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Osteochondral talar lesions and ankle biomechanics

Zengerink, M.

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Download date: 01 Mar 2020

Chapter 1

General introduction

Chapter 1

12

Broad perspective

The ankle joint is the most congruent joint of the human body. It is also one of the most common

joints to be injured.

As humans started to walk upright and assumed a bipedal instead of a quadrupedal locomotion,

the kinematics, kinetics and energetics changed. Advantages are that bipedalism is less

energetically expensive than quadrupedal walking [80, 91], and that it serves the purpose of

carrying things, as it leaves the hands free. A disadvantage may be that bipedal gait has made us

more prone to injury and falling. To stay upright, bipedal gait requires a more complex body

balance than quadrupedal gait. In case balance is lost, bodyweight is forcefully transmitted

through only one extremity, and the result may be that of ankle joint injury.

Many ankle joint injuries occur during sports. Over the past few decades, there has been an –

ongoing - (r)evolution in sports participation: it has been rising significantly [76]. First, men were

the frontrunners in this revolution, but today, women have caught up with men [76]. Sports like

long distance running and soccer have gained immense popularity among men and women. This

development is gladly seen, because the human body is made to move. Physical activity reduces

the risk for several diseases and may influence the course of several chronic diseases in a positive

way [77]. Although participating in sports in general is healthy, the risk of sports injuries is a

disadvantage of intensive physical activity.

In the Netherlands approximately 3.7 million sports injuries occur yearly. Of these, almost 40% is

treated medically [106]. In case of medically treated sports injuries it concerns acute sports

injuries in most cases, in other cases the injury developed gradually. Ankle injuries comprise a

large part of these sports injuries. In the Netherlands, in 2012, 770.000 sports injuries of the ankle

were sustained. This comprised 17% of all sports injuries in that year [106]. After knee injuries,

ankle injuries are the most common sports injuries. For almost 4 in 10 ankle injuries, medical

treatment is necessary [106].

Injury of the ankle joint may lead to ankle instability and intra-articular pathology. It is associated

with loose bodies, fractures, osteoarthritis, and osteochondral defects of the talus. Talar

osteochondral lesions are relatively common in patients with a history of ankle trauma [6, 56, 61,

70, 93, 94]. Because of the individual suffering and the burden on society they cause, these injuries

require optimal treatment.

Different terms are in use to describe bone-cartilage lesions, among these are: osteochondral

lesion (OCL), osteochondral defect (OCD), osteochondral lesion of the talus (OLT), transchondral

fracture and osteochondritis dissecans (OD). In this thesis the terms osteochondral lesion as well

as osteochondral defect are used.

Ankle anatomy

The specific anatomy of the ankle, with its high congruency, plays a large role in the development

of osteochondral defects of the talus. When the stabilizing structures are damaged, ankle

biomechanics are altered and damage to the cartilage may occur.

Introduction

13

The proximal articulation of the ankle is the mortise, which is made up of the lower end of the

tibia, its medial malleolus, the lateral malleolus of the fibula, and the transverse tibiofibular

ligament. These are the deep fibers of the posterior tibiofibular ligament. Its stability depends on

the integrity of the syndesmosis of the inferior tibiofibular joint. All articular surfaces are covered

with hyaline cartilage.

The lower articular surface of the tibia, wider in front than posteriorly, is concave antero-

posteriorly and is slightly convex from side to side. It articulates with the dorsal aspect or trochlea

of the body of the talus. The lateral malleolus is at the distal end of the fibula, and projects more

inferiorly and lies more posteriorly than the medial malleolus. There is a triangular articular facet

on the lateral aspect of the body of the talus. The malleolar fossa lies posterior to the articular

surface and gives attachment to the posterior tibiofibular and the posterior talofibular ligaments.

The talus consists of a rounded head anteriorly, a neck, and a body. The body forms the lower

articular surface, is cuboidal in shape, and has a trochlear articular surface. The trochlear surface

is wider anteriorly than posteriorly. It is convex from anterior to posterior and slightly concave

from side to side. The medial surface has a comma-shaped articular facet for the medial malleolus

and the lateral a triangular facet for the lateral malleolus [47].

When the ankle is dorsal flexed, the wider portion lies between the malleoli. This is the closepack,

or stable position, of the ankle. During plantar flexion, the narrow posterior area is in the mortise,

permitting some side-to-side movement. This is the least pack, or unstable position of the joint.

The talus has no muscles attached to it and has a very extensive articular surface. As a result,

fractures of the talus may result in avascular necrosis of either the body or the head. The relative

avascularity of the talus causes the bone more to be prone to the development of subchondral

cysts when the overlying cartilage is damaged. This process is not yet fully understood, though it is

thought that a crack in the cartilage may act as a pressure valve. Synovial fluid can enter the bone,

but not easily escape. Since fluid pressure is known to cause osteolysis [99], this mechanism could

be responsible for cyst formation in talar OCDs.

Biomechanics

The ankle joint complex, mainly formed by the ankle (tibiotalar) and subtalar joints, plays a

fundamental role in the human locomotor system, being involved in virtually every locomotion

activity [48]. Motion at the ankle and subtalar joints is guided by the osteoarticular and

ligamentous structures and induced by the forces and moments of the extrinsic muscles, in

addition to the external forces. The talus does not have tendon attachments, and is constrained

by ligament and contact forces [48]. When the limitis of normal ankle biomechanics are violated,

injury to stabilizing structures, and subsequent osteochondral lesions may occur.

The complex morphology of the ankle joint brings about a complex axis of rotation of the ankle

[107]. Since the 1950s, it has been recognized that the ankle joint axis during dorsal flexion is

different than that of plantar flexion [5, 33]. Barnett and Napier measured the trochlear surfaces of

152 human tali to discover that the medial and lateral curvatures of the talus are different,

1

Chapter 1

12

Broad perspective

The ankle joint is the most congruent joint of the human body. It is also one of the most common

joints to be injured.

As humans started to walk upright and assumed a bipedal instead of a quadrupedal locomotion,

the kinematics, kinetics and energetics changed. Advantages are that bipedalism is less

energetically expensive than quadrupedal walking [80, 91], and that it serves the purpose of

carrying things, as it leaves the hands free. A disadvantage may be that bipedal gait has made us

more prone to injury and falling. To stay upright, bipedal gait requires a more complex body

balance than quadrupedal gait. In case balance is lost, bodyweight is forcefully transmitted

through only one extremity, and the result may be that of ankle joint injury.

Many ankle joint injuries occur during sports. Over the past few decades, there has been an –

ongoing - (r)evolution in sports participation: it has been rising significantly [76]. First, men were

the frontrunners in this revolution, but today, women have caught up with men [76]. Sports like

long distance running and soccer have gained immense popularity among men and women. This

development is gladly seen, because the human body is made to move. Physical activity reduces

the risk for several diseases and may influence the course of several chronic diseases in a positive

way [77]. Although participating in sports in general is healthy, the risk of sports injuries is a

disadvantage of intensive physical activity.

In the Netherlands approximately 3.7 million sports injuries occur yearly. Of these, almost 40% is

treated medically [106]. In case of medically treated sports injuries it concerns acute sports

injuries in most cases, in other cases the injury developed gradually. Ankle injuries comprise a

large part of these sports injuries. In the Netherlands, in 2012, 770.000 sports injuries of the ankle

were sustained. This comprised 17% of all sports injuries in that year [106]. After knee injuries,

ankle injuries are the most common sports injuries. For almost 4 in 10 ankle injuries, medical

treatment is necessary [106].

Injury of the ankle joint may lead to ankle instability and intra-articular pathology. It is associated

with loose bodies, fractures, osteoarthritis, and osteochondral defects of the talus. Talar

osteochondral lesions are relatively common in patients with a history of ankle trauma [6, 56, 61,

70, 93, 94]. Because of the individual suffering and the burden on society they cause, these injuries

require optimal treatment.

Different terms are in use to describe bone-cartilage lesions, among these are: osteochondral

lesion (OCL), osteochondral defect (OCD), osteochondral lesion of the talus (OLT), transchondral

fracture and osteochondritis dissecans (OD). In this thesis the terms osteochondral lesion as well

as osteochondral defect are used.

Ankle anatomy

The specific anatomy of the ankle, with its high congruency, plays a large role in the development

of osteochondral defects of the talus. When the stabilizing structures are damaged, ankle

biomechanics are altered and damage to the cartilage may occur.

Introduction

13

The proximal articulation of the ankle is the mortise, which is made up of the lower end of the

tibia, its medial malleolus, the lateral malleolus of the fibula, and the transverse tibiofibular

ligament. These are the deep fibers of the posterior tibiofibular ligament. Its stability depends on

the integrity of the syndesmosis of the inferior tibiofibular joint. All articular surfaces are covered

with hyaline cartilage.

The lower articular surface of the tibia, wider in front than posteriorly, is concave antero-

posteriorly and is slightly convex from side to side. It articulates with the dorsal aspect or trochlea

of the body of the talus. The lateral malleolus is at the distal end of the fibula, and projects more

inferiorly and lies more posteriorly than the medial malleolus. There is a triangular articular facet

on the lateral aspect of the body of the talus. The malleolar fossa lies posterior to the articular

surface and gives attachment to the posterior tibiofibular and the posterior talofibular ligaments.

The talus consists of a rounded head anteriorly, a neck, and a body. The body forms the lower

articular surface, is cuboidal in shape, and has a trochlear articular surface. The trochlear surface

is wider anteriorly than posteriorly. It is convex from anterior to posterior and slightly concave

from side to side. The medial surface has a comma-shaped articular facet for the medial malleolus

and the lateral a triangular facet for the lateral malleolus [47].

When the ankle is dorsal flexed, the wider portion lies between the malleoli. This is the closepack,

or stable position, of the ankle. During plantar flexion, the narrow posterior area is in the mortise,

permitting some side-to-side movement. This is the least pack, or unstable position of the joint.

The talus has no muscles attached to it and has a very extensive articular surface. As a result,

fractures of the talus may result in avascular necrosis of either the body or the head. The relative

avascularity of the talus causes the bone more to be prone to the development of subchondral

cysts when the overlying cartilage is damaged. This process is not yet fully understood, though it is

thought that a crack in the cartilage may act as a pressure valve. Synovial fluid can enter the bone,

but not easily escape. Since fluid pressure is known to cause osteolysis [99], this mechanism could

be responsible for cyst formation in talar OCDs.

Biomechanics

The ankle joint complex, mainly formed by the ankle (tibiotalar) and subtalar joints, plays a

fundamental role in the human locomotor system, being involved in virtually every locomotion

activity [48]. Motion at the ankle and subtalar joints is guided by the osteoarticular and

ligamentous structures and induced by the forces and moments of the extrinsic muscles, in

addition to the external forces. The talus does not have tendon attachments, and is constrained

by ligament and contact forces [48]. When the limitis of normal ankle biomechanics are violated,

injury to stabilizing structures, and subsequent osteochondral lesions may occur.

The complex morphology of the ankle joint brings about a complex axis of rotation of the ankle

[107]. Since the 1950s, it has been recognized that the ankle joint axis during dorsal flexion is

different than that of plantar flexion [5, 33]. Barnett and Napier measured the trochlear surfaces of

152 human tali to discover that the medial and lateral curvatures of the talus are different,

Chapter 1

14

indicating that the axis of rotation of the ankle changes its position during the arc of motion [5,

107]. Hicks defined these different axes as the “dorsiflexion axis” and “plantar flexion axis”, stating

that movement cannot occur about these two axes simultaneously [33, 107]. In spite of these

findings, for a long period of time, combined motion at these two articulations was considered to

be a rotation about a single or a double fixed axis [15, 36, 37, 48, 90]. Patterns of joint motion were

investigated thoroughly, but basically with this same assumption [48, 55, 89, 107]. More recent

studies have reported that the instantaneous axis of rotation translates and rotates during passive

dorsal to plantar flexion [49, 50], suggesting that the hinge joint concept is an oversimplification

[48].

