MSK 2 Flashcards
Chondrocalcinosis
- HOGWASH
- Hyperparathyroidism.
- Ochronosis (Alkaptonuria)
- Gout
- Wilson Disease
- Arthritities
- pSeudogout: CPPD
- Haemocromatosis
https://dermnetnz.org/topics/alkaptonuria-and-ochronosis/
Hajdu-Cheney syndrome
Dr Máté Cs. Jánvári◉ and Dr Roma Patel et al.
Hajdu-Cheney syndrome is a very rare connective tissue disorder with only 50 cases reported in the literature 7.
Clinical presentation
It is mostly diagnosed in adulthood or adolescence with the presence of a positive family history. There has been no link between severity of disease and age of diagnosis 3. Clinical features include:
short stature; premature loss of dentition; short webbed neck
pseudoclubbing; shortening of digits; pain in digits
optical atrophy; optic disc oedema
hearing loss (conductive or sensorineural)
frontal and occipital headaches (due to basilar invagination)
craniofacial features: frontal bossing, widely spaced eyes, micrognathia, long philtrum, flat nasal bridge, coarse hair, low set ears and a low hairline
Pathology
It is associated with osteoporosis, bony deformities and acro-osteolysis. It follows an autosomal dominant inheritance but can also result from spontaneous de novo mutations.
Genetic markers
Diagnosis involves genetic testing searching for the truncating mutation in the terminal exon of NOTCH2 4.
Associations
congenital heart disease (VSD, ASD, PDA, Mitral regurgitation)
polycystic kidney disease
recurrent respiratory tract infections
Radiographic features
Hands and feet
acro-osteolysis
transverse band of osteolysis in distal phalanges is characteristic
distal to proximal osteolysis is also seen
Skull
bathrocephaly (bulging of squamous occipital bone)
delayed closure of sutures
thickening of the mastoids
aplasia of the frontal sinuses
J-shaped enlarged sella
dolichocephaly
platybasia with or without basilar invagination
Spine
kyphoscoliosis
spondylolisthesis
biconcave vertebrae
Maxillofacial
hypoplastic maxilla
malalignment of teeth
wide mandibular angle
Treatment and prognosis
Management is symptomatic and involves regular follow-up. Prevention of osteoporosis, vitamin D and bisphosphonates may also have a role 6.
History and etymology
First described by Nicholas Hajdu (1908–1987), Hungarian-English radiologist in 1948 as cranioskeletal dysplasia and later in 1965, by William D. Cheney (1899–1985), American radiologist as acro-osteolysis 1,2.
Differential diagnosis
These involve other causes of acro-osteolysis and can be differentiated radiologically 5. Amongst others, they include the following:
hyperparathyroidism
psoriasis
scleroderma
pyknodysostosis
Raynaud’s phenomenon
progeria
Segond fracture
Sign
Fracture of what?
Associations
Segond fracture
Dr Subhan Iqbal◉ and Assoc Prof Frank Gaillard◉◈ et al.
Segond fracture is an avulsion fracture of the knee that involves the lateral aspect of the tibial plateau and is very frequently (~75% of cases) associated with disruption of the anterior cruciate ligament (ACL). On the frontal knee radiograph, it may be referred to as the lateral capsular sign.
Clinical presentation
Contrary to the more common causes of an ACL tear, which typically involve a valgus stress 3, a Segond fracture usually occurs as a result of internal rotation and varus stress 1,4. Typically these injuries are seen in two settings:
falls
sports: especially soccer, skiing, basketball and baseball 4,10
Pathology
Somewhat surprisingly, the exact cause of a Segond fracture continues to be contentious. The conventional teaching has been that it is the result of avulsion of the middle third of the lateral capsular ligaments 7. Other candidate structures include the iliotibial band and anterior oblique band of the fibular collateral ligament 3.
In 2017, the ALL expert group released a consensus paper 8 recognising the presence of the anterolateral ligament 9, and noted a constant attachment to the lateral meniscus. However, the ALL is inconsistently identified on MRI 7.
Radiographic features
Plain radiograph
The classical appearance of a Segond fracture is that of a curvilinear or elliptic bone fragment projected parallel to the lateral aspect of the tibial plateau. This has been referred to as the lateral capsular sign 1, which is best seen on the anteroposterior view of the knee.
MRI
MRI is essential in all cases of Segond fractures to identify internal derangement. Disruption of the ACL is the most common, however, there are additional frequently encountered injuries.
Associated injuries include 1,3:
ACL tear
most common associated injury
75-100% of cases 6
medial or lateral meniscal tear
66-75% of cases 6
posterior horn most common
avulsion of ACL from the tibial attachment: rare
avulsion of fibular attachment of the long head of biceps femoris
avulsion of the fibular collateral ligament
Treatment and prognosis
Although the fracture itself is small, the extensive ligamentous injury associated with it usually requires surgical intervention, to correct anterior rotational instability 4. Healing of the Segond fracture is associated with a particular bone excrescence arising below the lateral tibial plateau.
History and etymology
First described by Paul Ferdinand Segond, French surgeon (1851-1912) based on cadaveric experiments 1,2,4.
Differential diagnosis
Imaging differential considerations include:
arcuate sign: avulsion fracture of the head of the fibula 5
fragment orientated more horizontally
Articular-sided rotator cuff tear
Dr Ammar Haouimi◉ and Dr Joachim Feger◉ et al.
Articular-sided rotator cuff tears are referred to as partial-thickness rotator cuff tears extending from the articular side into the rotator cuff.
Epidemiology
Articular-sided rotator cuff tears commonly occur in athletes with overhead activity 1.
They are more common than bursal-sided tears and most common in overhead athletes 4, but according to cadaver studies less common than intra-substance tears in the general population 5.
Risk factors
throwing sports
overhead sport activity
Pathology
Aetiology
Internal impingement is thought to have a significant role in the occurrence of a partial articular-sided rotator cuff tear and another extrinsic factor is glenohumeral instability. Intrinsic factors include the relative hypovascularity of the distal parts of tendon and the footprint and a decreased overall strength in relation to the bursal side, due to a more random fibre orientation 4,5. In addition trauma either as a single event or repetitive microtrauma is also thought to have a role in the development of articular sided tears 4,5.
Variants
an articular-sided rim rent tear or articular-sided tendon avulsion of the footprint, most commonly the tendon insertion of the supraspinatus tendon is called PASTA lesion.
a partial articular-sided rim rent tear, extending into the tendon substance is called PAINT lesion (partial articular tear with intratendinous extension)
Location
PASTA lesions are most commonly found in the anterior supraspinatus tendon 3
Radiographic features
Ultrasound
focal hypoechoic or anechoic defect of the rotator cuff, extending from the articular side into the tendon substance
MRI
focal non-transmural articular-sided defect of fluid signal intensity of the rotator cuff on fat-saturated T2- weighted or intermediate-weighted images with intact residual fibres
MR/CT arthrography
MR arthrography is preferred over CT arthrography since it is also able to depict bursal-sided or intrasubstance tears 2.
MR and CT arthrography can depict articular-sided tears with intraarticular contrast extending into the tear. The ABER (abduction and external rotation) position is particularly useful to demonstrate intratendinous extensions or PAINT lesion because the tendon fibres become loose when the muscles relax and the contrast fills the delaminated space 1.
Treatment and prognosis
Partial-articular sided tears can be initially treated conservatively for 2-3 months, especially if symptoms are minor or even asymptomatic and include cessation of throwing activities, physical therapy with the focus on rotator cuff strengthening and range of motion 4.
Surgery is indicated for patients, who failed conservative treatment and younger patients with a single acute injury and include debridement and repair the latter especially in larger tears, where more than 75% of the tendon diameter is affected 4,5. PAINT lesions might need more extensive debridement 4 or can be treated with non-absorbable mattress sutures 6.
See also
rotator cuff tear
full-thickness rotator cuff tear
partial-thickness rotator cuff tear
bursal-sided rotator cuff tear
intrasubstance tear
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Rim rent tear of rotator cuff
Dr Joachim Feger◉ and Dr Yuranga Weerakkody◉ et al.
A rim rent tear of the rotator cuff, also known as partial articular surface tendon avulsion (PASTA), is a specific subtype of partial-thickness rotator cuff tear that involves the articular surface footprint at the site of tendon attachment into the greater tubercle 2. This sort of tear is relatively common and also can involve the infraspinatus tendon 3.
History and etymology
The term “rim-rent” was first used by E A Codman in 1934 3-4.
Name this appearance and ddx
- Hair on end periosteal reaction
- ewings sarcoma
- Osteosarcoma
- mets
Jaccoud arthropathy is a deforming non-erosive arthropathy characterised by ulnar deviation of the second to fifth fingers with metacarpophalangeal joint subluxation.
Clinical presentation
Jaccoud arthropathy is characterised by marked ulnar subluxation and deviation at the metacarpophalangeal joints that is correctable or reducible with physical manipulation 7.
Pathology
It was traditionally described as occurring post-rheumatic fever. It is also seen in association with systemic lupus erythematosus (SLE) and other rheumatic and non-rheumatic conditions including psoriatic arthritis, inflammatory bowel disease and malignancy 5. It is thought to be related to ligamentous laxity 7.
Location
Typically affects the metacarpophalangeal joints but can also affect the proximal interphalangeal joints of the hands, wrists and knees 2.
Radiographic features
Plain radiograph
hand radiographs typically show marked ulnar subluxation and deviation at the metacarpophalangeal joints
absence of erosions is a notable feature, although occasionally “hook” erosions may be observed, which are similar to those seen in SLE and ankylosing spondylitis 6
evidence of muscle (soft tissue) atrophy also may be present
History and etymology
It is named after F S Jaccoud, a French physician, who described the entity in 1869 3.
Differential diagnosis
On imaging, possible considerations include:
rheumatoid arthritis: presence of erosions is a key distinction
Name this appearance and DDx
- Codmans triangle
- Osteosarcoma
- Ewings
- Osteomyeltis
Morquio syndrome
Dr Mostafa El-Feky and Dr Basab Bhattacharya et al.
Morquio syndrome (in older literature it is sometimes called Morquio-Brailsford syndrome) is an autosomal recessive mucopolysaccharidosis (MPS) type IV.
Epidemiology
Incidence estimated at ~1:40,000.
