2. INTRODUCTION
• The term osteomyelitis implies an infection of bone
and marrow.(osteo-myelo-itis).
• Most commonly results from bacterial and
mycobacterial infections, although fungi, parasites,
and viruses can infect the bone and the marrow.
4. OSTEOMYELITIS
Incidence is reduced - use of antibiotics
Causative organisms:
● S. aureus- Most common
● Immunocompromised patients:
○ H. influenzae, S. pneumoniae, Mycobacterium,
Pseudomonas, fungi, other gram negative organisms
● IV drug users:
○ S. aureus, Pseudomonas
● Infants:
○ With humerus involvement - Group B Streptococcus.
5. Pathways of infection
1. Hematogenous - most common source
2. Spread from contiguous source of
infection- skin, PNS, teeth
3. Direct implantation of infection -
penetrating or puncture wounds with
nail, splinter or glass, open fractures .
More common in feet
4. Post op infection - contamination of
surgical sites
6. ● Age group: 2 to 12 years
● Male : Female = 3:1
● Bones affected:
○ Large tubular bones : Femur (most common), tibia, humerus, radius
● Clavicle and pelvis - rarely involved. (Ilium bone- commonly involved in
pelvis)
● In IV drug users :
○ “S” joints - Spine, Sacroiliac, Symphysis pubis, Sternoclavicular joints.
● In diabetics:
○ Joints of the foot and toes - Sausage shaped deformities in toes .
CLINICAL FEATURES
7. CLINICAL FEATURES
Infants and children:
• Acute process
• Fever with chills, pain and swelling over the affected site, loss of limb function
• Elevated TLC, with left shift, raised ESR
Adults:
• Insidious or chronic process
• Fever, malaise, pain, edema, erythema.
• Pre existing infection of skin, respiratory system, genito urinary tract in 50%
cases
8. Vascular anatomy
Infantile pattern: Up to 1 year of age.
Metaphyseal vessels can penetrate growth plate
and supply epiphysis
Spread infection into epiphysis and joint.
Childhood pattern: Upto fusion of physis.
Metaphyseal vessels don’t cross growth plate.
Slow and turbulent flow in metaphyses -
proliferation of microbes.
Spare the epiphysis or joint
INFANT CHILD ADULT
9. Vascular anatomy
Adult pattern:
Metaphyseal vessels penetrate physis and reach
subarticular end of bone.
Increased incidence of septic arthritis
secondary to osteomyelitis in adult patients.
INFANT CHILD ADULT
10. Pathophysiology
Implantation of organism(usually in medullary tissues)
Vascular and cellular response
Localised edema and suppuration
Intramedullary pressure increases
Compression of capillaries and sinusoids in medullary
cavity
Infarction of fat, hematopoietic tissue and bone
●Active hyperaemia in the adjacent area and increased
osteoclastic activity
●Focal osteolysis and regional osteoporosis + inflammatory
exudate at the margin
11. Inflammation penetrates endosteum through
haversian canals and lacunae
Reaches periosteal space
(Occurs early in infants because of fewer sharpey’s fibres and easily
strippable periosteum from bone)
Periosteum and sub periosteal space involved +
increased pressure in sub periosteal space
Infarction of cortical bone and necrosis
Pathophysiology
12. ● Sequestrum: Dead bone – Due to cortical and
medullary infarcts.
○ Small Sequestrum removed by osteoclasts
● Involucrum: New bone formation from the
stripped surface of periosteum.
● Cloaca: Defect in involucrum- discharge of
inflammatory products from bone - Empyema
necessitatis
Pathophysiology
14. Radiologic features
Early signs
Latent period
10 days in the extremities
21 days in the spine
Soft tissue
Elevation and displacement of fat planes
Obliteration of fat planes
Bone
Moth-eaten or permeative medullary and cortical destruction
Periosteal new bone(solid, laminated, spiculated or Codman’s triangle)
15. Radiologic features
1. Latent period:
Radiographic latent period of 10 days (upto 3 weeks for spine)
Nuclear bone scan: Tc MDP and Gallium 67 citrate
■ first few hours of onset of symptoms
■ Increased uptake of radionuclide - “hot spot” on image
MRI:
■ Low signal on T1 and high signal on T2.
