VISITANTE

U. Szeimies

Osteoarthritis of the Ankle Joint or Subtalar Joint

Definition

Osteoarthritis is marked by patchy degenerative changes affect-ing the cartilage on both articular surfaces.

Symptoms

●Morning stiffness

●Pain after periods of inactivity

●Pain during exercise

●Pain at rest

●Limitation of motion

●Swelling

●Local warmth and redness over the joint

●Diffuse ankle or subtalar joint pain

Predisposing Factors

●Large, repetitive loads with inadequate recovery periods (competitive athletes)

●Strenuous exercise or exertion

●High body weight

●Trauma (unhealed capsuloligamentous injury with instability, step-off caused by an intra-articular fracture, such as a subta-lar injury in snowboarder’s ankle)

●Inflammatory joint disease

●Congenital factors

●Genetic disposition

●Disorders of cartilage metabolism (ochronosis, chondro-calcinosis)

Anatomy and Pathology

Osteoarthritis is the most common disease process affecting the joints. Its incidence increases as the population ages.

Under normal conditions a balance exists between the break-down and synthesis of articular cartilage matrix. The capacity for matrix synthesis declines with ageing, however. When high loads are placed upon the joint, synovial fluid is expressed from the joint space; this increases the friction between the cartilage surfaces, causing mechanical wear of the articular cartilage with delamination of the superficial cartilage layer, loss of cartilage thickness, subchondral sclerosis due to an abnormal pressure distribution, osteophyte formation, and fluid pene-tration of the subchondral bone layer causing cyst formation.

The wear-and-tear process initiates a kind of inflammatory response.

! Note

Cartilage status is not the only concern. Associated structures (joint capsule, ligaments, tendons, articulating bone ends, bur-sa) are also important, and changes in these structures may contribute to osteoarthritis.

Imaging

Radiographs

Typical radiographic findings in osteoarthritis are sclerosis of the subchondral cancellous bone, subchondral cysts, marginal osteophytes, joint space narrowing, articular surface remodel-ing after cartilage loss (surface grindremodel-ing), subluxation, capsular chondromas, and intra-articular loose bodies.

Ultrasound

A longitudinal scan through the anterior ankle joint will show effusion due to activated osteoarthritis, irregular thickening of the joint capsule, and an irregular, echogenic bone surface.

CT (▶Fig. 3.60)

CT with submillimeter isotropic voxels and MPRs in three planes are recommended for the optimum evaluation of bony structures. Findings may include osteophytes, subchondral cysts, erosion of the subchondral plate, joint space narrowing or bone-on-bone contact, and intra-articular loose bodies.

MRI

Imaging technology is particularly important in evaluations of articular cartilage, and the poor correlation between MRI and arthroscopy often reported in the literature most likely re-sults from less-than-optimal imaging equipment. A high field intensity (at least 1.5 T) should be combined with the use of

dedicated high-resolution joint coils, thin slice acquisition (2–3 mm), increased phase-encoding steps, and an increased image matrix. Unfortunately, the longer scan time and higher procurement costs of these systems are difficult to justify economically in most office settings.

Interpretation Checklist

●Carefully evaluate the articular cartilage; possible findings range from early signal changes and superficial fibrillations and ulcerations to deep ulcers or cartilage defects with ex-posed subchondral bone.

●Describe the extent of changes in millimeters and in at least two planes.

●Look for associated phenomena such as effusion, subchondral bone marrow edema, or synovitis as an expression of acti-vated osteoarthritis.

Examination Technique

●Standard protocol: prone position, high-resolution multi-channel coil

●Sequences:

○Coronal and sagittal PD-weighted fat-sat

○Coronal T1-weighted

○Axial T2-weighted

○T1-weighted fat-sat, true axial (angled to the joint plane) and sagittal after IV contrast administration

MRI Findings (▶Fig. 3.61)

●Cartilage evaluation:

○Areas of increased signal intensity

○Cartilage swelling

○Chondromalacia

○Fibrillations

○Fissures

○Erosions

○Ulcerations

○Indicate extent (superficial, deep, extending to subchondral bone, patchy cartilage defects)

○Measure the defect

○Exposed subchondral bone

●Evaluation/description of the subchondral bone:

○Edema formation

○Softening

○Chondromalacia

○Cortical fissures

○Cyst formation

○Subchondral cysts

○Marginal osteophytes

○Sclerosis

○Articular surface deformity

○Joint congruity

○Subluxation (degenerative arthritis)

○Measure subchondral defects and cysts

●Description of repair mechanisms:

○Intra-articular osteophytes

○Regenerative cartilage

●Evaluation of the synovium:

○Effusion

○Synovitis Fig. 3.60 Sagittal reformatted CT image of subtalar osteoarthritis.