In 1994, it was stated by Van den Bogert et al., that is was extremely difficult to determine the ankle

joint axes, around which the actual rotational movements occur [98]. And consequently, that it

was difficult to describe the movement of the ankle joint complex using functional axes. In 2002, it

was still concluded by Nigg and Hintermann, that is was practically impossible to estimate the

location of the talus during locomotion [66]. A lot of technical progress has been made since

however. With new techniques of imaging software and hardware it is possible to accurately

determine talar location during motion [23]. Furthermore, research of movement has gone from

invasive (insertion of tantalum bone markers), to minimally invasive (by generating CT scans of the

ankle and hindfoot).

Fundamental information about the biomechanical characteristics of the ankle joint may

contribute to a better understanding of the normal function of the ankle, the pathomechanics of

injury and resulting ankle instability, and subsequent intra-articular damage.

History

An osteochondral defect is a lesion involving articular cartilage and subchondral bone. The first

report on OCDs of the talus was by Monro in 1856 [62]. He discussed the presence of cartilaginous

bodies in the ankle joint. König, in 1888, suspected inflammation to be an etiologic factor. He

suggested that the loose bodies were caused by vascular occlusion, leading to spontaneous

osteonecrosis. He referred to the condition as osteochondritis dissecans. Inflammation has never

been demonstrated to be part of the pathology, however.

In the early 1950s, the cause of talar osteochondral lesions was unknown. In 1953, Rödén et al.

reported their series of osteochondral lesions of the talus. They were the first to conclude that

almost all lateral lesions were secondary to trauma. In their series, for medial lesions this

relationship was not found [79]. In 1959, Berndt and Harty laid a solid foundation, in their elegant

clinical and anatomic studies, supporting trauma as a primary cause, particularly of lesions of the

lateral talar dome [6]. In their study, 57% was located on the medial shoulder, mostly the posterior

third, and 43% of lesions were located on the lateral shoulder of the talus, mostly in the middle

third (Fig. 1). They also presented an enduring four-stage radiographic classification scheme.

Following their report, several authors reported of talar OCDs as a sequal to ankle sprain [9, 12, 22,

65].

Introduction

15

Figure 1 Superior view of the talar dome. Anterolateral (*) and posteromedial (**) locations of talar

osteochondral lesions as described by Berndt and Harty.

Etiology

Today, ankle trauma is accepted as the most frequent etiologic factor for OCDs of the talus [34, 82,

83]. The lesion can be caused by a single traumatic event, or by multiple, less intense

microtraumata. Although the origin of most lesions is traumatic, not all patients report a history of

ankle trauma. Atraumatic causes, including endocrine or metabolic factors [71], degenerative joint

disease [94], joint mal-alignment [28], genetic predisposition [63], and ischemia and necrosis [84]

have been proposed. The occurrence of OCDs in identical twins and siblings [1, 109], and the fact

that the defect is bilateral in 4 to 7% of patients [6, 9], further supports the hypothesis that some

lesions are of genetic origin.

During an ankle sprain or fracture, the talus twists inside the ankle mortise, and the cartilage of the

distal tibia and talar dome are forcefully pushed upon each other (Fig. 2). Ankle sprains usually

occur when the foot is forcefully inverted when the ankle is plantar flexed [24, 44, 46, 59]; in this

position the bony structure allows only minimal stability, the leverage is maximal, and the anterior

talofibular ligament (ATFL), which is the weakest component of the lateral ligament complex of

the ankle [3, 88], is taut and exposed to injury.

The degree of injury depends on the force exerted and on the range of abnormal motion that is

enforced on the ankle. This force could be modified by timely muscle activation, external

protection, and reasonable attention to the course or playing ground.

1

Chapter 1

14

indicating that the axis of rotation of the ankle changes its position during the arc of motion [5,

107]. Hicks defined these different axes as the “dorsiflexion axis” and “plantar flexion axis”, stating

that movement cannot occur about these two axes simultaneously [33, 107]. In spite of these

findings, for a long period of time, combined motion at these two articulations was considered to

be a rotation about a single or a double fixed axis [15, 36, 37, 48, 90]. Patterns of joint motion were

investigated thoroughly, but basically with this same assumption [48, 55, 89, 107]. More recent

studies have reported that the instantaneous axis of rotation translates and rotates during passive

dorsal to plantar flexion [49, 50], suggesting that the hinge joint concept is an oversimplification

[48].

In 1994, it was stated by Van den Bogert et al., that is was extremely difficult to determine the ankle

joint axes, around which the actual rotational movements occur [98]. And consequently, that it

was difficult to describe the movement of the ankle joint complex using functional axes. In 2002, it

was still concluded by Nigg and Hintermann, that is was practically impossible to estimate the

location of the talus during locomotion [66]. A lot of technical progress has been made since

however. With new techniques of imaging software and hardware it is possible to accurately

determine talar location during motion [23]. Furthermore, research of movement has gone from

invasive (insertion of tantalum bone markers), to minimally invasive (by generating CT scans of the

ankle and hindfoot).

Fundamental information about the biomechanical characteristics of the ankle joint may

contribute to a better understanding of the normal function of the ankle, the pathomechanics of

injury and resulting ankle instability, and subsequent intra-articular damage.

History

An osteochondral defect is a lesion involving articular cartilage and subchondral bone. The first

report on OCDs of the talus was by Monro in 1856 [62]. He discussed the presence of cartilaginous

bodies in the ankle joint. König, in 1888, suspected inflammation to be an etiologic factor. He

suggested that the loose bodies were caused by vascular occlusion, leading to spontaneous

osteonecrosis. He referred to the condition as osteochondritis dissecans. Inflammation has never

been demonstrated to be part of the pathology, however.

In the early 1950s, the cause of talar osteochondral lesions was unknown. In 1953, Rödén et al.

reported their series of osteochondral lesions of the talus. They were the first to conclude that

almost all lateral lesions were secondary to trauma. In their series, for medial lesions this

relationship was not found [79]. In 1959, Berndt and Harty laid a solid foundation, in their elegant

clinical and anatomic studies, supporting trauma as a primary cause, particularly of lesions of the

lateral talar dome [6]. In their study, 57% was located on the medial shoulder, mostly the posterior

third, and 43% of lesions were located on the lateral shoulder of the talus, mostly in the middle

third (Fig. 1). They also presented an enduring four-stage radiographic classification scheme.

Following their report, several authors reported of talar OCDs as a sequal to ankle sprain [9, 12, 22,

65].

Introduction

15

Figure 1 Superior view of the talar dome. Anterolateral (*) and posteromedial (**) locations of talar

osteochondral lesions as described by Berndt and Harty.

Etiology

Today, ankle trauma is accepted as the most frequent etiologic factor for OCDs of the talus [34, 82,

83]. The lesion can be caused by a single traumatic event, or by multiple, less intense

microtraumata. Although the origin of most lesions is traumatic, not all patients report a history of

ankle trauma. Atraumatic causes, including endocrine or metabolic factors [71], degenerative joint

disease [94], joint mal-alignment [28], genetic predisposition [63], and ischemia and necrosis [84]

have been proposed. The occurrence of OCDs in identical twins and siblings [1, 109], and the fact

that the defect is bilateral in 4 to 7% of patients [6, 9], further supports the hypothesis that some

lesions are of genetic origin.

During an ankle sprain or fracture, the talus twists inside the ankle mortise, and the cartilage of the

distal tibia and talar dome are forcefully pushed upon each other (Fig. 2). Ankle sprains usually

occur when the foot is forcefully inverted when the ankle is plantar flexed [24, 44, 46, 59]; in this

position the bony structure allows only minimal stability, the leverage is maximal, and the anterior

talofibular ligament (ATFL), which is the weakest component of the lateral ligament complex of

the ankle [3, 88], is taut and exposed to injury.

The degree of injury depends on the force exerted and on the range of abnormal motion that is

enforced on the ankle. This force could be modified by timely muscle activation, external

protection, and reasonable attention to the course or playing ground.

Chapter 1

16

When defects occur, they can be found on the medial and lateral sides of the talar dome.

Occasionally they are located centrally [25]. Approximately two-thirds of OCDs are located

medially, and one-third is located laterally [18]. Lateral lesions occur mostly on the anterolateral,

and medial lesions on the posteromedial shoulder of the talar dome [73]. Lateral lesions are

usually shallow and oval-shaped, and caused by a shear mechanism. Medial lesions, however, are

usually deeper and cup-shaped and caused by torsional impaction during axial loading of the

ankle [6].

Figure 2 During an ankle sprain, the talus twists inside its box-like housing, and the cartilage of the talar dome

is pushed forcefully upon the distal tibia, creating an osteochondral lesion (*).

According to Yao and Weis, medial lesions are most likely caused by an inversion of the foot and a

plantar flexed ankle. Lateral lesions are caused by eversion of the foot with the ankle in dorsal

flexion and the tibia internally rotated on the talus. These lesions are almost always secondary to

trauma [110].

The impact on the talus may lead to subchondral bruising and subsequent softening of the

cartilage, to a crack and subsequent cyst formation [38, 74, 101], or the shearing off of a chondral

or osteochondral fragment [6]. The formation of subchondral cysts is thought to be due to

intrusion of fluid through a bony defect, and may hamper effective treatment [75, 78, 87, 101].

To evaluate (osteo)chondral damage to the talar dome and tibial plafond after ankle injury, Van

Dijk performed ankle arthroscopies 4 to 7 days after trauma. He documented the arthroscopic

findings and treatment, especially lavage and, if necessary, ligament repair. During a 1,5 year

period he treated and recorded the progress of 30 patients, subsequently documenting his

findings. In the series of 30 consecutive patients with rupture of the lateral ankle ligaments after

acute supination trauma, 1 medial, 1 lateral and 4 tibial plafond osteochondral lesions were

Introduction

17

found. Apart from these lesions in the weight-bearing area, in 16 patients he also found a kissing

cartilage lesion between the medial talar facet and the anterior cartilage of the medial malleolus

[105].

Epidemiology

Osteochondral defects can occur in any joint. The most common location is the knee. It is

assumed that OCDs of the ankle account for approximately 4% of the total number of OCDs [13].

OCDs of the ankle used to occur most frequently in 20- to 30-year-old men [61], but with the rising

sports and work participation of women, the male-female ratio is now approximately 3:2 [96].

It is estimated that one ankle injury per 10,000 people per day occurs [41]. With this extremely high

occurrence, ankle sprains comprise 16 to 45% of sports-related injuries [19, 24, 54, 58, 64]. They

represent 25% of volleyball [24] and track and field injuries [57], 20 to 31% of soccer injuries [17,

24, 81], and 45% of basketball injuries [24]. In military training, the rates are even higher, and

reported to be 30 to 60% [4, 40].

The exact incidence of talar OCDs in the adult population is unknown. Because they mainly occur

after ankle injury, the incidence after ankle sprain and fracture has been determined by several

authors. Besides Van Dijk [105], two other investigators who routinely inspected the lateral talar

dome during surgery for lateral ankle ligament rupture, determined the rate of lateral OCDs after

this event. They reported it to be 5% [7] and 9% [53], respectively. The percentage of medial dome

lesions is unknown but estimated to be as high as lateral talar dome lesions [105].

Higher numbers of talar OCDs after ankle injury were published more recently by Takao et al. In a

group of 86 patients visiting the hospital for lateral ankle instability, osteochondral lesions were

found in 41% of patients. In case of patients with a distal fibular fracture requiring osteosynthesis,

the incidence was 71%. Diagnosis was performed by MRI and arthroscopy and included OCDs of

the tibial plafond as well [93]. Leontaritis et al. found chondral injuries in 73% of patients (61/84)

with an ankle fracture, confirmed during arthroscopy [51].

The incidence of OCDs of the ankle in children was investigated by Kessler et al. [42]. In their

population based cohort study they found an incidence of 4.6 per 100.000 in children aged 6 to 19

years. Patients aged 12 to 19 years represented the vast majority of those with OCD, with an

incidence of 6.8 per 100.000, compared to 1.1 per 100.000 in those 6 to 11 years of age. Teenagers

therefore had nearly 7 times the risk for ankle OCD compared with children 6 to 11 years of age.

