increasing numbers of patients over the coming decades and will be a substantial health challenge.7-10
Evolution of TAA DesignA brief history of the evolution of TAA greatly helps to understand the current issues with aseptic loosen-ing. TAAs are typically either two-component or three-component implants; the latter has a mobile bearing.4
The first generation of TAAs (the 1970s and early 1980s) had very poor results. They were predominantly two-component designs that were either too constrained or completely unconstrained and were also cemented. Although early reports showed good short-term results, the medium- and long-term results were very poor.17 A major reason for failure was the large bone resection re-quired to fit the components, thus exposing the weaker surfaces of the tibia and the talus, resulting in early loos-ening and subsidence of the prosthesis with subsequent failure.15 Cementation of the implants has also been im-plicated in their failure, although cementing implants to weak bone was not going to be successful (Figure 1).
Wynn and Wilde18 found that 60% of the Conaxial (Beck-Steffee) ankle replacements were loose at 5 years and 90% were loose at 10 years. Kitaoka and Patzer19 reported on 204 Mayo TAAs performed between 1974 and 1984 and found that the overall implant survival rate (defined as removal of the implant) was 79% at 5 years, 65% at 10 years, and 61% at 15 years, with a revi-
Dr. Dhar or an immediate family member is a member of a speakers’ bureau or has made paid presentations on behalf of LockDown Medical. Neither of the following authors nor any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this chapter: Dr. Sunderamoorthy and Dr. Majeed.
sion rate of 41% for persistent pain. Unger et al20 report-ed 93% loosening in 23 ankle replacements at a mean follow-up of 5.6 years. Bolton-Maggs et al21 reviewed 62 TAAs for rheumatoid arthritis performed at the London Hospital between 1974 and 1981 and noted substantial complications including loosening, component sinkage, and wound breakdowns and therefore recommended ankle fusion as the procedure of choice for end-stage ankle arthritis, irrespective of the etiology.
The second-generation TAAs were noncemented, fixed-bearing, three-component designs with some im-provements such as porous beads/hydroxyapatite coat-
ing for noncemented implant fixation and improved design for stability. The Agility TAA system (DePuy Synthes) is the prime example of this implant type with the longest follow-up; it was first used in 198422 (Fig-ure 2). The implant resurfaces the superior, medial, and lateral articular surfaces and requires arthrodesis of the syndesmosis for load sharing through the fibula. The implant was approved by the FDA in 1992, and until approximately 5 years ago, it was the most common TAA device in the US. The Agility has undergone sev-eral design changes; currently, the phase IV implant is available. Much has been written about the long-term outcome of the Agility, but its use has been severely cur-tailed because of the complexity of the procedure, high reoperation rates, axial malalignment issues, osteolysis, and the massive problem of salvage in failed cases.9,22
All third-generation (current) TAAs have three com-ponents: the tibial and talar components are most commonly composed of cobalt-chromium and have a porous backing for noncemented fixation. The compo-nents articulate with an ultra-high–molecular-weight polyethylene (UHMWPE) mobile bearing that helps re-duce shearing stresses and increases the contact surface area, thereby reducing polyethylene wear. The mobile-bearing concept was developed virtually simultane-ously around the mid 1980s in Europe (Scandinavian Total Ankle Replacement [STAR] Stryker) and in the US
F I G U R E 1
AP (A) and lateral (B) radiographs show a loose, unstable, two-component, first-generation unconstrained total ankle replacement. A consider-able amount of talar bone was excised to seat the talar component.
F I G U R E 2
Image of the Agility (DePuy Synthes) total ankle replacement.
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(Buechel-Pappas Total Ankle Replacement [BP] Endo-tec).1,2 Several mobile-bearing devices are now available with subtle design differences between them, although none has been shown to be vastly superior (Figure 3).
The short-term and medium-term survival results of the third-generation TAA implants have been more ac-ceptable. The 5-year survival results (defined as removal of one or more of the implants) range from 70% to 93% and the 10- to 12-year results range from 85% to 95%.2,5,10,12,14,16,23 The survival results from the New Zea-land, Swedish, and Norwegian national registries have been slightly inferior, with survival rates of 78% to 89% at 5 years and 62% to 72% at 10 years.24-26 In the studies based on these registries, aseptic loosening is the most common reason for revision. In the ninth annual report of the National Joint Registry in the UK, 471 primary and 21 revision TAAs were recorded; 25% of revisions were arthrodesis for a failed TAA. The indication for re-vision was aseptic loosening in 33%, lysis around the components in 33%, and malalignment in 24%.27
Osteolysis in TAA: Current Knowledge The loss of bone around the prostheses is known as periprosthetic osteolysis. This can result in loosening of the components, subsidence, and eventual failure of the joint arthroplasty, with catastrophic consequences.