Clinical presentation
Many cases present at ~2 years of age and have normal intelligence. Clinical features:
severe dwarfism (<4 foot)
joint laxity
corneal opacification/clouding
lymphadenopathy
progressive deafness
spinal kyphoscoliosis
prominent mandible and lower face
short neck
Pathology
It results from an excess of keratan sulphate due to a deficit in its degradation pathway. Keratan sulphate accumulates in various tissues inclusive of cartilage, the nucleus pulposus of the intervertebral disks and corneas.
Radiographic features
Plain radiograph / CT
Axial manifestations
platyspondyly
hypoplasia of odontoid peg
atlantoaxial subluxation
os odontoideum
anterior central vertebral body beaking
round vertebral bodies
coxa valga
goblet shaped flared iliac wings, increased acetabular angles and constricted iliac bone base
Calvarial manifestations
hypertelorism
dolichocephaly
Peripheral musculoskeletal manifestations
metaphyseal flaring in long bones
multiple epiphyseal centres
wide metacarpals with proximal pointing, irregular carpal bones
short and wide tubular bones
pointed proximal metacarpals of index to little finger
flattened femoral epiphyses; risk of lateral subluxation and dislocation
coxa valga
genu valgum
Thoracic manifestations
anterior sternal bowing, increased AP chest diameter, wide ribs
Echocardiography
late-onset aortic regurgitation
Treatment and Prognosis
Life expectancy ranges between 30-40 years. The most common cause of death is cervical myelopathy from C2 abnormality. Patients are also particularly vulnerable to respiratory infection.
History and etymology
Named after Luis Morquio, an Uruguayan paediatrician (1867-1935) 5. James Brailsford (1889-1961) 6 a renowned British radiologist made an important contribution to the understanding of the radiographic appearances of this condition.
what are the 3 dx criteria for this condition
Tenosynovial giant cell tumour
Tenosynovial giant cell tumour
- A well-defined focal oval-shaped, soft tissue swelling measuring roughly 3.0 x 2.0 cm is seen along the anterior aspect of the right ankle joint. No calcifications are seen in it. No significant abnormality is seen in the underlying bones and joints.
Findings: A well-defined soft tissue mass lesion measuring 3.0 x 3.0 x 5.0 cm is seen just anterior to the right ankle joint. This lesion has heterogeneous T1 and T2 signal intensity and well-defined outer margins showing smooth pressure erosions on the talar neck and distal anterior tibia. No fat component, haemorrhage, or calcifications are seen in it. The lesion shows significant enhancement in the post-contrast study and central degeneration. No bone marrow oedema is seen in the underlying bones. No abnormal ankle joint effusion is seen. The supporting ligaments of the ankle are preserved.
- Case Discussion
- Impression: Solitary localised soft tissue mass lesion in close relation to the right ankle joint, which is likely a tenosynovial giant cell tumour. Possible imaging differential diagnoses include Pigmented villonodular synovitis (PVNS), desmoid tumour, fibroma of the tendon sheath, and ganglion cyst.
- The case was reviewed by the musculoskeletal radiologist and oncologic orthopaedic surgeon. She underwent ultrasound guided biopsy of the lesion followed by its complete surgical excision.
- Histopathological analysis of both specimens (ultrasound guided biopsy as well as surgical excision): Tenosynovial giant cell tumour with a prominent xanthomatous component. No evidence of malignancy seen.
Tenosynovial giant cell tumours are usually benign lesions that arise from the tendon sheath. It is unclear whether these lesions represent neoplasms or merely reactive masses. On imaging, these lesions are commonly demonstrated as localised, solitary, subcutaneous soft tissue nodules, with low T1 and T2 signal and moderate enhancement.
Terminology
Tenosynovial giant cell tumour is the term used in the latest (2013) World Health Organisation classification 10,11. They have previously been known as giant cell tumours of the tendon sheath (GCTTS), pigmented villonodular tumour of the tendon sheath (PVNTS), extra-articular pigmented villonodular tumour of the tendon sheath or localised or focal nodular synovitis 11.
Epidemiology
Typically, they present in the 3rd to 5th decades and have a slight female predilection with an F:M ratio of 1.5-2.1:1 4. They are the second most common soft tissue mass of the hand and wrist.
Clinical presentation
Clinically these masses generally present in the hand (although they are found elsewhere also) as localised swelling with or without pain. They are slow-growing.
Pathology
Tenosynovial giant cell tumours can cause pressure erosion of adjacent bone, or rarely can invade the bone mimicking an intraosseous lesion 8.
Macroscopic appearance
Tenosynovial giant cell tumours have been divided macroscopically into localised or diffuse forms and appear as rubbery multinodular masses that are well circumscribed. They have an enveloping fibrous capsule, and the transected surface of the specimen is variably coloured depending on the relative proportions of fibrous tissue, haemosiderin, and pigmented foam cells 2.
Histology
The tumour is histologically identical to pigmented villonodular synovitis (PVNS) and is composed of fibroblasts and multinucleated giant cells, foamy histiocytes, and inflammatory cells on a background fibrous matrix 1,2.
Radiographic features
Plain radiograph
As these masses arise from tendons, commonly of the hand, they may cause pressure erosions on the underlying bone in 10-20% of cases. More commonly these masses arise from the palmar tendons. The mass itself is of soft tissue density. Periosteal reaction and calcification are uncommon 4,5.
Ultrasound
Ultrasound is useful as it allows not only the characterisation of the lesion but also is able to demonstrate the relationship with the adjacent tendon. On the dynamic scan, there is free movement of the tendon within the lesion. Typically they appear as:
associated with the volar surface of the digits
does not move with flexion or extension of adjacent tendons
usually homogeneously hypoechoic, although some heterogeneity may be seen in echotexture in a minority of cases 1
most will have some internal vascularity
MRI
Not surprisingly, given the histological similarity to PVNS, giant cell tumours of the tendon sheaths also share the same finding on MRI, mainly on account of haemosiderin accumulation.
Signal characteristics
T1: low signal
T2: low signal
T1 C+ (Gd): often show moderate enhancement 6
GE: low and may demonstrate blooming
Treatment and prognosis
Tenosynovial giant cell tumours are usually benign and local surgical excision usually suffices, with local recurrence (seen in 10-20% of cases) requiring more extensive surgery with or without radiotherapy being uncommon 1. Locally aggressive and malignant tenosynovial giant cell tumours can occur 11. Metastases can occur, most commonly to lymph nodes and lung 4.
Differential diagnosis
General imaging differential considerations include:
ganglion cyst
cystic component
attached to underlying joint capsule or tendon sheath 7
if previously ruptured may appear similar 1
pigmented villonodular synovitis (PVNS)
histologically identical
involves larger joints
desmoid tumour
fibroma of the tendon sheath
overlapping imaging features
no susceptibility artifact on gradient echo sequences
histologically diagnosis often needed 11
fibrosarcoma
rheumatoid arthritis nodules
If in the hand consider:
glomangioma: has high T2 signal on MRI
Subchondral insufficiency fracture of the knee
Dr Yuranga Weerakkody◉ and Assoc Prof Frank Gaillard◉◈ et al.
Subchondral insufficiency fracture of the knee (SIF/SIFK) are stress fractures in the femoral condyles or tibial plateau that occur in the absence of acute trauma, typically affecting older adults.
Terminology
The entity subsumes that previously known as spontaneous osteonecrosis of the knee (SONK/SPONK) or Ahlbäck disease. Recognising that spontaneous osteonecrosis of the knee was a misnomer and actually represents a subchondral insufficiency fracture that progressed to subchondral collapse with secondary osteonecrosis, the Society of Skeletal Radiology Subchondral Bone Nomenclature Committee recommended that “subchondral insufficiency fracture” be the preferred term 17.
Epidemiology
Subchondral insufficiency fracture of the knee is seen more frequently in women (M:F 1:3) and affects older patients, typically over the age of 55.
Clinical presentation
Patients often recall an acute onset of severe pain without significant trauma.
Pathology
By definition, secondary osteonecrosis of the knee occurs secondary to an insult. Subchondral insufficiency fracture of the knee is not thought to be caused by bone death but instead by osteoporosis and insufficiency fractures, with histopathologically proven origins in weakened trabeculae and applied microtraumatic forces 6,13.
Radiographic features
It is almost always unilateral, usually affects the medial femoral condyle (but can occasionally involve the tibial plateau 9) and is often associated with a meniscal tear.
Plain radiograph
In the later stages features seen include:
flattening of the medial femoral condyle
subchondral radiolucent focus
complicating subchondral fracture with periosteal reaction
MRI
Features can vary depending on the stage and are best characterised on T2-weighted and proton density-weighted sequences. The following criteria apply to lesions without overlying cartilage abnormalities:
subchondral bone plate fracture 13
in the weight-bearing area of the involved condyle
subtle flattening or a focal depressive deformity
an irregular, discontinuous hypointense line in the subarticular marrow, representing callus and granulation tissue
there may be a fluid-filled cleft within the subchondral bone plate (poor prognostic factor) 13
excavated defect of the articular surface (advanced cases)
focal subchondral area of low signal intensity subjacent to the subchondral bone plate representing local ischaemia (considered most important in early lesions and a specific MRI finding 12)
this area shows no enhancement on post-contrast; if it is thicker than 4 mm or longer than 14 mm, the lesion may be irreversible and may evolve into irreparable epiphyseal collapse and articular destruction
appears as a thickened subchondral bone plate, which represents a fracture with callus and granulation tissue and secondary osteonecrosis in the subarticular region 13
ill-defined bone marrow oedema and a lack of peripheral low signal intensity rim as seen in osteonecrosis and bone infarcts
Associated features that may predict prognosis include:
associated meniscal tear and degree of extrusion
chondrosis severity
Treatment and prognosis
Prognosis varies from complete recovery to total joint collapse 2. Treatment can either be operative or non-operative, with initial treatment often conservative and consisting of analgesia and protected weight bearing. Subchondral hypointense fracture lines tend to resolve with conservative therapy. In more advanced cases, subchondroplasty (where a bone substitute is injected) may be considered.
Differential diagnosis
Possible considerations include:
osteochondritis dissecans of the knee
subchondral stress/fatigue fracture: overuse injuries in patients without associated risk factors 17
History and etymology
It was first systematically described by Ahlbäck in 1968 2.