Clinical presentation

Patients with an OCD of the talus are typically young, active adults with deep ankle pain during or

after activity [21]. Other symptoms may include stiffness, swelling, and sometimes a locking

sensation of the ankle. Locking and catching are symptoms of a displaced fragment. In most

patients who have a non-displaced lesion after supination trauma, the symptoms in the acute

situation cannot be distinguished from the soft tissue damage [102].

1

Chapter 1

16

When defects occur, they can be found on the medial and lateral sides of the talar dome.

Occasionally they are located centrally [25]. Approximately two-thirds of OCDs are located

medially, and one-third is located laterally [18]. Lateral lesions occur mostly on the anterolateral,

and medial lesions on the posteromedial shoulder of the talar dome [73]. Lateral lesions are

usually shallow and oval-shaped, and caused by a shear mechanism. Medial lesions, however, are

usually deeper and cup-shaped and caused by torsional impaction during axial loading of the

ankle [6].

Figure 2 During an ankle sprain, the talus twists inside its box-like housing, and the cartilage of the talar dome

is pushed forcefully upon the distal tibia, creating an osteochondral lesion (*).

According to Yao and Weis, medial lesions are most likely caused by an inversion of the foot and a

plantar flexed ankle. Lateral lesions are caused by eversion of the foot with the ankle in dorsal

flexion and the tibia internally rotated on the talus. These lesions are almost always secondary to

trauma [110].

The impact on the talus may lead to subchondral bruising and subsequent softening of the

cartilage, to a crack and subsequent cyst formation [38, 74, 101], or the shearing off of a chondral

or osteochondral fragment [6]. The formation of subchondral cysts is thought to be due to

intrusion of fluid through a bony defect, and may hamper effective treatment [75, 78, 87, 101].

To evaluate (osteo)chondral damage to the talar dome and tibial plafond after ankle injury, Van

Dijk performed ankle arthroscopies 4 to 7 days after trauma. He documented the arthroscopic

findings and treatment, especially lavage and, if necessary, ligament repair. During a 1,5 year

period he treated and recorded the progress of 30 patients, subsequently documenting his

findings. In the series of 30 consecutive patients with rupture of the lateral ankle ligaments after

acute supination trauma, 1 medial, 1 lateral and 4 tibial plafond osteochondral lesions were

Introduction

17

found. Apart from these lesions in the weight-bearing area, in 16 patients he also found a kissing

cartilage lesion between the medial talar facet and the anterior cartilage of the medial malleolus

[105].

Epidemiology

Osteochondral defects can occur in any joint. The most common location is the knee. It is

assumed that OCDs of the ankle account for approximately 4% of the total number of OCDs [13].

OCDs of the ankle used to occur most frequently in 20- to 30-year-old men [61], but with the rising

sports and work participation of women, the male-female ratio is now approximately 3:2 [96].

It is estimated that one ankle injury per 10,000 people per day occurs [41]. With this extremely high

occurrence, ankle sprains comprise 16 to 45% of sports-related injuries [19, 24, 54, 58, 64]. They

represent 25% of volleyball [24] and track and field injuries [57], 20 to 31% of soccer injuries [17,

24, 81], and 45% of basketball injuries [24]. In military training, the rates are even higher, and

reported to be 30 to 60% [4, 40].

The exact incidence of talar OCDs in the adult population is unknown. Because they mainly occur

after ankle injury, the incidence after ankle sprain and fracture has been determined by several

authors. Besides Van Dijk [105], two other investigators who routinely inspected the lateral talar

dome during surgery for lateral ankle ligament rupture, determined the rate of lateral OCDs after

this event. They reported it to be 5% [7] and 9% [53], respectively. The percentage of medial dome

lesions is unknown but estimated to be as high as lateral talar dome lesions [105].

Higher numbers of talar OCDs after ankle injury were published more recently by Takao et al. In a

group of 86 patients visiting the hospital for lateral ankle instability, osteochondral lesions were

found in 41% of patients. In case of patients with a distal fibular fracture requiring osteosynthesis,

the incidence was 71%. Diagnosis was performed by MRI and arthroscopy and included OCDs of

the tibial plafond as well [93]. Leontaritis et al. found chondral injuries in 73% of patients (61/84)

with an ankle fracture, confirmed during arthroscopy [51].

The incidence of OCDs of the ankle in children was investigated by Kessler et al. [42]. In their

population based cohort study they found an incidence of 4.6 per 100.000 in children aged 6 to 19

years. Patients aged 12 to 19 years represented the vast majority of those with OCD, with an

incidence of 6.8 per 100.000, compared to 1.1 per 100.000 in those 6 to 11 years of age. Teenagers

therefore had nearly 7 times the risk for ankle OCD compared with children 6 to 11 years of age.

Clinical presentation

Patients with an OCD of the talus are typically young, active adults with deep ankle pain during or

after activity [21]. Other symptoms may include stiffness, swelling, and sometimes a locking

sensation of the ankle. Locking and catching are symptoms of a displaced fragment. In most

patients who have a non-displaced lesion after supination trauma, the symptoms in the acute

situation cannot be distinguished from the soft tissue damage [102].

Chapter 1

18

When an ankle sprain has occurred, a differentiation has to be made between the acute and the

chronic situation. In the acute situation, symptoms of OCDs compare with those of acute ankle

injuries. These are swelling, diffuse or localized ankle pain, and pain on weight-bearing. When it

concerns isolated ligament injury, pain and swelling usually resolve after a couple of weeks of

reduced loading of the ankle, sometimes in combination with tape or softcast. When symptoms

persist after this period, a talar OCD may be present. These patients typically present with deep

ankle pain on weight-bearing, and often a limited range of motion. Lateral lesions in general cause

more symptoms than medial ones [102].

The natural course of degenerative joint disease following an OCD has not been well defined.

However, it is known that subchondral cysts [101] may form and that when the lesion is large and

the affected piece is dissected, the joint mechanics are altered, which may lead to osteoarthritis.

Diagnosis

When after careful history taking and physical examination of the ankle an OCD is suspected,

weight-bearing anteroposterior, mortise, and lateral views are taken. A bone fragment may be

present in the joint space, and sometimes radiolucency of the talar dome is seen. Often there are

no abnormalities found at all during primary routine radiography. In a later stage, the defect

sometimes becomes visible when bone loss develops with subsequent radiolucency (Fig. 3). A

posteromedial or posterolateral defect may be revealed by a heelrise view with the ankle in

plantar flexed position [108]. When multiple injuries are present in the ankle, a bone scan can

differentiate between a symptomatic and an asymptomatic lesion [100].

Figure 3 Radiolucency at the medial talar dome, indicating an osteochondral lesion.

Introduction

19

Figure 4 Coronal and axial image of a computed tomography scan of a medial osteochondral talar lesion.

Figure 5 Coronal image of a magnetic resonance imaging scan indicating a lateral osteochondral talar lesion.

Computed tomography (CT) and magnetic resonance imaging (MRI) allow a 3-dimensional

evaluation of a lesion (Figs. 4 and 5, respectively). The sensitivity and specificity of CT to detect an

OCD are 0.81 and 0.99, respectively. Those of MRI are 0.96 and 0.96 [108]. MRI shows the

surrounding bony edema, if present. The exact size and location of the lesion are better defined by

CT, therefore CT is more valuable for preoperative planning [108].

Treatment

Several surgical techniques are available for the treatment of symptomatic OCDs of the ankle.

Non-surgical techniques, like immobilization in a cast, are almost out of use because of their low

overall success rates. When conservative therapy is still applied, it usually concerns a younger

patient with an acute partially detached lesion, or an acute lesion with a completely detached

fragment that is still in place [8].

1

Chapter 1

18

When an ankle sprain has occurred, a differentiation has to be made between the acute and the

chronic situation. In the acute situation, symptoms of OCDs compare with those of acute ankle

injuries. These are swelling, diffuse or localized ankle pain, and pain on weight-bearing. When it

concerns isolated ligament injury, pain and swelling usually resolve after a couple of weeks of

reduced loading of the ankle, sometimes in combination with tape or softcast. When symptoms

persist after this period, a talar OCD may be present. These patients typically present with deep

ankle pain on weight-bearing, and often a limited range of motion. Lateral lesions in general cause

more symptoms than medial ones [102].

The natural course of degenerative joint disease following an OCD has not been well defined.

However, it is known that subchondral cysts [101] may form and that when the lesion is large and

the affected piece is dissected, the joint mechanics are altered, which may lead to osteoarthritis.

Diagnosis

When after careful history taking and physical examination of the ankle an OCD is suspected,

weight-bearing anteroposterior, mortise, and lateral views are taken. A bone fragment may be

present in the joint space, and sometimes radiolucency of the talar dome is seen. Often there are

no abnormalities found at all during primary routine radiography. In a later stage, the defect

sometimes becomes visible when bone loss develops with subsequent radiolucency (Fig. 3). A

posteromedial or posterolateral defect may be revealed by a heelrise view with the ankle in

plantar flexed position [108]. When multiple injuries are present in the ankle, a bone scan can

differentiate between a symptomatic and an asymptomatic lesion [100].

Figure 3 Radiolucency at the medial talar dome, indicating an osteochondral lesion.

Introduction

19

Figure 4 Coronal and axial image of a computed tomography scan of a medial osteochondral talar lesion.

Figure 5 Coronal image of a magnetic resonance imaging scan indicating a lateral osteochondral talar lesion.

Computed tomography (CT) and magnetic resonance imaging (MRI) allow a 3-dimensional

evaluation of a lesion (Figs. 4 and 5, respectively). The sensitivity and specificity of CT to detect an

OCD are 0.81 and 0.99, respectively. Those of MRI are 0.96 and 0.96 [108]. MRI shows the

surrounding bony edema, if present. The exact size and location of the lesion are better defined by

CT, therefore CT is more valuable for preoperative planning [108].

Treatment

Several surgical techniques are available for the treatment of symptomatic OCDs of the ankle.

Non-surgical techniques, like immobilization in a cast, are almost out of use because of their low

overall success rates. When conservative therapy is still applied, it usually concerns a younger

patient with an acute partially detached lesion, or an acute lesion with a completely detached

fragment that is still in place [8].

Chapter 1

20

The type of surgical treatment needed, and the location of the lesion both determine the surgical

approach. Most primary lesions can be treated by means of arthroscopy, but lesions in the

posterior half of the talar dome may be hard to address arthroscopically. For secondary lesions,

often a different, more invasive treatment is chosen, requiring open surgery, with or without

osteotomy [32].

Surgery for primary lesions is mostly done by debridement and bone marrow stimulation. First it

was performed during an open surgical procedure; nowadays it is performed almost exclusively

arthroscopically. When possible, the OCD is approached by anterior ankle arthroscopy with the

ankle in full plantar flexion for adequate exposure of the defect [104]. When needed, noninvasive

intermittent distraction is used to improve exposure [103].

After debridement, the subchondral bone is penetrated by drilling or microfracturing. This may be

done by a chondral pick or K-wire. The sclerotic zone that is often present is partially destroyed

and multiple openings are created into the subchondral bone. This causes disruption of

intraosseous blood vessels and subsequent bleeding. Growth factors are released and a fibrin clot

forms inside the defect. Neovascularization causes marrow cells to be introduced into the defect

and fibrocartilaginous tissue is formed. In the case of large defects, a cancellous bonegraft can be

applied.

In 1986, Parisien [67] described the arthroscopic procedure to accomplish this formation of

fibrocartilaginous tissue. Good results were reported and have been confirmed by others [86, 95,

97]. Also more recent reports continue to show satisfactory results after arthroscopic debridement

and microfracturing [11, 52, 68].

Arthroscopic debridement and microfracturing, also known as bone marrow stimulation, remains

a popular option, because of the low-cost, minimally invasive character of the procedure. Ankle

arthroscopy is regarded a safe procedure, but complications rates need to be diminished [20].

Reduction of complications will contribute to making it an even more attractive procedure for

young active patients with ankle pathology.