18. Radiologic features
2. Soft tissue alterations -
○ Within 3 Days of bacterial contamination
○ Swelling of deep tissues - around metaphyses - children/infants -
Earliest radiographic sign
○ Elevation of Lucent fat planes from adjacent bone.
○ Myofascial marginal planes obliterated - adjacent soft tissue edema and
cellulitis
○ Mass like soft tissue density - obliterates soft tissue margins (neoplasm
= displaces and deforms soft tissue)
19.
20.
21. Radiologic features
3. Bone destruction:
○ Moth eaten or permeative pattern - focal loss of bone density in metaphyses
○ Can disseminate to epiphysis/diaphysis/growth plate.
○ Sequestrum: 3-6 weeks of onset of symptoms - more radiodense
○ Cortical disruption with cloaca.
22. Radiologic features
4. Periosteal response
○ Solid / unilamellated pattern
○ Multi-lamellated pattern - most common in infants/children
○ Spiculated / Codman’s triangle – occasional.
○ Large involucrum - rapidly formed woven bone - less radiodense.
23. Late signs
Soft tissue
Draining sinus(secondary carcinoma of tract)
Debris
Bone
Destruction of adjacent cortex.
Involucrum
Cloaca
Sequestrum
Sclerosis and moth-eaten sclerosis
Joint
Loss of joint space
Healing by bony ankylosis
24. MAGNETIC RESONANCE IMAGING
● Bone marrow oedema
● To assess extent of involvement
● To assess collections / abscess formation and its extent
● Assess involvement of adjacent soft tissue structures – muscles,
subcutaneous tissue, etc.
● MR imaging aids in planning surgery by delineating sinus
tracts and soft-tissue abscesses
25.
26.
27.
28.
29.
30. ULTRASOUND
● Assessment of soft tissues and joints adjacent to infected bone,
● Able to visualize soft tissue abscesses, cellulitis, subperiosteal collections
and joint effusion.
31. Computed Tomography
● Very limited role
● Gas within medulla : is an infrequent but reliable diagnostic sign of OM.
32. NUCLEAR IMAGING
● Radionuclide studies useful in examining patients with suspected
osteomyelitis include the 99mTc-MDP scan,111In-labeled WBC scan, and
67Ga-citrate scan
● Can detect osteomyelitic changes days or weeks before osseous changes
are apparent on standard radiographs.
Tc99
● Can detect as early as 24 – 48 hrs
33. NUCLEAR IMAGING
● Particularly valuable in looking for other sites of infection, because
multifocal osteomyelitis may occur, especially in neonates
● Not specific for osteomyelitis, and in the appropriate clinical setting may
suggest but cannot conclusively establish the diagnosis.
34. Management and prognosis of osteomyelitis
● Antibiotic therapy
● Surgical drainage and debridement
● Pathological fractures
● Septic arthritis
● Hematogenous spread - pyemic abscess, focal cellulitis
● Good prognosis overall
● Residual disability in 30% cases
● Mortality- 11%
35. ● Long standing discharging sinus
● Infection of surrounding soft tissues
● Malignant transformation-increasing severity of symptoms with rapid osteolysis:
○ Marjolin’s ulcer: Malignant transformation into squamous cell carcinoma of
ulcerative channel
■ In chronic osteomyelitis (20 to 30 years after onset of symptoms)
■ Deep lesion in the limb - commonly seen in Femur and tibia.
○ Osteosarcoma
Complications and Sequelae of OM
44. Brodie’s abscess
● Localised form of suppurative osteomyelitis
● Localised pain - Nocturnal, Reduces with Aspirin (mimics osteoid
osteoma)
● H/o recent infection or dental surgery
● Male children.