ABC
AO Spine TLICS Classificaiton
- Neurologic injury
- N0 neurological intact
- N1 Transient neuro deficit
- N2 Radicular symps
- N3 Incommplected SCI/Cauda equina
- N4 Complete SCI
- N5 unknow
- Modifies
- M1 designates fractures with an indetermin injruy to the tension band based on spinal imaging such as MRI or Clinical examiniation
HADD ddx
- CPPD: linear calc, mostly intra articular
- Gout: more faintly opacified, elevated urate
- Heterotopic ossification and myositis
- Soft tissue calcinosis
- Metastatic calcification: sarcoid, hyperparathyroidism, Hyper Vit D
*
Causes of Bilateral Distal clavicular osteolysis
PPP-ACRHS
- Atraumatic distal clavicular oseolysis: due to repetitive microtrauma, weightlifters/over head activities
- Hyperparathyroidism: subcondral bone resorption, usually suymmetric with osteopenia, abdnormal traecular pattern. the sacromian is normal, btut eh sternal clavi joint may be afected
- Rheymatoid arthritis: bilateral or unilateral changes with soft tissue swelling, subchondral osteoporosis and erosion of the outer third of the clavicle. Acromial erosions may occur later in the disease process.
- Scleroderma
- Psoriatic arthropathy
- Cleidocranial dysostosis
- pyknodysostosis
- progeria
Posterior Dislocation
- Trough line sign
Dr Henry Knipe◉◈ and Radswiki◉ et al.
The trough line sign is a sign of posterior shoulder dislocation on AP shoulder radiograph.
Pathology
In a posterior dislocation, the anterior aspect of the humeral head becomes impacted against the posterior glenoid rim. With sufficient force, this causes a compression fracture on the anterior aspect of the humeral head. This compression fracture is analogous to the Hill-Sachs compression fracture seen with anterior shoulder dislocation of the glenohumeral joint.
Radiographic features
Plain radiograph
Frontal radiographs reveal two nearly parallel lines in the superomedial aspect of the humeral head.
- https://radiopaedia.org/articles/trough-line-sign?lang=gb
Essex-Lopresti fracture-dislocation
Intra-articular radial head fracture with a large joint effusion (sail sign), with dorsal dislocation of the ulna at the distal radioulnar joint (DRUJ).
Dr Henry Knipe◉◈ and Assoc Prof Frank Gaillard◉◈ et al.
Essex-Lopresti fracture-dislocation is characterised by a fracture of the radial head, dislocation of the distal radioulnar joint and rupture of the antebrachial interosseous membrane 3.
Epidemiology
As little as 20% of Essex-Lopresti fracture-dislocations are recognised at the time of initial presentation 6.
Clinical presentation
The injury occurs due to the compressive force of trauma transmitted down the forearm through the proximal and distal radioulnar joints and the interosseous membrane 3,4. This usually occurs from a fall or high energy trauma with the elbow extended 4. As a result, there is axial and longitudinal loading that causes pain and instability. The distal radioulnar joint injury may be missed, leading to permanent wrist pain and stiffness or instability. Radiocapitellar impingement due to longitudinal instability may cause lateral elbow pain 4.
Classification
The proposed classification of Essex-Lopresti fracture-dislocation is based on the severity of radial head fracture 5.
type I: large fragments
type II: comminuted
type III: chronic injury with proximal migration of the radial head
Pathology
Rupture of the interosseous membrane results in perturbed transmission of force from the radius to the ulna 7. If not recognised acutely, chronic instability and proximal migration of the radius results in ulna abutment with increased force transmission across the ulnocarpal joint 4.
Radiographic features
Initial radiographs may be unremarkable for Essex-Lopresti fracture-dislocations 6.
Treatment and prognosis
There have been historically poor outcomes in the treatment of longitudinal forearm instability which is particularly complex in the chronic setting 3. The low incidence, late presentations and heterogeneity in study samples presented in the literature preclude researchers reaching safe conclusions and planning of clinical studies 3. A recent study found that radial head replacement with the reconstruction of the interosseous membranes and central band restores radioulnar displacement and ulna forces to near normal 3.
The proposed treatment may be based on the classification type 5.
type I: open reduction and internal fixation
type II: radial head excision and prosthetic replacement
type III: radial head replacement and ulnar shortening osteotomy
History and etymology
It is named after Peter Gordon Essex-Lopresti (1916-1951), a trauma surgeon at Birmingham accident hospital, England 2.
DDx of Enthesopathy
What is the Enthesis?
imaging features xray and uss
- DDx of Enthesopathy
- Seronegative Spondyloarthropaties
- Ank spond
- IBD Associated
- reactive arthritis
- repetitive mechanical stress
- Psoriatic arthritis
- Juvenile idiopathic arthritis
- Seronegative Spondyloarthropaties
- Pathology
- The causes of enthesopathy are broad.
- It may be localised and secondary to repetitive mechanical strain, or secondary to another condition which may be confined to a single system, or multisystem.
- Enthesopathy can incorporate:
- tendinopathy
- bursitis
- cyst-like erosions
- osteitis (reactive osseous inflammation)
- Plain radiograph / CT
- Chronic changes such as 2:
- enthesophytes
- erosions
- calcifications
- hyperostosis
- Chronic changes such as 2:
- Ultrasound
- The affected tendon/ligament can be thickened, hypoechoic with loss of the normal fibrillary pattern.
- Hyperaemia may be seen on colour Doppler.
- Mueller Weiss syndrome
- AKA
- also known as Brailsford disease
- Spontaneous multifactorial adult onset osteonecrosis of the tarsal navicular.
- This syndrome is distinct from Köhler disease, the osteonecrosis of the tarsal navicular bone that occurs in children.
- Epidemiology
- It occurs in adults between 40 and 60 years of age and is more common in females. Patients present with mid- and hind foot pain and pes planovarus.
- Plain radiographic features can include:
- comma-shaped deformity due to collapse of the lateral part of the bone
- medial or dorsal protrusion of a portion of the bone or the entire navicular bone
- The disease may be bilateral or asymmetric and associated with pathologic fractures.
- There is a radiographic staging.
4 stages of progression of Pagets
Sclerotic Mets
- Prostate
- Breast
- Hodkin lymphoma
- Neuroblastoma
- Carcinoid medulloblastoma
- Bladder
- Lung
Ghost sign in clay shovellers fracture. Stable
DOI:10.12671/JKFS.2018.31.2.57
Corpus ID: 134649937
Clay-Shoveler’s Fracture in an 18-Year-Old Cheerleader: A Case Report
Il-Yeong Hwang, S. J. Park, Jae-Ryong Cha
Published 2018
Medicine
Journal of the Korean Fracture Society
Financial support: None. Conflict of interests: None. Clay-Shoveler’s fracture refers to a fracture that is solely developed on the spinous process of the cervical spine or the thoracic vertebrae. This fracture rarely occurs during sporting activities. In this case, an 18-year-old female developed the fracture on the spinous process of the 7th cervical spine and 1st thoracic vertebrae due to the repetitive practice of cheerleading. The patient’s pain was improved by wearing a support device and taking an anti-inflammatory analgesic drug and muscle relaxant. Her case is being followed-up at the outpatient department
Sclerosis and collapse of the second metatarsal head.
Case Discussion
Freiberg infraction is the name of avascular necrosis of the second metatarsal head.
Four Characteristics of a benign Bone Lesion
and
Four Characteristics of a malignant bone lesion.
- Benign
- well defined sclerotic border
- lack of soft tissue mass
- Solid/no periosteal reaction
- Geographic bone destruction
- Malignant
- interrupted periosteal reaction
- moth-eaten or permeative destruction
- Soft tissue mass
- Wide zone of Transition.
What is a Chondroblastoma
- The ‘C’ in FEGNOMASHIC
- AKA a Codman Tumour.
- Rare benign cartilaginous neoplasm
- Arise in the epiphysis or ephphysis of long bones in young patients.
- Pateints < 20 years old.
- Less than 1% of all primary bone tumours.
- M>F
- Malignant transformation is possible.
- ASSOCIATATIONS: ABCS
- HISTOLOGY: Chondroblasts, chondroid matrix, cartilages with occasional giant multinucleated cells)
- LOCATION: 70% occur in the humerus, femour and ibia.
- 10% inthe hands and feet
What is this and what are the stages?
Stage 3 Pagets Disease
- Paget disease of the bone is a common, chronic bone disorder characterised by excessive abnormal bone remodelling. The classically described radiological appearances are expanded bone with a coarsened trabecular pattern. The pelvis, spine, skull, and proximal long bones are most frequently affected.
- Pathology
- The aetiology is not entirely known, but it is a disease of osteoclasts. Viral infection (paramyxovirus) 6 in association with genetic susceptibility has been postulated.
- There are three classically described stages, which are part of a continuous spectrum 22:
- early destructive stage
- incipient active
- lytic
- predominated by osteoclastic activity
- intermediate stage
- (active, mixed)
- osteoblastic as well as osteoclastic activity
- late stage
- inactive
- sclerotic/blastic
- early destructive stage
- These stages correlate well with the imaging findings.
- Markers
- elevated serum alkaline phosphatase
- normal calcium and phosphorus levels
- increased urine hydroxyproline
2019 Aug Q102
Enchondroma
Left hand x-rays demonstrate a fracture through an abnormality of the metaphyseal region of the third proximal phalange characterised by a non-aggressive lytic lesion expanding the local bone. No periosteal reaction. No matrix calcification or ossification.
Case Discussion
The patient went on to have a resection.
Pathology:
The specimen consists of multiple tan cartilaginous tissue fragments aggregating to 2.5 x 2.5 x 1 cm.
Histology confirmed multiple benign-appearing cartilaginous fragments, in keeping with an enchondroma.
Dr Yuranga Weerakkody◉ and Assoc Prof Frank Gaillard◉◈ et al.
Enchondromas, also known as chondromas 7, are relatively common intramedullary cartilage neoplasms with benign imaging features. They share histologic features with low-grade chondrosarcoma, and are sometimes classified under the umbrella term low-grade chondral series tumours.
Enchondromas account for the ‘E’ in the popular mnemonic for lytic bone lesions FEGNOMASHIC.
Epidemiology
most frequently diagnosed in childhood to early adulthood with a peak incidence of 10-30 years
most common primary benign bone tumour of hand/wrist
account for ~5% (range 3-10%) of all bone tumours, and ~17.5% (range 12-24%) of benign bone tumours 1
Associations
Two syndromes are associated with multiple enchondromas:
Ollier disease
Maffucci syndrome
Clinical presentation
Enchondromas are most commonly an incidental finding, most significant in that they shouldn’t be confused with more aggressive lesions.
