Treatment of osteochondral defects of the talus

R

TD

TT

C

D1

A

I

Afd

(

0d

© 2013 Elsevier Masson SAS. Tou

evue de chirurgie orthopédique et réparatrice de l’appareil moteur (2008) 94S, S398—S408

RAINING CONFERENCE, CONFÉRENCE D’ENSEIGNEMENT, CONGRÈS SFA, LYON,ÉCEMBRE 2007

reatment of osteochondral defects of the talusraitement des lésions ostéochondrales de l’astragale

.J.A. van Bergen, P.A.J. de Leeuw, C.N. van Dijk ∗

epartment of Orthopaedic Surgery, Academic Medical Center, University of Amsterdam, PO Box 22700,100 DD Amsterdam, The Netherlands

vailable online 11 November 2008

KEYWORDSOsteochondraldefect;Osteochondral lesion;Talus;Ankle;Treatment

Summary This review article provides a current concepts overview of osteochondral defectsof the talus, with special emphasis on treatment options, their indications and future develop-ments. Osteochondral defects of the talar dome are mostly caused by a traumatic event. Theymay lead to deep ankle pain on weight-bearing, prolonged swelling, diminished range of motionand synovitis. Plain radiographs may disclose the lesion. For further diagnostic evaluation,computed tomography (CT) and magnetic resonance imaging (MRI) have demonstrated simi-lar accuracy. Computed tomography is preferred for preoperative planning. Treatment optionsare diverse and up to the present there is no consensus. Based on the current literature, wepresent a treatment algorithm that is mainly guided by the size of the lesion. Asymptomatic orlow-symptomatic lesions are treated nonoperatively. The primary surgical treatment of defectsup to 15 mm in diameter consists of arthroscopic debridement and bone marrow stimulation.For large cystic talar lesions, retrograde drilling combined with a bone graft is an important
alternative. In adolescents or in (sub)acute situations, in which the fragment is 15 mm or larger,fixation of the fragment is preferred. Osteochondral autograft transfer and autologous chon-drocyte implantation (ACI), with or without a cancellous bone graft, are recommended forsecondary cases as well as large lesions.
. All

t

© 2008 Elsevier Masson SAS

ntroduction

n osteochondral defect (OD) is the collective term forocal lesions involving the articular cartilage and subchon-ral bone. If only cartilage is involved in the pathology,

∗ Corresponding author.E-mail addresses: [email protected]

C.J.A. van Bergen), [email protected] (C.N. van Dijk).

ufoobddto

035-1040/$ – see front matter © 2008 Elsevier Masson SAS. All rights reoi:10.1016/j.rco.2008.09.003

s droits réservés. - Document téléchargé le 08/03/2013

rights reserved.

he term chondral defect is used. Many synonyms aresed, including osteochondritis dissecans [1], transchondralracture [2], flake fracture [3], talar dome fracture [4],steochondral fracture [5], osteochondral lesion [6] andsteochondral defect [7]. A differentiation should be made
etween traumatic and nontraumatic origin (i.e. osteochon-ritis dissecans). A traumatic event may lead to (partial)etachment of an (osteo)chondral fragment, which may fur-her evolve in the formation of a subchondral cyst withr without osteonecrosis. There is sometimes confusion
served.

mailto:[email protected]

mailto:[email protected]

dx.doi.org/10.1016/j.rco.2008.09.003

M

Dmioofbssssrd

naldtrol

sBdaot

E

WnBctd3ldtdramfaaap

oa

© 2013 Elsevier Masson SAS.

Treatment of osteochondral defects of the talus

between traumatic and nontraumatic because a nontrau-matic OD may become symptomatic after trauma.

In 1856, Monro first reported the presence of cartilagi-nous bodies [8]. In 1888, König used the term osteochondritisdissecans for loose body formation associated with articu-lar cartilage and subchondral bone fracture [9]. He referredto an inflammatory process, although this has never beenproved to be involved in the pathology. It was not until 1922that the first report on osteochondritis dissecans in the anklewas published [10]. The talar dome is the secondly mostcommon location in the human body; most occur in the knee[11].

An OD is often not recognized and therefore not ade-quately treated. The nonrecognition is mainly due to thefact that the lesion produces symptoms of previous trauma,and it cannot always be identified on plain radiographs[12]. After standard treatment for acute ankle sprains,residual symptoms are reported in 33% of patients [13].In these cases the possibility of an OD should be consid-ered.

The talus has a limited reparative capacity because of itsrestricted vascular supply [14]. Inappropriate treatment ofOD may result in chronic ankle pain, functional impairment,subchondral cyst formation, and eventually osteoarthritis ofthe ankle [14—16].

For the last decade great developments have beenmade in the surgical treatment. Despite advancements inoptions like osteochondral autograft transfer system (OATS)or autologous chondrocyte implantation (ACI), arthroscopicdebridement and bone marrow stimulation remain the besttreatment that is currently available for defects up to 15 mmin diameter [17,18]. In larger (cystic) defects this treat-ment is less successful, and hence there is more debate[19,20].

The aim of this article is to provide an overview of treat-ment options and their indications for ODs of the talus, basedon the current evidence.

Etiology

In 1985, trauma was described in 98% of lateral lesions andin 70% of medial lesions [1]; more recently, 93% for lat-eral and 61% for medial lesions were reported [18]. As notall patients report a history of ankle injury, a subdivisioncan be made in the etiology of nontraumatic and traumaticdefects.

Ischemia, subsequent necrosis and possibly genetics areetiologic factors in nontraumatic ODs [14]. Furthermore,ODs in identical twins [21] and in siblings [22] have beendescribed. Less reported possible causes are metabolic,vascular, endocrine and degenerative factors, as well asmorphologic abnormalities [2,11,23].

In the etiology of traumatic ODs, ankle sprains play thelargest role. A severe ankle sprain may cause a small fractureand subsequent impaired vascularity, leading to the forma-tion of an OD. Alternatively, the cause may not be a single
event but may consist of a series of repeated, less intenseinjuries [14,23]. Microtraumas caused by repetitive surfaceloading or excessive stress can lead to cartilage cellulardegeneration or apoptosis and thickening of the subchondralbone [24].
[oc

b

Tous droits réservés. - Document téléchargé le 08/03/2013

S399

echanism of injury

uring an ankle sprain the talus twists inside the ankleortise, which may lead to a bruise and subsequent soften-

ng or even delamination of the cartilage. Separation mayccur in the upper layer, as a result of shearing forces,r may occur in the subchondral bone. Osteocartilaginousragments either remain partially attached or become looseodies in the ankle joint. The subchondral fracture has nooft tissue attachments and is highly susceptible to sub-equent avascular necrosis [11]. The repetitive forcing ofynovial fluid into the underlying cancellous bone with everytep of walking may create a subchondral cyst [25]. Theepetitive fluid pressure may prevent healing of a subchon-ral cyst.

Berndt and Harty clearly described the trauma mecha-ism in cadaver ankles [2]. They were able to reproducelateral defect by strong inversion of a dorsiflexed ankle,

eading to compression of the lateral border of the talarome against the face of the fibula. Partial detachment ofhe chip occurred when the lateral ligament ruptured. Theyeproduced medial lesions by plantar flexion and inversionf the ankle combined with slight anterior displacement andateral rotation of the tibia upon the talus.

