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Flashcards in Bones Deck (47)
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1
Q

generalised increased bone density 12

A

Most common
1. Metastases—prostate and breast most common. Heterogeneous;
generally not diffuse.
2. Sickle cell disease—medullary sclerosis and bone infarcts. Growth
arrest of long bones. H-shaped vertebrae.
3. Myelofibrosis—older patients. Diffuse medullary sclerosis, loss of
corticomedullary differentiation. No heterogeneity

Less common
4. Renal osteodystrophy—axial > appendicular. Rugger jersey spine.
5. Osteopetrosis—thickened cortices with reduced marrow space.
Pathological transverse fractures.
6. Paget’s disease—coarse trabeculae and bone expansion. Multiple
bones rather than generalized.
7. Systemic mastocytosis—lytic, sclerotic or mixed. Usually diffuse
affecting spine and epiphyses of long bones.

Rare
8. Fluorosis—diffuse osteosclerosis, particularly ribs and spine, with
entheseal ossification.
9. Pyknodysostosis—narrow medullary cavities with multiple long
bone fractures.
10. Hypoparathyroidism—diffuse sclerosis in 10%. Dense
metaphyseal bands and skull vault thickening.
11. Progressive diaphyseal dysplasia (Camurati-Engelmann
disease)—young patients. Fusiform enlargement and sclerosis of
long bones sparing the epiphyses.
12. Myeloma—rare osteosclerosing form. Associated with POEMS
syndrome ( Polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy myeloma, and skin changes)

2
Q

SOLITARY SCLEROTIC BONE LESION

15 (5-10)

A

Most common
1. Bone island (enostosis)—ovoid with long axis parallel to long axis
of bone and a feathered border.
2. Enchondroma—confluent punctate or nodular calcification, denser
centrally than peripherally. Enchondromas in the large long bones
are often more calcified than those in the fingers.
3. Metastasis—prostate, breast, mucinous adenocarcinoma of GI
tract, carcinoid, lymphoma, TCC in adults. Medulloblastoma and
neuroblastoma in children.
4. Callus—usually associated with a fusiform swelling in long bones.
5. Bone infarct—usually a central metadiaphyseal lucency with thin
serpentine calcified margins.

Less common
6. Paget’s disease—blastic phase causes sclerosis accompanied by
bone expansion, and cortical and trabecular thickening.
7. Osteoma—arises from membranous bone: skull and paranasal
sinuses. Ivory osteomas contain no trabeculae. Mature osteomas
have visible marrow. If multiple consider Gardner syndrome.
8. Osteoid osteoma/osteoblastoma—sclerosis caused by eccentric
periosteal thickening. Osteoid osteoma: radiolucent nidus <2 cm.
Osteoblastoma: more common in the posterior elements of
spine, larger nidus with thin shell.
9. Healed or healing bone lesion—treated metastasis, NOF, simple
bone cyst, brown tumour, eosinophilic granuloma.
10. Primary bone sarcoma—aggressive features: poorly defined
margins, aggressive periosteal reaction, Codman’s triangles, bone
destruction, soft tissue mass.
11. Fibrous dysplasia—usually lytic with ground glass areas but can
calcify in later life.
12. Chronic osteomyelitis—usually associated with an area of lysis,
chronic periosteal reaction and occasionally a sequestrum.
13. Chronic recurrent multifocal osteomyelitis (CRMO)—idiopathic
inflammatory disorder. Most commonly affects clavicles and tibias
in children. Often multifocal.
14. Lymphoma—primary bone lymphoma rare. More common as
secondary involvement. Large extraosseous soft tissue mass with
relative preservation of bone.
15. Cement and bone graft substitutes—history of surgery

3
Q

MULTIPLE SCLEROTIC BONE LESIONS

A

Most common
1. Metastases—prostate, breast, mucinous adenocarcinoma of GI
tract, carcinoid, lymphoma, TCC in adults. Medulloblastoma and neuroblastoma in children.
2. Multiple healed bone lesions—lytic metastases following
radiotherapy or chemotherapy. Eosinophilic granulomas and brown tumours following treatment.
3. Paget’s disease—often polyostotic.

