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  3. CLASSIFICATION of osteomyelitis Osteomyelitis is an infection in a bone 1) DURATION:- Acute, Subacute and Chronic Suppurative and Non-Suppurative 2) ORGANISM:- 3) HOST RESPONSE:- Pyogenic and Granulomatous
  4. • Acute osteomyelitis – present with bone infection of sudden onset associated with systemic illness . It develops rapidly over a period of 7-10 days. • It can be confirmed from blood culture or culture from specimen. • It is easier to treat and overall turns out better than chronic osteomyelitis.
  5. • Subacute osteomyelitis-insidious in onset , symptoms last for more than 2 weeks, no systemic symptoms . • Diagnosis of subacute osteomyelitis is difficult due to absence of obvious signs of local infection , absence of pyrexia and normal WBC counts. • Chronic osteomyelitis- infection had been present for more than 3 months
  6. CAUSATIVE ORGANISMS ⚫Staphylococcus aureus is responsible for more than 90% of all bone and joint infections. ⚫In immunosuppressed patients: H.influenza, Pneumococcus, Pseudomonas, Mycobacterium, Fungal & Gram-negative organisms are more commonly involved. ⚫In neonates: Group B streptococci is a common cause.
  7. INCIDENCE • Incidence in US population is 21.8/1lac/year • Incidence has reduced with the introduction of antibiotics • However, there has been an increased risk of osteomyelitis among Immunosuppressed patients, newborns, alcoholics and drug addicts.
  8. VASCULAR ANATOMY The blood flow through the metaphysis is slow and turbulent creating a natural environment for the proliferation of microbes • INFANTILE PATTERN: The metaphyseal and diaphyseal vessels penetrate the epiphyseal plate. Metaphyseal infections can thus pass to the epiphysis and then the joint. • CHILDHOOD PATTERN: No metaphyseal blood vessel penetrates the physis.The metaphysis is affected in hematogenous osteomyelitis with sparing of epiphysis and joints.
  9. • ADULT : Metaphyseal vessels penetrate the vanishing physis & anastomose with the vessels at the subarticular end of the bone. This explains increased incidence of septic arthritis secondary to osteomyelitis in adults.
  11. PATHOPHYSIOLOGY Four pathways of bone invasion:- 1) Hematogenous spread: Most common source of infection. 2) Spread from a contiguous source of infection: Cutaneous, Sinus and Dental infections are common sites. 3) Direct implantation of infection: Usually occurs as a result of direct penetrating injuries or puncture wounds. 4) Postoperative infection: Contamination of surgical sites.
  12. Implantationof organism in medullary tissue Vascularand cellular Response Increased intramedullarypressure Infarction of Bone Hyperemia Focal Osteolysis Penetration of inflammatory process through endosteum & Haversian canal Reaches the subperiosteal space PERIOSTITIS Loss of blood supply New bone formation Necrosis INVOLUCRUM SEQUESTRUM
  13. ⚫SEQUESTRUM: Dead bonewhich is denser than the surrounding bone resulting from the cortical & medullary infarcts. It is the hallmark of active infectious process. ⚫INVOLUCRUM: Periosteal new bonewhich is formed in an attempt to wall off the infective process. ⚫CLOACAE: are defects in the involucrum which allow the continued discharge (decompression) of inflammatory products from the bone. Most frequently associated with chronicosteomyelitis.
  14. CLINICAL FEATURES of ACUTE OSTEOMYELITIS ⚫AGE:- 2-12 years ⚫SEX:- Male predominance (3:1) ⚫Fever with chills, pain & swelling over the affected part and extensive loss of limb function. ⚫Pre-existing infection, most commonly skin, respiratory tract and genitourinary tract is seen in 50% cases. ⚫Femur is the m/c bone involved. Other common sites are tibia,humerus & radius. ⚫In adults pelvis and vertebrae are most commonly affected. In a person with DM bones of feet are affected, most commonly the calcaneum
  15. IMAGING MODALITIES • Bone scan and MRI are most sensitive modalities for detection of osteomyelitis however conventional radiology should always be the first imaging modality to start with as it provides overview of the anatomy and pathologic conditions of the bone and soft tissues of the region of the interest. • Sonography is the most useful in the diagnosis of fluid collections, periosteal involvement and surrounding soft tissue abnormalities.