The lateral lesions are typically shallow and wafer-haped, indicating the shear mechanism of injury [15].ecause of their shape, lateral lesions are more frequentlyisplaced than medial lesions. In contrast, medial lesionsre generally deep and cup-shaped, indicating a mechanismf torsional impaction [15]. These lesions are usually largerhan lateral lesions [26].

pidemiology

ith the increased awareness and newer diagnostic tech-iques, the incidence of OD seems to increase [27]. In 1955,osien et al. described an incidence of 7% in 113 patientsonservatively treated for acute lateral ankle ligament rup-ures [13]. Later, van Dijk et al. reported 4% fresh talarome lesions and 67% fresh chondral lesions of any kind in0 patients who had operative repair of acute ruptures ofateral ligaments [28]. More recently, an even higher inci-ence was reported, namely 41% of 86 patients with anterioralofibular ligament disruptions and 71% of 92 patients withistal fibular fractures [29]. However, the majority of theseeported lesions were located at the cartilage covering thenterior aspect of the medial malleolus and the oppositeedial talar facet or the anteromedial rim of the tibiapla-

ond [28,29]. Accordingly, talar ODs were found in 28% [30]nd 40% [31] of patients with ankle fractures treated byrthroscopically assisted open reduction and internal fix-tion. In these series the highest incidence was found inatients with distal fibular fractures [30,31].

Most ODs are localized on the posteromedial (58%)r anterolateral (42%) talar dome (Fig. 1) [18], althoughnteromedial, posterolateral and central lesions also occur
26]. In a large magnetic resonance imaging (MRI) surveyf 428 affected ankles 53% of the lesions were localizedentromedially and 26% centrolaterally [26].
In 4—7% of patients the occurrence of the defect isilateral [2,6,15], suggesting nontraumatic osteochondritis

S400

Figure 1 Three-dimensional CT-reconstruction of the leftankle of a 26-year-old male patient with a large osteochon-dral defect typically localized on the posteromedial (PM) talarda

do

C

Aabtopaawawmfsf

mssmst

D

Rc

Tase[saTlbp

tAsfpat1

C

ArTB

S

i

w1rgo

T

Vpt

•

•

•


ome. The usual localization of an anterolateral (AL) defect islso indicated (*).

issecans. Patients with an OD are frequently 20 to 30-year-ld men [2,17,18].

linical presentation

n OD often causes deep pain, swelling, recurrent synovitis,nd sometimes locking complaints. A differentiation has toe made between the acute and chronic situation [11]. Inhe acute situation symptoms of the OD compare to thosef acute ankle injuries, including lateral or medial ankleain, swelling and limited range of motion. In patients withn isolated ligamentous ankle injury these symptoms usu-lly resolve after functional treatment within two to threeeeks. If symptoms do not resolve after three to six weeksn OD should be suspected. These patients usually presentith persisting symptoms and sometimes a limited range ofotion. Locking and catching are symptoms of a displaced

ragment. In most patients with a nondisplaced lesion theymptoms in the acute situation cannot be distinguishedrom the soft tissue damage.

Chronic lesions typically present as persistent or inter-ittent deep ankle pain, during or after activity. Reactive

welling and stiffness may be present, but absence ofwelling, locking, or catching does not rule out an OD. Thereay be a normal range of motion, with the absence of

welling and absence of recognizable tenderness on palpa-ion.

iagnosis

outine radiographs of the ankle should be obtained afterareful history taking and physical examination of the ankle.

ob


C.J.A. van Bergen et al.

hese consist of weight-bearing anteroposterior (mortise)nd lateral views of both ankles. The sensitivity andpecificity of the combination of medical history, physicalxamination and radiography are 59 and 91%, respectively12]. The radiographs may not reveal any pathology, orhow an area of radiolucency (Fig. 2A). Initially the dam-ge may be too small to be visualized on a routine X-ray.he OD sometimes becomes apparent on radiographs at a

ater stage. A posteromedial or posterolateral defect maye revealed by a heelrise mortise view with the ankle inlantar flexion (Fig. 2C) [12].

For further diagnostic evaluation MRI or computedomography (CT) are often used, with similar accuracy [12].multislice helical CT-scan is useful for defining the exact

ize and location of the lesion and is therefore preferredor preoperative planning (Fig. 3) [11,32]. The scanningrotocol involves ‘‘ultrahigh resolution’’ axial slices withn increment of 0.3 mm and a thickness of 0.6 mm. Mul-iplanar coronal and sagittal reconstructions should bemm.

lassification

number of classifications have been proposed, based onadiography, CT, MRI, and arthroscopy [2,5,27,29,33,34].he first and most frequently used classification is fromerndt and Harty [2]:

Stage I A small compression fractureStage II Incomplete avulsion of a fragmentStage III Complete avulsion of a fragment without displace-

menttage IV Displaced fragment

Scranton and McDermott later added Stage V, represent-ng cystic lesions [25].

CT-scans are increasingly used in the preoperativeorkup. A CT-classification was therefore introduced in993, resembling the above classification, with stage V rep-esenting a radiolucent defect [27]. None of the currentrading systems, however, is sufficient to direct the choicef treatment.

reatment

arious surgical techniques for symptomatic ODs have beenublished. These are generally based on one of the followinghree principles [11]:

debridement and bone marrow stimulation (microfractur-ing, drilling, abrasion arthroplasty), with or without loosebody removal;securing a lesion to the talar dome (fragment fixation,retrograde drilling, cancellous bone grafting);development or replacement of hyaline cartilage (osteo-
chondral autograft transfer, ACI, allografts).
For years there has been an ongoing debate about theptimal treatment regime. Debridement of the lesion haseen performed progressively since the 1950s [2]. This

Treatment of osteochondral defects of the talus S401

adiogosteorrow

tpl

wtOoatpt

gc

S

Ts


Figure 2 Weight-bearing anteroposterior (A) and lateral (B) rradiolucency in the medial talar dome (arrow), indicating anreveals the posteromedial osteochondral defect more clearly (a

method was later combined with bone marrow stimula-tion, by means of drilling or microfracturing, with favorableresults [35]. With the development of ankle arthroscopy,this combined procedure gained much popularity [6,7,36].Nowadays, arthroscopic debridement and bone marrowstimulation are the mostly performed procedure for OD.Publications on treatment options for talar ODs were bun-dled in a systematic review performed in our institution inJuly 1998 [17] and updated in June 2000 [18]. Twenty-oneinvestigations with a total of 272 patients were identified.The success rate of debridement and bone marrow stim-ulation was superior to other methods. Arthroscopy wassuccessful in 87% and open procedures in 84% of the cases[18]. These good results were confirmed more recently[37,38]. However, OATS and ACI were not included dueto few studies, and sizes of the treated lesions were notdescribed.