Less common

  1. Multiple bone infarcts—consider an underlying disorder, e.g.
    sickle cell or Gaucher disease.
  2. Multiple stress fractures—callus formation around fractures.
  3. Lymphoma.
  4. Osteopoikilosis—multiple symmetrically distributed bone islands
    in the metaphyses and epiphyses of long bones and the pelvis.
    Some ovoid, some round.
  5. Multifocal osteosarcoma.
  6. Multiple osteomas—Gardner syndrome.
  7. Fibrous dysplasia—long lesions in long bones, often hemimelic
    (McCune-Albright syndrome). Usually lytic but can calcify.
  8. CRMO and SAPHO.

Rare

  1. Osteopathia striata (Voorhoeve disease)—linear striations along
    long axis of long bone.
  2. Erdheim-Chester disease—bilateral symmetrical metadiaphyseal
    sclerosis in long bones, most commonly femora and tibias.
  3. Multiple myeloma—sclerotic in 3%.
  4. Tuberous sclerosis.
  5. Intramedullary osteosclerosis—diaphyseal endosteal sclerosis
    typically involving the tibia or femur, usually bilateral and in women.
4
Q

BONE SCLEROSIS WITH A PERIOSTEAL REACTION 13
Most common 5
Less 6
Rare 2

A

Most common

  1. Healing fracture.
  2. Metastasis—osteoblastic metastases from prostate.
  3. Osteoid osteoma/osteoblastoma—solid or lamellated periosteal reaction.
  4. Chronic osteomyelitis—look for sequestrum.
  5. Osteosarcoma—classically sunray spiculation.

Less common

  1. Ewing sarcoma—often onion-skin or lamellated periosteal reaction.
  2. Chondrosarcoma—chondroid matrix with regions of enchondral
    ossification.
  3. Lymphoma.
  4. CRMO—clavicles and tibias in children and adolescents.
  5. SAPHO syndrome (synovitis–acne–pustulosis–hyperostosis–osteitis)—similar to CRMO but in adults. Although similar long bone changes may be seen, anterior chest wall and pelvic involvement predominate.
  6. Infantile cortical hyperostosis (Caffey’s disease)—infants <6
    months of age. Multiple bones, especially mandible, ribs and clavicles.

Rare

  1. Melorheostosis—sclerotomal distribution(The sclerotome forms the vertebrae and the rib cartilage and part of the occipital bone). Cortical and medullary sclerosis likened to dripping candle wax.
  2. Tertiary syphilis—usually bilateral periostitis involving skull, clavicles, ribs and tibias. Mixed sclerotic and lytic ‘gummatous’ lesions can also be seen.
5
Q
SOLITARY SCLEROTIC BONE LESION WITH 
A LUCENT CENTRE 9
MC 4
Less 3
Rare 2
A

Most common

  1. Osteoid osteoma/osteoblastoma—lucent nidus.
  2. Brodie’s abscess.
  3. Medullary bone infarct—irregular serpentine outline.
  4. Stress fracture—lucent fracture line may be visible.

Less common
5. Looser’s zone of osteomalacia.
6. Liposclerosing myxofibrous tumour—characteristic location in
the intertrochanteric region of the femur.
7. Tuberculosis.

Rare

  1. Syphilis.
  2. Yaws. (is a chronic skin infection characterized by papillomas (noncancerous lumps) and ulcers. It is caused by the bacterium Treponema pallidum subspecies pertenue)
6
Q

COARSE TRABECULAR PATTERN

6

A
  1. Paget’s disease.
  2. Osteoporosis.
  3. Osteomalacia.
  4. Haemoglobinopathies.
  5. Haemangioma.
  6. Gaucher disease
7
Q

SKELETAL METASTASES

Lytic 5

A
  1. Lung.
  2. Breast—usually lytic but can be sclerotic or mixed.
  3. Myeloma.
  4. Nonmucinous adenocarcinomas of the GI tract.
  5. Most other primary sources
8
Q

SKELETAL METASTASES

Lytic and expansile

A
  1. Renal cell carcinoma.
  2. Thyroid.
  3. Hepatocellular carcinoma.
  4. Melanoma.
  5. Phaeochromocytoma
9
Q

SKELETAL METASTASES

Sclerotic 7

A
  1. Prostate.
  2. Breast—particularly post treatment.
  3. Carcinoid.
  4. Mucinous adenocarcinomas of the GI tract.
  5. Transitional cell carcinoma.
  6. Small cell lung cancer.
  7. Lymphoma—particularly Hodgkin lymphoma; rare.
10
Q

SKELETAL METASTASES

Mixed 8

A
  1. Breast.
  2. Lung.
  3. Lymphoma.
  4. Cervix.
  5. Testis.
  6. Transitional cell carcinoma.
  7. Melanoma.
  8. Neuroblastoma—in children
11
Q