Rehabilitation after debridement and bone marrow stimulation may take up to 1 year post-

operatively. In most cases, surgery is followed by a period of non-weight-bearing, of 4 to 6 weeks.

Rationale for this is to give the fibrocartilage an optimal chance to develop and to become

secured to the surrounding bone and cartilage. The necessity of this non-weight-bearing period

has been debated lately by Li et al. [52], who reported successful outcomes after early weight-

bearing. Follow-up however was limited.

Securing the lesion to the talar dome is possible in case of a large loose fragment. One can choose

to secure it to the underlying bone using either a screw, a pin, a rod or fibrin glue [111]. In case of a

large cyst grafting may be necessary, using either autologous cancellous bone or demineralized

bone matrix (DBM) from donors, as an alternative to autologous bone grafting. DBM has

osteoconductive, osteoinductive, and osteogenic potential [14, 16, 72]. Its value in the treatment

of cystic osteochondral lesions has yet to be proven however.

Introduction

21

Retrograde drilling is done for primary OCDs when there is more or less intact cartilage with a large

subchondral cyst, or when the defect is hard to reach via the usual anterolateral and anteromedial

portals [27].

For stimulation of the development of hyaline cartilage, several options are available: allogenous

and autogenous osteochondral transplantation, bone grafting, and ACI. They have all been

developed in the past 2 decades [2, 10, 25, 26, 29-31, 35, 39, 43, 45, 60, 69, 85, 92]. These techniques

have specific indications according to the stage, location, and extent of damaged area. The age

and the lifestyle of the patient also influence the specific procedure that is recommended.

ACI with periosteal flapping of osteochondral lesions in the ankle joint is gaining more popularity,

since the increasing number of promising clinical reports [30, 69]. In contrast to the good clinical

outcome, the length of the rehabilitation, high laboratory costs, and technical problems appear to

be disadvantageous elements of this technique.

Treatment results vary widely in literature. It is unknown which strategy is most effective in the

treatment of talar OCDs, therefore further study on this topic is imperative. Most surgery for talar

OCDs is performed arthroscopically, but not without complications. To improve arthroscopic

treatment, increasing knowledge of the number and type of complications is mandatory. Finally,

none of the current treatment methods is completely successful, and secondary treatment

options have their limitations. This necessitates the search for better treatment methods, in order

to deliver optimal care for the individual patient.

Aims and outline of the thesis

This thesis aims at defining the appropriate surgical treatment for osteochondral talar lesions, and

how to improve this treatment by investigating ankle biomechanics, evaluating existing

techniques and developing new techniques. To accomplish this aim, treatment results,

complications in ankle arthroscopy, normal motion patterns of the ankle and arthroscopic access

to the talar dome were studied. Furthermore, a new treatment method for talar OCDs was

developed.

Part I describes the current concepts in the treatment of OCDs. Part II reviews the current

treatment options; it summarizes all eligible studies to compare the effectiveness of treatment

strategies for osteochondral lesions of the talus. It also aims at improving the technique of ankle

arthroscopy, which is still the most used technique in treatment of talar OCDs. It elucidates the

types of complications that may occur during ankle arthroscopy, and describes how the use of the

dorsiflexion method may prevent a significant number of complications. Part III presents a chapter

describing a computed tomography-based stress-test to determine the three-dimensional

position and orientation of the tibial, calcaneal and talar bones in eight extreme foot positions.

Talocrural and subtalar range of motion for healthy individuals was determined. Data of this study

were used in the next chapter to aim to define arthroscopic access to the talar dome. Part IV

describes two studies that led to the development of a new treatment strategy for osteochondral

lesions of the talus. Talar geometry and size and location of lesions was measured. With these

1

Chapter 1

20

The type of surgical treatment needed, and the location of the lesion both determine the surgical

approach. Most primary lesions can be treated by means of arthroscopy, but lesions in the

posterior half of the talar dome may be hard to address arthroscopically. For secondary lesions,

often a different, more invasive treatment is chosen, requiring open surgery, with or without

osteotomy [32].

Surgery for primary lesions is mostly done by debridement and bone marrow stimulation. First it

was performed during an open surgical procedure; nowadays it is performed almost exclusively

arthroscopically. When possible, the OCD is approached by anterior ankle arthroscopy with the

ankle in full plantar flexion for adequate exposure of the defect [104]. When needed, noninvasive

intermittent distraction is used to improve exposure [103].

After debridement, the subchondral bone is penetrated by drilling or microfracturing. This may be

done by a chondral pick or K-wire. The sclerotic zone that is often present is partially destroyed

and multiple openings are created into the subchondral bone. This causes disruption of

intraosseous blood vessels and subsequent bleeding. Growth factors are released and a fibrin clot

forms inside the defect. Neovascularization causes marrow cells to be introduced into the defect

and fibrocartilaginous tissue is formed. In the case of large defects, a cancellous bonegraft can be

applied.

In 1986, Parisien [67] described the arthroscopic procedure to accomplish this formation of

fibrocartilaginous tissue. Good results were reported and have been confirmed by others [86, 95,

97]. Also more recent reports continue to show satisfactory results after arthroscopic debridement

and microfracturing [11, 52, 68].

Arthroscopic debridement and microfracturing, also known as bone marrow stimulation, remains

a popular option, because of the low-cost, minimally invasive character of the procedure. Ankle

arthroscopy is regarded a safe procedure, but complications rates need to be diminished [20].

Reduction of complications will contribute to making it an even more attractive procedure for

young active patients with ankle pathology.

Rehabilitation after debridement and bone marrow stimulation may take up to 1 year post-

operatively. In most cases, surgery is followed by a period of non-weight-bearing, of 4 to 6 weeks.

Rationale for this is to give the fibrocartilage an optimal chance to develop and to become

secured to the surrounding bone and cartilage. The necessity of this non-weight-bearing period

has been debated lately by Li et al. [52], who reported successful outcomes after early weight-

bearing. Follow-up however was limited.

Securing the lesion to the talar dome is possible in case of a large loose fragment. One can choose

to secure it to the underlying bone using either a screw, a pin, a rod or fibrin glue [111]. In case of a

large cyst grafting may be necessary, using either autologous cancellous bone or demineralized

bone matrix (DBM) from donors, as an alternative to autologous bone grafting. DBM has

osteoconductive, osteoinductive, and osteogenic potential [14, 16, 72]. Its value in the treatment

of cystic osteochondral lesions has yet to be proven however.

Introduction

21

Retrograde drilling is done for primary OCDs when there is more or less intact cartilage with a large

subchondral cyst, or when the defect is hard to reach via the usual anterolateral and anteromedial

portals [27].

For stimulation of the development of hyaline cartilage, several options are available: allogenous

and autogenous osteochondral transplantation, bone grafting, and ACI. They have all been

developed in the past 2 decades [2, 10, 25, 26, 29-31, 35, 39, 43, 45, 60, 69, 85, 92]. These techniques

have specific indications according to the stage, location, and extent of damaged area. The age

and the lifestyle of the patient also influence the specific procedure that is recommended.

ACI with periosteal flapping of osteochondral lesions in the ankle joint is gaining more popularity,

since the increasing number of promising clinical reports [30, 69]. In contrast to the good clinical

outcome, the length of the rehabilitation, high laboratory costs, and technical problems appear to

be disadvantageous elements of this technique.

Treatment results vary widely in literature. It is unknown which strategy is most effective in the

treatment of talar OCDs, therefore further study on this topic is imperative. Most surgery for talar

OCDs is performed arthroscopically, but not without complications. To improve arthroscopic

treatment, increasing knowledge of the number and type of complications is mandatory. Finally,

none of the current treatment methods is completely successful, and secondary treatment

options have their limitations. This necessitates the search for better treatment methods, in order

to deliver optimal care for the individual patient.

Aims and outline of the thesis

This thesis aims at defining the appropriate surgical treatment for osteochondral talar lesions, and

how to improve this treatment by investigating ankle biomechanics, evaluating existing

techniques and developing new techniques. To accomplish this aim, treatment results,

complications in ankle arthroscopy, normal motion patterns of the ankle and arthroscopic access

to the talar dome were studied. Furthermore, a new treatment method for talar OCDs was

developed.

Part I describes the current concepts in the treatment of OCDs. Part II reviews the current

treatment options; it summarizes all eligible studies to compare the effectiveness of treatment

strategies for osteochondral lesions of the talus. It also aims at improving the technique of ankle

arthroscopy, which is still the most used technique in treatment of talar OCDs. It elucidates the

types of complications that may occur during ankle arthroscopy, and describes how the use of the

dorsiflexion method may prevent a significant number of complications. Part III presents a chapter

describing a computed tomography-based stress-test to determine the three-dimensional

position and orientation of the tibial, calcaneal and talar bones in eight extreme foot positions.

Talocrural and subtalar range of motion for healthy individuals was determined. Data of this study

were used in the next chapter to aim to define arthroscopic access to the talar dome. Part IV

describes two studies that led to the development of a new treatment strategy for osteochondral

lesions of the talus. Talar geometry and size and location of lesions was measured. With these

Chapter 1

22

data, a new metallic implant for medial osteochondral lesions was developed. Fitting and

accurate placement of the implant was tested in cadaver ankles. Part V finalizes the thesis with a

general discussion, conclusions and a summary.

Part I – Introduction

There are numerous surgical strategies for the treatment of OCDs. Chapter 2 provides an overview

of these treatment strategies, and describes in depth the techniques and rehabilitation protocols

of the three treatment options that are currently most used: debridement and bone marrow

stimulation (BMS), autologous chondrocyte implantation (ACI) and osteochondral autograft

transfer system (OATS). Based on the literature, a guideline for treatment is proposed for 6

different types of osteochondral talar lesions.

Part II – Current treatment

In spite of the many publications on treatment of osteochondral lesions of the talus, literature is

lacking randomized controlled trials and prospective comparative studies. However, on the

subject many case series were published. To provide the best available evidence, chapter 3

contains a systematic review of treatment strategies for osteochondral lesions of the talus. All

eligible studies were summarized to compare their effectiveness. The proportion of the patient

population successfully treated was noted, and study-size weighted success rates were

calculated. Based on outcome, recommendations for treatment were made.

In most treatment strategies, ankle arthroscopy is still used as main surgical technique - as

opposed to open surgery. The dual purpose of chapter 4 was therefore to determine the

complication rate for ankle arthroscopy in our institution, and to describe the dorsiflexion method

associated with this rate. Patients with a complication were examined to determine permanent

damage and persisting complaints. The complication rate was compared to what was found in

literature. The arthroscopic technique that was used was described in detail, with a rationale

presented clarifying how this technique may prevent a significant number of complications.

Chapter 5 contains a comment on our publication of complications in ankle arthroscopy and a

response to this comment. Authors Pau Golanó and Jordi Vega commented that the anatomy of

the joint may not have been sufficiently highlighted in the study. They underline the importance of

knowledge and identification of anatomical landmarks of the ankle, to facilitate orientation and

prevent damage during the procedure. Furthermore, they provide a clarifying picture of a

transverse section of the ankle at the level of the tibiofibular syndesmosis, showing important

structures susceptible to injury during ankle arthroscopy. In our comment we confirm knowledge

of anatomy as the basis for every surgical technique and affirm the importance of staying up to

date with the extensive literature on this subject.

Introduction

23

Part III – Ankle biomechanics and arthroscopic access

Up until recently, measuring ankle biomechanics wasn’t possible by using non-invasive

techniques. Technical progress however has made it possible to determine the range of motion of

a joint by using computed-tomography (CT). CT, together with specifically designed software, can

determine the three-dimensional (3D) orientation of bones. By scanning a joint in different

extreme positions, the orientations of the bones can be determined. From these, ranges of motion

are calculated. These are described as finite helical axis orientation, and rotations around and

translations along these axes.

The goal of chapter 6 was to establish a quantitative database of the normal ranges of motion of

the talocrural and subtalar joints by using a 3D computed tomography stress-test. A clinical case

on suspected subtalar instability demonstrates the relevance of the proposed method.

The optimal arthroscopic approach (i.e. anterior or posterior) can be unclear preoperatively.