In the case of a cystic lesion, debridement may be sup-plemented by cancellous bone grafting [11,38,39]. However,the limited availability of cancellous bone and pain at thedonor site remain disadvantages [40]. Large osteochondral
fragments can be fixed by screws, with a success rate of 73%(Fig. 4) [17].
Recently, more developments have taken place. OATS andACI as original procedures for osteochondral lesions of theknee have evolved to suitable treatment methods for cer-

pra[o

Figure 3 CT-scans of the right ankle of a 26-year-old female patieA. Axial slice. B. Coronal reconstruction. C. Sagittal reconstruction.


raphs of the right ankle of a 36-year-old male patient showingchondral defect. A 4 cm heelrise view (C) of the same ankle).

ain lesions of the talus [41—43]. Excellent results have beenublished, although numbers are still fairly small and noong-term follow-up is available [43—46].

In 2005 an expert consensus on the treatment of ODas achieved during the World Consensus Conference of

he International Society of Arthroscopy, Knee surgery andrthopaedic Sports medicine and International Federationf Sports Medicine (ISAKOS—FIMS) [47]. The expert groupgreed that debridement and bone marrow stimulation arehe first step in the treatment of most symptomatic OD andresented a useful guideline. For failed primary treatmenthey recommended to consider OATS.

Based on the current literature, a revised treatmentuideline is presented (Table 1), which will be further dis-ussed in the Discussion section.

urgical approach

he size and location of the lesion as well as the type ofurgical treatment determine the surgical approach. The
referred approach of most lesions is by means of ante-ior arthroscopy [48]. Alternative approaches are posteriorrthroscopy by means of a two-portal hindfoot approach49] and open arthrotomy with or without a medial malle-lar osteotomy [50,51]. Arthroscopy offers the advantages
nt showing a cystic posteromedial osteochondral ankle defect.

S402 C.J.A. van Bergen et al.

Figure 4 Weight-bearing radiographs of the left ankle of a 13-year-old male patient with progressive complaints of deep anklepain over 18 months without preceding trauma. Preoperative anteroposterior (A) and lateral (B) radiographs show a large lateralradiolucent area involving more than 50% of the talar dome, represeby means of two compression screws. The radiographs C and D represhas healed. Screw removal was performed three months later.

Table 1 Guideline for treatment of osteochondral defectsof the talus.

Lesion type Treatment options

Asymptomatic or lowsymptomatic

Conservative

Symptomatic, < 15 mm Conservativea, debridementand drilling/microfracturing

Symptomatic, ≥ 15 mm Fragment fixation, OATS, ACI,debridement anddrilling/microfracturing

Cystic, ≥ 15 mm Debridement ± (retrograde)drilling/microfracturing withcancellous bone, OATS, ACIwith cancellous bone

Secondary OATS, ACI, HemiCAP®b,TruFit®b

Massive lesion Allograft, ankle arthrodesis,total ankle replacement

OATS: osteochondral autograft transfer system; ACI: autologouschondrocyte implantation.

a A trial period of six months conservative treatment isrecommended.

b

omrmio

uaAipte

D

Wutsbdavtbt

abcc

douw2tie

d(aimtrs

Operative technique


Resurfacing of the medial talar dome by a metal implant(HemiCAP®) and biodegradable double-layer implants (TruFit®)might become valuable alternatives in the future.

f outpatient treatment and possibly less postoperativeorbidity, faster and functional rehabilitation, and earlier

esumption of sports [48]. Lateral lesions seldom require aalleolar osteotomy. In the rare case of a posteriorly local-

zed lateral lesion, a fibular osteotomy provides the bestpen exposure [52].

In the situation of debridement and bone marrow stim-lation the majority of lesions can be treated by means ofnterior arthroscopy with the ankle in full plantar flexion.s a rule of thumb, lesions located in the anterior half or

n the anterior part of the posterior half of the talus in
atients with unlimited plantar flexion can be reached andreated this way [48]. Some ligament laxity will improve thexposure.
Tap


nting partial talar necrosis. The lesion was secured to the talusent the situation six months postoperatively in which the lesion

ebridement and bone marrow stimulation

ith this technique, all unstable cartilage including thenderlying necrotic bone is removed. Any cysts underlyinghe defect are opened and curetted. After debridement,everal connections with the subchondral bone are createdy drilling or microfracturing. The objective is to partiallyestroy the calcified zone that is often present and to cre-te openings into the subchondral bone. Intraosseous bloodessels are disrupted and the release of growth factors leadso the formation of a fibrin clot. The formation of local newlood vessels is stimulated, marrow cells are introduced inhe defect and fibrocartilaginous tissue is formed [53].

Advantages of this technique are the possibility ofrthroscopy, the relatively easy procedure, and early reha-ilitation. A disadvantage is the formation of fibrousartilage rather than hyaline cartilage. Although often suc-essful, this may be insufficient for large defects [19].

Preoperatively the approach to the defect should beetermined (see section: Surgical approach). In the casef arthroscopic treatment it has to be decided whether tose a 4.0 mm arthroscope and treat the OD in the anteriororking area by full plantar flexion of the ankle, or to use a.7 mm arthroscope in combination with mechanical distrac-ion [36]. Arthroscopy with the foot in full plantar flexions the preferred method in most cases, although skill andxperience are required [7,48].

The subchondral bone can be perforated using a 2 mmrill, a microfracture awl or a 1.4 mm Kirschner-wireK-wire). A K-wire has the advantage of flexibility, whereas

drill may break more easily if the position of the ankles changed during drilling. Microfracturing by means of aicrofracture awl offers the possibility to work ‘‘around

he corner’’ and results in microfractures of the trabeculaeather than destruction of the bone [54], but any createdmall bony particles should be carefully removed [55].

he standard anteromedial and anterolateral approachesre created in the fully dorsiflexed position, as describedreviously [36,48]. Introduction of the 4.0 mm arthroscope

Treatment of osteochondral defects of the talus S403

Figure 5 Arthroscopic images of the right talus of a 17-year-old female patient with a lateral osteochondral defect (OD) that istreated by debridement and drilling. A. The arthroscope is in the anteromedial portal. With the ankle in the neutral position the ODis out of the arthroscopic view. B. By bringing the ankle in plantarflexion the OD can be seen. C. The size of the lesion is identified

tedles ae tou

iOmta[

toctirtttsAaif(

O

Frptbth


by palpating the cartilage with a probe (arrows), which is inserdebridement of the defect. E. With the use of a K-wire small hotreated lesion after switching portals. G. During loosening of th

and a 4.5 or 5.5 mm bonecutter shaver is performed with theankle in the fully dorsiflexed position to prevent iatrogeniccartilage damage. If osteophytes or synovitis are present,they are removed first by a chisel, burr or bonecutter shaverwith the ankle in the dorsiflexed position. The completenessof removal is checked by plantarflexing the ankle. Duringthis part of the procedure a soft tissue distractor may beapplied (Fig. 5A) [36,56]. It should now be possible to visu-alize the lesion in the forced plantarflexed position (Fig. 5B)and to identify the defect by palpating the cartilage witha probe or hook (Fig. 5C). Debridement is performed byusing the bonecutter shaver or a small closed cup curette(Fig. 5D). It is important to remove all necrotic bone andoverlying unstable cartilage [57]. After full debridement,the sclerotic zone is perforated several times at intervals ofapproximately 3 mm (Fig. 5E and F). Sufficient hemorrhagecan be checked by loosening of the tourniquet (Fig. 5G).