As a rule, enchondromas should be asymptomatic; however, lesions of the hands/feet may present with pain from pathological fracture or impending fracture 8.
Malignant transformation into low-grade chondrosarcoma is rare and may present with pain.
Pathology
Enchondromas comprise lobules of mature hyaline cartilage which are partially or completely encased by surrounding normal bone 9. The cartilaginous lobules may undergo endochondral ossification, often resulting in the characteristic ‘rings and arcs’ pattern of mineralisation.
They arise from rests of growth plate cartilage/chondrocytes which become isolated within mature bone. Hence, they may be seen in any bone formed from cartilage.
By definition, they show no histologic evidence of local invasion (which would suggest low-grade chondrosarcoma). However, it is important to be aware that enchondroma cannot be reliably distinguished from chondrosarcoma by histology, and diagnosis depends on correlation of clinical, imaging, and pathology findings 9.
Grossly, lesions are usually <3 cm, translucent, nodular, and are grossly greyish-blue.
Location
Enchondromas are typically located in a central or eccentric position within the medullary cavity of tubular bones:
small tubular bones of the hands and feet (~50%) 4
proximal phalanx most common 8
large tubular bones
e. g. femur, tibia, humerus
rare: (consider chondrosarcoma)
pelvis
ribs
scapula
Rarely an enchondroma may extend through the cortex and demonstrate an exophytic growth pattern. This is known as an enchondroma protuberans, and may either be seen sporadically or as part of Ollier disease 2.
Radiographic features
Enchondromas have a somewhat variable appearance by imaging, although characterisation by excluding suspicious features is key. Since most are asymptomatic incidental findings, lesions in a characteristic location and appearance are not usually further investigated.
Imaging is generally less helpful in corroborating benignity of lesions in the hands/feet, as well as in enchondromatosis or skeletally immature patients 9.
Radiograph and CT
Enchondromas have a variable appearance, although typically they are small <5 cm lytic lesions with non-aggressive features:
narrow zone of transition
sharply defined margins
+/- chondroid calcification (rings and arcs calcification)
often no matrix mineralisation (purely lytic) in the hands/feet
+/- expansile
more commonly in hands/feet
may have mild endosteal scalloping
should not “grow” through cortex (unless pathologic fracture)
pertinent negatives 9:
no gross bone destruction
no periosteal reaction
no soft tissue mass
The majority of enchondromas more frequently arise in the metaphyseal region, owing presumably to their origin from the growth plate 1, although they are frequently seen in the diaphysis. They only rarely are seen in the epiphysis, and a cartilaginous lesion in an epiphysis is more likely to be a chondrosarcoma 3.
MRI
MRI is useful in evaluating soft tissue extension and for confirming the diagnosis. Enchondromas appear as well-circumscribed somewhat lobulated masses replacing marrow 1.
T1
intermediate to low-signal
internal foci of low signal of “rings and arcs” characteristic of a chondroid matrix
T1 C+ (Gd)
enhancement is variable and may be seen both peripherally or of translesional septae
similar pattern of enhancement may be seen in chondrosarcomas 3,6
T2
sharply defined
predominantly high signal
internal foci of low signal of “rings and arcs” characteristic of a chondroid matrix
no bone marrow or soft tissue oedema
Descriptions should include
location i.e. central or peripheral
presence and amount of endosteal scalloping
Differentiation of an enchondroma from low-grade chondrosarcoma is problematic, as they can have similar appearances. See enchondroma vs low-grade chondrosarcoma.
Nuclear medicine
Increased uptake on the bone scan can be seen with enchondromas. Intense uptake occurs with an underlying pathological fracture or cortical expansion in small bones 5.
Treatment and prognosis
The majority of enchondromas remain asymptomatic and require no treatment.
Pathologic fractures are commonly treated by curettage and bone grafting, with follow-up x-rays to monitor for healing and recurrence. An incisional biopsy is obtained intraoperatively. Recurrence is reported in 2-15% and suggests malignancy 8.
If malignant transformation is suspected, which occurs in less than 5% of cases, then treatment is more aggressive 4.
Complications
pathological fracture
malignant transformation into chondrosarcoma
Differential diagnosis
The differential is significantly affected by the modality in question, and most entities below can be excluded with MRI. The exception is chondrosarcoma.
bone infarct
chondrosarcoma
difficult to distinguish
see: enchondroma vs low grade chondrosarcoma
intraosseous ganglion
other benign lytic bone lesions
lytic metastasis to bone
granulomatous disease
skeletal sarcoidosis
skeletal tuberculosis
what is this
ligament of wrisberg pseudotear
seen at posterior horn/root of lateral meniscus
The carpal boss is a hypertrophied bony protuberance on the dorsal surfaces of the base of the second or third metacarpals, near the capitate and trapezium. It may be bilateral.
Pathology
The condition may represent one or more of:
degenerative osteophyte formation
os styloideum (an accessory ossicle of the wrist)
bony prominence at the base of the second or third metacarpals (which is often called “styloid process”)
Pain may be the result of a ganglion, inflamed bursa or extensor tendon slipping over the bony prominence.
Radiographic features
The radiographic appearance of a carpal boss is characteristic, however optimal visualisation of the boss may be difficult to obtain due to superimposed bony structures.
CT may show degenerative disease at a pseudoarthrosis, and MRI may show oedema related to abnormal motion.
Bone Island
AKA: Enostosis
Intro:
- Cortical bone within cancellous bone
- 1-4cm
- homogenously dense
- well marginated
- may be “warm” on bone scan
Multi centric osteosarcoma
multicentric osteosarcoma:
- synchronous osteoblastic OSA at multiple sites.
- has a tendancy to be multi-centric, metaphyseal, and symmetric
- occurs exclusively in children ages 5-10 yrs
- extremely poor prognosis
DIFFUSE BONEY SCLEROSIS
MMMSPROOF
- METS(osteoblastic) + lyphoma + leukaemia
- Myelofibrosis
- Mastocytosis
- Sickle Cell
- Pajets/Piknodisostosis
- Renal osteodystrophy
- Osteopetrosis
- Osteopoikilosis, osteopathica striata
- Flurosis
6 Ddx interupted periosteal reaction
6 Ddx interupted periosteal reaction
- Osteosarcoma
- Ewings Sarcoma
- Osteomyelitis
- Chondrosarcoma
- LCH
- Subperiosteal Haemorrage
Rugger jersey spine (hyperparathyroidism)
Dr Mostafa El-Feky and Assoc Prof Frank Gaillard◉◈ et al.
Rugger jersey spine describes the prominent endplate densities at multiple contiguous vertebral levels to produce an alternating sclerotic-lucent-sclerotic appearance. This mimics the horizontal stripes of a rugby jersey. This term and pattern are distinctive for hyperparathyroidism.
Pathology
In response to increased bone resorption due to excess parathyroid hormone (PTH) secretion and subsequent loss of bone mass, osteoblasts form an increased amount of osteoid that does not contain hydroxyapatite but does appear opaque on radiographs. The sclerotic bands on the superior and inferior endplates of the vertebral bodies represent accumulations of excess osteoid and appear opaque because of their increased volume when compared to normal bone.
Differential diagnosis
Paget disease
picture frame vertebral body
osteopetrosis
sandwich vertebrae
severe osteoporosis with compression fractures
Note: confusingly some authors use the term rugger jersey for osteopetrosis, although most would assume the term refers to hyperparathyroidism.
Quiz questions
Fibrous cortical defect
Dr Mohamed Saber and Assoc Prof Frank Gaillard◉◈ et al.
Fibrous cortical defects (FCD) are benign bony lesions and are a type of fibroxanthoma, histologically identical to the larger non-ossifying fibroma (NOF).
Epidemiology
Fibrous cortical defects typically occur in children (usually 2-15 years), and indeed are one of the most common benign bony lesions, which combined with non-ossifying fibromas are seen in up to 40% of skeletally immature children/adolescents 3. There is a male predilection by a ratio of 2:1 3.
Clinical presentation
They are asymptomatic and self-limiting, completely healing by adulthood.
Pathology
Fibrous cortical defects macroscopically appear as fleshy, fibrous, yellow or tan-brown lesions with variable areas of haemorrhage 3.
Microscopic examination reveals the lesions to be highly cellular containing spindle-shaped cells on a background of stromal tissue in a prominent storiform pattern. Foamy histiocytes and multinucleated giant cells are also seen. Mitotic figures and/or cellular dysplasia should not be seen 3.
During the healing phase, there is an increase in osteoblastic activity as new bone replaces the defect, gradually being remodelled and completely disappearing 2.
Radiographic features
FCDs are benign lytic bone lesions, and, along with fibrous dysplasia share the F in the popular mnemonic FEGNOMASHIC.
They typically occur in the metaphysis or diametaphyseal junction and appear as small (<2-3 cm) lucent defects within the cortex that over time become sclerotic as they heal. They are typically located in the distal femur or proximal or distal tibia. They are much less frequently seen in the upper limb 2,3.
Importantly, there is no associated soft tissue mass 3.
Plain radiograph and CT
lucent intracortical defects
outlined by a thin rim of sclerosis
no involvement of the underlying medullary cavity
no periosteal reaction
MRI
Signal characteristics include:
T1: hypointense
T2: variable, depending on the phase of healing 3
Nuclear medicine (bone scan)
Appearance depends on the phase of the lesion. In general they are negative; however, mild hyperaemia and moderate bone uptake are present during healing. If extensive uptake or hyperaemia is present, then an alternative diagnosis or superimposed fracture should be considered 3.
Treatment and prognosis
As these lesions are benign, characteristic in appearance and self-limiting, no treatment, biopsy or even follow-up is required in typical cases. If associated with pathological fracture (more common in non-ossifying fibromas) then cast immobilisation until the fracture has healed, followed by biopsy with or without curettage, and bone grafting may be necessary 3.
History and etymology
Fibrous cortical defect was first described by Dallas Burton Phemister (1882-1951) 5, an American orthopaedic surgeon in 1929 4.
Differential diagnosis
Possible differential considerations include
non-ossifying fibroma (NOF): larger (by definition >3 cm), bubbly
cortical desmoid: posteromedial aspect of the distal femur
osteoid osteoma: night pains
osteomyelitis
stress fracture
intracortical osteosarcoma
haemangeoma
Meniscal root tear
Meniscal root tear
Dr Magdalena Chmiel-Nowak◉ and Dr Yuranga Weerakkody◉ et al.