  16. 1) PLAIN RADIOGRAPHS:  No plain film changes are seen in the early phase of osteomyelitis.  Only 5% of radiographs are positive in the early course of the disease.  Most accurate means for early detection is a nuclear bone scan.  The radiological latent period on a plain film is upto 10 days for extremities and 21 days for spinal lesions.  The plain film radiographic diagnosis is made on the basis of abnormalities of soft tissue and bone.
  17. SOFT TISSUE ALTERATIONS: ⚫Earliest radiographic signs involve the soft tissues rather than the bone ⚫Seen within 3 days of bacterial contamination of bone ⚫Swelling of thedeep soft tissues usually around the metaphysis may be the earliestsign. ⚫Elevation and displacement of fat planes. ⚫Obliteration of fat planes. ⚫Increased density. ⚫Draining sinus.
  18. OSSEOUS ALTERATIONS ⚫BONE DESTRUCTION: Early lesion is that of a moth-eaten or permeative destructive pattern usually affecting the metaphysis. Bone sequestrum formation appears 3-6 weeks after the initial onset of symptoms. The necrotic fragments retain their original radiographic density. As a result, they appear more SCLEROTIC RELATIVE TO THE ADJACENT OSTEOPENIC BONE. Large involucrum may be seen which is composed of more rapidly formed woven bone & is therefore LESS DENSE RADIOGRAPHICALLY.
  19. ⚫PERIOSTEAL RESPONSE:  Periosteal new bone formation may beof the following types- 1) Solid 2)Laminated or lamellar pattern 3)Codman’s triangle  A soft tissue component, subperiosteal abscess and dense involucrum are more striking in infants than in adults.
  23. 2) ULTRASONOGRAPHY: 1) Deep soft tissue swelling- earliest sign. • Periosteal elevation- seen as a hyperechoic line • Subperiosteal fluid collection. • Cortical breech- seen as a focal defect in the cortex. • Joint effusion • Abscess or sinus tract formation in soft tissues which are characteristic of acute osteomyelitis.
  24. Osteomyelitis of tibia showing soft tissue swelling with collection
  25. 3) RADIONUCLIDE IMAGING: • Most sensitive investigation fordetecting early destructive activity . Howeverspecificity is low. • 99mTc-MDP, 99mTc-HMDP and Gallium 67 citrate are the m/c used radionuclide agents. • Indium 111 labelled WBC are more sensitive & specific. • Theaccretion of radionuclide in bone is related to the blood flow and local bone turnover. • On triple phase scans, it shows increased uptake of “hot spots” on all phases. • False-positive results are seen in degenerative disease, healing fracture, soft tissue infection and loose prosthesis.
  26. • Gallium scan may reveal abnormal accumulation of radiotracer in patients who has active osteomyelitis where Tc scan showed decreased activity or cold lesions • Gallium accumulation seems to correlate more accurately with activity of osteomyelitis than Tc uptake. • Disadvantage of Gallium can’t distinguish bone and soft tissue uptake clearly.
  27. Three Phase/Triphasic Bone Scan The first phase /nuclear angiogram/ flow phase. • Serial scans are taken during the first 2 to 5 seconds after injection of the Technetium-99m-MDP. This phase typically shows perfusion to a lesion. • Cellulitis shows uptake more in phase 1 and phase 2 scan, but not in phase 3. • Pathology that is more moderate to severe will show more uptake in the first two phases. • Pathology that is chronic or partially treated will be more pronounced in the third phase of a triphasic scan.
  28. The second phase/ blood pool phase • Obtained 5 minutes after injection. This shows the relative vascularity to the area. • Areas with moderate to severe inflammation have dilated capillaries, which is where the blood flow is stagnant and the radioisotope can "pool". • This phase shows areas of intense or acute inflammation more definitively compared with the third phase.
  29. The third phase, delayed phase • Obtained 3 hours after the injection, when the majority of the radioisotope has been metabolized. • This phase best shows the amount of bone turnover associated with a lesion.
  30. ⦿Gallium concentrates avidly at the site of infection following local accumulation of leucocytes and proteins that are labelled in vivo. ⦿ The radiation dose is higher and the image quality poorer.
  31. 4) COMPUTED TOMOGRAPHY: ⚫ Early detection of bonychanges ⚫Bettervisualization of axial skeletal involvement ⚫Betterdelineation of periosteal reaction and sequestra. ⚫ Sequestra are shown as areas of dense or high attenuation spicules of bone in areas of osteolysis. ⚫Cloacae, periostitis and soft tissue masses are shown. These may enhancewith ivcontrast.