● Metaphyses of long bones
● Distal tibia> proximal tibia> distal femur > proximal/distal fibula> distal
radius
45. Brodie’s abscess
PATHOLOGY:
Abscess within bone cavity - contains necrotic debris and purulent/mucous fluid
Surrounded by inflammatory granulation tissue
Sclerosis of adjacent spongy bone
● S. aureus - most common
● Culture - negative in some cases
● Mimics chronic recurrent multifocal osteomyelitis
46. Radiographic features
● Oval/ elliptical/ serpigenous radiolucency ( usually >1 cm)
● Surrounding reactive sclerosis - halo or doughnut rim
● Lytic lesion often oriented along the long axis of the bone surrounded by thick dense
rim of reactive sclerosis that fades imperceptibly into surrounding bone
● Periosteal new-bone formation
47. ● Radiolucent finger like extension into epiphysis: ‘tunnelling’ (pathognomonic).
● As a rule sequestrum is absent.
● Abscess if located in the cortex, surrounding sclerosis and periostitis simulate an
osteoid osteoma or stress fracture.
● No bony enlargement/ cortical breakthrough/ visible matrix
Radiographic features
50. Brodie’s abscess
• X-ray: circular lucent area
without calcification > 1
cm
• Enhances typically on
delayed isotope scan.
• MRI:necrotic tissue gives
less signal intensity.
Osteoid osteoma
• Xray: circular lucent area
with or without
calcification < 1 cm.
• Central nidus
• Enhances centrally both on
blood pool and delayed
scan.
• MRI: central vascular
material gives brighter
signal intensity.
51.
52. Brodie’s abscess
MRI:
Penumbra Sign :
T1 - high signal intensity lesion
surrounded by relatively less hyper intense
signal rim - confirms infectious agent - rules
out tumor
Treatment- Surgical decompression
curettage
53. Garre’s Sclerosing Osteomyelitis
● Rare condition
● Chronic low grade diffuse non purulent
osteomyelitis
● Culture - negative
● In children and young adults
● Moderate nocturnal pain
● Hard bony mass
● Long tubular bones - Fusiform thickening of
bone
54. Garre’s Sclerosing Osteomyelitis
● Cortical lesion + significant ossifying periostitis + reactive
new bone formation
● No sequestrum/ bony destruction
● Gross sclerosis and contour irregularity in absence of
apparent bone destruction.
● Resemble osteoid osteoma , fibrous dysplasia, Ewings
sarcoma radiologically
55. SEPTIC ARTHRITIS
Usually Mono articular
Source: Blood borne from other infection/ traumatic implantation/ Secondary to
joint replacement surgery
Causative organisms:
● S. aureus - most common overall
● Gonococcus - Most common in <30 years age
● Others : Salmonella, Streptococcus (alpha, beta haemolytic, S. pneumoniae),
Brucella, Serratia
● Nocardia, Mycobacteria, Fungi
56. Clinical features
● Common age group: 1 month to 5 years
● Severe pain and capsular edema - Reduced joint movements
● Acute Fever +/- chills, erythema
● Weight bearing joints - change in gait
● Raised ESR/CRP, raised TLC with left shift
● Culture positive - blood/ joint aspirate
Treatment:
● Antibiotic therapy and joint decompression
57. Pathologic features
Organism within vasculature of synovial membrane
Contamination of synovial fluid
Acute inflammatory response begins
Capsule distends
Reduced cartilage nutrition and death of chondrocytes
Proteolytic enzymes from inflammatory cells and chondrocytes
Progressive destruction of articular surface
Process continues - eventual joint dislocation in advanced stages
With continued use of joint - rapid disintegration- total loss of articular space
58. Pathologic features
● Rapidly progressing
● Infection penetrates sub chondral bone
● Destruction of articular cortex
● Regional hyperaemia + joint disuse - juxta articular osteoporosis
● Greater destruction of bone - ankylosis of joint
● Sites - common - Knee, ankle, hip
● Rare - shoulder, hands and feet - post traumatic - human or animal bites
60. Radiologic features
1. Soft tissue alterations:
● Displacement of juxta articular fat - distension of joint capsule
Hip-deviation of fat folds of obturator internus, psoas major, gluteus
medius.
● Waldenstrom’s sign
61.