Rehabilitation

Active plantar flexion and dorsiflexion are encouraged. Par-tial weight-bearing (eggshell) is allowed as tolerated. It isthe senior author’s practice to allow progress to full weight-bearing within two to four weeks in patients with central orposterior lesions of up to 1 cm. Larger lesions and anteriorlesions require partial weight-bearing up to six weeks. Run-ning on even ground is permitted after 12 weeks [11]. Sportis resumed after an average of 15.1 weeks [38]. Full returnto normal and sporting activities is usually possible four tosix months after surgery [19].

Osteochondral autograft transfer

OATS consists of the harvesting of one or more osteochon-dral plugs in a lesser-weight-bearing area of the knee andtransplanting them into the talar defect [41,58]. The aim

ud

cO


through the anterolateral portal. D. A shaver is introduced forre drilled in the subchondral bone. F. Arthroscopic view of therniquet sufficient hemorrhage in the defect is checked.

s to restore the articular surface with hyaline cartilage.ne single graft or several smaller grafts (i.e. mosaicplasty)ay be used. The use of several grafts provides a bet-

er match to the curvature of the talar dome and surfacerea of the defect, and may reduce donor site morbidity45,59].

Although X-ray evaluation and CT may help to determinehe extent of the lesion, indication of OATS is rather basedn the size determined after excision of the defect. OATSan also be offered to patients in case of failed primaryreatment (Table 1). An essential aspect of the procedures insertion of the osteochondral plugs perpendicular to theecipient site. Due to the constrained configuration of thealocrural joint with its highly contoured articular surfaces,he best approach is by means of open arthrotomy, most ofhe times using a malleolar osteotomy. The primary harvestite is the medial upper part of the medial femoral condyle.s a less frequent option, the lateral supracondylar ridge canlso be used through a miniarthrotomy [11]. In case the knees precluded as a donor site, the ipsilateral talar articularacet may also be used as a harvest site of small-sized grafts2.7 or 3.5 mm in diameter) [60].

perative technique

or medial lesions a medial malleolar osteotomy is usuallyequired. Once the lesion is exposed, all diseased and sus-ect cartilage is removed by curette and scalpel dissectiono a sharply defined rim. After debridement of the bonyase of the defect by curettage or abrasion arthroplasty,he sharp cutting edge of the appropriate-sized drill guideelps to determine an ideal filling rate of the defect. The
sual size of the drill holes in the talus is 4.5 or 6.5 mm iniameter (Fig. 6).
Upon completion of the recipient site preparation, osteo-hondral grafts are harvested from the ipsilateral knee.nce the site has been clearly identified, the proper size

S404

Figure 6 Osteochondral defect of the anterolateral talard(t

tfM[fd

awbAuFcibeih

R

Pwpiseam

A

Aditt

9Bgo

ptawtw

lmtt

O

AoAs2ap

wmAtbt

otiaaicrptwh

R

Tppiwagraphic evidence of osteotomy healing. At six weeks, the


ome after treatment with two osteochondral autograftsarrows), measuring 6.5 and 4.5 mm in diameter, harvested fromhe knee.

ubular chisel is directed perpendicular to the articular sur-ace and driven by a hammer to the appropriate depth.inimal graft length should be at least twice its diameter

11]. Three to four plugs can be obtained by flexing the kneerom 0 to 100◦. At the end of the graft harvesting a suctionrain is left behind in the knee joint.

After the graft harvest the recipient site is again evalu-ted. The first hole is drilled through the tubular drill guide,hich also serves as the delivery tube. The depth shoulde 3—4 mm deeper than the length of the selected plug.t this stage the hole is enlarged by 0.1—0.2 mm with these of a conical dilator, allowing easy insertion of the graft.or each graft, drilling, dilation and delivery are done as aombined step accordingly. After the entire set of grafts ismplanted (Fig. 6), the ankle is lavaged, observed for looseodies, and sent through a range of motion to ensure congru-ncy of the mosaicplasty. The osteotomy site is reduced andnternal fixation is performed utilizing the predrilled screwoles.

ehabilitation

atients are kept nonweight-bearing for three weeks; sixeeks for those with a malleolar osteotomy. Following thiseriod, partial weight-bearing up to 30 kg for three weekss allowed to promote integration of the grafts. An ortho-is may improve comfort. Range of motion exercises arencouraged. Unprotected weight-bearing is subsequentlyllowed. Athletic activities may begin at approximately sixonths.

utologous chondrocyte implantation

CI is the implantation of in vitro cultured autologous chon-rocytes using a periosteal tissue cover after expansion ofsolated chondrocytes. ACI has been popularized by Brit-berg et al. and Petersen et al. since 1994 [42,43]. Sincehat time, ACI has been performed in over 25,000 patients;

ptri



5% in the knee, 3% in the ankle, and 2% in other joints [11].ased on promising early results with ACI in the knee, sur-eons have now started using ACI for osteochondral lesionsf the talus.

For patients with an OD who remain symptomatic afterrimary surgical treatment ACI is considered a valuablereatment option. The defect should be focal, contained,nd preferably more than 1.5 cm in diameter. Large lesionsith subchondral cysts may also be treated with ACI, using

he ‘‘sandwich technique’’, i.e. filling the base of the defectith autologous cancellous bone [43,46].

Contraindications to ACI are bipolar lesions (‘‘kissingesions’’) and diffuse degenerative joint changes. Skeletalalalignment and ligamentous instability are also con-

raindications, unless they are concomitantly corrected athe time of surgery [46].

perative technique

CI is a staged procedure. The initial surgery consistsf ipsilateral knee arthroscopy for cartilage harvesting.rticular cartilage is harvested from nonweight-bearingurfaces such as the intercondylar notch. Approximately00—300 mg of cartilage is harvested with the use of curettesnd sent to the laboratory for chondrocyte isolation androliferation.

The second stage of the procedure is usually at least foureeks after the harvesting procedure. A medial or lateralalleolar osteotomy is necessary to provide access for theCI procedure [46]. All pathologic fibrous and cartilaginousissue is debrided. One should not penetrate the subchondralone during this step, as this would enable marrow elementso contaminate the cultured chondrocyte population.

The periosteal graft, oversized by 1—2 mm, is nextbtained from the ipsilateral proximal or distal tibia. Withhe cambium side facing toward bone, the periosteal grafts placed over the defect and sutured with multifilamentbsorbable sutures, size 5.0 or 6.0. Fibrin glue is placedt the interface to help seal the graft. A small open-ng at the interface is left patent. Saline is injected, toonfirm a watertight compartment, and subsequently aspi-ated from the defect. The cultured chondrocytes are thenlaced into the defect and the insertion site is closed withhe last stitch and fibrin glue. The osteotomy is repairedith two malleolar screws inserted through predrilledoles.

ehabilitation

he patient is kept nonweight-bearing and placed in a well-added short leg cast during the immediate postoperativeeriod. At two weeks postoperatively, the patient is placedn a controlled action motion (CAM) walker boot. Partialeight-bearing and gentle ankle range of motion exercisesre permitted. Weight-bearing is advanced based on radio-

atient discontinues the use of the CAM walker. Repeti-ive impact activities, such as jogging and aerobics, can beesumed after six to eight months. Return to high level sportss permitted after 12 months.

padtaim

nvlOmctlsdco

tmbrnclallba

p1as

[ro

lteaca

titems[



Future developments

To overcome the disadvantages of current treatment optionsvarious attempts are undertaken, aimed at the improvementof current techniques or the development of alternativemethods.