During anterior arthroscopy for an OCD, the ankle is held in full plantar flexion to optimize

exposure of the talar dome, increasing the chance of reaching the lesion. When a lesion is located

in a part of the talar dome that remains covered by the tibial plafond in any position, osteotomy

might be necessary. Chapter 7 uses the data of the 3D computed tomography stress-test of the

ankle to determine and visualize arthroscopic access to the talus. Coverage of the talus by the

distal tibia is determined for the neutral position and eight extreme foot positions, among which

are maximum plantar flexion and maximum dorsiflexion. The area of the talar surface that may be

hard to reach is visualized and described.

Part IV- Future treatment

The disadvantages associated with secondary treatment options, like donor-site morbidity and

high costs, leads to the search for new strategies. To treat larger cystic and secondary lesions,

current techniques aim to replace the defected cartilage with harvested cartilage or in-vitro

cultured cartilage. It was hypothesized that defect can also be covered by a metal device, as is

done before in the knee. To develop a metallic resurfacing implant, knowledge of talar geometry,

lesion size and location is necessary. Chapter 8 describes in detail the measurements of the sizes

of medial and lateral talar OCDs. Furthermore, it describes the measurements of talar radius and

angle of the talar shoulder at the location where the osteochondral lesion occurs. These data

served as the basis for the development of the talar HemiCAP, a prosthetic device consisting of a

screw and a metallic cap, which is able to restore the continuity of the talar articular surface, and

cover a subchondral lesion. Fifteen offset sizes were developed and it was hypothesized that there

would be a matching offset size for each talus, that the prosthetic device can be implanted slightly

recessed to the cartilage level, and that excessive contact pressures on the opposite tibial

cartilage can be avoided. Chapter 9 aims to test these hypotheses by implanting the prosthetic

device on the medial talar surface of 11 intact fresh-frozen human cadaver ankles, aiming its

surface 0.5 mm below cartilage level.

1

Chapter 1

22

data, a new metallic implant for medial osteochondral lesions was developed. Fitting and

accurate placement of the implant was tested in cadaver ankles. Part V finalizes the thesis with a

general discussion, conclusions and a summary.

Part I – Introduction

There are numerous surgical strategies for the treatment of OCDs. Chapter 2 provides an overview

of these treatment strategies, and describes in depth the techniques and rehabilitation protocols

of the three treatment options that are currently most used: debridement and bone marrow

stimulation (BMS), autologous chondrocyte implantation (ACI) and osteochondral autograft

transfer system (OATS). Based on the literature, a guideline for treatment is proposed for 6

different types of osteochondral talar lesions.

Part II – Current treatment

In spite of the many publications on treatment of osteochondral lesions of the talus, literature is

lacking randomized controlled trials and prospective comparative studies. However, on the

subject many case series were published. To provide the best available evidence, chapter 3

contains a systematic review of treatment strategies for osteochondral lesions of the talus. All

eligible studies were summarized to compare their effectiveness. The proportion of the patient

population successfully treated was noted, and study-size weighted success rates were

calculated. Based on outcome, recommendations for treatment were made.

In most treatment strategies, ankle arthroscopy is still used as main surgical technique - as

opposed to open surgery. The dual purpose of chapter 4 was therefore to determine the

complication rate for ankle arthroscopy in our institution, and to describe the dorsiflexion method

associated with this rate. Patients with a complication were examined to determine permanent

damage and persisting complaints. The complication rate was compared to what was found in

literature. The arthroscopic technique that was used was described in detail, with a rationale

presented clarifying how this technique may prevent a significant number of complications.

Chapter 5 contains a comment on our publication of complications in ankle arthroscopy and a

response to this comment. Authors Pau Golanó and Jordi Vega commented that the anatomy of

the joint may not have been sufficiently highlighted in the study. They underline the importance of

knowledge and identification of anatomical landmarks of the ankle, to facilitate orientation and

prevent damage during the procedure. Furthermore, they provide a clarifying picture of a

transverse section of the ankle at the level of the tibiofibular syndesmosis, showing important

structures susceptible to injury during ankle arthroscopy. In our comment we confirm knowledge

of anatomy as the basis for every surgical technique and affirm the importance of staying up to

date with the extensive literature on this subject.

Introduction

23

Part III – Ankle biomechanics and arthroscopic access

Up until recently, measuring ankle biomechanics wasn’t possible by using non-invasive

techniques. Technical progress however has made it possible to determine the range of motion of

a joint by using computed-tomography (CT). CT, together with specifically designed software, can

determine the three-dimensional (3D) orientation of bones. By scanning a joint in different

extreme positions, the orientations of the bones can be determined. From these, ranges of motion

are calculated. These are described as finite helical axis orientation, and rotations around and

translations along these axes.

The goal of chapter 6 was to establish a quantitative database of the normal ranges of motion of

the talocrural and subtalar joints by using a 3D computed tomography stress-test. A clinical case

on suspected subtalar instability demonstrates the relevance of the proposed method.

The optimal arthroscopic approach (i.e. anterior or posterior) can be unclear preoperatively.

During anterior arthroscopy for an OCD, the ankle is held in full plantar flexion to optimize

exposure of the talar dome, increasing the chance of reaching the lesion. When a lesion is located

in a part of the talar dome that remains covered by the tibial plafond in any position, osteotomy

might be necessary. Chapter 7 uses the data of the 3D computed tomography stress-test of the

ankle to determine and visualize arthroscopic access to the talus. Coverage of the talus by the

distal tibia is determined for the neutral position and eight extreme foot positions, among which

are maximum plantar flexion and maximum dorsiflexion. The area of the talar surface that may be

hard to reach is visualized and described.

Part IV- Future treatment

The disadvantages associated with secondary treatment options, like donor-site morbidity and

high costs, leads to the search for new strategies. To treat larger cystic and secondary lesions,

current techniques aim to replace the defected cartilage with harvested cartilage or in-vitro

cultured cartilage. It was hypothesized that defect can also be covered by a metal device, as is

done before in the knee. To develop a metallic resurfacing implant, knowledge of talar geometry,

lesion size and location is necessary. Chapter 8 describes in detail the measurements of the sizes

of medial and lateral talar OCDs. Furthermore, it describes the measurements of talar radius and

angle of the talar shoulder at the location where the osteochondral lesion occurs. These data

served as the basis for the development of the talar HemiCAP, a prosthetic device consisting of a

screw and a metallic cap, which is able to restore the continuity of the talar articular surface, and

cover a subchondral lesion. Fifteen offset sizes were developed and it was hypothesized that there

would be a matching offset size for each talus, that the prosthetic device can be implanted slightly

recessed to the cartilage level, and that excessive contact pressures on the opposite tibial

cartilage can be avoided. Chapter 9 aims to test these hypotheses by implanting the prosthetic

device on the medial talar surface of 11 intact fresh-frozen human cadaver ankles, aiming its

surface 0.5 mm below cartilage level.

Chapter 1

24

Part V – General discussion

Chapter 10 provides a general discussion and conclusions. In chapter 11 provides a summary of

the thesis.

References

1. Anderson DV, Lyne ED (1984) Osteochondritis dissecans of the talus: case report on two

family members. J Pediatr Orthop 4:356-357 2. Assenmacher JA, Kelikian AS, Gottlob C, Kodros S (2001) Arthroscopically assisted

autologous osteochondraltransplantation for osteochondral lesions of the talar dome: an MRI and clinical follow-up study. Foot Ankle Int 22:544-551

3. Attarian DE, McCrackin HJ, Devito DP, McElhaney JH, Garrett WE,Jr (1985) A biomechanical study of human lateral ankle ligaments and autogenous reconstructive grafts. Am J Sports Med 13:377-381

4. Balduini FC, Vegso JJ, Torg JS, Torg E (1987) Management and rehabilitation of ligamentous injuries to the ankle. Sports Med 4:364-380

5. Barnett CH, Napier JR (1952) The axis of rotation at the ankle joint in man; its influence upon the form of the talus and the mobility of the fibula. J Anat 86:1-9

6. Berndt AL, Harty M (1959) Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg Am 41-A:988-1020

7. Bosien WR, Staples OS, Russell SW (1955) Residual disability following acute ankle sprains. J Bone Joint Surg Am 37-A:1237-1243

8. Buda R, Pagliazzi G, Castagnini F, Cavallo M, Giannini S (2016) Treatment of Osteochondritis Dissecans of the Talus in Skeletally Immature Population: A Critical Analysis of the Available Evidence. Foot Ankle Spec 9:265-270

9. Canale ST, Belding RH (1980) Osteochondral lesions of the talus. J Bone Joint Surg Am 62:97-102

10. Christel P, Versier G, Landreau P (1998) Les greffes osteo-chondrales selon la technique de la mosaicplasty. [Osteochondral grafts according to the mosaicplasty technique]. Matrise Orthopedique 76:1-13

11. Clanton TO, Johnson NS, Matheny LM (2014) Outcomes Following Microfracture in Grade 3 and 4 Articular Cartilage Lesions of the Ankle. Foot Ankle Int 35:764-770

12. Davidson AM, Steele HD, MacKenzie DA, Penny JA (1967) A review of twenty-one cases of transchondral fracture of the talus. J Trauma 7:378-415

13. DeBerardino TM, Arciero RA, Taylor DC (1997) Arthroscopic treatment of soft-tissue impingement of the ankle in athletes. Arthroscopy 13:492-498

14. Drosos GI, Kazakos KI, Kouzoumpasis P, Verettas DA (2007) Safety and efficacy of commercially available demineralised bone matrix preparations: a critical review of clinical studies. Injury 38 Suppl 4:S13-21

15. Dul J, Johnson GE (1985) A kinematic model of the human ankle. J Biomed Eng 7:137-143 16. Edwards JT, Diegmann MH, Scarborough NL (1998) Osteoinduction of human demineralized

bone: characterization in a rat model. Clin Orthop Relat Res (357):219-228 17. Ekstrand J, Tropp H (1990) The incidence of ankle sprains in soccer. Foot Ankle 11:41-44 18. Elias I, Zoga AC, Morrison WB, Besser MP, Schweitzer ME, Raikin SM (2007) Osteochondral

lesions of the talus: localization and morphologic data from 424 patients using a novel anatomical grid scheme. Foot Ankle Int 28:154-161

Introduction

25

19. Evans DL (1953) Recurrent instability of the ankle; a method of surgical treatment. Proc R Soc Med 46:343-344

20. Ferkel RD (2016) Editorial Commentary: Ankle Arthroscopy: Correct Portals and Distraction Are the Keys to Success. Arthroscopy 32:1375-1376

21. Ferkel RD, Zanotti RM, Komenda GA, Sgaglione NA, Cheng MS, Applegate GR, Dopirak RM (2008) Arthroscopic treatment of chronic osteochondral lesions of the talus: long-term results. Am J Sports Med 36:1750-1762

22. Flick AB, Gould N (1985) Osteochondritis dissecans of the talus (transchondral fractures of the talus): review of the literature and new surgical approach for medial dome lesions. Foot Ankle 5:165-185

23. Foumani M, Strackee SD, Jonges R, Blankevoort L, Zwinderman AH, Carelsen B, Streekstra GJ (2009) In-vivo three-dimensional carpal bone kinematics during flexion-extension and radio-ulnar deviation of the wrist: Dynamic motion versus step-wise static wrist positions. J Biomech 42:2664-2671

24. Garrick JG (1977) The frequency of injury, mechanism of injury, and epidemiology of ankle sprains. Am J Sports Med 5:241-242

25. Gautier E, Jung M, Mainil-Varlet P (1999) Articular surface repair in the talus using autogenous osteochondral plug transplantation. A preliminary report. Int Cartilage Rep Soc Newslett 1:19-20

26. Gobbi A, Mahajan S, Tuy B (June 15-18, 2002) Osteochondral lesions of the talus. A four year follow-up study in athletes. Presented at the 4th Symposium of the International Cartilage Repair Society Toronto, Canada

27. Gras F, Marintschev I, Muller M, Klos K, Lindner R, Muckley T, Hofmann GO (2010) Arthroscopic-controlled navigation for retrograde drilling of osteochondral lesions of the talus. Foot Ankle Int 31:897-904