62. Waldenstroms sign:
• Increased distance between the
Kohler's teardrop(inferior and
medial surface of
acetabulum) and the femoral
head
• A measurement of >11mm or
difference of >2mm with
opposite side
• Age
63. Radiologic features
2. Osseous alterations
● Loss of normal subcortical cortical bone
● Moth eaten type destruction of medulla in metaphyses
● Complete resorption of articulating ends of bones
● Lamellated type periosteal reaction
● Complete ankylosis of joint (fibrous/ bony)
● Healing - articular surface remodelling but deformity persists.
66. TOM SMITH’S ARTHRITIS
● Joints with metaphyses included within adjacent joint capsule - more prone to
rapid development of septic arthritis
○ Proximal and distal femur, distal tibia, proximal and distal humerus
Osteomyelitis
Rupture metaphyseal cortex
Enter joint space
Spread via synovial fluid to epiphyses or subarticular end of bone
Tom smith arthritis
● Hip, knee, ankle, shoulder, elbow
67. Tubercular osteomyelitis
●Respiratory primary infection
●Hematogenous spread to MSK system
●Thoracic and lumbar spine
●M. bovis - causes more bone and joint TB (but number of M.tuberculosis
cases >>> M.bovis)
●Diagnosis by culture - joint aspirate, tissue exudation, tissue biopsy
68. ●Insidious and chronic course
●Pre pubertal children
●Mild pain in the joint + stiffness
●TB spine - insidious back pain, reduced ROM, focal tenderness, +/-
neurological impairment
●Pott’s paraplegia - sudden onset paraplegia in TB spine
●Pus discharging sinuses
Tubercular osteomyelitis
69. ●Appendicular joints - lower limb >> upper limb
●Most common - Knee and hip
●Tenderness, soft tissue swelling, joint effusion, local rise of temperature
●Limping gait - painful movements of weight bearing joint.
●Muscle contractures - reduced ROM.
●Muscle atrophy and deformity.
Tubercular osteomyelitis
70. Tubercular Arthritis
● Mono articular
● Middle aged/ elderly
● Infection focus in metaphysis - spread to joint
● Extensive inflammation in synovial membrane- thickened membrane
● Granulation tissue spreads to free surface articular cartilage - erosions and
destruction
● Cartilage and bone destruction- sequestrum formed
● Both surfaces of joint affected - Kissing sequestrum
● Increased vascularity in low grade Tb - hyperaemic osteoporosis
71. TB ARTHRITIS
• Typically affects large joints: hip and knee
• Monoarticular disease is the rule.
• Radiographic triad : PHEMISTER’S TRIAD
• Progressive slow joint space narrowing
• Juxta articular osteoporosis
• Peripheral erosive defects of articular surfaces
72. TB ARTHRITIS
• Juxta-articular osteoporosis.
• Peripherally located osseous erosions
• Gradual narrowing of joint space
• Wedge-shaped areas of necrosis (kissing sequestra) may be present on both
sides of the affected joint
• EventuallyFibrous ankylosis
74. Marginal erosions - corners of bone without cartilage but exposed to
synovial membrane
Joint widening - joint effusion, distension, soft tissue swelling
Bone destruction - sub chondral cortex + moth eaten destruction of bones of
either sides of joint
Narrowing of joint - articular cartilage and bone destroyed
Juxta articular osteoporosis - hyperaemia and disuse atrophy
Fibrous ankylosis - end stage
Tubercular Arthritis - Radiologic features
75. Unusual Presentations of Tuberculosis
● Caries sicca: tuberculous erosions of the humeral head.
● Cystic tuberculosis: multiple, symmetric, well-defined round or oval lytic lesions of
the appendicular skeleton.
● Tuberculous dactylitis: tubercular destruction of the short tubular bones of the hand
and feet; often called spina ventosa.
● Pott’s puffy tumor: a tubercular calvarial lesion forming a button sequestrum and a
fluctuant cold abscess of the scalp.
76. Unusual Presentations of Tuberculosis
● Weaver’s bottom: tubercular involvement of the subgluteal bursae allowing direct
extension to the ischial tuberosity.