Most current knowledge regarding this process is from studies of total hip arthroplasty (THA) and total knee arthroplasty. However, with increasing numbers of TAA procedures being performed and greater length of follow-up, more TAA literature is being published. One of the most common reported causes for failure in TAA is aseptic loosening of the components. The New Zealand National Registry reviewed 202 TAAs with a follow-up of 6 years and a failure rate of 7%. Compo-nent loosening was the main reason for the failure in 10 patients.24 An analysis of 531 ankle athroplasty pro-cedures between 1993 and 2005 in the Swedish ankle arthroplasty register showed that 101 ankles (19%) un-derwent revision; 31 ankles underwent revision for talar or tibial component loosening.25 Wood and Deakin10 reviewed 200 STAR TAAs and showed a 5-year survival of 93.3% and a 10-year survival of 80.3%. One of the most common reasons for failure was component loos-ening. Karantana et al5 reviewed 52 STAR TAAs at 9-year follow-up and showed aseptic loosening in one patient and lucency lines in three more. Radiographic loosening of STAR prostheses occurred in 34 of 376 ankles (9%) in six studies with a mean follow-up of 3.8 years. Rippstein et al23 reviewed 240 consecutive primary TAAs with the Mobility prosthesis (DePuy Synthes) and found that nonprogressive radiolucency ranged from 1.8% to 37.3% in the 10 zones surrounding the tibial compo-
F I G U R E 3
AP radiographs show the Mobility (A, DePuy Synthes) and Scandinavian Total Ankle Replacement (B, Stryker) third-generation, three-component devices.
nent, and from 0 to 2.2% in the three zones surrounding the talar component.
Based on the literature, it is difficult to reach any firm conclusions regarding the etiology of these lesions or prevention strategies. Knecht et al22 detected osteolytic lesions in up to 76% of ankles with the Agility TAA; how-ever, most lesions were small and stable with little or no progression. Lytic lesions were separated into two cat-egories, expansile and mechanical. Pyevich et al9 previ-ously referred to expansile lesions as ballooning lysis. The authors reported lucency around the tibial component seen on mortise radiographs of 25 of 98 Agility ankles (26%). The lucency lines were rarely progressive after 2 years. Circumferential lucency around the tibial compo-nent on the lateral radiograph was noted to be associated with syndesmotic nonunion. These radiolucent lines were characterized as early onset and were rarely progres-sive (mechanical). Ballooning, expansile osteolysis was characterized as a late-onset, progressive lesion, prob-ably resulting from implant wear. Koivu et al28 studied Ankle Evolutive System ([AES] Biomet) TAAs and found that expansile lesions occurred early and were rapidly progressive. No relationship was detected between age, weight, or preoperative diagnosis and the development of lysis, lucency, or component migration (Figure 4).
The AES DeviceThe AES prosthesis is a striking example of the devastat-ing effects of osteolysis (Figure 5). The AES expanded on the design of the BP prosthesis. The AES was designed in 1998 and had a three-component mobile-bearing de-sign. The cobalt-chromium tibial and talar components were grit blasted and coated with hydroxyapatite. The mobile bearing was composed of UHMWPE sterilized with ethylene oxide. Two successive versions of the AES were developed: the first had a modular tibial implant, and in August 2004, the tibial component was made in a single piece and the implant was dual coated with hydroxyapatite sprayed over a thick layer of plasma-sprayed titanium.
A short-term study by the designers of the AES pros-thesis outlined the surgical technique and reported good preliminary results.29 Henricson et al30 reported promising midterm results in 93 patients who under-went AES TAA between 2002 and 2007. However, con-cerns regarding osteolysis were beginning to arise.