To improve ACI, researchers are experimenting withalternatives. The detached osteochondral fragment hasbeen proposed as a source of osteocytes to result in lessmorbidity [61]. Furthermore, different scaffolds that canbe implanted with cultured chondrocytes have been devel-oped, obviating the need for periosteal grafting for fixation[62—64]. Matrix-induced autologous chondrocyte implanta-tion (MACI) makes use of a collagen type I—III membrane,which serves as the scaffold for implanted chondrocytes.Although this is promising in animal and human knees[64,65], only two short-term ankle cases have been reported[63]. Using Hyalograft C as the scaffold, Giannini et al. per-formed arthroscopic ACI in 30 patients with good short-termresults [20].

Regarding OATS, the postoperative application of pulsedelectromagnetic fields has been recently shown to limit graftresorption and cyst formation in sheep [66].

As a tissue engineering technique of cartilage, bonemarrow-derived mesenchymal stem cells have been suc-cessfully implanted using different scaffolds. The majorityof this research, however, is still experimental [67—70].Jancewicz et al. were the first to report a clinical seriesin the talus [71]. Demineralized bone matrix has been pro-posed as an alternative to autologous bone grafts for thetreatment of OD [72].

Experimental progress is made with the use of biodegrad-able composite implants. Müller et al. reported the use ofdouble-layer biodegradable implants consisting of poly-dl-lactide and a polyglactin/polydioxanon fleece [73]. Jianget al. investigated repair with a biphasic osteochon-dral composite consisting of b-tricalcium phosphate anddl-polylactide-co-glycolide seeded with autologous chondro-cytes using single stage surgery [74]. Commercially availablecomposite implants have become available for the treat-ment of ODs of the knee (TruFit Plug®, Smith & Nephew, SanAntonio, TX, USA) [75].

Our research group is currently investigating the appli-cability of a novel resurfacing technique of the medial talardome by means of a contoured metal implant (HemiCAP®,Arthrosurface Inc., Franklin, MA, USA) [76].

Alignment and potential correction osteotomy are impor-tant issues. In case of persistent complaints after initialtreatment, check the overall alignment and hindfoot align-ment. The future role of correction osteotomy in thetreatment algorithm of OD has to be established.

Discussion

The choice of treatment depends on several factors, suchas the patient’s age, symptoms, duration of complaints,
location and size of the defect, and whether it concernsa primary or secondary OD [6,11,19,20].
Asymptomatic or low-symptomatic lesions are treatednonoperatively by rest, ice, temporarily reduced weight-bearing, and an orthosis in case of giving way, for a trial

tlotd


S405

eriod of six months [7,11]. Although nonoperative ther-py yields only 45% successful results [18], a trial periodoes not adversely affect the outcome of surgery [35]. Car-ilage lesions have demonstrated to deteriorate slowly in thenkle joint. Hence, the advice is to be conservative; theres always time to test the effect of debridement and bonearrow stimulation.Surgical treatment is considered in the case of failure of

onoperative treatment or continuing symptoms after pre-ious surgery (secondary OD). According to reviews of theiterature the best currently available treatment for primaryDs is the combination of excison, debridement and bonearrow stimulation [17,18]. According to the ISAKOS—FIMS

onsensus debridement and drilling or microfracturing arehe first step in the treatment of symptomatic osteochondralesions that are too small to consider fixation [47]. Hence,ymptomatic lesions up to 15 mm are treated primarily byebridement and bone marrow stimulation. Subchondralystic lesions smaller than 15 mm do not influence the post-perative prognosis [77].

In the case of a (cystic) defect sized 15 mm or largerhis technique might also be considered as a primary treat-ent option. In these cases a cancellous bone graft maye placed in the defect after debridement [20,38,78]. Ret-ograde drilling, combined with cancellous bone grafting ifecessary, may be performed if there is a (large) subchondralyst with intact cartilage [34,79]. Alternatively, the cancel-ous bone graft may be placed underneath the cartilage flapfter debridement of the subchondral bone [78]. A cancel-ous bone graft is harvested from the ipsilateral iliac crest orocally from the distal tibial metaphysis [39]. Possible draw-acks of this procedure are the limited availability and paint the donor site [40].

Fragment fixation with one or two screws or K-wires isreferred in (sub)acute situations in which the fragment is5 mm or larger. In adolescents, fixation of an OD shouldlways be considered in case of failure of a period of con-ervative treatment (Fig. 4) [32].

In case of failed primary surgical treatment, OATS41,45,80] and the more recently introduced ACI [43,44] areeasonable options. They both aim at creating a new layerf hyaline cartilage.

OATS was originally developed to treat osteochondralesions in the knee [81]. After promising early experiences,he indication was extended to the talus [45]. Christel et al.mphasized the difficulty of restoring the curvature of therticular surface and reported less favorable clinical out-ome in the ankle compared to the knee [82], whereas otheruthors published promising results [45,80,83,84].

Although hyaline cartilage of the donor area located inhe knee is different from the talar hyaline cartilage, theres no evidence this would represent a negative influence onhe results. However, the integration of donor and recipi-nt hyaline cartilage can be impaired because of differentechanical properties and thickness [82,85,86]. Other pos-

ible disadvantages are the limited availability of grafts85] and the risk of donor site morbidity [87]. Furthermore,
he use of a medial malleolar osteotomy to approach theesion has been associated with a worse outcome, i.e. localsteoarthritis and higher morbidity [88]. A randomized con-rolled trial with two years follow-up comparing OATS withebridement (with or without microfracture) showed similar

S

raoau

nh[tiacdsaoad

aeti[ivt

C

TtIm

baeOepaiptemf

R

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[


406

esults among the methods [89]. However, the debridementnd microfracture techniques were recommended becausef less postoperative pain. Possible alternatives includingrtificial osteochondral plugs and metal implants may besed in the future.

The newer ACI offers a promising treatment alter-ative, but long-term data are lacking. Several authorsave reported favorable results at short-term follow-up11,43,44,90—92]. However, long-term studies are neededo evaluate the efficacy of this technique. Incomplete heal-ng of subchondral cysts has been noted in some patientsfter ACI, although this did not adversely influence clini-al outcomes at short-term follow-up [11]. Other possibleisadvantages are insufficient graft integration, two-stageurgery and high costs [85,92,93]. Until further data arevailable, we cannot advocate ACI as an initial treatmentption for most cases of OD. However, in patients who havelarge OD or failed prior surgical treatment, the short-termata suggest that ACI can provide good results.