The image shows complete loss of the subtalar joint space with subchondral sclerosis and multiple subchondral cysts.

Fig. 3.61 a, b Activated osteoarthritis of the ankle joint.

a Sagittal T1-weighted fat-sat image after con-trast administration demonstrates synovitis with subchondral bone marrow edema and the devel-opment of subchondral cysts.

b Coronal T1-weighted fat-sat image after contrast administration shows joint incongruity resulting from cartilage loss with exposure of subchondral bone. The linear signal void in the joint space is caused by a vacuum phenomenon.

○Synovial villi

●Evaluation of the capsule and ligaments:

○Thickened joint capsule

○Capsular chondromas

○Osteomas

○Intra-articular loose bodies

○Adjacent ligament structures

●Sequelae of osteoarthritis:

○Degenerative changes in neighboring joints

○Signs of overload in tendons and in adjacent ligaments and capsule-ligament attachments

Chondropathy can be classified, but there is no uniform system for grading cartilage lesions. The best approach is to give a pre-cise description of the cartilage lesion in the radiology report.

The Outerbridge system is widely used for the classification of cartilage lesions (▶Table 3.8).

Imaging Recommendation

Modality of choice: varies with the treatment approach. The initial study is radiography. MRI is used to evaluate early forms of osteoarthritis and determine degree of activation, while CT is used to exclude ossified intra-articular loose bodies.

●Pigmented villonodular synovitis

Treatment

Conservative

●Nonsteroidal anti-inflammatory drugs

●Physical therapy

●Ankle brace

●Intra-articular injection of steroids or hyaluronic acid

Operative

●Grades I and II: arthroscopic debridement, synovectomy, osteophyte removal, cartilage stabilization; with > 5° mala-lignment: axial correction

●Grade III or higher: arthrodesis of the ankle joint or endoprosthesis

Prognosis, Complications

Prognosis

Secondary axial malalignment may result from local wear. The rate of progression of the disease cannot be predicted. More-over, the complaints do not always correlate with the degree of joint damage revealed by imaging.

Possible Complications

●Chronic activated osteoarthritis

●Subluxation

●Dislocation

●Complete destruction of the joint and adjacent structures

Chondromatosis, Multiple Intra-Articular Loose Bodies

Definition

Chondromatosis is characterized by the formation of benign cartilage neoplasms (chondromas) within the joint capsule and in tendon sheaths and bursae. The chondromas may ossify, creating a condition known as synovial osteochondromatosis.

Synonyms for chondromatosis are articular chondromatosis, synovial chondromatosis, and Reichel disease.

Symptoms

●Locking of the joint

●Limited motion

●Pain

●Joint swelling

●Palpable intra-articular bodies

●Crepitation

Predisposing Factors

●Poorly understood

●Recurrent microtrauma

●Genetic disposition is known (familial synovial chondromato-sis with dwarfism)

Anatomy and Pathology

●Chondromatosis: rare in the ankle joint; most common in the hip, knee, and elbow. The precise cause is unknown. It is char-acterized by multiple calcified or ossified sites of cartilage proliferation and by metaplasia of the synovial membrane in joints, tendon sheaths, and bursae.

○Primary chondromatosis: synovial metaplasia

○Secondary chondromatosis: small, loose cartilage fragments detached from the synovial membrane in a setting of joint degeneration, trauma, or an osteochondral fracture

●Isolated intra-articular loose bodies: posttraumatic or, more commonly, in a setting of degenerative joint disease

Imaging

Radiographs

Classic findings of multiple calcifications and isolated intra-articular loose bodies are not always seen and may be obscured Table 3.8 Outerbridge classification of cartilage lesions

Grade Description

I MRI signal changes with no loss of cartilage thickness II Superficial cartilage lesions affecting no more than 50% of

the cartilage thickness

III Cartilage lesions affecting more than 50% of the cartilage thickness but without exposure of subchondral bone IV Full-thickness cartilage defect with exposure of subchondral

bone

by superimposed bony structures. Cartilage fragments are not visible unless calcified or ossified.