Morgan et al31 presented the outcomes of 38 consecu-tive patients who underwent AES TAA between 2002 and 2004 at a minimum follow-up of 4 years. Most patients presented with substantially improved function and pain relief, but substantial osteolysis was seen around the components in nine patients. No further revisions were suggested because the symptoms were nonpro-gressive. Despite high patient satisfaction, the authors reported some concerns about osteolysis. Rodriguez et al32 reported on 18 ankles that underwent TAA with the AES implant and observed a high frequency of delayed appearance of osteolysis (77%) at a mean follow-up of 39.4 months.
Besse et al33 reported midterm results of a prospective study that included 50 TAAs with AES implants per-formed from 2003 to 2006 at a mean follow-up of 40
F I G U R E 4
AP radiograph of a Scandinavian Total Ankle Replacement (Stryker) impant with osteolysis between the tibial rails and the medial tibia. Note the medial edge loading resulting in wear of the insert.
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months; 82% of patients had good functional outcome. However, progressive ballooning lysis was seen as soon as 2 years following implantation. The radiographic bone-implant interface was classified as normal, lucent (radiolucent lines < 2 mm), or ballooning lysis. The ballooning lysis was further classified into five catego-ries based on the size of the radiolucent area using the 30-mm tibial stem as a reference. Radiographically, the AP and lateral ankle views were divided into 10 zones and data were summarized for the tibial (1-2-6-7) and the talar (5-8-9) zones. Tibia-implant interface cysts (> 5 mm) were reported in 62% of cases, and talus- implant interface cysts were reported in 43%, suggesting a substantial risk of subsidence. Although the functional outcome and patient satisfaction were comparable with published results using other third-generation pros-theses, the authors stopped implantation of this pros-thesis because of the massive lesions observed. A high osteolysis rate was also noted by Koivu et al,28 with 130 consecutive AES devices implanted between 2002 and 2008. Radiolucent lines or osteolytic lesions were seen on plain radiographs in 48 ankles (37%). Marked os-teolytic lesions were found in 27 ankles (21%). The ta-lar component migrated in 9 ankles; a shift of the tibial component was observed in 2 other ankles. Of 27 ankles with marked osteolysis, 16 underwent revision surgery (revision rate, 15.5%). The contents of the osteolytic cavities histologically were interpreted as a foreign-body
reaction. The authors concluded that the use of AES im-plants should be avoided until the causes of osteolytic had been determined. Further, a report by Koivu et al34 showed that peri-implant osteolysis in early TAA im-plant failure seems to be caused by receptor activator of nuclear factor-κB ligand (RANKL)–driven chronic foreign body inflammation directed against necrotic autologous tissues and not implant-derived particles. The AES prosthesis has since been withdrawn from the market.
Aseptic Loosening Lucencies (cysts) in modern TAAs can occur in either the malleolar region or the main bodies of the tibia and talus or both and seem to follow different progression patterns. Malleolar cysts tend to be more benign, are slowly progressive, and tend not to threaten the integ-rity of the metal implants. However, the cysts may be symptomatic. Their etiology is debated considerably because often, they do not seem to occur as a result of polyethylene wear (Figure 6). Cysts have been seen more often with the STAR prosthesis, and the possibility remains that they occur due to breaches in the surfaces of the medial or lateral malleoli as a result of prepara-tion of the gutters for seating the talar implant. Synovial pressure during gait could possibly force fluid through these breaches, causing eventual cyst formation (Hakon Kofoed, MD, personal communication).
Main body lucencies tend to be one of two types. The first, possibly a result of stress shielding, manifests as a lucent line less than 2 mm wide and is rarely progres-sive.14 The second is the development of an osteolytic cavity on the tibial or talar side or both. The lucency on the tibial side is usually around or between the central fixation bars (STAR) or tibial fixation stems (Mobility), whereas on the talar side the lucencies are often hidden and become apparent only when large.5,11,14 Although several studies have described changes in radiolucencies on the basis of serial radiographs, CT is the definitive modality for outlining such lesions35 (Figure 7). Hanna et al36 showed that CT is a more accurate method for early detection and quantification of periprosthetic lu-cency than plain radiography. Accurate evaluation of lucent lesions can also help identify patients at high risk.
An initial cohort reported on 124 Mobility TAA pro-cedures performed in 116 patients (unpublished results,
F I G U R E 5
AP (A) and lateral (B) radiographs show the Ankle Evolutive System (Biomet) three-component mobile-bearing implant.