For massive ODs the transplantation of fresh or frozenllografts has been described. A number of experts havexpressed their concerns of use in the talus, based uponhe gradual deterioration of the hyaline part of such graftsn the knee and resorption and fragmentation of the graft94]. Therefore, transplantation of osteochondral allograftss only indicated for massive osteochondral lesions [95]. Sal-age procedures for massive ODs or recurrent failure ofreatment are ankle arthrodesis or total ankle replacement.

onclusion

he choice of treatment is hindered by the fact that none ofhe grading systems is related to current treatment options.n Table 1 we present a guideline for treatment that is pri-arily based on the size of the lesion.Arthroscopic debridement and bone marrow stimulation,

y nature of the minimally invasive approach, have greatdvantage in treating typical defects of up to 1.5 cm in diam-ter. For larger ODs, the optimal treatment may consist ofATS, cancellous bone graft and/or ACI. The medium-termncouraging results of OATS and cancellous bone grafts holdromise for these procedures in lasting relief of symptomsnd prevention of ankle osteoarthritis. ACI has encourag-ng short-term results in the ankle joint. Much research iserformed to improve this method, and its place in thereatment algorithm remains to be further defined. Tissuengineering techniques, artificial plugs and resurfacing byetal implants might become reasonable alternatives in the

uture.

eferences

[1] Flick AB, Gould N. Osteochondritis dissecans of the talus (tran-schondral fractures of the talus): review of the literature andnew surgical approach for medial dome lesions. Foot Ankle1985;5(4):165—85.

[2] Berndt AL, Harty M. Transchondral fractures (osteochondritisdissecans) of the talus. J Bone Joint Surg Am 1959;41-A:988—1020.

[3] Ittner G, Jaskulka R, Fasol P. Treatment of flake fracture of thetalus. Z Orthop Ihre Grenzgeb 1989;127(2):183—6.

[

[



[4] Baker Jr CL, Morales RW. Arthroscopic treatment of tran-schondral talar dome fractures: a long-term follow-up study.Arthroscopy 1999;15(2):197—202.

[5] Anderson IF, Crichton KJ, Grattan-Smith T, Cooper RA, BrazierD. Osteochondral fractures of the dome of the talus. J BoneJoint Surg Am 1989;71(8):1143—52.

[6] Kumai T, Takakura Y, Higashiyama I, Tamai S. Arthroscopicdrilling for the treatment of osteochondral lesions of the talus.J Bone Joint Surg Am 1999;81(9):1229—35.

[7] Schuman L, Struijs PA, van Dijk CN. Arthroscopic treatment forosteochondral defects of the talus. Results at follow-up at 2 to11 years. J Bone Joint Surg Br 2002;84(3):364—8.

[8] Monro A, Billroth T. Microgeologie, Berlin; 1856. p. 236 [citedby Berndt and Harty].

[9] König F. Über freie Körper in den Gelenken. Dtsch Z Chir1888;27:90—109.

10] Kappis M. Weitere Beiträge zur traumatisch-mechanischenEntstehung der ‘‘spontanen’’ Knorpelablösungen (sogen.Osteochondritis dissecans). Dtsch Z Chir 1922;171:13—29.

11] Zengerink M, Szerb I, Hangody L, Dopirak RM, Ferkel RD, vanDijk CN. Current concepts: treatment of osteochondral ankledefects. Foot Ankle Clin 2006;11(2):331—59, vi.

12] Verhagen RA, Maas M, Dijkgraaf MG, Tol JL, Krips R, van DijkCN. Prospective study on diagnostic strategies in osteochondrallesions of the talus. Is MRI superior to helical CT? J Bone JointSurg Br 2005;87(1):41—6.

13] Bosien WR, Staples OS, Russel SW. Residual disabilityfollowing acute ankle sprains. J Bone Joint Surg Am 1955;37-A(6):1237—43.

14] Schachter AK, Chen AL, Reddy PD, Tejwani NC. Osteochondrallesions of the talus. J Am Acad Orthop Surg 2005;13(3):152—8.

15] Canale ST, Belding RH. Osteochondral lesions of the talus. JBone Joint Surg Am 1980;62(1):97—102.

16] Mankin HJ. The response of articular cartilage to mechanicalinjury. J Bone Joint Surg Am 1982;64(3):460—6.

17] Tol JL, Struijs PA, Bossuyt PM, Verhagen RA, van Dijk CN. Treat-ment strategies in osteochondral defects of the talar dome: asystematic review. Foot Ankle Int 2000;21(2):119—26.

18] Verhagen RA, Struijs PA, Bossuyt PM, van Dijk CN. Systematicreview of treatment strategies for osteochondral defects of thetalar dome. Foot Ankle Clin 2003;8(2):233—42.

19] Chuckpaiwong B, Berkson EM, Theodore GH. Microfracture forosteochondral lesions of the ankle: outcome analysis and out-come predictors of 105 cases. Arthroscopy 2008;24(1):106—12.

20] Giannini S, Buda R, Faldini C, Vannini F, Bevoni R, Grandi G,et al. Surgical treatment of osteochondral lesions of the talusin young active patients. J Bone Joint Surg Am 2005;87(Suppl.2):28—41.

21] Woods K, Harris I. Osteochondritis dissecans of the talus inidentical twins. J Bone Joint Surg Br 1995;77(2):331.

22] Anderson DV, Lyne ED. Osteochondritis dissecans of thetalus: case report on two family members. J Pediatr Orthop1984;4(3):356—7.

23] Bruns J. Osteochondrosis dissecans. Orthopade 1997;26(6):573—84.

24] Frenkel SR, Di Cesare PE. Degradation and repair of articularcartilage. Front Biosci 1999;4:D671—85.

25] Scranton Jr PE, McDermott JE. Treatment of type V osteochon-dral lesions of the talus with ipsilateral knee osteochondralautografts. Foot Ankle Int 2001;22(5):380—4.

26] Elias I, Zoga AC, Morrison WB, Besser MP, Schweitzer ME, RaikinSM. Osteochondral lesions of the talus: localization and mor-phologic data from 424 patients using a novel anatomical grid
scheme. Foot Ankle Int 2007;28(2):154—61.
27] Loomer R, Fisher C, Lloyd-Smith R, Sisler J, Cooney T. Osteo-chondral lesions of the talus. Am J Sports Med 1993;21(1):13—9.

28] van Dijk CN, Bossuyt PM, Marti RK. Medial ankle pain after lat-eral ligament rupture. J Bone Joint Surg Br 1996;78(4):562—7.

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[



[29] Takao M, Ochi M, Uchio Y, Naito K, Kono T, Oae K. Osteochondrallesions of the talar dome associated with trauma. Arthroscopy2003;19(10):1061—7.

[30] Aktas S, Kocaoglu B, Gereli A, Nalbantodlu U, Guven O. Inci-dence of chondral lesions of talar dome in ankle fracture types.Foot Ankle Int 2008;29(3):287—92.

[31] Loren GJ, Ferkel RD. Arthroscopic assessment of occultintraarticular injury in acute ankle fractures. Arthroscopy2002;18(4):412—21.