● Long vertebra: as a result of an extensive gibbus deformity, the vertebra caudal to the
gibbus may become taller than it is broad.
● Gouge defects: anterior vertebral erosions secondary to subligamentous dissection and
spread of the tubercular process.
77. Unusual Presentations of Tuberculosis
● Kissing sequestrum: represents cartilage and bone destruction leading to complete
joint obliteration.
● Pott’s paraplegia: a pressure paraplegia secondary to collapse of vertebral bodies,
extensive granulation tissue, and detached sequestra from the vertebral bodies.
● Scrofula: Bovine tuberculosis affecting the cervical lymph nodes.
79. Cystic TB
• Symmetric well defined ,round or oval lytic lesions with little or no
periosteal reaction initially
• Children > adults
• Peripheral skeleton
• Good prognosis
80.
81. TB dactylitis
• TB involvement of short tubular bones of hands and feet.
• Frequent in children.
• Soft tissue swelling is the initial manifestation
• Multiple foci with periostitis
• Soft tissue swelling,bone expansion and thinning of cortex: spina ventosa
84. Feature Suppurative Non-suppurative(TB)
Age Prepubertal Prepubertal and debilitated geriatric
Clinical features Fever, acute pain and swelling;
onset and progression is rapid
(2 weeks)
Staphylococcus
Insidious onset;fever, prostration;
very slow, relentless progression
(months)
Cause Staphylococcus aureus Mycobacterium tuberculosis
Sequestrum formation Common Less common
Psoas abscess formation Uncommon Occurs (5%)
Marjolin’s ulcer Occurs rarely Does not occur
Sinus formation Common Less common
Discovertebral disease Occurs Most common site
Multiple segmental involvement Rare Common
Gouge defects Do not occur Occur
Osteoporosis Mild Extensive
Periosteal reaction Common Usually absent
Sacroiliac involvement Rare Occurs occasionally U/L
End stage Bony ankylosis Fibrous ankylosis
85. SYPHILITIC OSTEOMYELITIS
Causative organism: Treponema pallidum
Angiitis of vasa vasorum/ small arterioles
Endarteritis- necrosis of vessel wall - infarction of tissue supplied by that
vessel
Areas of coagulative necrosis + infiltration of plasma cells and TLCs
Skeletal syphilis - congenital or acquired
86. CONGENITAL SYPHILIS
● Placental transmission in 2nd and 3rd trimester
● Langhans layer of chorion - barrier to pathogen upto 4 months of gestation
● Untreated = 25% fetus- die in utero and 25-30% die after birth
● Majority - symptoms within 4 months of birth
● 40% - late symptomatic syphilis
● Master masquerader
● Sites: Knees, Shoulders, Wrists
● Epiphyseal centres- avascular cartilages - not affected -formation and maturation of
cartilage not affected.
87. Radiologic features of congenital syphilis
Phase 1- Metaphysitis
● At birth
● Infection beneath growth plates - normal vasculature is replaced by syphilitic
granulation tissue
● Bilateral symmetrical changes
● Radiolucent metaphyseal bands: Mimic lucent bands of leukaemia and mets from
neuroblastoma.
88. Radiologic features of congenital syphilis
Phase 1- Metaphysitis
● Metaphyseal irregularity + fragmentation and infarction at metaphysis- physis junction
- Saw toothed appearance - Mimics scurvy on radiograph
● Wimberger’s sign of congenital syphilis : symmetrical erosive defects on medial
surfaces of proximal ends of tibia
● Spontaneous resolution can occur. Heals in 2 weeks to 2 months post treatment
91. Phase 2 - Periostitis
● Periosteum infiltration by granulation tissue
● Solid/ lamellated periosteal reaction - diffuse symmetrical- affecting all
long bones
● Completely resolves with treatment
Radiologic features of congenital syphilis
92.