Sunil Dhar, Dakshinamurthy Sunderamoorthy, Haroon Majeed; Nottingham, England). The mean patient age was 65 years (range, 22 to 88 years); the mean follow-up was 37 months (range, 12 to 78 months). Cystlike osteolysis was present in 10 patients (8%). In five pa-tients, the cyst size increased in a gradually progressive manner around the Mobility implants, whereas in the other five, these cysts were nonprogressive. These cysts were initially noted on routine follow-up radiographs. After a cystlike change was identified in any patient in the presence of ongoing pain, appropriate investigations were conducted to exclude the possibility of infection or aseptic loosening of implants including complete blood count, C-reactive protein levels, erythrocyte sedi-mentation rate, and CT scanning. These patients were followed up more frequently to monitor any change in their symptoms or radiographic appearances. Cyst dimensions were measured between 5 to 18 mm. No explosive cysts were identified in any patient. In six pa-tients, the cysts were located anterior to the stem of the tibial prostheses, three were located medially, and one was located anterolaterally. One patient had cystic ap-
pearance around the talar implant in addition to the tibial cyst. Three patients developed pain that was con-sidered to be the result of the cyst; two of these patients underwent curettage and bone grafting of the lesions with resolution of symptoms. The mean time of appear-ance of cystlike change in symptomatic patients was 9 months (range, 8 to 10 months), whereas in asymp-tomatic patients the mean time of appearance of cysts was 12 months (range, 9 to 15 months).
Periprosthetic OsteolysisPeriprosthetic osteolysis and subsequent aseptic loosen-ing is a well-known complication after prosthetic joint arthroplasty.37 Both mechanical and biologic factors are thought likely to contribute to the pathogenesis of the osteolysis. Although the end result of both factors is similar (such as loss of fixation), their pathways are totally different.
Mechanical FactorsImplant fixation is an important factor, and aseptic loosening can be the result of inadequate initial fixa-tion or mechanical loss of fixation over time. More than 100 years ago, Wolff38 described the response of bone to mechanical forces (Wolff law), and stress shielding of bone is well recognized in the literature on THA and total knee arthroplasty. In the ankle, this process is best seen in the STAR prosthesis, for which an increase in density is often observed above the anchoring bolts of the tibial implant and a decrease is observed centrally above the tibial plate. Strain-adaptive bone remodel-ing, the phenomenon by which it is thought that bone remodels in response to dynamic strains within the matrix, manifests a progressively increasing osteogenic response to progressively increased loading (that is, low strains are associated with the loss of bone), whereas el-evated strains result in a proportional increase in bone area. The fixation of the tibial component is achieved with two anchoring bars that cause force transmission from the two bars into the bone. This can result in stress shielding between the anchoring bolts and the area above the tibial plate.39
The Biologic Process of OsteolysisThe biologic process of osteolysis is generally agreed to be the result of the production of wear debris from the
F I G U R E 6
AP radiograph of a Scandinavian Total Ankle Replacement (Stryker) implant in situ with no evidence of loosening demonstrates medial and lateral malleolar cysts.
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prosthetic articulation, resulting in an inflammatory response that causes bone resorption.40 This process was originally described somewhat erroneously follow-ing THA as “cement disease,” because it was thought that the polymethyl methacrylate used in THA was principally responsible for the particles of wear.41 It is now known that any particulate debris from metal, ce-ment, or polyethylene can produce periprosthetic os-teolysis, either alone or in concert. Osteolysis also has been reported in conjunction with metal-on-metal and ceramic-on-ceramic bearing surfaces.42
Periprosthetic osteolysis is considered a foreign-body reaction to particulate debris. The size of the wear par-ticles, their load and composition, access to peripros-thetic bone, and the cellular response to the particulate debris are important factors. Wear particles incite a
chronic inflammatory process that results in osteoly-sis. This sustained chronic inflammatory response is manifested by recruitment of a wide array of cell types that includes macrophages, fibroblasts, giant cells, neu-trophils, lymphocytes, and most important, osteoclasts, which are the principal bone-resorbing cells. The cel-lular response entails secretion of osteoclastogenic and inflammatory cytokines that increase osteoclast activity and enhanced osteolysis. Studies have shown that at the core of the biologic response that results in osteolysis is activation of the receptor activator of nuclear factor-κB (RANK)/RANKL axis, which is indicated by expression of RANK, RANKL, and osteoprotegerin (OPG) proteins in periprosthetic membranes. The RANK/RANKL/OPG pathway, discovered in the late 1990s, is thought to play a crucial role in osteoclastogenesis and osteolysis. This
F I G U R E 7
AP radiograph (A) and coronal CT scan (B) of a Scandinavian Total Ankle Replacement (Stryker) implant in situ. The cyst appears much larger on CT.