[32] Stone JW. Osteochondral lesions of the talar dome. J Am AcadOrthop Surg 1996;4(2):63—73.

[33] Hepple S, Winson IG, Glew D. Osteochondral lesionsof the talus: a revised classification. Foot Ankle Int1999;20(12):789—93.

[34] Taranow WS, Bisignani GA, Towers JD, Conti SF. Retrogradedrilling of osteochondral lesions of the medial talar dome. FootAnkle Int 1999;20(8):474—80.

[35] Alexander AH, Lichtman DM. Surgical treatment of tran-schondral talar dome fractures (osteochondritis dissecans).Long-term follow-up. J Bone Joint Surg Am 1980;62(4):646—52.

[36] van Dijk CN, Scholte D. Arthroscopy of the ankle joint.Arthroscopy 1997;13(1):90—6.

[37] Hankemeier S, Muller EJ, Kaminski A, Muhr G. 10-yearresults of bone marrow stimulating therapy in the treat-ment of osteochondritis dissecans of the talus. Unfallchirurg2003;106(6):461—6.

[38] Saxena A, Eakin C. Articular talar injuries in athletes: resultsof microfracture and autogenous bone graft. Am J Sports Med2007;35(10):1680—7.

[39] Kolker D, Murray M, Wilson M. Osteochondral defects of thetalus treated with autologous bone grafting. J Bone Joint SurgBr 2004;86(4):521—6.

[40] Silber JS, Anderson DG, Daffner SD, Brislin BT, Leland JM, Hili-brand AS, et al. Donor site morbidity after anterior iliac crestbone harvest for single-level anterior cervical discectomy andfusion. Spine 2003;28(2):134—9.

[41] Hangody L, Fules P. Autologous osteochondral mosaic-plasty for the treatment of full-thickness defects ofweight-bearing joints: 10 years of experimental and clinicalexperience. J Bone Joint Surg Am 2003;85-A(Suppl. 2):25—32.

[42] Brittberg M, Lindahl A, Nilsson A, Ohlsson C, Isaksson O,Peterson L. Treatment of deep cartilage defects in the kneewith autologous chondrocyte transplantation. N Engl J Med1994;331(14):889—95.

[43] Petersen L, Brittberg M, Lindahl A. Autologous chon-drocyte transplantation of the ankle. Foot Ankle Clin2003;8(2):291—303.

[44] Baums MH, Heidrich G, Schultz W, Steckel H, Kahl E,Klinger HM. Autologous chondrocyte transplantation for treat-ing cartilage defects of the talus. J Bone Joint Surg Am2006;88(2):303—8.

[45] Hangody L, Kish G, Modis L, Szerb I, Gaspar L, Dioszegi Z, et al.Mosaicplasty for the treatment of osteochondritis dissecans ofthe talus: two to seven year results in 36 patients. Foot AnkleInt 2001;22(7):552—8.

[46] Bazaz R, Ferkel RD. Treatment of osteochondral lesions ofthe talus with autologous chondrocyte implantation. Tech FootAnkle Surg 2004;3(1):45—52.

[47] van Dijk CN. Osteochondral defect. In: Chan KM, Karlson J,editors. ISAKOS—FIMS World consensus conference on ankleinstability; 2005. p. 68—9.

[48] van Dijk CN, van Bergen CJ. Advancements in anklearthroscopy. J Am Acad Orthop Surg.

[49] van Dijk CN, Scholten PE, Krips R. A 2-portal endoscopicapproach for diagnosis and treatment of posterior ankle pathol-ogy. Arthroscopy 2000;16(8):871—6.

[


S407

50] Mendicino RW, Lee MS, Grossman JP, Shromoff PJ. Obliquemedial malleolar osteotomy for the management of talar domelesions. J Foot Ankle Surg 1998;37(6):516—23.

51] Jarde O, Trinquier-Lautard JL, Garate F, De LM, Vives P. Osteo-chondral lesions of the talar dome: surgical treatment in aseries of 30 cases. Rev Chir Orthop Reparatrice Appar Mot2000;86(6):608—15.

52] Garras DN, Santangelo JA, Wang DW, Easley ME. A quan-titative comparison of surgical approaches for posterolat-eral osteochondral lesions of the talus. Foot Ankle Int2008;29(4):415—20.

53] O’Driscoll SW. The healing and regeneration of articular carti-lage. J Bone Joint Surg Am 1998;80(12):1795—812.

54] Steadman JR, Rodkey WG, Rodrigo JJ. Microfracture: surgicaltechnique and rehabilitation to treat chondral defects. ClinOrthop Relat Res 2001;391(Suppl.):S362—9.

55] van Bergen CJ, de Leeuw PA, van Dijk CN. Potential pitfall inthe microfracturing technique during the arthroscopic treat-ment of an osteochondral lesion. Knee Surg Sports TraumatolArthrosc. 2008; doi:10.1007/s00167-008-0594-y.

56] van Dijk CN, Verhagen RA, Tol HJ. Technical note: Rester-ilizable noninvasive ankle distraction device. Arthroscopy2001;17(3):E12.

57] Takao M, Uchio Y, Kakimaru H, Kumahashi N, Ochi M. Arthro-scopic drilling with debridement of remaining cartilage forosteochondral lesions of the talar dome in unstable ankles. AmJ Sports Med 2004;32(2):332—6.

58] Scranton Jr PE, Frey CC, Feder KS. Outcome of osteochon-dral autograft transplantation for type-V cystic osteochondrallesions of the talus. J Bone Joint Surg Br 2006;88(5):614—9.

59] Choung D, Christensen JC. Mosaicplasty of the talus: a jointcontact analysis in a cadaver model. J Foot Ankle Surg2002;41(2):65—75.

60] Kreuz PC, Steinwachs M, Erggelet C, Lahm A, Henle P, NiemeyerP. Mosaicplasty with autogenous talar autograft for osteo-chondral lesions of the talus after failed primary arthroscopicmanagement: a prospective study with a 4-year follow-up. AmJ Sports Med 2006;34(1):55—63.

61] Giannini S, Buda R, Grigolo B, Vannini F, De FL, Facchini A.The detached osteochondral fragment as a source of cells forautologous chondrocyte implantation (ACI) in the ankle joint.Osteoarthritis Cartilage 2005;13(7):601—7.

62] Marcacci M, Berruto M, Brocchetta D, Delcogliano A, GhinelliD, Gobbi A, et al. Articular cartilage engineering with Hyalo-graft C: three-year clinical results. Clin Orthop Relat Res2005;435:96—105.

63] Cherubino P, Grassi FA, Bulgheroni P, Ronga M. Autologouschondrocyte implantation using a bilayer collagen mem-brane: a preliminary report. J Orthop Surg (Hong Kong)2003;11(1):10—5.

64] Willers C, Chen J, Wood D, Xu J, Zheng MH. Autologouschondrocyte implantation with collagen bioscaffold for thetreatment of osteochondral defects in rabbits. Tissue Eng2005;11(7—8):1065—76.

65] Bartlett W, Skinner JA, Gooding CR, Carrington RW, FlanaganAM, Briggs TW, et al. Autologous chondrocyte implantation ver-sus matrix-induced autologous chondrocyte implantation forosteochondral defects of the knee: a prospective, randomisedstudy. J Bone Joint Surg Br 2005;87(5):640—5.

