Cysts: Osteolysis and Stress Shielding: More Than Just Filling A Void

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CHAPTER 18
© 2015 American Academy of Orthopaedic Surgeons 197
Cysts: Osteolysis and Stress
Shielding; More Than Just
Filling a Void
Sunil Dhar, MBBS, MS, MCh Orth, FRCS Ed Orth
Dakshinamurthy Sunderamoorthy, MBBS, MRCS Ed, FRCS Ed
(Tr & Orth)
Haroon Majeed, MBBS, MRCS
Introduction
Total 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 Design
A 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.

TO T AL A NKLE A R T HROPLAST Y
198 © 2015 American Academy of Orthopaedic Surgeons
sion rate of 41% for persistent pain. Unger et al20 repor t-
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
FIGURE 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.
FIGURE 2
Image of the Agility (DePuy Synthes) total ankle replacement.

CHAPTER 18 C YSTS: OSTEOLYSIS AND S TRESS S HIELDING
© 2015 American Academy of Orthopaedic Surgeons 199
(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-
FIGURE 3
AP radiographs show the Mobility (A, DePuy Synthes) and Scandinavian Total Ankle Replacement (B, Stryker) third-generation, three-component
devices.

TO T AL A NKLE A R T HROPLAST Y
200 © 2015 American Academy of Orthopaedic Surgeons
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 Device
The 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
FIGURE 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.

CHAPTER 18 C YSTS: OSTEOLYSIS AND S TRESS S HIELDING
© 2015 American Academy of Orthopaedic Surgeons 201
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,
FIGURE 5
AP (A) and lateral (B) radiographs show the Ankle Evolutive System
(Biomet) three-component mobile-bearing implant.

TO T AL A NKLE A R T HROPLAST Y
202 © 2015 American Academy of Orthopaedic Surgeons
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 Osteolysis
Periprosthetic 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 Factors
Implant 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 Osteolysis
The biologic process of osteolysis is generally agreed to
be the result of the production of wear debris from the
FIGURE 6
AP radiograph of a Scandinavian Total Ankle Replacement (Stryker)
implant in situ with no evidence of loosening demonstrates medial
and lateral malleolar cysts.

CHAPTER 18 C YSTS: OSTEOLYSIS AND S TRESS S HIELDING
© 2015 American Academy of Orthopaedic Surgeons 203
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
FIGURE 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.

TO T AL A NKLE A R T HROPLAST Y
204 © 2015 American Academy of Orthopaedic Surgeons
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 E2, 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 Strategies
The current literature suggests the surgeon choose two
complementary approaches, nonsurgical and surgical.
Nonsurgical Interventions
Although 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 Intervention
Little 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

CHAPTER 18 C YSTS: OSTEOLYSIS AND S TRESS S HIELDING
© 2015 American Academy of Orthopaedic Surgeons 205
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
FIGURE 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.

TO T AL A NKLE A R T HROPLAST Y
206 © 2015 American Academy of Orthopaedic Surgeons
the authors of this chapter is markedly different with
the Mobility implant, they will continue to follow the
current management regimen.
Conclusion
Periprosthetic 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.
References
1. Kofoed H: Cylindrical cemented ankle arthroplasty: A
prospective series with long-term follow-up. Foot Ankle
Int 1995;16(8):474-479.
2. Buechel FF, Pappas MJ: Survivorship and clinical
evaluation of cementless, meniscal-bearing total ankle
replacements. Semin Arthroplasty 1992;3(1):43-50.
3. Kumar A, Dhar S: Total ankle replacement: Early results
during learning period. Foot Ankle Surg 2007;13(1):
19-23.
4. Hintermann B: Total Ankle Arthroplasty: History Over-
view, Current Concepts and Future Perspectives. New
York, NY, Springer, 2005, pp 59-89.
5. Karantana A, Hobson S, Dhar S: The scandinavian
total ankle replacement: Survivorship at 5 and 8 years
FIGURE 9
Intraoperative photograph demonstrating curettage and bone graft-
ing of a medial malleolar cyst.
FIGURE 10
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