CT

CT can accurately define and localize calcified intra-articular loose bodies for preoperative planning.

Ultrasound

Sonography is useful for evaluating effusion and synovitis. A dy-namic examination is performed. The location and mobility of intra-articular bodies can be determined by their acoustic shad-ows, depending on their density.

MRI

Interpretation Checklist

●Chondromatosis:

○Evaluate extent

○Associated synovitis

○Early cartilage lesions

○Preosteoarthritic changes

○Secondary osteoarthritis

○Evaluate tendon sheaths and bursae

○Exclude malignant change

●Intra-articular loose bodies:

○Extent of synovitic irritation

○Evaluate cartilage quality

○Exclude osteochondritis dissecans

○Accurate preoperative localization

Examination Technique

●Standard protocol: prone position, high-resolution multi-channel coil

●Sequences:

○Coronal and sagittal PD-weighted fat-sat

○Coronal T1-weighted

○Axial T2-weighted

○T1-weighted fat-sat, true axial (angled to the joint plane) and sagittal after IV contrast administration

MRI Findings (▶Fig. 3.62)

●Marked effusion.

●Signal characteristics of chondromas vary depending on de-gree of calcification.

●Noncalcified lesions have high signal intensity in the proton-density image (interactive window!); they may appear, for example, as myriad small, scattered, bright nodules floating in the effusion.

●Calcified chondromas have low signal intensity in T1- and T2-weighted sequences.

●Ossified lesions may be hyperintense in T1- and T2-weighted sequences due to fatty bone marrow.

●Synovitis enhances on postcontrast images.

Imaging Recommendation

Modalities of choice: initial study is radiography. If x-rays are equivocal, MRI is performed. MRI gives an excellent view of noncalcified chondromas.

! Note

Bone erosion without marginal sclerosis on radiographs is suspi-cious for a malignant process.

Differential Diagnosis

Osteoarthritis with capsular chondromas and osteomas or ossi-fied foci. Differentiating feature: capsular chondromas are usually isolated, unlike the multiple tiny spheres in synovial chondromatosis. Intra-articular loose bodies and capsular chondromas always occur in an advanced stage of degenera-tive joint disease.

Treatment

Intra-articular loose bodies are removed at surgical synovec-tomy. This can be done arthroscopically in the ankle joint. An open procedure may be indicated for the smaller joints.

Fig. 3.62 a, b A 41-year-old man with locking and pain in the posterior ankle joint.

a Sagittal T1-weighted fat-sat image after con-trast administration reveals an intra-articular loose body in the posterior joint recess with sur-rounding synovitic enhancement.

b Axial T1-weighted fat-sat image after contrast administration. Contrast imaging can distinguish between a sessile and loose or symptomatic in-tra-articular body, with increased enhancement in the adjacent tissue.

Prognosis, Complications

Pressure from the synovial chondromas may damage the bone and cartilage, giving rise to secondary osteoarthritis. Malignant transformation to low-grade chondrosarcoma rarely occurs. A large percentage of noncalcified synovial chondromas signify an active proliferative process, associated with an increased risk of malignant degeneration. The incidence of recurrence is 3 to 23%.

Osteochondral Lesions of the Talus

It is common to find posttraumatic osteochondral lesions on the talar dome as the result of a sprain (talar rim lesion, chondritis dissecans, flake fracture) as well as ischemic osteo-necrosis of the talar trochlea. Lesions of the cartilage and bone located on the medial or lateral shoulder of the talus are currently referred to as osteochondral lesions of the talus. In-creasingly, this term is replacing the older blanket term “osteo-chondritis dissecans.”

A somewhat less common entity is epiphyseal developmental disorder or maturation disorder of the talus (abnormal ossifica-tion of the talar rim). A small porossifica-tion of the epiphysis remains separate and does not undergo further maturation with the rest of the epiphysis. This leads to the formation of an intra-articular loose body with a bony defect in the talar shoulder with possible remodeling of the articular surface and fibro-cartilage formation.