28. Guettler JH, Demetropoulos CK, Yang KH, Jurist KA (2004) Osteochondral defects in the human knee: influence of defect size on cartilage rim stress and load redistribution to surrounding cartilage. Am J Sports Med 32:1451-1458

29. Hangody L, Kish G, Modis L, Szerb I, Gaspar L, Dioszegi Z, Kendik Z (2001) Mosaicplasty for the treatment of osteochondritis dissecans of the talus: two to seven year results in 36 patients. Foot Ankle Int 22:552-558

30. Hangody L, Kish G (2000) Surgical treatment of osteochondritis dissecans of the talus. In: Duparc J (ed) European textbook on surgical techniques in orthopaedics and traumatology, Editions Scientifiques et Medicales edn. Elsevier, pp 1-5

31. Hangody L, Kish G, Karpati Z, Szerb I, Eberhardt R (1997) Treatment of osteochondritis dissecans of the talus: use of the mosaicplasty technique--a preliminary report. Foot Ankle Int 18:628-634

32. Hannon CP, Smyth NA, Murawski CD, Savage-Elliott I, Deyer TW, Calder JD, Kennedy JG (2014) Osteochondral lesions of the talus: aspects of current management. Bone Joint J 96-B:164-171

33. Hicks JH (1953) The mechanics of the foot. I. The joints. J Anat 87:345-357 34. Hintermann B, Regazzoni P, Lampert C, Stutz G, Gachter A (2000) Arthroscopic findings in

acute fractures of the ankle. J Bone Joint Surg Br 82:345-351 35. Imhoff AB, Oettl GM, Burkart A (Boston, November, 16-18, 1998) Extended indication for

osteochondral autografts in different joints. Presented at the 2nd Symposium of the International Cartilage Repair Society

36. Inman VT (1976) The joints of the ankle. Lippincott Williams and Wilkins, Baltimore 37. Isman RE, Inman VT (1969) Anthropometric studies of the human foot and ankle. Bull

Prosthet Res 7:97-129

1

Chapter 1

24

Part V – General discussion

Chapter 10 provides a general discussion and conclusions. In chapter 11 provides a summary of

the thesis.

References

1. Anderson DV, Lyne ED (1984) Osteochondritis dissecans of the talus: case report on two

family members. J Pediatr Orthop 4:356-357 2. Assenmacher JA, Kelikian AS, Gottlob C, Kodros S (2001) Arthroscopically assisted

autologous osteochondraltransplantation for osteochondral lesions of the talar dome: an MRI and clinical follow-up study. Foot Ankle Int 22:544-551

3. Attarian DE, McCrackin HJ, Devito DP, McElhaney JH, Garrett WE,Jr (1985) A biomechanical study of human lateral ankle ligaments and autogenous reconstructive grafts. Am J Sports Med 13:377-381

4. Balduini FC, Vegso JJ, Torg JS, Torg E (1987) Management and rehabilitation of ligamentous injuries to the ankle. Sports Med 4:364-380

5. Barnett CH, Napier JR (1952) The axis of rotation at the ankle joint in man; its influence upon the form of the talus and the mobility of the fibula. J Anat 86:1-9

6. Berndt AL, Harty M (1959) Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg Am 41-A:988-1020

7. Bosien WR, Staples OS, Russell SW (1955) Residual disability following acute ankle sprains. J Bone Joint Surg Am 37-A:1237-1243

8. Buda R, Pagliazzi G, Castagnini F, Cavallo M, Giannini S (2016) Treatment of Osteochondritis Dissecans of the Talus in Skeletally Immature Population: A Critical Analysis of the Available Evidence. Foot Ankle Spec 9:265-270

9. Canale ST, Belding RH (1980) Osteochondral lesions of the talus. J Bone Joint Surg Am 62:97-102

10. Christel P, Versier G, Landreau P (1998) Les greffes osteo-chondrales selon la technique de la mosaicplasty. [Osteochondral grafts according to the mosaicplasty technique]. Matrise Orthopedique 76:1-13

11. Clanton TO, Johnson NS, Matheny LM (2014) Outcomes Following Microfracture in Grade 3 and 4 Articular Cartilage Lesions of the Ankle. Foot Ankle Int 35:764-770

12. Davidson AM, Steele HD, MacKenzie DA, Penny JA (1967) A review of twenty-one cases of transchondral fracture of the talus. J Trauma 7:378-415

13. DeBerardino TM, Arciero RA, Taylor DC (1997) Arthroscopic treatment of soft-tissue impingement of the ankle in athletes. Arthroscopy 13:492-498

14. Drosos GI, Kazakos KI, Kouzoumpasis P, Verettas DA (2007) Safety and efficacy of commercially available demineralised bone matrix preparations: a critical review of clinical studies. Injury 38 Suppl 4:S13-21

15. Dul J, Johnson GE (1985) A kinematic model of the human ankle. J Biomed Eng 7:137-143 16. Edwards JT, Diegmann MH, Scarborough NL (1998) Osteoinduction of human demineralized

bone: characterization in a rat model. Clin Orthop Relat Res (357):219-228 17. Ekstrand J, Tropp H (1990) The incidence of ankle sprains in soccer. Foot Ankle 11:41-44 18. Elias I, Zoga AC, Morrison WB, Besser MP, Schweitzer ME, Raikin SM (2007) Osteochondral

lesions of the talus: localization and morphologic data from 424 patients using a novel anatomical grid scheme. Foot Ankle Int 28:154-161

Introduction

25

19. Evans DL (1953) Recurrent instability of the ankle; a method of surgical treatment. Proc R Soc Med 46:343-344

20. Ferkel RD (2016) Editorial Commentary: Ankle Arthroscopy: Correct Portals and Distraction Are the Keys to Success. Arthroscopy 32:1375-1376

21. Ferkel RD, Zanotti RM, Komenda GA, Sgaglione NA, Cheng MS, Applegate GR, Dopirak RM (2008) Arthroscopic treatment of chronic osteochondral lesions of the talus: long-term results. Am J Sports Med 36:1750-1762

22. Flick AB, Gould N (1985) Osteochondritis dissecans of the talus (transchondral fractures of the talus): review of the literature and new surgical approach for medial dome lesions. Foot Ankle 5:165-185

23. Foumani M, Strackee SD, Jonges R, Blankevoort L, Zwinderman AH, Carelsen B, Streekstra GJ (2009) In-vivo three-dimensional carpal bone kinematics during flexion-extension and radio-ulnar deviation of the wrist: Dynamic motion versus step-wise static wrist positions. J Biomech 42:2664-2671

24. Garrick JG (1977) The frequency of injury, mechanism of injury, and epidemiology of ankle sprains. Am J Sports Med 5:241-242

25. Gautier E, Jung M, Mainil-Varlet P (1999) Articular surface repair in the talus using autogenous osteochondral plug transplantation. A preliminary report. Int Cartilage Rep Soc Newslett 1:19-20

26. Gobbi A, Mahajan S, Tuy B (June 15-18, 2002) Osteochondral lesions of the talus. A four year follow-up study in athletes. Presented at the 4th Symposium of the International Cartilage Repair Society Toronto, Canada

27. Gras F, Marintschev I, Muller M, Klos K, Lindner R, Muckley T, Hofmann GO (2010) Arthroscopic-controlled navigation for retrograde drilling of osteochondral lesions of the talus. Foot Ankle Int 31:897-904

28. Guettler JH, Demetropoulos CK, Yang KH, Jurist KA (2004) Osteochondral defects in the human knee: influence of defect size on cartilage rim stress and load redistribution to surrounding cartilage. Am J Sports Med 32:1451-1458

29. Hangody L, Kish G, Modis L, Szerb I, Gaspar L, Dioszegi Z, Kendik Z (2001) Mosaicplasty for the treatment of osteochondritis dissecans of the talus: two to seven year results in 36 patients. Foot Ankle Int 22:552-558

30. Hangody L, Kish G (2000) Surgical treatment of osteochondritis dissecans of the talus. In: Duparc J (ed) European textbook on surgical techniques in orthopaedics and traumatology, Editions Scientifiques et Medicales edn. Elsevier, pp 1-5

31. Hangody L, Kish G, Karpati Z, Szerb I, Eberhardt R (1997) Treatment of osteochondritis dissecans of the talus: use of the mosaicplasty technique--a preliminary report. Foot Ankle Int 18:628-634

32. Hannon CP, Smyth NA, Murawski CD, Savage-Elliott I, Deyer TW, Calder JD, Kennedy JG (2014) Osteochondral lesions of the talus: aspects of current management. Bone Joint J 96-B:164-171

33. Hicks JH (1953) The mechanics of the foot. I. The joints. J Anat 87:345-357 34. Hintermann B, Regazzoni P, Lampert C, Stutz G, Gachter A (2000) Arthroscopic findings in

acute fractures of the ankle. J Bone Joint Surg Br 82:345-351 35. Imhoff AB, Oettl GM, Burkart A (Boston, November, 16-18, 1998) Extended indication for

osteochondral autografts in different joints. Presented at the 2nd Symposium of the International Cartilage Repair Society

36. Inman VT (1976) The joints of the ankle. Lippincott Williams and Wilkins, Baltimore 37. Isman RE, Inman VT (1969) Anthropometric studies of the human foot and ankle. Bull

Prosthet Res 7:97-129

Chapter 1

26

38. Jackson DW, Lalor PA, Aberman HM, Simon TM (2001) Spontaneous repair of full-thickness defects of articular cartilage in a goat model. A preliminary study. J Bone Joint Surg Am 83-A:53-64

39. Jakob RP, Mainil-Varlet P, Saager C (Fribourg, Switzerland, October 29-31, 1997) Mosaicplasty in cartilaginous lesions over 4 cm2 and indications outside the knee. Cartilage Repair. Presented at the 2nd Fribourg International Symposium

40. Kahn G (1998) Ankle sprain prevention with an over-shoe brace in the military set-up. Directed by Mann, G., Nyska, M. and Dvir, Z. Dissertation or Thesis, Sackler Tel Aviv University Medical School, Tel Aviv, Israel

41. Katcherian D (1994) Soft-tissue injuries of the ankle. In: Lufter LD, Mizel MS, Pfeffer GB (eds) Orthopaedic knowledge update: foot and ankle. American Academy of Orthopaedic Surgeons, Rosemont (IL), pp 241-253

42. Kessler JI, Weiss JM, Nikizad H, Gyurdzhyan S, Jacobs JC,Jr, Bebchuk JD, Shea KG (2014) Osteochondritis Dissecans of the Ankle in Children and Adolescents: Demographics and Epidemiology. Am J Sports Med 42:2165-2171

43. Kim CW, Bugbee W (Anaheim, California, February 7, 1999) Ankle osteochondral allografts. Presented at the 29th Annual Meeting of the American Orthopaedic Foot and Ankle Society

44. Knight KL (1978) Identification of ligaments torn by forceful inversion of cadaver ankles in plantar and dorsiflexion. Med Sci Sports 10:38-42

45. Kolker D, Wilson MG (Toronto, Canada, June 15-18, 2002) Autologous osteochondral grafting for cartilage defects of the talar dome. Presented at the 4th Symposium of the International Cartilage Repair Society

46. Kristiansen B (1981) Evans' repair of lateral instability of the ankle joint. Acta Orthop Scand 52:679-682

47. Last RJ (1984) Ankle anatomy. In: Last RJ (ed) Anatomy, regional and applied., 7th edn. Churchill Livingstone, London, pp 182-189

48. Leardini A, O'Connor JJ, Giannini S (2014) Biomechanics of the natural, arthritic, and replaced human ankle joint. J Foot Ankle Res 7(1):8

49. Leardini A, Stagni R, O'Connor JJ (2001) Mobility of the subtalar joint in the intact ankle complex. J Biomech 34:805-809

50. Leardini A, O'Connor JJ, Catani F, Giannini S (1999) Kinematics of the human ankle complex in passive flexion; a single degree of freedom system. J Biomech 32:111-118