93. Phase 3- Osteitis:
● Granulation tissue extend from metaphysis to diaphysis
● Osteolytic lesion with reactive sclerosis + periostitis of long tubular bones
● Extensive periostitis + cortical overgrowth - undulating dense contour of
long bones
● Anterior bowing of tibia with osteolytic defects (gumma) throughout the
bone
● Saber shin - both tibia involved
Radiologic features of congenital syphilis
94.
95. Other features of congenital syphilis
CLUTTON’S JOINTS:
Bilateral painless swellings around knee joints - Syphilitic synovitis -
especially Knees
HUTCHINSON’S SIGN:
Deformity of teeth - peg shaped hypoplastic and notched tooth
96. ACQUIRED SYPHILIS
● Tertiary syphilis
● Superficial portions of skeleton - skull, tibia, clavicle
● <10% patients of acquired syphilis - develop Osseous syphilis
Bowing of tibia
● Pseudo bowing - in acquired syphilis - outer diameter of bone enlarged -
due to periosteal proliferation
● True bowing - in congenital syphilis
97. Radiographic features of Acquired syphilis
● Long bones involved
● Proliferative periostitis: Diffuse thickening of both inner and outer cortices
● Periosteal reaction: Solid / laminated / lace like appearance (more
aggressive).
● Lytic gummatous lesions in cortex or medulla + surrounding sclerosis
● Sequestrum - rare.
● Skull - most common - frontal bone - outer table
104. ACTINOMYCOSIS - A. israelii and A. bovis
● Commensals in mouth and bowel
● Post penetrating wound / surgery / secondary to osteoradionecrosis
● Osseous Actinomycosis- in 15% cases - extension from adjacent soft tissue/
hematogenous
105. ACTINOMYCOSIS - A. israelii and A. bovis
2 types:
1. Cervico- facial type: Most common
Poor oral hygiene
Biopsy
2. Chest and abdominal type:
Ileocecal disease - rare
Pulmonary symptoms- 15% cases
Treatment - Specific antibiotic therapy + surgical debridement
106. Radiologic features
Common - mandible( tooth extraction / socket infection) , spine, ribs,
pelvis
Lytic destructive lesion (at angle of mandible)
No periosteal reaction
Abscess with draining sinuses
ACTINOMYCOSIS - A. israelii and A. bovis
107. SPINAL ACTINOMYCOSIS
● Infection from adjacent retroperitoneal/mediastinal lymph node
● Thoracic and lumbar.
● Multiple vertebrae involved.
● Lytic destruction +/- sclerosis
● Disc spared.
● Neural arch + adjacent rib
● Paravertebral abscess - smaller than TB and no calcification.
● Sawtooth outline of vertebral bodies - periosteal reaction.
108. MADURAMYCOSIS
Causative organisms:
Nocardia madurae,Madurella madurae, N. brasiliensis, Monospermium
apiosermium
Source : Soil
TRIAD :
Foot involved + Localised swelling + purulent grainy discharge from sinus
tracts
Long standing soft tissue swelling - penetrates muscles, tendons and synovial
membranes
Tarso metatarsal region >>> hand , wrist, arm, leg
109. Radiologic features
Localised: Poorly defined lesions
Advanced: Widespread lytic destructive lesions
No or minimal periosteal reaction
Deformity- Bizarre undulating or filiform
● Fistula formation
● Diffuse intra articular osseous ankylosis- of all joints of
foot
MADURAMYCOSIS
110. ● Mimics Neurotrophic arthropathy of diabetic patients (but more
sclerotic reaction with destruction and collapse)
Xray:
○ Widespread lytic destruction and deformity.
○ Periosteal reaction is minimal ,sequestration is rare
MRI:
Dot in circle sign: Small low intensity focus within high signal
lesions - SPECIFIC
Generalised low intensity signal of matrix with lesions of high
intensity interspersed throughout
MADURAMYCOSIS
111.
112. LEPROSY
• Caused by M.leprae.
• Abnormalities
• Directly due to the presence of bacilli.
• Indirectly due to neuropathy
• Face,hands and feet are commonly involved.
• Face-Nasal destruction
• Hands and feet: Metaphysis of the phalanges are involved.
113. • Neuropathic resorption gives a ‘licked candy stick appearance’ because
of bone loss both longitudinally and circumferentially.