activation culminates in enhanced osteoclast recruit-ment and activity adjacent to bone-implant interfaces, resulting in osteolysis.42-44
Most polyethylene particles are produced by abra-sion, adhesion, microfatigue, and third-body wear mechanisms.44-47 Dumbleton et al45 conducted a litera-ture review of the association between wear rate and osteolysis in THA and showed that wear-induced oste-olysis increases as the rate of wear increases. Particles of polyethylene and other debris are dispensed through the joint fluid. Fluid flows according to pressure gradi-ents, and any area of bone accessed by joint fluid is a potential site for debris deposition. Although increased fluid pressure and implant motion may play a role, the final pathway seems to be related to the host response to particulate debris of all types.44,46,47
Wear debris is formed at prosthetic joint articula-tions, modular interfaces, and nonarticulating inter-faces.47-49 Most particles are less than 5 µm in diameter and the cellular response to particles may vary with size, shape, composition, charge, and number of particles.50,51 The size of these particles is important, and several re-ports have estimated that particles ranging from 0.2 to 10.0 µm in diameter undergo phagocytosis by macro-phages.52 In vitro studies of macrophage cultures clearly indicate that smaller polymethyl methacrylate and polyethylene particles (< 20 µm) elicited a substantially greater inflammatory cytokine response, as indicated by increased release of tumor necrosis factor (TNF), interleukin (IL)-1, IL-6, prostaglandin E
2, matrix metal-
loproteinases, and other factors.50,53-55 Although particle phagocytosis has been identified as a critical compo-nent of this biologic response, recent studies in human macrophages indicate that direct interactions between particle and cell surface are sufficient to activate osteo-clastogenic signaling pathways50 (Figure 8).
Management StrategiesThe current literature suggests the surgeon choose two complementary approaches, nonsurgical and surgical.
Nonsurgical InterventionsAlthough the mainstay of treatment of osteolysis and aseptic loosening is surgical, because of the consider-able ongoing research into the cellular and inflamma-tory responses resulting in periprosthetic bone loss,
therapeutic interventions can potentially be developed. Bisphosphonates inhibit osteoclast metabolic activity and their ability to resorb bone. Because of this potent antiresorptive efficacy and high uptake in the skeleton, bisphosphonates are being used in the treatment of periprosthetic osteolysis. Several bisphosphonates have promise as therapeutic agents. Alendronate has proved efficacious in both rat and dog models of polyethylene-induced periprosthetic osteolysis.43,56 In a clinical case study, O’Hara et al57 reported that oral alendronate halt-ed the progression of osteolysis over the course of 1 year before revision surgery to replace the polyethylene liner.
Targeting osteoclasts may prove valuable in prevent-ing or treating osteolysis. For example, anti-RANKL strategies could be effective in blocking osteolysis. OPG inhibits bone-resorbing activity of isolated mature os-teoclasts, probably by suppressing osteoclast survival, and has been shown to suppress both UHMWPE and titanium particle–induced osteolysis in the mouse cal-varial model.43 Another approach is to treat the under-lying inflammation with the inflammatory suppressor IL-10, probably by using an anti-TNF action, which prevented a fibrotic reaction and allowed bone growth in the presence of polyethylene particles in an animal model.56 Also, anti–TNF-α gene therapy was able to in-hibit a resorptive response to titanium particles in the mouse calvarial model.43,56
Transferring such interventions from the laboratory to human patients may be ineffective, or at least not generally applicable. Prophylactic treatment begins im-mediately postoperatively to optimize the osteointegra-tion of the implant and therefore reduce access to the bone of wear particles that can inhibit the initiation and progression of particle-induced osteolysis.56 Further, although nonsurgical approaches may not replace the lost bone, therapeutic medical intervention can help prevent further osteolysis following surgical restoration of bone stock.