LUCENT BONE LESIONS
Well-defined, sclerotic margin
12

A
  1. Nonossifying fibroma—young patients, eccentric metaphyseal
    location. Consider benign fibrous histiocytoma if patient >25
    years or atypical location.
  2. Bone cysts—both SBCs and ABCs usually have a thin sclerotic
    margin. ABCs are more eccentric and expansile.
  3. Fibrous dysplasia—variable appearance, typically diaphyseal.
  4. Chondroblastoma—epiphyseal location, young patients. If
    patient >20 years, consider clear cell chondrosarcoma.
  5. Brodie’s abscess—typically young patients, most common in
    metaphysis. Discrete lucency with surrounding ill-defined
    sclerosis.
  6. Healing metastases or primary malignant bone
    lesions—sclerotic rim indicates a good response to treatment.
  7. Osteoblastoma—large lucent nidus with a sclerotic margin. Most
    common in spine.
  8. Intraosseous lipoma—typically in calcaneus or intertrochanteric
    region of femur. Thin sclerotic margin. Focus of central
    calcification is pathognomonic but not always present.
  9. Liposclerosing myxofibrous tumour—characteristic location:
    intertrochanteric region of femur. Usually a thick sclerotic margin.
  10. Adamantinoma/osteofibrous dysplasia (OFD)—characteristic
    location: anterior cortex of tibial diaphysis. Both can look
    identical but OFD occurs in a younger age group (<10 years).
  11. Chondromyxoid fibroma—rare; can mimic NOF, BFH and ABC.
  12. Haemophilic pseudotumour—usually very expansile + other
    signs of haemophilia
12
Q

LUCENT BONE LESIONS
Well-defined, nonsclerotic margin
9

A
  1. Metastasis—usually older patients, in axial or proximal
    appendicular skeleton.
  2. Myeloma/plasmacytoma—older patients, usually in axial or
    proximal appendicular skeleton. Typically ‘punched-out’
    appearance, may be expansile.
  3. Low-grade chondral lesions—e.g. enchondroma, low-grade
    chondrosarcoma. Both can be lytic without chondroid matrix.
  4. Giant cell tumour—typically has a well-defined nonsclerotic
    margin. Adults 20–50 years.
  5. Simple/aneurysmal bone cyst—both may have no perceptible
    sclerotic margin.
  6. Eosinophilic granuloma—may appear well-defined.
  7. Brown tumour—often expansile. Look for other signs of
    hyperparathyroidism.
  8. Lytic phase of Paget’s disease—well-defined flame-shaped
    advancing edge without sclerosis.
  9. Desmoplastic fibroma—rare. Often contains pseudotrabeculations
13
Q

LUCENT BONE LESIONS

Poorly defined margin

A
  1. Metastasis—usually ill-defined.
  2. Myeloma—usually discrete but may appear ill-defined.
  3. Osteomyelitis—ill-defined and lytic in the acute phase.
  4. Bone lymphoma—typically ill-defined subtle bone destruction
    with a large soft tissue mass. Can occur at any age but more
    common in older patients.
  5. Primary bone sarcomas—e.g. Ewing sarcoma, osteosarcoma,
    chondrosarcoma, fibrosarcoma, undifferentiated pleomorphic
    sarcoma, angiosarcoma. Internal matrix may be absent.
  6. Eosinophilic granuloma—patients <30 years. Can occur
    anywhere, often has an aggressive appearance indistinguishable
    from infection or malignancy.
  7. Giant cell tumour—can appear ill-defined. Adults 20–50 years
14
Q

GROSSLY EXPANSILE LUCENT

BONE LESION 12

A

Most common

  1. Plasmacytoma—older patients, usually in axial or proximal appendicular skeleton.
  2. Metastases—RCC, thyroid, HCC, phaeochromocytoma, melanoma. Usually in axial or proximal appendicular skeleton.
  3. Aneurysmal bone cyst—in children and young adults. Usually has a thin sclerotic margin.
  4. Giant cell tumour—usually older patients than ABC. Often abuts articular surface, no sclerotic margin.

Less common
5. Telangiectatic osteosarcoma—mimics ABC.
6. Fibrous dysplasia—usually fusiform expansion rather than a
discrete expansile mass.
7. Brown tumour—look for other signs of hyperparathyroidism.
8. Haemangioma—often expansile when in flat bones, e.g. skull or
pelvis, with a sunburst periosteal reaction.
9. Chordoma—in sacrum, clivus or vertebral bodies.