CHAPTER 18 C YSTS: OSTEOLYSIS AND S TRESS S HIELDING
© 2015 American Academy of Orthopaedic Surgeons 207
comparable to other series. Clin Orthop Relat Res
2010;468(4):951-957.
6. Hobson SA, Karantana A, Dhar S: Total ankle re-
placement in patients with significant pre-operative
deformity of the hindfoot. J Bone Joint Surg Br
2009;91(4):481-486.
7. Haddad SL, Coetzee JC, Estok R, Fahrbach K, Banel D,
Nalysnyk L: Intermediate and long-term outcomes of
total ankle arthroplasty and ankle arthrodesis:
A systematic review of the literature. J Bone Joint Surg
Am 2007;89(9):1899-1905.
8. Gougoulias N, Khanna A, Maffulli N: How successful
are current ankle replacements?: A systematic review of
the literature. Clin Orthop Relat Res 2010;468(1):
199-208.
9. Pyevich MT, Saltzman CL, Callaghan JJ, Alvine FG: To-
tal ankle arthroplasty: A unique design. Two to twelve-
year follow-up. J Bone Joint Surg Am 1998;80(10):
1410-1420.
10. Wood PL, Deakin S: Total ankle replacement: The
results in 200 ankles. J Bone Joint Surg Br 2003;85(3):
334-341.
11. Wood PL, Prem H, Sutton C: Total ankle replacement:
Medium-term results in 200 Scandinavian total ankle
replacements. J Bone Joint Surg Br 2008;90(5):605-609.
12. Buechel FF Sr, Buechel FF Jr, Pappas MJ: Ten-year
evaluation of cementless Buechel-Pappas meniscal bear-
ing total ankle replacement. Foot Ankle Int 2003;24(6):
462-472.
13. Wood PL: Experience with the STAR ankle arthro-
plasty at Wrightington Hospital, UK. Foot Ankle Clin
2002;7(4):755-764, vii.
14. Mann JA, Mann RA, Horton E: STAR™ ankle: Long-
term results. Foot Ankle Int 2011;32(5):S473-S484.
15. van den Heuvel A, Van Bouwel S, Dereymaeker G: Total
ankle replacement: Design evolution and results. Acta
Orthop Belg 2010;76(2):150-161.
16. Anderson T, Montgomery F, Carlsson A: Uncemented
STAR total ankle prostheses: Three to eight-year follow-
up of fifty-one consecutive ankles. J Bone Joint Surg Am
2003;85-A(7):1321-1329.
17. Helm R, Stevens J: Long-term results of total ankle
replacement. J Arthroplasty 1986;1(4):271-277.
18. Wynn AH, Wilde AH: Long-term follow-up of the
Conaxial (Beck-Steffee) total ankle arthroplasty. Foot
Ankle 1992;13(6):303-306.
19. Kitaoka HB, Patzer GL: Clinical results of the
Mayo total ankle arthroplasty. J Bone Joint Surg Am
1996;78(11):1658-1664.
20. Unger AS, Inglis AE, Mow CS, Figgie HE III: Total
ankle arthroplasty in rheumatoid arthritis: A long-term
follow-up study. Foot Ankle 1988;8(4):173-179.
21. Bolton-Maggs BG, Sudlow RA, Freeman MA: To-
tal ankle arthroplasty: A long-term review of the
London Hospital experience. J Bone Joint Surg Br
1985;67(5):785-790.
22. Knecht SI, Estin M, Callaghan JJ, et al: The Agility total
ankle arthroplasty. Seven to sixteen-year follow-up.
J Bone Joint Surg Am 2004;86-A(6):1161-1171.
23. Rippstein PF, Huber M, Coetzee JC, Naal FD: Total
ankle replacement with use of a new three-component
implant. J Bone Joint Surg Am 2011;93(15):1426-1435.
24. Hosman AH, Mason RB, Hobbs T, Rothwell AG: A New
Zealand national joint registry review of 202 total ankle
replacements followed for up to 6 years. Acta Orthop
2007;78(5):584-591.
25. Henricson A, Skoog A, Carlsson A: The Swedish Ankle
Arthroplasty Register: An analysis of 531 arthroplasties
between 1993 and 2005. Acta Orthop 2007;78(5):569-574.
26. Fevang BT, Lie SA, Havelin LI, Brun JG, Skredder-
stuen A, Furnes O: 257 ankle arthroplasties performed
in Norway between 1994 and 2005. Acta Orthop
2007;78(5):575-583.
27. National Joint Registry for England, Wales, and North-
ern Ireland. 9th Annual Report, 2012, p 19. Available at:
www.njrcentre.org.uk. Accessed October 7, 2014.
28. Koivu H, Kohonen I, Sipola E, Alanen K, Vahlberg T,
Tiusanen H: Severe periprosthetic osteolytic lesions af-
ter the Ankle Evolutive System total ankle replacement.
J Bone Joint Surg Br 2009;91(7):907-914.
29. Asencio JG, Leonardi C: Ankle Evolutive System pros-
thesis: A simple, accurate, and reliable specific concept
for primary and revision surgery. Tech Foot & Ankle
2005;4:119-124.
30. Henricson A, Knutson K, Lindahl J, Rydholm U: The
AES total ankle replacement: A mid-term analysis of 93
cases. Foot Ankle Surg 2010;16(2):61-64.
31. Morgan SS, Brooke B, Harris NJ: Total ankle replace-
ment by the Ankle Evolution System: Medium-term
outcome. J Bone Joint Surg Br 2010;92(1):61-65.
32. Rodriguez D, Bevernage BD, Maldague P, Deleu PA,
Tribak K, Leemrijse T: Medium term follow-up of the