66] Benazzo F, Cadossi M, Cavani F, Fini M, Giavaresi G, Setti S,et al. Cartilage repair with osteochondral autografts in sheep:effect of biophysical stimulation with pulsed electromagneticfields. J Orthop Res 2008;26(5):631—42.

67] Hui JH, Chen F, Thambyah A, Lee EH. Treatment of chondrallesions in advanced osteochondritis dissecans: a comparativestudy of the efficacy of chondrocytes, mesenchymal stem cells,periosteal graft, and mosaicplasty (osteochondral autograft) inanimal models. J Pediatr Orthop 2004;24(4):427—33.

http://dx.doi.org/10.1007/s00167-008-0594-y

S

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[


408

68] Liu Y, Shu XZ, Prestwich GD. Osteochondral defect repair withautologous bone marrow-derived mesenchymal stem cells in aninjectable, in situ, cross-linked synthetic extracellular matrix.Tissue Eng 2006;12(12):3405—16.

69] Kayakabe M, Tsutsumi S, Watanabe H, Kato Y, TakagishiK. Transplantation of autologous rabbit BM-derived mes-enchymal stromal cells embedded in hyaluronic acid gelsponge into osteochondral defects of the knee. Cytotherapy2006;8(4):343—53.

70] Shao X, Goh JC, Hutmacher DW, Lee EH, Zigang G. Repairof large articular osteochondral defects using hybrid scaffoldsand bone marrow-derived mesenchymal stem cells in a rabbitmodel. Tissue Eng 2006;12(6):1539—51.

71] Jancewicz P, Dzienis W, Pietruczuk M, Skowronski J, BieleckiM. Osteochondral defects of the talus treated by mesenchymalstem cell implantation: early results. Rocz Akad Med Bialymst2004;49(Suppl. 1):25—7.

72] Gao J, Knaack D, Goldberg VM, Caplan AI. Osteochondral defectrepair by demineralized cortical bone matrix. Clin Orthop RelatRes 2004;427(Suppl.):S62—6.

73] Muller PE, Schrimpf F, Milz S, Kircher J, Durr HR, Wegener B, etal. Repair of osteochondral defects in the knee by resorbablebioimplants in a rabbit model. Acta Orthop 2006;77(6):981—5.

74] Jiang CC, Chiang H, Liao CJ, Lin YJ, Kuo TF, Shieh CS, et al.Repair of porcine articular cartilage defect with a biphasicosteochondral composite. J Orthop Res 2007;25(10):1277—90.

75] Williams RJ, Gamradt SC. Articular cartilage repair using aresorbable matrix scaffold. Instr Course Lect 2008;57:563—71.

76] van Bergen CJ, Zengerink M, Blankevoort L, van Dijk CN. Par-tial resurfacing for osteochondral defects of the medial talardome: A biomechanical cadaver study. Presented at the 54thNordic Orthopaedic Federation Congress, Amsterdam, 11—13June 2008.

77] Han SH, Lee JW, Lee DY, Kang ES. Radiographic changesand clinical results of osteochondral defects of thetalus with and without subchondral cysts. Foot Ankle Int2006;27(12):1109—14.

78] Draper SD, Fallat LM. Autogenous bone grafting for thetreatment of talar dome lesions. J Foot Ankle Surg2000;39(1):15—23.

79] Kono M, Takao M, Naito K, Uchio Y, Ochi M. Retrograde drillingfor osteochondral lesions of the talar dome. Am J Sports Med2006;34(9):1450—6.

80] Assenmacher JA, Kelikian AS, Gottlob C, Kodros S. Arthroscop-
ically assisted autologous osteochondral transplantation forosteochondral lesions of the talar dome: an MRI and clinicalfollow-up study. Foot Ankle Int 2001;22(7):544—51.
81] Hangody L, Kish G, Karpati Z, Szerb I, Udvarhelyi I. Arthroscopicautogenous osteochondral mosaicplasty for the treatment of

[

[



femoral condylar articular defects. A preliminary report. KneeSurg Sports Traumatol Arthrosc 1997;5(4):262—7.

82] Christel P, Versier G, Landreau PH, Djian P. Osteochondralgrafting using the mosaicplasy technique. Maitrise Orthop1998;76:1—13.

83] Baltzer AW, Arnold JP. Bone-cartilage transplantation from theipsilateral knee for chondral lesions of the talus. Arthroscopy2005;21(2):159—66.

84] Gautier E, Kolker D, Jakob RP. Treatment of cartilage defectsof the talus by autologous osteochondral grafts. J Bone JointSurg Br 2002;84(2):237—44.

85] Giannini S, Vannini F. Operative treatment of osteochondrallesions of the talar dome: current concepts review. Foot AnkleInt 2004;25(3):168—75.

86] Lane JG, Massie JB, Ball ST, Amiel ME, Chen AC, Bae WC,et al. Follow-up of osteochondral plug transfers in a goatmodel: a six-month study. Am J Sports Med 2004;32(6):1440—50.

87] Reddy S, Pedowitz DI, Parekh SG, Sennett BJ, Okereke E. Themorbidity associated with osteochondral harvest from asymp-tomatic knees for the treatment of osteochondral lesions ofthe talus. Am J Sports Med 2007;35(1):80—5.

88] Gaulrapp H, Hagena FW, Wasmer G. Postoperative evaluationof osteochondrosis dissecans of the talus with special refer-ence to medial malleolar osteotomy. Z Orthop Ihre Grenzgeb1996;134(4):346—53.

89] Gobbi A, Francisco RA, Lubowitz JH, Allegra F, Canata G.Osteochondral lesions of the talus: randomized controlled trialcomparing chondroplasty, microfracture, and osteochondralautograft transplantation. Arthroscopy 2006;22(10):1085—92.

90] Giannini S, Buda R, Grigolo B, Vannini F. Autologous chondro-cyte transplantation in osteochondral lesions of the ankle joint.Foot Ankle Int 2001;22(6):513—7.

91] Koulalis D, Schultz W, Heyden M. Autologous chondrocytetransplantation for osteochondritis dissecans of the talus. ClinOrthop Relat Res 2002;395:186—92.

92] Whittaker JP, Smith G, Makwana N, Roberts S, HarrisonPE, Laing P, et al. Early results of autologous chondrocyteimplantation in the talus. J Bone Joint Surg Br 2005;87(2):179—83.

93] Caumo F, Russo A, Faccioli N, Vecchini E, Costa A, RicciM, et al. Autologous chondrocyte implantation: prospectiveMRI evaluation with clinical correlation. Radiol Med (Torino)2007;112(5):722—31.

94] Gross AE, Agnidis Z, Hutchison CR. Osteochondral defects ofthe talus treated with fresh osteochondral allograft transplan-tation. Foot Ankle Int 2001;22(5):385—91.

95] Raikin SM. Stage VI: massive osteochondral defects of the talus.Foot Ankle Clin 2004;9(4):737—44 [vi].

Documents

Treatment of osteochondral defects of the talus