Rare

  1. Haemophilic pseudotumour—look for other signs of haemophilia.
  2. Slow growing central bone sarcoma.
  3. Hydatid cyst
15
Q

LUCENT EPIPHYSEAL BONE LESION 7

A

This includes carpal and tarsal bones since they are epiphyseal
equivalents.
1. Lesions related to joint pathology—e.g. geode, intraosseous
ganglion, erosion, osteochondral defect, PVNS.
2. Giant cell tumour—nonsclerotic margin, extends from metaphysis
to epiphysis. Mainly in adults.
3. Chondroblastoma—perilesional sclerosis ± chondroid calcification.
Typically 10–20 years.
4. Infection—including Brodie’s abscess.
5. Clear cell chondrosarcoma—mimics chondroblastoma but usually
occurs >20 years.
6. Location-specific lesions—e.g. intraosseous lipoma (calcaneus,
central calcification), simple bone cyst (calcaneus, no central
calcification), osteoblastoma (talus).
7. Bone lesions which can occur anywhere—e.g. metastasis, brown
tumour, lymphoma, myeloma, haemophilic pseudotumour

16
Q

LUCENT BONE LESION CONTAINING
CALCIUM OR BONE 14
MC 4
LC 10

A

Most common
1. Enchondroma—chondroid matrix.
2. Osteoid osteoma and osteoblastoma—lucent nidus can contain
calcification.
3. Avascular necrosis and bone infarction.
4. Metastases—some are mixed lytic and sclerotic.

Less common
5. Chondroblastoma—chondroid matrix. Epiphyseal location.
6. Chondrosarcoma—chondroid matrix. Usually metaphyseal.
7. Osteosarcoma—osteoid matrix. Usually metaphyseal.
8. Fibrous dysplasia—usually ground-glass density but can be sclerotic.
9. Osteomyelitis with sequestrum.
10. Eosinophilic granuloma—‘button sequestrum’ (central density with surrounding lucency)
11. Intraosseous lipoma—characteristic central focus of calcification,
especially in calcaneus.
12. Haemangioma—contains coarsened trabeculae. Most common
in spine.
13. Liposclerosing myxofibrous tumour—classically intertrochanteric
region of femur.
14. Fibrosarcoma/undifferentiated pleomorphic sarcoma.

17
Q

EXOPHYTIC AND JUXTACORTICAL
BONE LESIONS
8

A
  1. Callus—can be profuse, e.g. after an avulsion fracture, if bones
    misaligned or in malunion.
  2. Osteochondroma—well-defined exophytic bony mass (sessile or
    pedunculated), usually arising from metaphysis and pointing away from the joint. The cortex and trabeculae within the lesion should be continuous with those in the metaphysis. Can transform to chondrosarcoma: worrying features include continued growth or change in morphology after physeal
    closure, bone destruction, soft tissue mass and cartilage cap >1 cm thick (on ultrasound/MRI).
  3. Heterotopic ossification and myositis ossificans—well-defined with dense ossification in the periphery and less density centrally. May mimic surface osteosarcoma in the early stage; follow up can help differentiate by showing maturation of ossification.
  4. Surface osteosarcoma—three types:
    (a) Parosteal—low grade, arises from outer periosteum, usually metaphyseal. Pedunculated ‘cauliflower’ appearance with a narrow stalk + partial cleft between the mass and underlying bone. Mature osteoid matrix within the mass which is more dense centrally (in contrast to myositis ossificans).
    (b) Periosteal—intermediate grade, arises from inner periosteum, usually diaphyseal. Broad-based with cortical erosion and spiculated periosteal reaction. Less organized osteoid matrix.
    (c) High grade—amorphous osteoid matrix + larger soft tissue
    mass ± underlying cortical destruction. Usually diaphyseal.
  5. Periosteal chondroma/chondrosarcoma—both typically arise on
    the metaphyseal surface as a soft tissue mass ± chondroid matrix.
    The underlying cortex is mildly scalloped. Difficult to differentiate
    the two on imaging; size >3 cm is more suggestive of
    chondrosarcoma.
  6. Cortical desmoid—characteristic location: distal posteromedial
    femoral metaphyseal cortex (at muscle insertion site).
    Well-defined scalloping of cortical surface, typically small.
  7. Parosteal lipoma—juxtacortical radiolucent mass with an
    associated irregular bony excrescence arising perpendicularly
    from the periosteum. Characteristic bony spur at base.
  8. Bizarre parosteal osteochondromatous proliferation (BPOP)—
    typically arises from the periosteum of bones in the hands
18
Q