Surgical InterventionLittle has been published regarding the surgical man-agement of osteolysis and aseptic loosening in TAAs to assist decision making. However, it seems obvious that management strategies for osteolysis depend on the stability of the prosthesis and whether it is loose and therefore unstable. If the prosthesis is loose, it must be
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determined whether it is salvageable or a conversion to arthrodesis is required. This depends on the amount of bone loss and displacement of the implants. Conversion to fusion is a major undertaking because of the substan-tial space left by the removed prostheses and accompa-nying bone loss. In these situations, it is highly unlikely that the subtalar joint is salvageable, so a tibiotalocal-caneal fusion is commonly undertaken with massive bone graft incorporated into the gap. Fixation is usually achieved with an intramedullary nail or an external fix-ator such as the Ilizarov or Taylor spatial frames. More recently, plating systems and metallic cages are available to fill the void and prevent late graft collapse.
Custom prostheses have been reported for use with substantial bone loss.58 Further, use of a long-stemmed prosthesis to bypass tibial defects has also been report-ed.59 However, no recommendations have been made
because the numbers reported are small and long-term outcomes are unknown.
Not all radiolucencies reduce implant survivorship. Nonprogressive radiolucent lines that are asymptom-atic and less than 2 mm wide do not require surgical treatment. However, patients with ballooning or ex-pansile osteolysis require careful attention because of concern regarding progression and eventual loosening. An isolated talar or tibial lesion can be observed with serial radiographs and CT scans at 6-month intervals. Surgical treatment is determined on the basis of expan-sion, particularly rapid expansion over 6 to 12 months. Progressive lucencies or cysts can be bone-grafted with retention of the implants, provided the implant is well fixed at the time of reoperation. The polyethylene in-sert is changed at the time of grafting. If radiographs show osteolytic lesions in multiple areas, immediate surgical intervention should be considered. Multiple studies have reported favorable survivorship despite the radiographic evidence of the impending or threatening failure of the implant because of progressive radiolu-cency.4,14
Curettage and bone grafting of osteolytic lesions requires careful planning. CT scans are invaluable in planning approaches and defining the extent of the lesions.35,36 The cavity is exposed by making a cortical window over the lesion and a thorough curettage is per-formed. Material from the cavity is sent for histologic examination. Autograft can be used for smaller cavi-ties, but for larger or multiple cavities, allograft is used. The graft is packed tightly and the window is replaced. Patients are treated in a plaster cast for 6 weeks of toe-touch weight bearing and then mobilized out of the cast as the patient progresses (Figures 9 and 10).
The results of bone grafting for osteolysis performed by the authors of this chapter have been satisfactory in eliminating the cavities and relieving pain; none of the patients who underwent bone grafting in this series have progressed to revision (unpublished results, Sunil Dhar, Dakshinamurthy Sunderamoorthy, Haroon Ma-jeed; Nottingham, England). This experience has been reported in the literature, although Besse et al60 recently published poor results following bone grafting of osteo-lytic lesions in AES ankles. The authors theorized that the possibly defective backing of the implants resulted in continuing delamination. Because the experience of
F I G U R E 8
Photograph of a damaged polyethylene insert from a Scandinavian Total Ankle Replacement (Stryker). Note the severe erosion and de-lamination, a source of particulate debris.
the authors of this chapter is markedly different with the Mobility implant, they will continue to follow the current management regimen.
ConclusionPeriprosthetic bone loss around TAAs is becoming an increasingly important health issue. However, little re-
search has been published regarding this situation. The same cellular processes studied in osteolysis of the hip and knee are likely also at work in the ankle. A better understanding of the effect of instability and deformity of the arthritic ankle, improved prosthetic design and backing surfaces, perhaps even the use of polymethyl methacrylate with modern prostheses, improved surgi-cal techniques, and medical therapeutic advances may help reduce the incidence of osteolysis and mitigate its effects.
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F I G U R E 9
Intraoperative photograph demonstrating curettage and bone graft-ing of a medial malleolar cyst.
F I G U R E 1 0
Flowchart for the surgical management of periprosthetic osteolysis following total ankle arthroplasty.
Prosthesis stable
Lucent lines < 2 mm: observe
Periprosthetic osteolysis
Prosthesis loose
Ballooning lysis Multiple lucencies Tibiotalocalcaneal fusion with bone
grafting
Revision ± custom prosthesis ± bone
graft
Observe 6–12 months; surgery if
expanding
Surgery
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