  33. Figure 8–8 This 13-year-old boy presented with fever, leukocytosis, and severe left hip pain. (A) A T1-weighted coronal MR image of the pelvis demonstrates decreased signal in the bone marrow of the left femoral neck. (B) A T2-weighted image demonstrates a left hip joint effusion and increased signal (edema) within the left femoral neck. This represented a combination of septic arthritis and osteomyelitis.
  34. COMPLICATIONS  LOCAL COMPLICATIONS: 1) Chronic Osteomyelitis- most common 2) Acute pyogenic arthritis 3) Pathological fracture 4) Growth-plate disturbances- lengthening, shortening and deformity of limb.  SYSTEMIC COMPLICATIONS: Septicemiaand metastatic abscess.
  35. CHRONIC OSTEOMYELITIS ⚫FACTORS RESPONSIBLE FOR CHRONICITY- 1) General factors: nutritional status, vascular disease, DM 2) Local factors: foreign body, sinus 3) Virulence of organism 4) Treatment: delayed, inadequate, inappropriate or non-compliance to treatment 5) Risk factors- prosthesis, penetrating trauma
  36. ⚫C/F:- chronic discharging sinus is m/c presenting symptom, minimal pain, low grade fever, tenderness ⚫Tibia is most commonly involved ⚫May be associated with SAPHO syndrome ⚫RADIOLOGICAL EXAMINATION- 1) Increased density ( sclerosis) of bone 2) Thickening and irregularity of bone 3) Periosteal new bone 4) Areas of destruction 5) Dense sequestra
  37. ⚫ COMPLICATIONS:- 1) Acute exacerbations 2) Pathological fracture 3) Growth disturbances 4) Joint stiffness 5) MARJOLIN’S ULCER: squamous cell carcinoma within a cloaca usually 10-25 years later & painless. 6) Amyloidosis 7) SAPHO SYNDROME : Synovitis, acne, pustulosis , hyperostosis and osteitis.
  38. BRODIE’S ABSCESS • Defined as a localized form of suppurative osteomyelitis. • C/F:- localized nocturnal limb pain, & relieved byaspirin. • Staph. aureus is the m/c bacterial agent. • Metaphysisof tubular bones. • Distal tibia is m/c site. Othersare proximal tibia, distal femur, fibula & distal radius.
  39. RADIOGRAPHIC FEATURES: A well circumscribed area of bonedestruction with a surrounding zone of reactive sclerosis (Doughnut Rim) • Usually > 1 cm • A metaphyseal serpinginous tractwith sclerotic border marks the tractof infection.
  40. BRODIE ‘S ABSCESS OSTEOID OSTEOMA Radiolucency >1cm. Radiolucent nidus <1 cm and may have a target centre of calcification. Enhances on only delayed isotope scan. Enhances centrally both on blood pool and delayed scan due to central vascularity. MRI: The necrotic tissue does not enhance. Penumbra sign is seen MRI : The central vascular material will have a brighter signal and enhancement. ARTERIOGRAM: Vascular Blush in the radiolucent nidus confirms diagnosis.
  41. GARRE’S SCLEROSING OSTEOMYELITIS • Chronic, low-grade, diffuse, non-purulent osteomyelitischaracterized by the striking absence of visible pathogens on tissue culture. • Only in children and young adults
  42. • Found in the long tubular bones with fusiform thickening of the bone. • Lesion is cortical with significant periostitis & reactive new bone formation. • No bonedestruction or sequestrum is noted.
  43. SUPPURATIVE SPONDYLITIS ⚫Affected only in 2-4% of thecases of osteomyelitis. ⚫M/c involves the lumbar vertebrae>thoracic ⚫In ivdrug abusers, Cervical spine is involved ⚫C/F- backache(m/c), decreased motion, local tenderness.
  44. ⚫Routeof infection:
  45. ⚫The age of the patient determines the location and rate of spread and thus the radiological features. ⚫<20 years: vascular channels to the disc exist and disc infection occurs before vertebral disease. ⚫Decrease in disc height, paraspinal edema. ⚫Eventually vertebral end plate destruction occurs creating patchy areas of osteolysis throughout the vertebral body.
  46. ⚫ADULTS: initial focus occurs at anterior vertebral endplate-radiolucent & irregular lesion. ⚫As the adult disc is avascular, the organisms lodge adjacent to the subchondral plates and involve the disc secondarily. ⚫Vertebral destruction & collapse occurs, with soft-tissue paraspinal swelling. ⚫Intradiscal gas may be seen on CT in clostridia, brucellosis, tuberculosis & streptococcal infection.