‘MOTH-EATEN BONE’ IN AN ADULT

8

A
  1. Metastases.
  2. Multiple myeloma—numerous punched-out lytic lesions.
  3. Bone sarcomas—e.g. Ewing sarcoma, osteosarcoma,
    chondrosarcoma.
  4. Bone lymphoma—subtle ill-defined bone destruction, usually with
    a large soft tissue mass.
  5. Langerhans cell histiocytosis—young adults only.
  6. Osteomyelitis.
  7. Osteoporosis—extensive cortical tunnelling can mimic an
    aggressive process.
  8. Hyperparathyroidism—extensive subperiosteal bone resorption +
    brown tumours can mimic malignancy
19
Q

REGIONAL OSTEOPENIA

A

Most common

  1. Disuse—typically distal foot and ankle, hand and wrist.
  2. Complex regional pain syndrome—typically unilateral upper limb. Triple phase uptake on bone scintigraphy.
  3. Inflammatory arthropathy.
  4. Septic arthritis.

Less common

  1. Transient osteoporosis of the hip.
  2. Regional migratory osteoporosis.
  3. Haemophilic arthropathy.
  4. Soft tissue arteriovenous malformation
20
Q

GENERALIZED OSTEOPENIA 4

A
  1. Osteoporosis.
  2. Diffuse infiltrative bone disease—multiple myeloma in adults,
    leukaemia in children.
  3. Osteomalacia/rickets.
  4. Hyperparathyroidism
21
Q

OSTEOPOROSIS

RF 5

A
  1. Increased radiolucency of bone—can be affected by radiographic
    factors.
  2. Cortical thinning—most commonly endosteal resorption in the
    elderly. Pencil-line cortex, vertebral picture framing.
  3. Prominent secondary trabeculae—caused by preferential
    resorption of primary trabeculae.
  4. Vertebral fractures—anterior wedge or biconcave vertebral
    compression.
  5. Insufficiency fractures—sacrum, pubis, femoral neck, tibial
    plateau, ankle and foot
22
Q

OSTEOPOROSIS
Causes
Primary 3
Secondary 6

A

Primary

  1. Postmenopausal.
  2. Age-related.
  3. Juvenile—rare self-limiting condition occurring in children of 8–12
    years. Spontaneous improvement is seen.

Secondary
1. Endocrine—e.g. hypogonadism, Cushing’s, diabetes, acromegaly,
hyperprolactinaemia, Addison’s disease, hyperthyroidism,
hyperparathyroidism (subperiosteal resorption), mastocytosis (mast
cells produce heparin; may also produce diffuse sclerosis).
2. Disuse.
3. Iatrogenic—e.g. steroids, heparin, aromatase inhibitors, androgen
deprivation, antiepileptics, proton pump inhibitors.
4. Deficiency states—e.g. vitamin C (scurvy), protein, chronic renal/
liver disease, anorexia, malabsorption, alcohol excess.
5. Chronic and systemic disease—e.g. rheumatoid arthritis, amyloidosis, COPD.
6. Congenital—e.g. osteogenesis imperfecta, Turner syndrome,
homocystinuria, neuromuscular diseases, mucopolysaccharidoses,
trisomy 13 and 18, pseudo and pseudopseudohypoparathyroidism,
glycogen storage diseases, progeria

23
Q

OSTEOMALACIA AND RICKETS

causes 5

A

Most common causes
1. Vitamin D deficiency—either low dietary intake, poor sunlight exposure or malabsorption.

Other causes
2. Renal disease.
(a) Glomerular disease—results in renal osteodystrophy.
(b) Tubular disease—e.g. renal tubular acidosis, Fanconi
syndrome or hypophosphataemic rickets.