Definition

An osteochondral lesion is an ischemic condition that pro-gresses in stages culminating in osteonecrosis of the subchon-dral bone and adjacent cartilage. It is a chronic, persistent lesion of the talar rim that typically develops after an ankle sprain. A subtype is ischemic osteonecrosis, a circumscribed fragmenta-tion of cartilage and bone that predominantly affects convex ar-ticular surfaces in adolescents.

Symptoms

●Activated lesions cause persistent joint pain, which is often independent of the lesion site

●Pain

●Locking (joint mouse)

●Recurrent effusions

●Limited motion

Differentiation is required from silent lesions that are detected incidentally, especially in children. Even higher-grade lesions may be completely asymptomatic.

Predisposing Factors

●Prior history of a single lateral ankle sprain, recurrent medial sprains, high level of athletic activity, high body weight

●Most lateral lesions result from osteochondral flake fractures

●Up to 30% of patients with a medial lesion have bilateral lesions

●Genetic predisposition has been postulated; hemoglobinopa-thies, Gaucher disease

Males are predominantly affected.

Anatomy and Pathology

●Posttraumatic osteochondral lesion: Direct trauma and repeti-tive microtrauma may cause lesions of the bone and overlying cartilage. Repetitive shear forces are also considered a risk factor in patients with joint instability. The activated stage is marked by the development of extensive bone edema ranging to osteonecrosis. Subchondral sclerosis develops around the necrotic zone, resulting in dissection. Joint pressures force synovial fluid through the damaged cartilage surface into the subchondral bone, leading to the cystic form of osteochondri-tis dissecans. The devitalized fragment may increasingly sepa-rate from its base and become an intra-articular loose body.

●Ischemic osteonecrosis: According to the prevailing theory of pathogenesis, ischemic osteonecrosis results from a subchon-dral fatigue fracture causing diminished blood flow at the end-artery level.

Traumatic osteochondral lesions are most commonly located on the lateral border of the talus, while ischemic lesions pre-dominantly affect the medial talar shoulder and central portion of the trochlea. Often it is difficult to distinguish be-tween a traumatic and ischemic cause, and both forms exist on a continuum.

Classification is based on intraoperative assessment of carti-lage and bone lesions (Outerbridge, Cheng-Ferkel, International Cartilage Research Society [ICRS] Classification;▶Table 3.9).

Imaging

Radiographs

The Berndt and Harty classification is most commonly used for lesion classification on conventional radiographs. The Arcq grading system is less widely used (▶Table 3.10).

Table 3.9 Classification of osteochondral lesions of the talus Grade Description

I Smooth and intact, soft II Rough surface III Fissures

IV Flaplike detachment with exposed bone V Loose bone fragment, not displaced VI Loose fragment displaced within the joint

Table 3.10 Radiographic grading system for osteochondral lesions of the talus

Grade Description

I Subchondral lucent zone

II Sclerotic focus with a peripheral lucent line and sclerotic rim III Partial separation of the fragment

IV Complete separation of the fragment

Radiographs are often negative in the early stage. Later they show a faint lucency with ill-defined central density in the shoulder or trochlear surface of the talus. The end stage is marked by an intra-articular loose body and an associated sub-chondral defect with sclerotic margins.

Ultrasound

Not indicated. At most, sonography may show a nonspecific re-active effusion.

MRI

Before the advent of MRI, very little was known about the path-ophysiology of osteochondral lesions of the talus. Conventional radiographs could depict only the end-stage features of a crater base and loose body. With its capability for water-sensitive imaging of the subchondral bone, MRI can now demonstrate all stages from early bone marrow edema to necrosis, sclerosis, and cartilage disruption.

Interpretation Checklist

●Evaluation of the subchondral region

●Bone marrow edema

●Demarcation

●Viability of the osteochondral fragment

●Cartilage quality

●Differentiation between a stable or unstable lesion

●Extent of necrosis

●Associated changes

●Synovitis

●Effusion

●Evaluation of progression

●Comparison with prior images

Examination technique

Contrast administration is not strictly necessary; necrosis can also be evaluated with fat-suppressed water-sensitive sequen-ces and unenhanced T1-weighted images. Contrast administra-tion is helpful for evaluating synovitis, however.