51. Leontaritis N, Hinojosa L, Panchbhavi VK (2009) Arthroscopically detected intra-articular lesions associated with acute ankle fractures. J Bone Joint Surg Am 91:333-339

52. Li S, Li H, Liu Y, Qu F, Wang J, Liu C (2014) Clinical outcomes of early weight-bearing after arthroscopic microfracture during the treatment of osteochondral lesions of the talus. Chin Med J (Engl) 127:2470-2474

53. Lippert MJ, Hawe W, Bernett P (1989) Surgical therapy of fibular capsule-ligament rupture. Sportverletz Sportschaden 3:6-13

54. Liu SH, Jason WJ (1994) Lateral ankle sprains and instability problems. Clin Sports Med 13:793-809

55. Lundberg A, Goldie I, Kalin B, Selvik G (1989) Kinematics of the ankle/foot complex: plantarflexion and dorsiflexion. Foot Ankle 9:194-200

56. Ly PN, Fallat LM (1993) Trans-chondral fractures of the talus: a review of 64 surgical cases. J Foot Ankle Surg 32:352-374

57. Mack RP (1982) Ankle injuries in athletics. Clin Sports Med 1:71-84 58. Maehlum S, Daljord OA (1984) Acute sports injuries in Oslo: a one-year study. Br J Sports Med

18:181-185

Introduction

27

59. Mann G, Elishuv O, Nyska M, Chaimsky G, Finterbush A, Perry C (1993) Recurrent ankle sprain: experience with modification of Williams reefing technique. J Orthop Tech 8(3):361-376

60. Martin TL, Wilson MG, Robledo J (Anaheim, California, February 7, 1999) Early results of autologous bone grafting for large talar osteochondritis dissecans lesions. Presented at the 29th Annual Meeting of the American Orthopaedic Foot and Ankle Society

61. McCullough CJ, Venugopal V (1979) Osteochondritis dissecans of the talus: the natural history. Clin Orthop Relat Res (144):264-268

62. Monro A (1856) Microgeologie. Dissertation or Thesis, Berlin: Th. Billroth 63. Mubarak SJ, Carroll NC (1979) Familial osteochondritis dissecans of the knee. Clin Orthop

Relat Res (140):131-136 64. Mukherjee K, Gangopadhyay P (1983) Extensor digitorum brevis transfer in chronic unstable

ankles. J R Coll Surg Edinb 28:250-255 65. Nash WC, Baker CL,Jr (1984) Transchondral talar dome fractures: not just a sprained ankle.

South Med J 77:560-564 66. Nigg BM, Hintermann B (2002) Biomechanics of the ankle joint complex and the shoe. In:

Nyska M, Mann G (eds) The unstable ankle., 1st edn. Human kinetics publishers, Champaign, IL, pp 42-50

67. Parisien JS (1986) Arthroscopic treatment of osteochondral lesions of the talus. Am J Sports Med 14:211-217

68. Park HW, Lee KB (2015) Comparison of chondral versus osteochondral lesions of the talus after arthroscopic microfracture. Knee Surg Sports Traumatol Arthrosc 23:860-867

69. Petersen L, Brittberg M, Lindahl A (2003) Autologous chondrocyte transplantation of the ankle. Foot Ankle Clin 8:291-303

70. Pettine KA, Morrey BF (1987) Osteochondral fractures of the talus. A long-term follow-up. J Bone Joint Surg Br 69:89-92

71. Pick MP (1955) Familial osteochondritis dissecans. J Bone Joint Surg Br 37-B:142-145 72. Pietrzak WS, Woodell-May J, McDonald N (2006) Assay of bone morphogenetic protein-2,-4,

and -7 in human demineralized bone matrix. J Craniofac Surg 17:84-90 73. Prokuski LJ, Saltzman CL (1997) Challenging fractures of the foot and ankle. Radiol Clin

North Am 35:655-670 74. Reilingh ML, Blankevoort L, van Eekeren IC, van Dijk CN (2013) Morphological analysis of

subchondral talar cysts on microCT. Knee Surg Sports Traumatol Arthrosc 21:1409-1417 75. Reilingh ML, Van Bergen CJ, Van Dijk CN (2009) Diagnosis and treatment of osteochondral

defects of the ankle. South Afr Orthop J 8(2):44-50 76. RIVM (2016) Sport Kernindicatoren [Key indicators Sports].

In: https://www.volksgezondheidenzorg.info/onderwerp/sport-en-bewegen 77. RIVM (2014) Nationaal kompas volksgezondheid. Lichamelijke activiteit. [National compass

public health. Physical activity.] www.nationaalkompas.nl/gezondheidsdeterminanten/leefstijl/lichamelijke-activiteit/

78. Robinson DE, Winson IG, Harries WJ, Kelly AJ (2003) Arthroscopic treatment of osteochondral lesions of the talus. J Bone Joint Surg Br 85:989-993

79. Rödén S, Tillegard P, Unanderscharin L (1953) Osteochondritis dissecans and similar lesions of the talus: report of fifty-five cases with special reference to etiology and treatment. Acta Orthop Scand 23:51-66

80. Rodman PS, McHenry HM (1980) Bioenergetics and the origin of hominid bipedalism. Am J Phys Anthropol 52:103-106

81. Sandelin J, Santavirta S, Lattila R, Vuolle P, Sarna S (1988) Sports injuries in a large urban population: occurrence and epidemiological aspects. Int J Sports Med 9:61-66

1

Chapter 1

26

38. Jackson DW, Lalor PA, Aberman HM, Simon TM (2001) Spontaneous repair of full-thickness defects of articular cartilage in a goat model. A preliminary study. J Bone Joint Surg Am 83-A:53-64

39. Jakob RP, Mainil-Varlet P, Saager C (Fribourg, Switzerland, October 29-31, 1997) Mosaicplasty in cartilaginous lesions over 4 cm2 and indications outside the knee. Cartilage Repair. Presented at the 2nd Fribourg International Symposium

40. Kahn G (1998) Ankle sprain prevention with an over-shoe brace in the military set-up. Directed by Mann, G., Nyska, M. and Dvir, Z. Dissertation or Thesis, Sackler Tel Aviv University Medical School, Tel Aviv, Israel

41. Katcherian D (1994) Soft-tissue injuries of the ankle. In: Lufter LD, Mizel MS, Pfeffer GB (eds) Orthopaedic knowledge update: foot and ankle. American Academy of Orthopaedic Surgeons, Rosemont (IL), pp 241-253

42. Kessler JI, Weiss JM, Nikizad H, Gyurdzhyan S, Jacobs JC,Jr, Bebchuk JD, Shea KG (2014) Osteochondritis Dissecans of the Ankle in Children and Adolescents: Demographics and Epidemiology. Am J Sports Med 42:2165-2171

43. Kim CW, Bugbee W (Anaheim, California, February 7, 1999) Ankle osteochondral allografts. Presented at the 29th Annual Meeting of the American Orthopaedic Foot and Ankle Society

44. Knight KL (1978) Identification of ligaments torn by forceful inversion of cadaver ankles in plantar and dorsiflexion. Med Sci Sports 10:38-42

45. Kolker D, Wilson MG (Toronto, Canada, June 15-18, 2002) Autologous osteochondral grafting for cartilage defects of the talar dome. Presented at the 4th Symposium of the International Cartilage Repair Society

46. Kristiansen B (1981) Evans' repair of lateral instability of the ankle joint. Acta Orthop Scand 52:679-682

47. Last RJ (1984) Ankle anatomy. In: Last RJ (ed) Anatomy, regional and applied., 7th edn. Churchill Livingstone, London, pp 182-189

48. Leardini A, O'Connor JJ, Giannini S (2014) Biomechanics of the natural, arthritic, and replaced human ankle joint. J Foot Ankle Res 7(1):8

49. Leardini A, Stagni R, O'Connor JJ (2001) Mobility of the subtalar joint in the intact ankle complex. J Biomech 34:805-809

50. Leardini A, O'Connor JJ, Catani F, Giannini S (1999) Kinematics of the human ankle complex in passive flexion; a single degree of freedom system. J Biomech 32:111-118

51. Leontaritis N, Hinojosa L, Panchbhavi VK (2009) Arthroscopically detected intra-articular lesions associated with acute ankle fractures. J Bone Joint Surg Am 91:333-339

52. Li S, Li H, Liu Y, Qu F, Wang J, Liu C (2014) Clinical outcomes of early weight-bearing after arthroscopic microfracture during the treatment of osteochondral lesions of the talus. Chin Med J (Engl) 127:2470-2474

53. Lippert MJ, Hawe W, Bernett P (1989) Surgical therapy of fibular capsule-ligament rupture. Sportverletz Sportschaden 3:6-13

54. Liu SH, Jason WJ (1994) Lateral ankle sprains and instability problems. Clin Sports Med 13:793-809

55. Lundberg A, Goldie I, Kalin B, Selvik G (1989) Kinematics of the ankle/foot complex: plantarflexion and dorsiflexion. Foot Ankle 9:194-200

56. Ly PN, Fallat LM (1993) Trans-chondral fractures of the talus: a review of 64 surgical cases. J Foot Ankle Surg 32:352-374

57. Mack RP (1982) Ankle injuries in athletics. Clin Sports Med 1:71-84 58. Maehlum S, Daljord OA (1984) Acute sports injuries in Oslo: a one-year study. Br J Sports Med

18:181-185

Introduction

27

59. Mann G, Elishuv O, Nyska M, Chaimsky G, Finterbush A, Perry C (1993) Recurrent ankle sprain: experience with modification of Williams reefing technique. J Orthop Tech 8(3):361-376

60. Martin TL, Wilson MG, Robledo J (Anaheim, California, February 7, 1999) Early results of autologous bone grafting for large talar osteochondritis dissecans lesions. Presented at the 29th Annual Meeting of the American Orthopaedic Foot and Ankle Society

61. McCullough CJ, Venugopal V (1979) Osteochondritis dissecans of the talus: the natural history. Clin Orthop Relat Res (144):264-268

62. Monro A (1856) Microgeologie. Dissertation or Thesis, Berlin: Th. Billroth 63. Mubarak SJ, Carroll NC (1979) Familial osteochondritis dissecans of the knee. Clin Orthop

Relat Res (140):131-136 64. Mukherjee K, Gangopadhyay P (1983) Extensor digitorum brevis transfer in chronic unstable

ankles. J R Coll Surg Edinb 28:250-255 65. Nash WC, Baker CL,Jr (1984) Transchondral talar dome fractures: not just a sprained ankle.

South Med J 77:560-564 66. Nigg BM, Hintermann B (2002) Biomechanics of the ankle joint complex and the shoe. In:

Nyska M, Mann G (eds) The unstable ankle., 1st edn. Human kinetics publishers, Champaign, IL, pp 42-50

67. Parisien JS (1986) Arthroscopic treatment of osteochondral lesions of the talus. Am J Sports Med 14:211-217

68. Park HW, Lee KB (2015) Comparison of chondral versus osteochondral lesions of the talus after arthroscopic microfracture. Knee Surg Sports Traumatol Arthrosc 23:860-867

69. Petersen L, Brittberg M, Lindahl A (2003) Autologous chondrocyte transplantation of the ankle. Foot Ankle Clin 8:291-303

70. Pettine KA, Morrey BF (1987) Osteochondral fractures of the talus. A long-term follow-up. J Bone Joint Surg Br 69:89-92

71. Pick MP (1955) Familial osteochondritis dissecans. J Bone Joint Surg Br 37-B:142-145 72. Pietrzak WS, Woodell-May J, McDonald N (2006) Assay of bone morphogenetic protein-2,-4,

and -7 in human demineralized bone matrix. J Craniofac Surg 17:84-90 73. Prokuski LJ, Saltzman CL (1997) Challenging fractures of the foot and ankle. Radiol Clin

North Am 35:655-670 74. Reilingh ML, Blankevoort L, van Eekeren IC, van Dijk CN (2013) Morphological analysis of

subchondral talar cysts on microCT. Knee Surg Sports Traumatol Arthrosc 21:1409-1417 75. Reilingh ML, Van Bergen CJ, Van Dijk CN (2009) Diagnosis and treatment of osteochondral

defects of the ankle. South Afr Orthop J 8(2):44-50 76. RIVM (2016) Sport Kernindicatoren [Key indicators Sports].