Meniscal root tears are a type of meniscal tear in the knee where the tear extends to either the anterior or posterior meniscal root attachment to the central tibial plateau. They often tend to be radial tears extending into the meniscal root.
Epidemiology
According to one source, they are thought to account for ~10% of all arthroscopic meniscectomies 5.
Pathology
While they can arise from a number of mechanisms, root tears are generally thought to be chronic 5.
Associations
ACL tears are associated with posterior horn root tears of the lateral meniscus
Radiographic features
MRI
Best assessed on T2 weighted sequences. When it involves the posterior root, medial root tears are easier to diagnose than lateral root tears.
On medial posterior root tears there is often 2:
shortening or absence of the root on sagittal images
vertical fluid cleft on coronal fluid-sensitive (T2) images
On posterior root radial tears of the lateral meniscus, the appearance may be similar to radial tears in other locations.
For root tears in general, sagittal imaging may demonstrate a meniscal ghost sign.
Other features include:
truncation sign on coronal images 4
features meniscal extrusion on coronal plane 4
History and etymology
They were first described by M J Pagnani et al. in 1991 6.
Calcifications and arthropathy
- Periarticular
- Scleroderma
- SLE
- Articular
- CPPD
- Chondrocalcinosis
- Joint space-related
- neuropathic arthropathy
- Synovial osteoenchondromatosis
- Osteochondritis dissecans
- Osteochondral fracture.
- The achilles tendon is formed by the confluence of the gastrocnemious and the soleus
- The critical zone the site of most acute tears is 2-6cm proximal to its calcaneal insertion site
- x-ray shows marked soft tissue swelling behind the distal tibial and akle with obliteration of the pre-achilles fat pad
- MRI in partial tears shows tendon enlargement and edema, intratendinous areas of increased signal intensity on T2W, and surrounding soft tissue edema
- In complete tear: a tendinous gap is present and is filled with high signal blood and edema.
- Achilles tendon tear
- Achilles tendon tears are the most common ankle tendon injuries, and are most commonly seen secondary to sports-related injury, especially squash and basketball.
- Epidemiology
- There is strong male over-representation presumably as a result of the predominantly sport related aetiology. Patients are typically aged 30-50 years and have no antecedent history of calf or heel pain.
- There are however numerous recognised predisposing factors including:
- intratendinous steroid injection
- diabetes mellitus
- systemic inflammatory illnesses
- rheumatoid arthritis
- systemic lupus erythematosus
- repeated microtrauma
- gout
- fluoroquinolone antibiotics
- ochronosis 4
- hyperparathyroidism
- Clinical presentation
- Typically patients present with sudden onset of pain and swelling in the Achilles region, often accompanied by an audible snap during forceful dorsiflexion of the foot. A classic example is that of an unfit ‘weekend warrior’ playing squash.
- If complete a defect may be felt and the patient will have only minimal plantar flexion against resistance.
- Pathology
- The spectrum of tears ranges from microtears to interstitial tears (parallel to the long axis of the Achilles), to partial tears, and eventually to complete tears.
- Tears can be acute or chronic, with repeated minor trauma. At the mildest end of the spectrum all that may be present is peritendonitis.
- Location
- Typically, in a young ‘normal’ individual, the Achilles tendon ruptures in the ‘critical zone’, which is a region of relative watershed hypovascularity 2-6 cm proximal to insertion.
- Classification
- The Achilles tendon tear classification is primarily based on the degree of retraction.
- Radiographic features
- Plain radiograph
- Plain radiographs may show soft tissue swelling and obliteration of pre-Achilles fat pad (Kager’s triangle).
- Ultrasound
- For partial thickness tears
- there is often enlargement of the tendon ( >1 cm) with abnormally hypoechoic or anechoic areas within which correspond to the tear and associated adjacent tendinosis
- For full thickness tears
- often shows separation of the torn ends with a contour change of the tendon
- there is acoustic shadowing at the margins of the tear from sound beam refraction, and adjacent hypoechoic tendinosis
- For partial thickness tears
- MRI
- Appearances can vary:
- a full-thickness tear often shows a tendinous gap filled with oedema or blood
- complete rupture shows retraction of tendon ends
- T2: partial thickness or interstitial tears may show high signal on long TR, and tendon swelling to >7 mm AP
- When a plantaris muscle is present then its tendon is usually spared due to its more anterior insertion on the calcaneum.
- Appearances can vary:
- Post-operative
- post-operative MR imaging may show a tendon gap although this tends to resolve in around 12 weeks 8
- post-operatively, Achilles tendon may appear thicker on MR follow up 9
- Plain radiograph
- Treatment and prognosis
- Treatment depends on the extent of the tear. Partial thickness tears can initially be treated conservatively, with surgery reserved for failure of conservative management, on in some cases for high-performance athletes. Full-thickness tears are normally surgically repaired. If the patient is not deemed suitable for surgical repair (frail, ill, etc.) casting of the ankle in the talipes equinus position may be an alternative.
- Surgical repair results in a shorter Achilles tendon and better greater calf muscle strength (less soleus atrophy) than non-surgical treatment 10.
- History and etymology
- A true rupture of the Achilles tendon was first described by Ambroise Pare in 1575 and first reported in the medical literature in 1633 3.
Adamantinoma
- Adamantinomas are rare, low-grade malignant tumors of unknown etiology that are almost always located in the diaphysis of the mid-tibia.
- Clinical
- The condition usually presents in patients who are between 20 and 40 years old with regional pain and a palpable mass.
- Diagnosis
- is made with a biopsy showing nests of epithelial-like cells arranged in palisading or glandular pattern, in a background of fibrous stroma.
- Incidence
- less than 300 cases have been documented
- Demographics
- occurs in young adults (20 - 40 years of age)
- Anatomic location
- almost always located in mid-tibia
- Radiographs
- multiple sharply circumscribed lucent lesions (“soap bubble” appearance) with interspersed sclerotic bone in mid-tibia
- some lesions may destroy cortex
- may see bowing of the tibia
- radiographic evolution of lesions is helpful in the diagnosis as lesions may continue to grow and erode thru the cortex
- unlike other primary bone tumors, adamantinoma typically shows no periosteal reaction
RE Charcot Spinal arthropathy
a. Neurosyphillis is the most common cause
b. Destruction of entire vertebral level
c. Deep sensation and proprioception loss
d. Differential diagnosis is infection and adjacent segment disease
e. Increased sclerosis and fragmentation
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5934971/#:~:text=Charcot%20spinal%20arthropathy%20(CSA)%2C,of%20deep%20pain%20and%20proprioceptive
2019 Aug Q96
Abstract
Charcot spinal arthropathy (CSA) is a rare progressive disorder of vertebral joint degeneration that occurs in the setting of any condition characterized by decreased afferent innervation with loss of deep pain and proprioceptive sensation in the vertebral column. While surgical circumferential arthrodesis remains the most effective treatment modality, it is associated with multiple complications, including hardware construct failure. This manuscript represents an up-to-date narrative review of the treatment of CSA, its associated complications, and complication prevention.
Keywords: Bone morphogenetic protein, Charcot spinal arthropathy, circumferential arthrodesis, spinal cord injury
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INTRODUCTION
Charcot spinal arthropathy (CSA), also commonly known as spinal neuroarthropathy or neuropathic spinal arthropathy, is a rare progressive disorder of vertebral joint degeneration that occurs in the setting of any condition characterized by decreased afferent innervation, involving loss of deep pain and proprioceptive sensation in the vertebral column. Neuropathic arthropathy was first described by Jean-Martin Charcot in 1868.[1] The first case of CSA was reported in 1884 by Kronig in a patient with tabes dorsalis secondary to tertiary syphilis.[2] Historically, CSA was most commonly reported in the setting of tertiary syphilis. Nowadays, as a consequence of low incidence of syphilis due to improved antibiotic therapy, CSA presents almost exclusively in patients who have suffered traumatic spinal cord injury (SCI).[3,4,5,6,7] CSA secondary to traumatic SCI occurs 17 years after injury on average.[8] Less commonly, CSA may present secondary to syringomyelia, meningocele, myelomeningocele, diabetes mellitus, peripheral neuropathies, anesthetic leprosy, congenital analgesia, Parkinson’s disease, arachnoiditis, transverse myelitis, and others.[8,9,10,11,12] In cases of CSA involving gross spinal instability and absence of medical comorbidities that would otherwise cause contraindication, surgery has become the preferred treatment modality. While posterior-only reconstruction has been indicated in mild cases with minimal bony involvement, the majority of CSA today is treated by circumferential arthrodesis. In addition to improvements in surgical technique, the application of a multimodal treatment model, including the use of bone morphogenetic protein (BMP), has reduced the rates of treatment failure.[13] We present a comprehensive narrative review describing the treatments for CSA, associated complications, and their prevention, with an emphasis on circumferential arthrodesis involving both an anterior and posterior-column construct.
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PATHOPHYSIOLOGY/DIAGNOSTICS
While the etiology of CSA remains disputed, two theories have gained prominence. The neurotraumatic theory hypothesizes that abnormal motion and spinal instability secondary to loss of deep pain and proprioceptive sensation in the posttraumatic SCI vertebral column results in repetitive microtrauma that leads to inflammation of the subchondral bone and articular cartilage.[9,14] Ultimately, the chronic inflammation results in facet joint destruction, intervertebral disc degeneration, progressive deformity, and spinal instability [Figure 1].[13] Conversely, the neurovascular theory describes the onset of hypervascular regions in the subchondral bone due to underlying systemic pathologies such as diabetic neuroarthropathy or autonomic dysfunction. This leads to increased osteoclastic resorption, causing microfractures that ultimately result in facet joint destruction and gross instability.[8]
which are false regarding this condition?
A/ Affects the 4th and 5th metacarpals
B/ causes chondrocalcinosis
C/ Bilateral and symmetrical
D/ subchondral sclerosis and cysts
E/ more common in females
Case courtesy of Dr Chris O’Donnell, Radiopaedia.org, rID: 58172
E is false.
Hemochromatosis (skeletal manifestations)
Dr Dai Roberts◉ and Assoc Prof Frank Gaillard◉◈ et al.
Hemochromatosis is a systemic disease which affects many organs systems, including the joints, characterized by hemosiderin and calcium pyrophosphate deposition.
For a general discussion, and for links to other system specific manifestations, please refer to the article on hemochromatosis.