• Diffuse osteoporosis
• Nerve calcifications (rare)
114. References
• Yochum and Rowe’s Essentials of skeletal radiology
• Yu Jin Lee, Sufi Sadigh, Kshitij Mankad, Nikhil Kapse, Gajan Rajeswaran. The
imaging of osteomyelitis.Quant Imaging Med Surg 2016;6(2):184-198.
Increased inflammation and destruction within bone.
Increased inflammation and destruction within bone.
BONE SCAN: EARLY DETECTION OF OSTEOMYELITIS. A. Initial Plain Film. Note that the initial radiographic examination shows no destructive changes in this 12-year-old patient who presented with pain in the wrist.
B. 10-Day Follow-Up. Note the permeative pattern of bone destruction in the metaphysis of the distal radius.
C. Bone Scan, Initial Presentation. Note that this examination, performed at the same time as panel A, reveals an area of
increased uptake (a hot spot) (arrow) of technetium.
COMMENT: On initial physical examination, this patient presented with signs and symptoms suggesting infection; thus
the bone scan was performed immediately after the initial radiographs were reviewed as normal. With such a clinical
presentation, when there is even a remote suspicion of infection, a bone scan should be obtained, even if initial radiographs appear normal. (Courtesy of David P. Thomas, MD,
Melbourne, Australia.)
BONE SCAN: EARLY DETECTION OF OSTEOMYELITIS. A. Plain Film. Note that diffuse soft tissue swelling is evident over the tarsometatarsal junction. A few subtle bone erosions can be appreciated (arrows).
B and C. Bone Scan. Note the diffuse increase in uptake over the tarsometatarsal region (arrows). COMMENT: In this diabetic
patient, the bone scan was decisive in identifying an infection that could rapidly progress and place the limb at risk.
On bone scan, a second infective site was isolated in the shoulder.
Humerus. Note the large soft tissue swelling (arrows) representing an early radiographic sign of osteomyelitis in this
pediatric patient. Observe also the lifting of the periosteum as a result of the infectious process, creating a solid-type
periosteal reaction (arrowhead).
A. AP Tibia. Note the grossly destructive osteolytic lesion in the diametaphyseal area of the distal tibia. B. Lateral Tibia. Observe the lytic destructive lesion on the anterior surface of the tibia, associated with a large, lobulated soft tissue mass (arrows).
COMMENT: Marjolin’s ulcer represents the complication of a squamous cell carcinoma developing within the ulcerative channel of the draining sinus (cloaca).This is found only in chronic osteomyelitis and is a rare complication. A 20- to 30-year latent period is typical from the onset of osteomyelitis
to the development of neoplasm.
Circumferential thickening of cortex with Charecteristic absence of destructive foci
Displacement of capsular and obturator fat planes (solid arrows).
Obliteration of iliopsoas fat plane(arrowhead) and metaphyseal focus of infection(open arrow)
A. Initial Film. Note that radiographic examination of
the hip joint reveals a lytic destructive lesion in the lateral
margin of the cortex of the acetabular surface (arrow).
There is a subtle suggestion of early symmetric loss of the
joint space. Of incidental notation is a benign bone cyst
(arrowhead) present in the supra-acetabular area. B. 1-Month
Follow-Up. Observe the nearly complete obliteration of the
articular joint space, with extensive destruction of the cortical
margins surrounding the acetabular rim. C. 2-Month
Follow-Up. Note the severe resorption of the femoral head,
with lateral displacement of the femur from the acetabulum.
There is extensive disorganization of the bony structures
of the acetabulum and the femoral head. D. 3-Month
Follow-Up. Note the complete resorption of the femoral
head and destruction of the acetabulum. Persistent lateral
displacement of the femur from the acetabulum is noted.
Of incidental notation, observe the spotty loss of bone
density present in the visualized portion of the shaft of
the femur as the result of disuse osteoporosis (arrow).
COMMENT: This 25-year-old patient presented with localized
pain in the hip joint
well defined lytic lesion in medullary and cortical areas of metaphysis and diaphysis of humerus.Absent sclerosis although periosteitis can be seen.