  47. • Soft tissue swelling-  In cervical spine infections: Widening of the retropharyngeal & retrotracheal spaces.  In thoracic spine- Displacement of paraspinal lines  In lumbar spine- Paravertebral or psoas abscess • Epidural abscess may occur. • Osseous ankylosis may occur as a late sequelae
  48. ⚫BRUCELLA SPONDYLITIS: Lumbar vertebra m/c 1. Diminished disc height 2. Loss of vertebral endplate 3. Anterior disco-vertebral erosions 4. Anterior osteophytes 5. Intradiscal gas
  49. • SI JOINT INFECTION Less common Ivdrug abusers Loss of articularcortex Erosions of subchondral bone Reactive sclerosis
  50. CHILDHOOD INFLAMATORY DISCITIS ⦿Is a distinct entity from osteomylelitis of the spine. ⦿Occurs from 1-16 yrs of age. ⦿Clinical presentation is similar to acute osteomyelitis but less severe. ⦿Xray: latent period of 3-4 weeks. ⦿Disc space narrowing , fragmentation and destruction of adjacent subchondral endplate.
  51. ⚫Reactive end plate sclerosis occursas disease progresses. ⚫Posteriorelements are spared. ⚫A mild spinal flexion deformity mayoccur ⚫MRI is the most sensitive technique. Cortical destruction is seen on T1. Disc & marrow inflammation is seen on T1,T2 and STIR sequences.
  52. SEPTIC ARTHRITIS • More common in children, Male predominance ⚫Monoarticular involvement- knee (50%), hip and ankle are most common sites of involvement ⚫Staph aureus is the commonest causative organism ⚫Others are:- gonococcus, H.influenza, E. coli, pneumococcus, salmonella, brucella.
  54. CLINICAL FEATURES: • High grade feverand malaise • Erythema, swelling and pain overaffected joint • Altered gait- if weight bearing jointsare involved • Restricted rangeof movements • LAB INVESTIGATIONS- raised ESR, leucocytosis, positive blood or joint fluid cultures
  55. RADIOLOGIC FEATURES: ⚫PLAIN RADIOGRAPH:- Soft tissuealterations- 1) Displacementof juxta-articular fat-early sign 2)Waldenstrom’s sign- in arthritis of hip joint 3)Rapid narrowing of joint space followed by complete loss within few weeks Osseousalterations- 1) Earliestsign is loss of normal subchondral cortical bone 2)Moth eaten destructive pattern in metaphysis 3)Laminated periosteal response 4)Completeankylosisof joint in laterstages.
  57. ⦿WALDENSTROM’S SIGN: Measurement from inferiorand medial surface of acetabulum (Kohlers teardrop) to the medial margin femoral head is taken. A measurement of >11 mm ora differenceof >2 mm compared with opposite hip is a positive sign.
  58. COMPLICATIONS:- 1) Deformity and stiffness 2) Pathological dislocation 3) Secondary osteoarthritis
  59. TOM SMITH’S ARTHRITIS • Septic arthritis of hip seen in infants. • Osteomyelitis can rupture the metaphyseal cortex enter the articulation and spread via the synovial fluid to the epiphysis and subarticular bone. • D/D- DDH.
  60. • Bones that have metaphysis within the adjacent joint capsule are predisposed to rapid development of septic arthiritis • Head of femur is completely destroyed by the pyogenic process. • C/F- unstable gait, affected leg is shorter & hip movements are increased in all directions.
  62. TUBERCULOSIS OF BONES ⚫ Radiographic changes are seen at presentation. ⚫ Accounts for 3% of all cases of extrapulmonary TB ⚫ Targets the hips, knees, spine ⚫ Spinal tuberculosis is most common, accounts for 50% all skeletal TB cases ⚫ Metaphysis is commonly involved,when long bones are involved. ⚫ There is no surrounding zone of sclerosis. ⚫ Sequestra are small and absorbed by granulation tissue. ⚫ Periosteal reaction is not a prominent feature.