Radiographic features
chondrocalcinosis: particularly knees and triangular fibrocartilage
arthropathy
symmetrical loss of joint space, subchondral cysts
close association with CPPD which is often seen concurrently
most commonly hands (MCP, carpal, PIP) with the characteristic hook like/ beak-like osteophytes projecting from radial ends of 2nd and 3rd metacarpals
more extensive involvement from the second to the fifth MCP and radial hook-like/drooping osteophytes are more characteristic than in CPPD 3
can also affect the knee, hip, and elbow
generalized osteoporosis (~25%) or osteopaenia (~40%) 4
Differential diagnosis
On imaging consider:
calcium pyrophosphate deposition disease (CPPD)
osteoarthritis
distal hand joints rather than MCP joints
psoriatic arthritis
15 Ddx non-interupted periosteal reaction
15 Ddx non-interupted periosteal reaction
- Caffy disease
- Thyroid acropachy/Gauchers/Treated scurvy/pachydermoperiostosis etc
- Chondrosarcoma
- osteoid osteoma
- osteoblastoma
- ABC
- Chondromyxoid fibroma
- periosteal chondroma
- chondroblastoma
- OM
- LCH
- Healing fracture
- juxtacortical myositis ossificans
- Hypertrophic Osteoarthropathy
- Haemophila
https://www.youtube.com/watch?v=otDM3-fHnzc
List the different types of meniscal tears
Melorheostosis
- Dr Robert Foley and Dr Hani Makky ALSALAM et al.
- Melorheostosis, also known as Leri disease, is an uncommon mesenchymal dysplasia manifesting as regions of sclerosing bone with a characteristic dripping wax appearance (a.k.a. flowing candle wax appearance).
- Epidemiology
- Although changes occur in early childhood, age at presentation is often later, and the condition often remains occult until late adolescence or early adulthood. In only approximately half of the cases is the diagnosis made before the age of 20 2.
- There is no recognised familial predisposition 3.
- Clinical presentation
- The condition, especially in childhood, is usually asymptomatic, being diagnosed as an incidental finding on radiographs obtained for another purpose 1,3. When melorheostosis does manifest clinically, the most common presentation is of joint contracture or pain, which are more common in adults 3.
- Pathology
- Distribution
- Melorheostosis can be either monostotic or polyostotic and tends to be monomelic. It has a predilection for long bones of the limbs, although it can be seen almost anywhere. Hands and feet are not infrequently involved whereas involvement of the axial skeleton is rare 1,2. The condition has a tendency to give a sclerotome distribution. Uncommonly, it can present with a mineralised peri-articular mass.
- Distribution
- Associations
- sclerodermic skin changes: thickening and fibrosis of overlying skin
- hyperpigmentation of overlying skin 4
- muscle atrophy
- vascular tumours and malformations
- other tumours, e.g. osteosarcoma, malignant fibrous histiocytoma 4
- Buschke-Ollendorff syndrome
- Radiographic features
- Plain radiograph
- Radiographs are considered sufficient for establishing the diagnosis.
- Five patterns have been described 1:
- classic
- periosteal cortical thickening is characteristic, but endosteal thickening is also seen in many cases, especially when the age of onset is in adolescence, where it may be purely endosteal 5
- thick undulating ridges of bone, reminiscent of molten wax (dripping wax appearance or flowing candle wax appearance)
- confined to sclerotomes, and can be seen apparently flowing across joints to the next bone
- osteoma-like
- myositis ossificans-like
- osteopathia striata-like
- Plain radiograph
- mixed
- Not infrequently features of melorheostosis, osteopathia striata and osteopoikilosis may co-exist in a so-called overlap syndrome, termed mixed sclerosing bone dysplasia. These conditions may share an underlying aetiology (loss of function mutations in the LEMD3 gene) 1.
- MRI
- Usually, the lesions show low signal on all imaging sequences, with no enhancement.
- Nuclear medicine
- An increase in radiotracer uptake is usually present on late phase bone scans 2.
- Treatment and prognosis
- The disease is of variable severity, but in general follows a chronic progressive course in adults and a faster course in children, occasionally resulting in substantial disability from contractures or deformity.
- Conservative management is often unrewarding, and in severe cases, surgical intervention may be required, including tendon release, osteotomies and even amputation 1-3.
- The disease is of variable severity, but in general follows a chronic progressive course in adults and a faster course in children, occasionally resulting in substantial disability from contractures or deformity.
- History and etymology
- The condition was first written up in the literature by the French neurologist Andre Leri (1875-1930) 7 and J Joanny in 1922 6.
- The name is derived from the Ancient Greek words for limb (melos) and flow (rhe), due to its characteristic appearance of flowing hyperostosis 1,3.
Flowing ossifications
Dr Praveen Jha and Dr René Pfleger◉ et al.
Flowing ossifications are seen in diffuse idiopathic skeletal hyperostosis (DISH).
They are defined as heterotopic ossifications involving the anterior longitudinal ligament, paraspinal connective tissues and annulus fibrosus of at least four contiguous vertebral bodies and are originally described on lateral radiographs of the spine. Typically there are radiolucencies between the anterior aspect of the vertebral bodies and the flowing ossifications of the anterior longitudinal ligament. The radiolucencies again classically end at the level of the vertebral endplates.
See also
syndesmophytes
parasyndesmophytes
Although often used synonymously, they actually have their own definition.
As always in those cases, one has to decide for oneself, if one wants to be a “lumper” or a “splitter”.
Parasyndesmophytes
Dr Henry Knipe◉◈ and Dr René Pfleger◉ et al.
Parasyndesmophytes or floating syndesmophytes are, as the name suggests, paravertebral dystrophic soft tissue calcifications or heterotopic ossifications.
Pathology
They are known to be seen in psoriatic arthritis and reactive arthritis 4.
Radiographic features
Initially they begin at a distance from the vertebral body and intervertebral space. In early disease they are best described as thick and fluffy or thin and curvilinear densities on one side of the spine, parallelling lateral surface of vertebrae and disci. Eventually they will grow to form large and bulky masses, merging with the underlying bone and disc.
Differential diagnosis
Late stages can render differentiation from the related counterparts syndesmophytes and flowing ossifications somewhat difficult.
Syndesmophyte
Mrs. Syeda Salma Talib and Dr Prashant Mudgal et al.
Syndesmophytes are calcifications or heterotopic ossifications inside a spinal ligament or of the annulus fibrosus. They are seen in only a limited number of conditions including:
ankylosing spondylitis
ochronosis
fluorosis
reactive arthritis
psoriatic arthritis
They can be classified as marginal (along the margins of the vertebral bodies) or non marginal (larger and bulky away from the vertebral bodies). Ankylosing spondylitis classically displays symmetrical marginal syndesmophytes.
Radiographic features
Appearance on plain radiographs comprises vertical and symmetrical calcification of the lateral margins of the intervertebral disc space.
Differential diagnosis
syndesmophyte: paravertebral ossifications that run parallel with the spine c.f. osteophytes which typically protrude perpendicular to the spine
enthesophyte: located at an attachment of a ligament or tendon, not associated with a joint
Name this appearance and DDx
- Solid periosteal reaction
- osteoid osteoma
- Stress fracture
PVC exposure Transverse Acro-osteolysis case:
https://journals.sagepub.com/doi/pdf/10.1177/003591577606900419
Acro-osteolysis
Dr Daniel J Bell◉ and Dr Yuranga Weerakkody◉ et al.
Acro-osteolysis (plural: acro-osteolyses) refers to resorption of the distal phalanx. The terminal tuft is most commonly affected. It is associated with a heterogeneous group of pathological entities and, some of which can be remembered by using the mnemonic PINCH FO.
When there is linear bone resorption of the midshaft of the distal phalanx with a relatively spared terminal tuft, the condition is also referred to as band acro-osteolysis and carries a more limited differential diagnosis.
Pathology
Multiple digits
Terminal tuft resorption
scleroderma 4
Raynaud disease
psoriatic arthritis
thermal injury
extreme cold: frostbite
extreme heat: burns, electricity
trauma
hyperparathyroidism
epidermolysis bullosa
porphyria
drugs
phenytoin (occurs in infants of epileptic mothers treated with phenytoin) 7
ergot poisoning/abuse
insensitivity to pain, e.g. leprosy, congenital insensitivity to pain
juvenile chronic arthritis
dermatomyositis
vascular occlusion 5
reactive arthritis 6
pityriasis rubra pilaris (very rare skin condition) 8
pachydermoperiostosis 9
sarcoidosis 16
Midshaft resorption (band acro-osteolysis)
polyvinyl chloride (PVC) exposure 10
primary acro-osteolysis: Hajdu-Cheney syndrome
hyperparathyroidism (also causes terminal tuft resorption)
scleroderma 11 (also causes terminal tuft resorption)
idiopathic non-familial acro-osteolysis 15
pyknodysostosis 13, 14 (also causes terminal tuft hypoplasia)
biomechanical in guitar players 11
Single digit
epidermal inclusion cyst 3
glomus tumour of digit 3
Osteochondral defect
Dr Yahya Baba◉ and Assoc Prof Frank Gaillard◉◈ et al.
Osteochondral defects (OCD) or lesions (OCL) are focal areas of damage with articular cartilage damage and injury of the adjacent subchondral bone plate and subchondral cancellous bone.
Terminology
Osteochondral defect is a broad term that describes the morphological change of a localised gap in the articular cartilage and subchondral bone 5. It is often used synonymously with osteochondral injury/defect and in the paediatric population. Isolated lesions of cartilage or subchondral bone are not considered an OCD 6.
Please note that OCD is a commonly used abbreviation for both osteochondral defect and osteochondritis dissecans, two closely related conditions.
Pathology
Aetiology
osteochondritis dissecans: thought to be due to repeated microtrauma
articular collapse secondary to avascular necrosis or subchondral insufficiency fracture
osteochondral impaction fracture
postsurgical (e.g. following anterior cruciate ligament repair)
Location
The recognised sites of osteochondral defects are:
femoral condyle (most common in the lateral aspect of the medial femoral condyle)
humeral head
talus
capitellum of the humerus
Staging
Osteochondral injuries are graded according to the stability and location of the fragment and presence of secondary degenerative changes (see: osteochondral injury staging).
Radiographic features
Plain radiograph and CT
Both x-rays and CT are able to detect displaced defects with ease. However, they are insensitive to grading lower stage lesions and are inadequate in predicting stability.