MRI Findings (▶Fig. 3.63,▶Fig. 3.64,▶Fig. 3.65,

▶Fig. 3.66)

Various classifications have been developed, most of which are based on radiographic features. At present there is no uniform MRI classification system, so reporting must rely on an accurate description of findings:

●Early stage: diffuse, faint, subchondral bone marrow edema in the lateral or medial talar dome, an intact cortical layer, nor-mal hyaline articular cartilage; measure extent of edema, ef-fusion, and reactive synovitis.

●Edema zone is demarcated by a fairly well-defined “jump” in intensity from normal fatty marrow signal to bone marrow edema with no fluid detection. T1-weighted sequence shows preservation of fatty marrow signal without necrosis (= sta-ble lesion), which is important for directing transchondral drilling.

●Incipient separation: water image shows hyperintense fluid around the osteochondral lesion indicating the development of a crater base; fragment undergoes necrosis with loss of

T1-weighted fatty marrow signal, often with continued detec-tion of edema (= unstable lesion).

●Separation: the detached fragment may be whole or frag-mented, with cyst formation deep to the base.

●Assessment of cartilage surface: initial signal changes, fibrilla-tion and fissuring; look for undermining cartilage lesions, fol-lowed later by fibrocartilage formation and articular surface remodeling.

●Associated changes: effusion, reactive synovitis, cartilage le-sions at other sites caused by the osteochondral fragment.

●Two sites of predilection: ischemic osteonecrosis is usually located on the medial side and produces deeper lesions; post-traumatic osteochondritis dissecans usually affects the anterolateral dome and is more superficial.

Imaging Recommendation

Modality of choice: MRI for early detection, follow-up, assess-ment of cartilage quality, assessassess-ment of stability, and determin-ing the degree of activation.

Fig. 3.63 Chondral flake fracture on the lateral shoulder of the talus following an acute ankle sprain. The 44-year-old woman presented with a lateral ankle sprain and patchy hematoma in the soft tissues.

Coronal PD-weighted fat-sat MR image shows a faint zone of bone contusion on the lateral talar shoulder with fresh delamination of the overlying articular cartilage.

Differential Diagnosis (▶ Fig. 3.67)

●Osteochondral lesion of the tibial articular surface

●Talar fracture

●Inflammatory joint disease

●Transient bone marrow edema syndrome

●Ossification disturbance of the talar dome

Treatment

Conservative

●Grades I–III: activity modification, stress reduction

●Fresh injuries: immobilization

Operative

●Arthroscopic debridement of unstable cartilage

●Microfracturing Fig. 3.64 a–c Osteochondral lesion on the medial talar dome.

a Coronal T1-weighted image shows preservation of fatty marrow signal in the osteochondral fragment with no evidence of necrosis.

b Coronal T1-weighted fat-sat image after contrast administration shows enhancement in the fragment with no signs of necrosis. Even if the overlying articular cartilage appears sound, it is important to describe even the slightest signal changes in the cartilage since it is common to find compromised (soft) cartilage adjacent to an osteochondral lesion.

c Sagittal T1-weighted fat-sat image after contrast administration shows an intact cortical layer with no subchondral fissures.

Fig. 3.65 a, b Osteochondral lesion on the medial talar dome in a woman with chronic complaints and pain that is aggravated by physical activity.

a Coronal T1-weighted image shows flattening of the medial talar dome with joint incongruity. Ab-sence of fatty marrow signal indicates necrosis of the osteochondral fragment.

b Coronal T1-weighted fat-sat image after con-trast administration shows no enhancement of the fragment. Adjacent mild bone marrow ede-ma indicates chronic activation.

Fig. 3.66 a, b Osteonecrosis of the medial talar dome.

a Coronal PD-weighted fat-sat image shows a rel-atively large subchondral lesion in the medial shoulder of the talus.

b Unenhanced coronal T1-weighted image shows a large necrotic area with absence of fatty mar-row signal.

●For larger defects: cancellous bone grafting

●Autologous chondrocyte transplantation

●Coverage with a membrane or repair with an osteochondral autograft taken from the knee

●Coverage with a membrane or repair with an osteochondral autograft taken from the knee

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