  1. Hepatic disease—parenchymal failure or chronic cholestasis.
  2. Anticonvulsants—phenytoin and phenobarbital.
  3. Tumour-associated—paraneoplastic phenomenon, usually due to
    a benign phosphaturic mesenchymal tumour which may be small
    and hard to find; PET-CT can aid localization.
24
Q

Conditions which mimic rickets/osteomalacia

2

A
  1. Hypophosphatasia.
  2. Metaphyseal chondrodysplasia (Schmid type)—metaphyseal
    cupping and irregularity, bowed long bones, short-limbed
    dwarfism
25
Q

OSTEOMALACIA AND RICKETS

In infants <6 months of age

A
  1. Biliary atresia.
  2. Metabolic bone disease of prematurity—combined dietary
    deficiency and hepatic hydroxylation of vitamin D.
  3. Hypophosphatasia.
  4. Vitamin D-dependent rickets—rachitic changes are associated
    with a severe myopathy in spite of adequate dietary intake of
    vitamin D.
26
Q
PERIOSTEAL REACTIONS
Parallel spiculated (‘hair-on-end’) 3
A
  1. Ewing sarcoma.
  2. Infantile cortical hyperostosis (Caffey’s disease).
  3. Syphilis.
27
Q

PERIOSTEAL REACTIONS
Divergent spiculated (‘sunray’)
7

A
  1. Osteosarcoma.
  2. Metastases—especially from sigmoid colon and rectum.
  3. Ewing sarcoma.
  4. Haemangioma—when in flat bones, e.g. skull, pelvis.
  5. Meningioma—skull only.
  6. Tuberculosis.
  7. Tropical ulcer—typically involves the foot or lower leg ( chronic ulcerative skin lesion thought to be caused by polymicrobial infection with a variety of microorganisms, including mycobacteria. It is common in tropical climates)
28
Q
PERIOSTEAL REACTIONS
Codman triangle (single lamina or lamellated)
A
  1. Aggressive malignant bone tumour.

2. Osteomyelitis

29
Q

PERIOSTEAL REACTIONS—SOLITARY

AND LOCALIZED

A
  1. Trauma—fracture, periosteal haematoma.
  2. Insufficiency and stress fractures.
  3. Inflammatory.
  4. Neoplastic—e.g. malignant primary bone tumour, metastasis, or
    benign bone lesion + pathological fracture.
30
Q

PERIOSTEAL REACTION—BILATERALLY
SYMMETRICAL IN ADULTS
6

A
  1. Hypertrophic osteoarthropathy (HOA)—
  2. Vascular insufficiency—most common in lower limbs due to
    venous stasis/varicose veins. Often associated with phleboliths.
  3. Thyroid acropachy—predominantly radial sided in the thumbs
    and index fingers.
  4. Pachydermoperiostosis—aka primary HOA. Solid periosteal
    reaction + skin thickening.
  5. Fluorosis—solid undulating periosteal new bone along long bones
    with calcification/ossification of tendon and ligament insertions.
  6. Hypervitaminosis A
31
Q

PERIOSTEAL REACTIONS—BILATERALLY

ASYMMETRICAL

A
  1. Metastases.
  2. Osteomyelitis.
  3. Reactive and psoriatic arthritis.
  4. Nonaccidental injury—in infants and children.
  5. Osteoporosis—increased liability to fracture.
  6. Osteomalacia—associated with Looser’s zones.
  7. Bleeding diathesis.
  8. Sickle cell dactylitis—in young children due to infarction of persistent red marrow in long bones of hands and feet. Hard to differentiate from osteomyelitis
32
Q

HYPERTROPHIC OSTEOARTHROPATHY

A

Primary
Pachydermoperiostosis—rare, autosomal dominant inheritance.
Presents in children and young adults, mainly males.African. Skin
thickening is also seen.

Secondary
Most common

  1. Lung cancer—>60% of cases.
  2. Bronchiectasis—frequently due to cystic fibrosis.
  3. Lung metastases.

Less common

  1. Other pleuropulmonary causes—e.g. pleural fibroma (rare, but
    has the highest incidence of accompanying HOA), mesothelioma,
    COPD, pulmonary fibrosis, sarcoidosis, chronic infection (e.g.
    abscess, empyema, TB), pulmonary AVM.
  2. GI disorders—irritable bowel disease, coeliac disease, Whipple’s
    disease, polyposis, malignancy.
  3. Cyanotic congenital heart disease—produces clubbing but only
    rarely a periosteal reaction.
  4. Cirrhosis and hepatobiliary malignancies.
  5. Other malignancies—lymphoma, nasopharyngeal carcinoma,
    RCC, breast phyllodes tumour, thymic carcinoma, melanoma
33
Q

EXCESSIVE CALLUS FORMATION

8

A

Most common
1. Hypertrophic fracture nonunion.
2. Neuropathic arthropathy—including congenital insensitivity to
pain. Accompanied by joint destruction, fragmentation, sclerosis
and osteophyte formation. (Dense,degeneration,debris, destruction, deformity, dislocation
3. Steroid therapy and Cushing’s syndrome.