TO T AL A NKLE A R T HROPLAST Y
208 © 2015 American Academy of Orthopaedic Surgeons
AES ankle prosthesis: High rate of asymptomatic oste-
olysis. Foot Ankle Surg 2010;16(2):54-60.
33. Besse JL, Brito N, Lienhart C: Clinical evaluation and
radiographic assessment of bone lysis of the AES total
ankle replacement. Foot Ankle Int 2009;30(10):964-975.
34. Koivu H, Mackiewicz Z, Takakubo Y, Trokovic N, Paja-
rinen J, Konttinen YT: RANKL in the osteolysis of AES
total ankle replacement implants. Bone 2012;51(3):
546-552.
35. Kohonen Ia, Koivu H, Pudas T, Tiusanen H, Vahlberg
T, Mattila K: Does computed tomography add informa-
tion on radiographic analysis in detecting periprosthetic
osteolysis after total ankle arthroplasty? Foot Ankle Int
2013;34(2):180-188.
36. Hanna RS, Haddad SL, Lazarus ML: Evaluation of peri-
prosthetic lucency after total ankle arthroplasty: Helical
CT versus conventional radiography. Foot Ankle Int
2007;28(8):921-926.
37. Gruen TA, McNeice GM, Amstutz HC: “Modes of
failure” of cemented stem-type femoral components:
A radiographic analysis of loosening. Clin Orthop Relat
Res 1979;141:17-27.
38. Wolff J: Das Gesetz der Transformation der Knochen.
Berlin, Germany, Hirschwald, 1892.
39. Bouguecha A, Weigel N, Behrens BA, Stukenborg-
Colsman C, Waizy H: Numerical simulation of strain-
adaptive bone remodelling in the ankle joint. Biomed
Eng Online 2011;10:58.
40. Willert HG, Semlitsch M: Reactions of the articular
capsule to wear products of artificial joint prostheses.
J Biomed Mater Res 1977;11(2):157-164.
41. Jones LC, Hungerford DS: Cement disease. Clin Orthop
Relat Res 1987;225:192-206.
42. Archibeck MJ, Jacobs JJ, Roebuck KA, Glant TT: The
basic science of periprosthetic osteolysis. Instr Course
Lect 2001;50:185-195.
43. Abu-Amer Y, Darwech I, Clohisy JC: Aseptic loosening
of total joint replacements: Mechanisms underlying
osteolysis and potential therapies. Arthritis Res Ther
2007;9(Suppl 1):S6.
44. Purdue PE, Koulouvaris P, Nestor BJ, Sculco TP: The
central role of wear debris in periprosthetic osteolysis.
HSS J 2006;2(2):102-113.
45. Dumbleton JH, Manley MT, Edidin AA: A literature re-
view of the association between wear rate and osteolysis
in total hip arthroplasty. J Arthroplasty 2002;17(5):
649-661.
46. Jacobs JJ, Roebuck KA, Archibeck M, Hallab NJ, Glant
TT: Osteolysis: Basic science. Clin Orthop Relat Res
2001;393:71-77.
47. Harris WH: The problem is osteolysis. Clin Orthop Relat
Res 1995;311:46-53.