MRI
MRI is the modality of choice, with high sensitivity and specificity for the detection of separation of the osteochondral fragment (see: osteochondral injury staging and osteochondritis dissecans surgical staging). This is essential in determining management.
T1
the signal is variable with intermediate to low signal adjacent to fragment and variable fragment signal
T2
high signal line (rim sign) demarcating fragment from bone usually indicates an unstable lesion, however, false positives can result from oedema
low signal loose bodies, outlined by high signal fluid
donor defect filled with high signal fluid
high signal subchondral cysts
Treatment and prognosis
Treatment depends on the location and size of the defect as well as the presence of secondary degenerative changes. When the latter is present, then joint replacement is often the only feasible treatment.
At earlier stages (stage 1 to 4), a number of options exist including:
osteochondral autograft (same patient)
osteochondral allograft (cadaveric donor)
subchondral bone drilling
chondral shaving and abrasion
Osteochondral injury staging
Dr Mostafa El-Feky◉ and Assoc Prof Frank Gaillard◉◈ et al.
Osteochondral injury staging system for MRI attempts to grade the stability and severity of osteochondral injury and is used to plan management.
stage I
injury limited to articular cartilage
MRI findings: subchondral oedema
x-ray findings: none
stage II
cartilage injury with associated subchondral fracture but without detachment
thin sclerotic margin
x-ray findings: usually none; may see fracture as sclerotic or osteopenic area
two subtypes 2,3
type A: cystic on CT and/or oedema on MRI
type B: non-displaced and incompletely undercut by fluid (MR) or lucency (CT), with an open connection to the articular cartilage (essentially 2a without oedema on MRI)
stage III
detached, non-displaced fragment
MRI findings: high signal around osteochondral fracture (rim sign) but not displaced
x-ray findings: slight lucency between osteochondral fragment and remainder of the bone
stage IV
osteochondral fragment displaced
usually joint effusion present, surrounding fragment and filling donor site
x-ray findings: increased lucency between osteochondral fragment and remainder of the bone, or loose body with donor site irregularity
stage V
subchondral cyst formation
secondary degenerative change
x-ray findings: secondary osteoarthritis
Meniscal flounce
Dr Andrew Dixon◉ and Assoc Prof Frank Gaillard◉◈ et al.
Meniscal flounces refer to the “ruffled” appearance of the inner margin of knee menisci. They were initially thought to be only an arthroscopic finding, as a result of joint distension and anaesthetic muscle relaxants but they are occasionally seen on MRI.
Epidemiology
Meniscal flounces are uncommon with initial studies suggesting a frequency of around 0.2% on MRI scans, however more recently a frequency of up to 5% in relation to the medial meniscus has been reported.1,4 It is far more common to be seen with the medial meniscus than the lateral meniscus.
Pathology
They are not associated with an increased incidence of meniscal tears, but can be mistaken for one. They reflect a degree of redundancy in the medial meniscus and are typically seen in the flexed knee.
Radiographic features
MRI
In the sagittal plane the flounce is seen as a wave or kink in the inner margin of the meniscus. In the coronal plane, they may make the inner margin of the meniscus appear truncated or blurred and simulate a small radial tear.
Whenever a flounce is identified it is important to check that there are no ligamentous or capsular injuries that may be resulting in the laxity. This is particularly important if a lateral meniscal flounce is seen, as these are rare and may be a sign of popliteomeniscal fascicle injury/deficiency with hypermobile meniscus.
History and etymology
Out of interest, a flounce is a ruffle placed around a garment (often undergarment) as a decoration.
Differential diagnosis
radial-type meniscal tear
Unilateral facet dislocation
The vertebral body of C6 is anteriorly displaced relative to C7. The C6/7 facet joints are abnormally aligned, with one dislocated anteriorly (locked), and the other almost perched.
Case Discussion
A radiograph was performed at a rural centre before the patient was transferred to a tertiary trauma, where a CT confirmed the diagnosis (scan not available).
Classically as one of the facets is still normally aligned, the amount of anterolisthesis is limited to less that 25 - 50%. Both facets would need to be dislocated to achieve greater anterolisthesis.
Name of this appearance and ddx
- Onion skin Periosteal reaction
- Ewings Sarcoma
- LCH
- Osteosarcoma
- Osteomyelitis
An olecranon spur is an extra-articular enthesophyte seen at the posterior portion of the proximal ulna’s olecranon within the superficial aspect of the central triceps tendon insertion point.
Epidemiology
Olecranon spurs are commonly seen in patients with conditions such as tendinitis of the triceps, bursitis and gout. It is also believed to be more prevalent in patients who have a history of elbow trauma, or those who partake in repetitive forceful elbow extension activities 1. They can be an incidental finding.
Clinical presentation
They can be found in asymptomatic individuals or in patients who present with posterior midline elbow pain.
Radiographic features
The spur often curves upwards and possesses a faint radiolucent line at the base, which is thought to be due to the spur’s formational developmental process as the calcified fibrocartilage thickens and forms small osseous nodules that overtime will fuse 1,2. Careful inspection of the base is therefore warranted to ensure it is not fractured 3.
In the case of an incidental finding, one should look for secondary signs of inflammation such as swelling, or clarifying if the patient has midline posterior elbow pain, as the patient may be asymptomatic.
Mimic of NOF
This is OM
Jumper’s knee
Dr Mostafa El-Feky◉ and Assoc Prof Frank Gaillard◉◈ et al.
Jumper’s knee is a chronic insertional injury of the posterior and proximal fibres of the patellar tendon at the site of its origin at the inferior pole of the patella.
Many authors consider jumper’s knee to be the adult form of Sinding-Larsen-Johansson disease 1 . Some suggest instead that jumper’s knee is a mid-substance patellar tendinopathy.
2019 AUg Q102
Chondrosarcoma
- Low grade chondrosarcoma.
- Case Discussion
- Differential diagnosis is bone infarct (on plain film) and enchondroma.
Dr Bahman Rasuli◉ and R Bronson et al.
Chondrosarcomas are malignant cartilaginous tumours that account for ~25% of all primary malignant bone tumours. They are most commonly found in older patients within the long bones and can arise de novo or secondary from an existing benign cartilaginous neoplasm. On imaging, these tumours have ring-and-arc chondroid matrix mineralisation with aggressive features such as lytic pattern, deep endosteal scalloping and soft-tissue extension.
Epidemiology
The typical presentation is in the 4th and 5th decades and there is a slight male predominance of 1.5-2:1.
Clinical presentation
Patients usually present with pain, pathological fracture, a palpable lump or local mass effect. Hyperglycaemia can occur as a paraneoplastic syndrome.
Pathology
The histology of chondrosarcomas can differ according to their subtype (see below). In general, these tumours are multilobulated (due to hyaline cartilage nodules) with central high water content and peripheral endochondral ossification. This accounts not only for the high T2 MRI signal (see below) but also for rings and arcs calcification or popcorn calcification.
Grading
Chondrosarcomas are divided into three (sometimes four) grades based primarily on cellularity (see: chondrosarcoma grading).
Subtypes
Chondrosarcomas are either primary, arising de novo, or secondary and arise from a pre-existent cartilaginous mass (see: secondary chondrosarcoma).
Primary
conventional intramedullary chondrosarcoma (or central chondrosarcoma): low, intermediate or high grade (see: chondrosarcoma grading)
juxtacortical chondrosarcoma: low, intermediate or high grade
clear cell chondrosarcoma
myxoid chondrosarcoma: usually intermediate grade
mesenchymal chondrosarcoma: usually high grade
extraskeletal chondrosarcoma
dedifferentiated chondrosarcoma
Secondary
Arising from pre-existing cartilaginous lesions:
osteochondroma
solitary osteochondroma
hereditary multiple exostoses
enchondroma
solitary enchondroma
Ollier disease
Maffucci syndrome
Distribution
long bones: 45% (the reason is that the cartilage is more abundant in the long, tubular bones)
femur: 20-35%
tibia: 5%
upper limb (especially proximal humerus): 10-20%
pelvis: 25% especially around the triradiate cartilage
ribs: 8%
patients often younger than at other sites
anterior ribs/costochondral junction
spine: 7%
greater male predominance 2-4:1
thoracic most common
location
posterior elements and vertebral body 45%
posterior elements only 40%
vertebral body only 15%
scapula: 5%
sternum: 2%
head and neck (including cervical spine): 6-7%
craniofacial: 2% (see chondrosarcoma of the skull base)
hands and feet: rare cf. enchondromas
Radiographic features
Imaging findings vary somewhat with different subtypes but do have some general features. Below are typical imaging appearances which are best demonstrated by conventional chondrosarcomas.
In general chondrosarcomas are large masses at the time of diagnosis, usually >4 cm in diameter and >10 cm in 50% of cases.
Plain radiograph
lytic (50%)
intralesional calcifications: ~70% (rings and arcs calcification or popcorn calcification)
endosteal scalloping: affecting more than two-thirds of the cortical thickness (c.f. less than two-thirds in enchondromas)
moth-eaten appearance or permeative appearance in higher grade tumours (see chondrosarcoma grading), e.g. myxoid, dedifferentiated and mesenchymal chondrosarcomas
cortical remodelling, thickening and periosteal reaction are also useful in distinguishing between an enchondroma and low-grade chondrosarcoma (see enchondroma vs. low-grade chondrosarcoma)
CT
The features seen on CT are the same as on plain film, but are simply better seen:
94% of cases demonstrate matrix calcification, c.f. 60-78% on plain film
endosteal scalloping
cortical breach, seen in ~90% of long bone chondrosarcoma, c.f. only ~10% of enchondromas
soft tissue mass: tumour cellularity, and therefore density, increases with increased grade of the tumour
heterogenous contrast enhancement
MRI
T1: low to intermediate signal
iso- to slightly hyperintense cf. muscle
iso- to slightly hypointense cf. grey matter (see chondrosarcoma of the base of skull)
T2: very high intensity in non-mineralised/calcified portions
gradient echo/SWI: blooming of mineralised/calcified portions
T1 C+ (Gd)
most demonstrate heterogeneous moderate to intense contrast enhancement.
enhancement can be septal and peripheral rim-like corresponding to fibrovascular septation between lobules of hyaline cartilage
Nuclear medicine
Typically chondrosarcomas demonstrate increased uptake on bone scan, seen in over 80% of cases, and usually the uptake is quite intense. This is useful in helping to distinguish low-grade chondrosarcoma from an enchondroma as the latter has increased uptake in ~20% of cases, and usually to a lesser degree (see: enchondroma vs low grade chondrosarcoma).