In: https://www.volksgezondheidenzorg.info/onderwerp/sport-en-bewegen 77. RIVM (2014) Nationaal kompas volksgezondheid. Lichamelijke activiteit. [National compass

public health. Physical activity.] www.nationaalkompas.nl/gezondheidsdeterminanten/leefstijl/lichamelijke-activiteit/

78. Robinson DE, Winson IG, Harries WJ, Kelly AJ (2003) Arthroscopic treatment of osteochondral lesions of the talus. J Bone Joint Surg Br 85:989-993

79. Rödén S, Tillegard P, Unanderscharin L (1953) Osteochondritis dissecans and similar lesions of the talus: report of fifty-five cases with special reference to etiology and treatment. Acta Orthop Scand 23:51-66

80. Rodman PS, McHenry HM (1980) Bioenergetics and the origin of hominid bipedalism. Am J Phys Anthropol 52:103-106

81. Sandelin J, Santavirta S, Lattila R, Vuolle P, Sarna S (1988) Sports injuries in a large urban population: occurrence and epidemiological aspects. Int J Sports Med 9:61-66

Chapter 1

28

82. Santrock RD, Buchanan MM, Lee TH, Berlet GC (2003) Osteochondral lesions of the talus. Foot Ankle Clin 8:73-90, viii

83. Saxena A, Eakin C (2007) Articular talar injuries in athletes: results of microfracture and autogenous bone graft. Am J Sports Med 35:1680-1687

84. Schachter AK, Chen AL, Reddy PD, Tejwani NC (2005) Osteochondral lesions of the talus. J Am Acad Orthop Surg 13:152-158

85. Schaefer DB, Martin I, Dick W (Toronto, Canada, June 15-18, 2002) Mosaicplasty for the treatment of osteochondral lesions of the talus. Presented at the 4th Symposium of the International Cartilage Repair Society

86. Schuman L, Struijs PA, van Dijk CN (2002) Arthroscopic treatment for osteochondraldefects of the talus. Results at follow-up at 2 to 11 years. J Bone Joint Surg Br 84:364-368

87. Scranton PE,Jr, McDermott JE (2001) Treatment of type V osteochondral lesions of the talus with ipsilateral knee osteochondral autografts. Foot Ankle Int 22:380-384

88. Siegler S, Block J, Schneck CD (1988) The mechanical characteristics of the collateral ligaments of the human ankle joint. Foot Ankle 8:234-242

89. Siegler S, Chen J, Schneck CD (1988) The three-dimensional kinematics and flexibility characteristics of the human ankle and subtalar joints--Part I: Kinematics. J Biomech Eng 110:364-373

90. Singh AK, Starkweather KD, Hollister AM, Jatana S, Lupichuk AG (1992) Kinematics of the ankle: a hinge axis model. Foot Ankle 13:439-446

91. Sockol MD, Raichlen DA, Pontzer H (2007) Chimpanzee locomotor energetics and the origin of human bipedalism. Proc Natl Acad Sci U S A 104:12265-12269

92. Speck M, Schweinfurt M, Boerner T (Toronto, Canada, June 15-18, 2002) Osteochondral autograft transplantation for traumatic and degenerative lesions of the talus. Presented at the 4th Symposium of the International Cartilage Repair Society

93. Takao M, Ochi M, Uchio Y, Naito K, Kono T, Oae K (2003) Osteochondral lesions of the talar dome associated with trauma. Arthroscopy 19:1061-1067

94. Thordarson DB (2001) Talar body fractures. Orthop Clin North Am 32:65-77, viii 95. Tol JL, Struijs PA, Bossuyt PM, Verhagen RA, van Dijk CN (2000) Treatment strategies in

osteochondral defects of the talar dome: a systematic review. Foot Ankle Int 21:119-126 96. van Bergen CJ, Kox LS, Maas M, Sierevelt IN, Kerkhoffs GM, van Dijk CN (2013) Arthroscopic

treatment of osteochondral defects of the talus: outcomes at eight to twenty years of follow-up. J Bone Joint Surg Am 95:519-525

97. van Buecken K, Barrack RL, Alexander AH, Ertl JP (1989) Arthroscopic treatment of transchondral talar dome fractures. Am J Sports Med 17:350-356

98. van den Bogert AJ, Smith GD, Nigg BM (1994) In vivo determination of the anatomical axes of the ankle joint complex: an optimization approach. J Biomech 27:1477-1488

99. van der Vis HM, Aspenberg P, Marti RK, Tigchelaar W, van Noorden CJ (1998) Fluid pressure causes bone resorption in a rabbit model of prosthetic loosening. Clin Orthop Relat Res 350:201-208

100. van Dijk CN (2014) Ankle arthroscopy. Techniques developed by the Amsterdam Foot and Ankle School. Springer, New York

101. van Dijk CN, Reilingh ML, Zengerink M, van Bergen CJ (2010) The natural history of osteochondral lesions in the ankle. Instr Course Lect 59:375-386

102. van Dijk CN, Reilingh ML, Zengerink M, van Bergen CJ (2010) Osteochondral defects in the ankle: why painful?. Knee Surg Sports Traumatol Arthrosc 18:570-580

103. van Dijk CN, Verhagen RA, Tol HJ (2001) Technical note: Resterilizable noninvasive ankle distraction device. Arthroscopy 17:1-5

104. van Dijk CN, Scholte D (1997) Arthroscopy of the ankle joint. Arthroscopy 13:90-96

Introduction

29

105. van Dijk CN (1994) On diagnostic strategies in patients with severe ankle sprain. Thesis, University of Amsterdam

106. Veiligheid NL (2012) Sports ankle injuries. [Safety NL, Enkelblessures door sport]. www.veiligheid.nl

107. Veillette C (2011) Biomechanics of the foot and ankle. In: www.orthopaedicsone.com/display/Main/Biomechanics+of+the+foot+and+ankle

108. Verhagen RA, Maas M, Dijkgraaf MG, Tol JL, Krips R, van Dijk CN (2005) Prospective study on diagnostic strategies in osteochondral lesions of the talus. Is MRI superior to helical CT?. J Bone Joint Surg Br 87:41-46

109. Woods K, Harris I (1995) Osteochondritis dissecans of the talus in identical twins. J Bone Joint Surg Br 77:331

110. Yao J, Weis E (1985) Osteochondritis dissecans. Orthop Rev 14:190-204 111. Zelent ME, Neese DJ (2006) Talar dome fracture repaired using bioabsorbable fixation. J Am

Podiatr Med Assoc 96:256-259

1

Chapter 1

28

82. Santrock RD, Buchanan MM, Lee TH, Berlet GC (2003) Osteochondral lesions of the talus. Foot Ankle Clin 8:73-90, viii

83. Saxena A, Eakin C (2007) Articular talar injuries in athletes: results of microfracture and autogenous bone graft. Am J Sports Med 35:1680-1687

84. Schachter AK, Chen AL, Reddy PD, Tejwani NC (2005) Osteochondral lesions of the talus. J Am Acad Orthop Surg 13:152-158

85. Schaefer DB, Martin I, Dick W (Toronto, Canada, June 15-18, 2002) Mosaicplasty for the treatment of osteochondral lesions of the talus. Presented at the 4th Symposium of the International Cartilage Repair Society

86. Schuman L, Struijs PA, van Dijk CN (2002) Arthroscopic treatment for osteochondraldefects of the talus. Results at follow-up at 2 to 11 years. J Bone Joint Surg Br 84:364-368

87. Scranton PE,Jr, McDermott JE (2001) Treatment of type V osteochondral lesions of the talus with ipsilateral knee osteochondral autografts. Foot Ankle Int 22:380-384

88. Siegler S, Block J, Schneck CD (1988) The mechanical characteristics of the collateral ligaments of the human ankle joint. Foot Ankle 8:234-242

89. Siegler S, Chen J, Schneck CD (1988) The three-dimensional kinematics and flexibility characteristics of the human ankle and subtalar joints--Part I: Kinematics. J Biomech Eng 110:364-373

90. Singh AK, Starkweather KD, Hollister AM, Jatana S, Lupichuk AG (1992) Kinematics of the ankle: a hinge axis model. Foot Ankle 13:439-446

91. Sockol MD, Raichlen DA, Pontzer H (2007) Chimpanzee locomotor energetics and the origin of human bipedalism. Proc Natl Acad Sci U S A 104:12265-12269

92. Speck M, Schweinfurt M, Boerner T (Toronto, Canada, June 15-18, 2002) Osteochondral autograft transplantation for traumatic and degenerative lesions of the talus. Presented at the 4th Symposium of the International Cartilage Repair Society

93. Takao M, Ochi M, Uchio Y, Naito K, Kono T, Oae K (2003) Osteochondral lesions of the talar dome associated with trauma. Arthroscopy 19:1061-1067

94. Thordarson DB (2001) Talar body fractures. Orthop Clin North Am 32:65-77, viii 95. Tol JL, Struijs PA, Bossuyt PM, Verhagen RA, van Dijk CN (2000) Treatment strategies in

osteochondral defects of the talar dome: a systematic review. Foot Ankle Int 21:119-126 96. van Bergen CJ, Kox LS, Maas M, Sierevelt IN, Kerkhoffs GM, van Dijk CN (2013) Arthroscopic

treatment of osteochondral defects of the talus: outcomes at eight to twenty years of follow-up. J Bone Joint Surg Am 95:519-525

97. van Buecken K, Barrack RL, Alexander AH, Ertl JP (1989) Arthroscopic treatment of transchondral talar dome fractures. Am J Sports Med 17:350-356

98. van den Bogert AJ, Smith GD, Nigg BM (1994) In vivo determination of the anatomical axes of the ankle joint complex: an optimization approach. J Biomech 27:1477-1488

99. van der Vis HM, Aspenberg P, Marti RK, Tigchelaar W, van Noorden CJ (1998) Fluid pressure causes bone resorption in a rabbit model of prosthetic loosening. Clin Orthop Relat Res 350:201-208

100. van Dijk CN (2014) Ankle arthroscopy. Techniques developed by the Amsterdam Foot and Ankle School. Springer, New York

101. van Dijk CN, Reilingh ML, Zengerink M, van Bergen CJ (2010) The natural history of osteochondral lesions in the ankle. Instr Course Lect 59:375-386

102. van Dijk CN, Reilingh ML, Zengerink M, van Bergen CJ (2010) Osteochondral defects in the ankle: why painful?. Knee Surg Sports Traumatol Arthrosc 18:570-580

103. van Dijk CN, Verhagen RA, Tol HJ (2001) Technical note: Resterilizable noninvasive ankle distraction device. Arthroscopy 17:1-5

104. van Dijk CN, Scholte D (1997) Arthroscopy of the ankle joint. Arthroscopy 13:90-96

Introduction

29

105. van Dijk CN (1994) On diagnostic strategies in patients with severe ankle sprain. Thesis, University of Amsterdam

106. Veiligheid NL (2012) Sports ankle injuries. [Safety NL, Enkelblessures door sport]. www.veiligheid.nl

107. Veillette C (2011) Biomechanics of the foot and ankle. In: www.orthopaedicsone.com/display/Main/Biomechanics+of+the+foot+and+ankle

108. Verhagen RA, Maas M, Dijkgraaf MG, Tol JL, Krips R, van Dijk CN (2005) Prospective study on diagnostic strategies in osteochondral lesions of the talus. Is MRI superior to helical CT?. J Bone Joint Surg Br 87:41-46

109. Woods K, Harris I (1995) Osteochondritis dissecans of the talus in identical twins. J Bone Joint Surg Br 77:331

110. Yao J, Weis E (1985) Osteochondritis dissecans. Orthop Rev 14:190-204 111. Zelent ME, Neese DJ (2006) Talar dome fracture repaired using bioabsorbable fixation. J Am

Podiatr Med Assoc 96:256-259