Central (tibial) and eccentric(fibular) lytic lesions
A. PA Wrist. Note the ankylosis of all joint compartments.
B. Lateral Lumbar Spine. Note that at the L3–L4 level there
has been destruction of the vertebral endplates and intervertebral
disc (arrow). Note the small area of calcification within
a previous psoas abscess (arrowhead).
CONGENITAL SYPHILIS: SKELETAL INVOLVEMENT,
PHASE 1, METAPHYSITIS (RADIOLUCENT BANDS).A. Lower Extremity. Observe the extensive bilateral radiolucent metaphyseal bands (arrows) in both ends of the femora, tibiae, and fibulae. Of incidental notation is a baby identification anklet around the distal tibia and fibula ofone leg. B. Upper Extremity. Note the extensive radiolucent metaphyseal bands in the proximal humerus, radius, and ulna (arrows). COMMENT: The early lesions in phase 1 (metaphysitis) congenital syphilis are those of bilateral radiolucent metaphyseal bands, which may be broad and/or horizontal, occasionally mimicking the lucent bands in leukemia or metastatic disease of neuroblastoma. These bands often lead to metaphyseal irregularity, with fragmentation and infractions that
CONGENITAL SYPHILIS: WIMBERGER’S SIGN. Note the bilateral destruction at the medial margins of the tibial metaphyses (arrows). This is caused by metaphyseal foci of spirochetal infection and is diagnostic for congenital syphilis.
CONGENITAL SYPHILIS: SKELETAL INVOLVEMENT, PHASE 2, PERIOSTITIS. A. Upper Extremity. Observe the diffuse periosteal new bone formation about the distalhumeri bilaterally (arrows). B. Lower Extremity. Note the extensive amount of periosteal new bone formation about the femur and proximal tibia and fibula (arrows). Metaphyseal irregularity with lytic destruction is noted. The opposite lower extremity is not visualized, as a result of poor patient positioning because of the patient’s painful condition.
CONGENITAL SYPHILIS: SKELETAL INVOLVEMENT,
PHASE 3, OSTEITIS. Note the extensive destruction, with metaphyseal (arrows) and diaphyseal radiolucencies throughout the humerus, radius, and ulna. Observe the exuberant periosteal overgrowth, with expansile deformity of the bones of the upper extremity. COMMENT: Infants who have not received therapy or for whom therapy has proven ineffective may develop osteitis. Syphilitic granulation tissue may extend from the metaphysis to the diaphysis, creating an extension of the infectious focus. Reactive sclerosis often surrounds the osteolytic lesions, with associated periostitis of the long tubular bones. The most frequently involved bone
in this stage of the disease process is the tibia, creating the classic saber shin anterior bowing deformity.
ACQUIRED SYPHILIS: SKELETAL INVOLVEMENT.
A. Tibia and Fibula. B and C. Radius and Ulna. Observe the extensive proliferative periostitis in the distal tibia, fibula, radius, and ulna, which has created some thickening of both the inner and outer cortices of these bones. This type of periosteal new bone formation in acquired syphilis has been
referred to as a lace-like pattern.
ACQUIRED SYPHILIS: FRONTAL BONE INVOLVEMENT.
A and B. Skull. Observe the scalloped, large lytic lesions scattered throughout the frontal bone in this
patient with acquired skeletal syphilis. COMMENT: Skull involvement is somewhat rare in syphilis; however, when
it occurs, the frontal bone is the target site. Of incidental notation is the approximation of the anterior and posterior
clinoids of the sella turcica, creating a bridging appearance.
This is a normal variant.
MADURA FOOT.
A. Early Phase. Observe the osteolytic foci within the calcaneus and cuboid (arrows).
B. Late Involvement. Note the advanced destruction of the tarsus and metatarsus regions. Note the undulating surface
that at some locations has filiform bone spicules radiating away from the parent bone. These features are characteristic
of long-standing mycetoma.
LICKED CANDY STICK appearances associated with thickening and irregularity of soft tissues.