Treatment and prognosis
Prognosis varies with both grade and location. In general:
grade
grade 1: 90% 5-year survival
grade 3: 29% 5-year survival
location
long bones have a better prognosis than axial skeleton
Quiz questions
What should you look for?
What is injured?
Segond Fracture
Osteochondroma
Dr Mohammad Taghi Niknejad and Assoc Prof Frank Gaillard◉◈ et al.
Osteochondromas are a relatively common imaging finding, accounting for 10-15% of all bone tumours and approximately 35% of all benign bone tumours. Although usually thought of as a benign bone tumour, they may be thought of as a developmental anomaly. They are frequently asymptomatic and have very low malignant potential if sporadic and solitary.
Epidemiology
Osteochondromas develop during childhood (period of most rapid skeletal growth), but once formed remain for the rest of the individual’s life. They can present at any age and are most frequently found incidentally.
They are usually sporadic, but can be part of:
hereditary multiple exostoses (HME): also known as diaphyseal aclasis
Trevor disease: also known as dysplasia epiphysealis hemimelica
Malignant transformation occurs in the cartilage cap, and is uncommon in sporadic solitary osteochondromas (~1%), whereas in the setting of hereditary multiple exostoses the rate is much higher (5-25%) 5.
Clinical presentation
Symptomatic presentation is either due to mechanical effects of the lesion, fracture, or malignant transformation.
Mechanical symptoms include:
impingement upon nearby structures:
nerve compression
vascular compression
reactive myositis
palpable lump
bursal formation and bursitis
Fractures occur typically through the neck of pedunculated lesions.
Ongoing growth and or pain after skeletal maturity has been reached is suspicious for malignant degeneration.
Pathology
Osteochondromas are considered a chondroid neoplasm and are primarily a part of the growth plate which separates and continues growing independently, without an associated epiphysis, usually away from the nearby joint. The medullary cavity is continuous with the parent bone, and hyaline cartilage caps them. Osteochondromas can be congenital or occur as a result of previous trauma to the growth plate, including previous irradiation 3,4.
Location
They most commonly arise from the appendicular skeleton, especially around the knee 3:
lower limb: 50% of all cases 3
femur (especially distal): most common: 30%
tibia (especially proximal): 15-20%
less common locations: feet, pelvis
upper limb
humerus: 10-20%
less common locations: hands, scapula
spine: the posterior elements of the spine are an uncommon but not rare site for these tumours
Radiographic features
Plain radiograph
An osteochondroma can be either sessile or pedunculated and is seen in the metaphyseal region typically projecting away from the epiphysis. There is often associated broadening of the metaphysis from which it arises. The cartilage cap is variable in appearance. It may be thin and difficult to identify, or thick with rings and arcs calcification and irregular subchondral bone.
New cortical irregularity or continued growth after skeletal maturity has been reached, as well as frankly aggressive features (e.g. bony destruction, large soft tissue component, metastases) are all worrying for malignant transformation.
CT
CT demonstrates the same findings as on radiograph but is better able to demonstrate medullary continuity and the cartilage cap.
Ultrasound
Ultrasound is able to demonstrate the cartilage cap very accurately as a hypoechoic region bounded by bone on its deep surface and muscle/fat superficially.
MRI
MRI is the best imaging modality to assess cartilage thickness (and thus assessing for malignant transformation), the presence of oedema in bone or adjacent soft tissues, and visualising neurovascular structures in the vicinity.
The cartilage cap of osteochondromas appears the same as cartilage elsewhere, with intermediate to low signal on T1 and high signal on T2 weighted images.
A cartilage cap of over 1.5 cm in thickness is suspicious for malignant degeneration 3.
With intravenous gadolinium administration, enhancement of benign lesions is normally seen in the tissue that covers the cartilaginous cap which is fibrovascular in nature, however, the cartilaginous cap itself should not enhance.
Nuclear medicine
During growth, osteochondromas demonstrate increased uptake on bone scans, but with time they become no more active than normal bone. Presence of increased activity in adulthood should raise the possibility of a complication (e.g. fracture, malignancy).
Treatment and prognosis
As they represent normal growth of a growth plate in an abnormal direction, they often stop growing with the rest of the skeleton 3.
In most instances, no treatment is required. The osteochondroma can be locally resected for cosmetic or mechanical reasons.
If malignant transformation occurs (~1% in solitary osteochondromas and ~5-25% with hereditary multiple exostoses) then the resultant chondrosarcoma is usually of low grade (67-85% of cases), and surgery is usually curative (70-90%) 3,5. Limb-sparing wide local excision usually suffices. The features associated with sarcomatous transformation can be remembered by the mnemonic GLAD PAST 1:
growth after skeletal maturity
lucency (new)
additional scintigraphic activity
destruction (cortical)
pain after puberty
and
soft tissue mass
thickened cartilage cap greater than 1.5cm
Local recurrence is seen in both benign and malignant lesions, due to spillage of cartilage cells into the resection bed. Rates are estimated at 2% and up to 15% respectively 3.
Differential diagnosis
Imaging differential considerations include:
hands: bizarre parosteal osteochondromatous proliferation (BPOP): arises from the bone cortex and lacks medullary continuity
humerus: supracondylar spur: projects towards the elbow joint
malunited fracture
Cortical desmoid
tumour mimic
Ewing sarcoma
Dr Tee Yu Jin◉ and Assoc Prof Frank Gaillard◉◈ et al.
Ewing sarcomas are the second most common malignant primary bone tumors of childhood after osteosarcoma, typically arising from medullary cavity with invasion of the Haversian system. They usually present as moth-eaten destructive permeative lucent lesions in the shaft of long bones with large soft tissue component without osteoid matrix and typical onion skin periostitis. It may also involve flat bones and appears sclerotic in up to 30% of cases.
Epidemiology
Ewing sarcoma typically occurs in children and adolescents between 10 and 20 years of age (95% between 4 and 25 years of age), and has a slight male predilection (M:F 1.5:1) 1,2.
The Ewing sarcoma family of tumors primarily occurs in white patients. In the United States, the incidence in Asians/Pacific Islanders is about one-half that in Caucasians, while the incidence among African Americans is one-ninth that in Caucasians 12.
Clinical presentation
Presentation is non-specific with local pain being by far the most common symptom. Occasionally a soft tissue mass may be palpable. Pathological fractures also occur. Systemic symptoms including fever may be present. ESR is also elevated.
Pathology
Ewing sarcoma is a small round blue cell tumor with regular sized primitive appearing cells. It is closely related to the soft tissue tumors pPNET, Askin tumor and neuroepithelioma, which collectively are referred to as Ewing sarcoma family of tumors (ESFT) 1. They share not only microscopic appearances but also demonstrate a non-random t(11;22)(q24;q12) chromosome rearrangement.
Location
lower limb: 45%
femur most common
pelvis: 20%
upper limb: 13%
spine and ribs: 13% (see thoracic Ewings sarcoma)
sacrococcygeal region most common 4
skull/face: 2%
Alternatively 3:
long bones: 50-60%
femur: 25%
tibia: 11%
humerus: 10%
flat bones: 40%
pelvis: 14%
scapula
ribs: 6% (thoracic Ewing sarcoma)
As far as location within long bones, the tumor is almost always metadiaphyseal or diaphyseal 2-3:
mid-diaphysis: 33%
metadiaphysis: 44%
metaphysis: 15%
epiphysis: 1-2%
Radiographic features
Ewing sarcomas tend to be large with poorly marginated tumors, with over 80% demonstrating extension into adjacent soft tissues. It should be noted that pPNET often extend into bone, making the distinction difficult.
Plain radiograph and CT
The appearance of these tumors is very variable, but they usually have clearly aggressive appearance. Common findings include 2:
permeative: 76%
laminated (onion skin) periosteal reaction: 57%
sclerosis: 40%
They occasionally demonstrate other appearances, including Codman triangles, spiculated (sunburst) or thick periosteal reaction and even bone expansion or cystic components.
Soft tissue calcification is uncommon, seen in less than 10% of cases 2.
MRI
T1: low to intermediate signal
T1 C+ (Gd): heterogeneous but prominent enhancement
T2: heterogeneously high signal, may see hair on end low signal striations
Nuclear medicine
Ewing sarcomas demonstrate increased uptake on both Gallium67-citrate and all three phases of the Technetium99m methylene diphosphonate bone scans 6.
Treatment and prognosis
Systemic chemotherapy is the mainstay of treatment with surgery and/or radiotherapy playing a role depending on the location and size of the tumor.
What was once a uniformly fatal tumor now has respectable survival rates, although these vary with location. Spinal tumors for example have up to 86% long term survival compared to 25% of sacrococcygeal tumors 4. The overall 5 year survival is in the order of 50-75% of patients with local disease only at the time of presentation 5.
Prognosis is significantly impacted by the presence of distant metastases at the time of diagnosis, which is far more common for the pelvis (25-30%) compared to extremities (<10%) 5. Metastases most frequently go to bone or lungs.
History and etymology
It is named after James Stephen Ewing (1866-1943), an American pathologist, who first described his eponymous tumor in 1920 8,11.
Differential diagnosis
other Ewing sarcoma family of tumors
pPNET: large soft tissue component with extension into bone
Askin tumor: chest wall
osteosarcoma:
more often has amorphous calcified matrix
classically perimetaphyseal, Ewing sarcoma also occurs in other locations
more prevalent around the knee and in the proximal humerus, in other locations Ewing sarcoma is the more frequent of the two
osteomyelitis
metastatic disease
hematological malignancy
eosinophilic granuloma 9
neuroblastoma (
Causes of Unilateral erosion/abscence of the clavicles
PROMM
- Rheumatoid
- post-traumatic distal slavicular osteolysis
- Myeloma
- Mets
- Osteomyelitis
X-ray Interpretation: Shoulder Injuries | Radiopaedia.org
Key Points
post-traumatic osteolysis of the distal end of the clavicle may be seen in patients following AC joint injuries
these injuries can be unilateral or bilateral as the result of a single traumatic event or repetitive strain
history of trauma or repetitive strain is important, otherwise, differential diagnoses may be considered
a useful mnemonic to remember the differentials is SHIRT Pocket:
S: scleroderma
H: hyperparathyroidism
I: infection (osteomyelitis)
R: rheumatoid arthritis
T: trauma
P: progeria