Less common

  1. Osteogenesis imperfecta.
  2. Paralysis—more common in lower extremities.
  3. Renal osteodystrophy.
  4. Multiple myeloma.

Children
8. Nonaccidental injury

34
Q

OSTEONECROSIS/AVASCULAR NECROSIS
Common 5
Less common 8

A

Common

  1. Corticosteroids—both exogenous and endogenous (Cushing’s syndrome).
  2. Alcohol.
  3. Idiopathic—e.g. Perthes’ disease in children.
  4. Fractures—especially femoral neck, talus and scaphoid.
  5. Chemotherapy.

Less common
6. Haemoglobinopathies—especially sickle cell anaemia.
7. Radiotherapy—localized to the treatment field, e.g. pelvis/sacrum.
8. Metabolic and endocrine—e.g. pregnancy, diabetes, hyperlipidaemia, gout, Gaucher disease.
9. Connective tissue diseases—e.g. SLE, rheumatoid arthritis, scleroderma.
10. Toxic—e.g. immunosuppressives, anti-inflammatories (NSAIDs).
11. Haemopoietic disorders—e.g. polycythaemia vera, haemophilia.
12. Thrombotic and embolic—including vasculitis, fat embolism and
dysbaric osteonecrosis.
13. Others—e.g. pancreatitis, severe burns, amyloidosis

35
Q

EROSIONS OF THE MEDIAL METAPHYSIS

OF THE PROXIMAL HUMERUS

A
  1. Normal variant.
  2. Chronic rotator cuff tear—results in elevation of humeral head
    and impingement of medial metaphysis on glenoid, causing
    mechanical erosion.
  3. Hyperparathyroidism—subperiosteal resorption.
  4. Rheumatoid arthritis.
  5. Malignancy—e.g. leukaemia, metastases (including neuroblastoma
    in children).
  6. Lysosomal storage disorders—e.g. Gaucher disease, Hurler
    syndrome, Niemann-Pick disease
36
Q

EROSION OR ABSENCE OF THE OUTER
END OF THE CLAVICLE
Common 3
LC 7

A

Common

  1. Posttraumatic osteolysis.
  2. Postoperative—e.g. following subacromial decompression.
  3. Rheumatoid arthritis—typically bilateral and symmetrical.

Less common
4. Malignancy—metastasis, myeloma.
5. Septic arthritis—erosion involves both sides of joint.
6. Hyperparathyroidism—typically bilateral and symmetrical, ±
resorption at other sites, e.g. coracoclavicular ligament insertion,
sternoclavicular joint, greater and lesser tuberosities of humerus.
7. Cleidocranial dysplasia.
8. Pyknodysostosis—hypoplastic clavicles also associated with
hypoplastic mandibles, acroosteolysis and osteosclerosis.
9. Scleroderma—juxtaarticular soft tissue calcification highly
suggestive.
10. Gout.

37
Q

MADELUNG DEFORMITY

A

Short bowed distal radius with increased radiocarpal angle.
• Long dorsally subluxed ulna.
• V-shaped proximal carpal row.

Secondary

  1. Growth arrest following radial growth plate injury or infection.
  2. Multiple hereditary exostoses.
  3. Turner syndrome.
  4. Achondroplasia.
  5. Leri-Weill dyschondrosteosis.
38
Q

CARPAL FUSION

isolated

A
  1. Lunate-triquetral—most common site. 1% of the population.
  2. Capitate-hamate.
  3. Trapezium-trapezoid.
39
Q

CARPAL FUSION

Syndrome-related

A
  1. Acrocephalosyndactyly (Apert syndrome)—craniosynostosis, syndactyly.
  2. Arthrogryposis multiplex congenita—multiple congenital contractures.
  3. Diastrophic dwarfism—short-limbed dwarfism.
  4. Ellis-van Creveld syndrome—short-limbed dwarfism, polydactyly.
  5. Dyschondrosteosis—mesomelic dwarfism + bilateral Madelung deformities.
  6. Hand-foot-genital syndrome—scaphoid-trapezium coalition.
  7. Nievergelt syndrome—mesomelic dwarfism, club foot, metatarsal synostoses.
  8. Oto-palato-digital syndrome—deformed carpals, ear and palatal anomalies.
  9. Holt-Oram syndrome—radial ray anomalies and cardiac malformations.
  10. Turner syndrome—Madelung deformity and lunate-triquetral
    coalition may be seen.
  11. Symphalangism—interphalangeal joint fusions and carpal coalitions.
  12. Fetal alcohol syndrome—capitate-hamate coalition + radioulnar
    synostoses.
40
Q