48. Schmalzried TP, Jasty M, Harris WH: Periprosthetic
bone loss in total hip arthroplasty: Polyethylene wear
debris and the concept of the effective joint space.
J Bone Joint Surg Am 1992;74(6):849-863.
49. Harris WH: Wear and periprosthetic osteolysis: The
problem. Clin Orthop Relat Res 2001;393:66-70.
50. González O, Smith RL, Goodman SB: Effect of size,
concentration, surface area, and volume of poly-
methylmethacrylate particles on human macrophages in
vitro. J Biomed Mater Res 1996;30(4):463-473.
51. Sabokbar A, Pandey R, Athanasou NA: The effect of par-
ticle size and electrical charge on macrophage-osteoclast
differentiation and bone resorption. J Mater Sci Mater
Med 2003;14(9):731-738.
52. Gelb H, Schumacher HR, Cuckler J, Ducheyne P, Baker
DG: In vivo inflammatory response to polymethylmeth-
acrylate particulate debris: Effect of size, morphology,
and surface area. J Orthop Res 1994;12(1):83-92.
53. Shanbhag AS, Jacobs JJ, Glant TT, Gilbert JL, Black J,
Galante JO: Composition and morphology of wear de-
bris in failed uncemented total hip replacement. J Bone
Joint Surg Br 1994;76(1):60-67.
54. Abbas S, Clohisy JC, Abu-Amer Y: Mitogen-activated
protein (MAP) kinases mediate PMMA-induction of
osteoclasts. J Orthop Res 2003;21(6):1041-1048.
55. O’Keefe RJ, Rosier RN, Teot LA, Stewart JM, Hicks DG:
Cytokine and matrix metalloproteinase expression in
pigmented villonodular synovitis may mediate bone and
cartilage destruction. Iowa Orthop J 1998;18:26-34.
56. Atkins GJ, Haynes DR, Howie DW, Findlay DM: Role of
polyethylene particles in peri-prosthetic osteolysis:
A review. World J Orthop 2011;2(10):93-101.
57. O’Hara LJ, Nivbrant B, Röhrl S: Cross-linked poly-
ethylene and bisphosphonate therapy for osteolysis
in total hip arthroplasty: A case report. J Orthop Surg
(Hong Kong) 2004;12(1):114-121.
58. DeVries JG, Berlet GC, Lee TH, Hyer CF, Deorio JK:
Revision total ankle replacement: An early look at agility
to INBONE. Foot Ankle Spec 2011;4(4):235-244.

CHAPTER 18 C YSTS: OSTEOLYSIS AND S TRESS S HIELDING
© 2015 American Academy of Orthopaedic Surgeons 209
59. Myerson MS, Won HY: Primary and revision total ankle
replacement using custom-designed prostheses. Foot
Ankle Clin 2008;13(3):521-538, x.
60. Besse JL, Lienhart C, Fessy MH: Outcomes following
cyst curettage and bone grafting for the management
of periprosthetic cystic evolution after AES total ankle
replacement. Clin Podiatr Med Surg 2013;30(2):157-170.