CARPAL FUSION

Acquired

A
  1. Inflammatory arthritides—especially juvenile idiopathic arthritis and rheumatoid arthritis.
  2. Pyogenic arthritis.
  3. Chronic tuberculous arthritis.
  4. Posttraumatic.
  5. Postsurgical.
41
Q
SHORT METACARPAL(S) OR METATARSAL(S)
5
A
  1. Idiopathic.
  2. Posttraumatic—iatrogenic, fracture, growth plate injury, thermal
    or electrical.
  3. Postinfarction—e.g. sickle cell anaemia.
  4. Turner syndrome—4th ± 3rd and 5th metacarpals.
  5. Pseudo and pseudopseudohypoparathyroidism—4th and 5th
    metacarpals.
42
Q

ARACHNODACTYLY

A

Most common
1. Marfan syndrome—although arachnodactyly is not necessary for
the diagnosis.
2. Normal variant—constitutional tall stature.

Less common
There are several disorders that have a marfanoid phenotype that
can include arachnodactyly. These include:
3. Homocystinuria.
4. Ehlers-Danlos syndrome.
5. Klinefelter syndrome.
6. Loeys-Dietz syndrome.
7. Congenital contractural arachnodactyly (Beals syndrome).
8. MEN 2B.
9. Myotonic dystrophy.
10. Stickler syndrome

43
Q

DISTAL PHALANGEAL DESTRUCTION
Resorption of the tuft (acroosteolysis)
MC 5
LC 6

A

Most common

  1. Scleroderma—look for soft tissue thinning and calcification.
  2. Raynaud disease—and other vasculopathies, e.g. SLE.
  3. Psoriatic arthropathy—look for joint erosions.
  4. Hyperparathyroidism—look for subperiosteal bone resorption.
  5. Trauma—including burns and frostbite.

Less common
6. Peripheral neuropathy—e.g. due to diabetes, leprosy, congenital
insensitivity to pain. Results in recurrent trauma.
7. Other arthritides—e.g. juvenile idiopathic arthritis, reactive
arthritis, multicentric reticulohistiocytosis.
8. Other skin disorders—dermatomyositis, epidermolysis bullosa,
congenital erythropoietic porphyria.
9. Phenytoin toxicity—in infants of treated epileptic mothers.
10. Snake and scorpion venom.
11. Pyknodysostosis (mimic)—look for diffuse bony sclerosis

44
Q

DISTAL PHALANGEAL DESTRUCTION

Resorption of the midportion

A
  1. Hyperparathyroidism.
  2. Polyvinyl chloride tank cleaners.
  3. Acroosteolysis of Hajdu and Cheney—very rare.
45
Q

LYTIC LESIONS OF THE PHALANGES
poorly defined 2
well defined 5+

A

Poorly defined

  1. Osteomyelitis—particularly in diabetic feet. Also consider tuberculous dactylitis(spina ventousa), sickle cell dactylitis and syphilitic dactylitis.
  2. Metastasis—lung is the most common primary site.

Well-defined

  1. Enchondroma—often purely lytic without chondroid matrix.
  2. Joint-based lesions—e.g. subchondral cysts, erosions.
  3. Implantation epidermoid—palmar scalloping, distal phalanx only.
  4. Glomus tumour—dorsal scalloping, distal phalanx only.
  5. Sarcoidosis—multiple well-defined lace-like lytic lesions.
  6. Other rare lesions not specific to the phalanges—e.g. fibrous dysplasia, ABC, GCT, SBC, brown tumour, LCH, fibrous cortical defect
46
Q

FLUID–FLUID LEVELS IN BONE LESIONS

ON CT AND MRI

A

Benign

  1. Aneurysmal bone cyst.
  2. Chondroblastoma.
  3. Giant cell tumour.
  4. Simple bone cyst.
  5. Fibrous dysplasia.

Malignant

  1. Telangiectatic osteosarcoma.
  2. Any necrotic bone tumour.
47
Q

Camurati-Engelmann disease (diaphyseal dysplasia)

A

diffuse and somewhat irregular thickening of the cortical bone in the diaphyses of all of the long bones, with no involvement of the epiphyses.

delayed skeletal maturity.

Calvarial thickening with a dense diploic space and absence of the frontal and sphenoid sinuses.