  63. TUBERCULAR ARTHRITIS • COMMON SITES: Hip and knee joints. Early features: • Joint widening secondary to effusion. • Soft tissue swelling. • Marginal erosions. • Destruction of cortical white line. Tuberculous arthritis of the knee joint. Frontal radiograph demonstrates periarticular osteopenia (black arrow), peripheral osseous erosions (white arrow), and relative preservation of the joint space. A triad of radiologic abnormalities (Phemister triad) consisting of periarticular osteoporosis, peripherally located osseous erosion, and gradual diminution of the joint space suggests the diagnosis of tuberculosis
  64.  LATE FEATURES: Symmetrical narrowing of joint space.  Moth eaten osteolytic bone destruction.  Juxta articular osteoporosis  End stage is fibrous ankylosis of the joint.
  66. 1) Slow , insidious onset. 2) Severe Juxta articular osteoporosis 3) Slow and asymmetrical Joint Space narrowing 4) Bony sclerosis uncommon. 5) End Stage—fibrous ankylosis. Pyogenic 1) Acute presentation 2) Juxta articular osteoporosis less severe 3) Early joint Space narrowing 4) Bony sclerosis common 5) Bony ankylosis. 70 Tuberculous
  67. UNUSUAL PRESENTATIONS OF TUBERCULOSIS • CARRIES SICCA: Tubercular destruction of the humeral head with multiple erosive defects. • CYSTIC TUBERCULOSIS: Multiple, symmetric, well defined lytic lesions of the appendicular skeleton. • POTTS PUFFY TUMOR: A tubercular calvarial lesion forming a button sequestrum and fluctuant cold abscess on the scalp. • WEAVER’S BOTTOM: Tubercular involvement of the subgluteal bursae allowing direct extension to the ischial tuberosity.
  68.  TUBERCULOUS DACTYLITIS: Tubercular destruction of the tubular bones of the hand and feet with soft tissue swelling, bone expansion and thinning of cortex. Also known as spina ventosa.
  69. TUBERCULAR SPONDYLITIS ⦿Spine is the most frequent site of skeletal TB. ⦿Radiological latent period 21 days. ⦿Most common site: lower thoracic and upper lumbar vertebrae.  GENERAL: Insidious onset with constitutional symptoms like low grade fever, anorexia, weight loss and night sweats.  LOCAL:Back pain, tenderness, paraplegia or paraparesis, and kyphotic or scoliotic deformities
  70. Risk factors of spinal infections  Advanced age > 50  Intravenous drug abuse  Immunosuppression or immune deficiency  Long-term steroid administration  Diabetes mellitus  Organ transplantation  Malnutrition  Malignancy  HIV infection  Previous TB infection
  71. Types of spinal involvement 1. Paradiscal 2. Central 3.Anterior Atypical : – Neural arch involvement only – Spinal canal granulomas without bony involvement  Involvement of posterior elements is rare
  72. ⚫ In the more common paradiscal type ⚫ Infection begins in the metaphyseal areas ⚫ Bone softensgets compressed ⚫ anterior wedging or total collapse ⚫ Spreads under the anterior longitudinal ligament to involve adjacent Vertebra Total collapse
  73.  Approx. 75% of infected individuals develop a soft tissue infection ⚫ PARA VERTEBRAL ABSCESS CERVICAL : Retropharyngeal THORACIC : Paravertebral & along ribs LUMBAR : Psoas abscess ⚫ Commonly occurs in the psoas muscle “ cold abscess ”Known as cold abscess because forms slowly and does not normally present with heat, inflammation or pain. ⚫ Paraspinal fistula which may form a communication with the chest wall or pelvic floor ⚫ Left untreated, degeneration and inflammation of the vertebrae causes Herniation into the cord space cord compression and cauda equina(NEUROLOGICAL COMPLICATION ,more in thoracic (narrowest canal) ⚫ Kyphosis gibbous (severe kyphosis) ⚫ Paraplegia
  74. FEATURES OF POTT’S SPINE ON RADIOGRAPH EARLY FEATURES: ⦿ lytic destruction at the anterior subchondral endplate ⦿ Loss of disc height ⦿ Paraspinal swelling LATE FEATURES: ⦿ Vertebral body collapse. ⦿ Obliteration of the disc. ⦿ Gibbus formation. ⦿ Biomechanical stress on the uninvolved vertebral body caudal to the gibbus leads to increase in height : width ratio known as LONG VERTEBRA.
  75. Atypical features – Involvement of only one vertebral body –Involvement of several vertebral bodies without intervertebral discitis – Bowing of rib cage secondary to collapse of multiple vertebral bodies – Destruction of lateral or posterior aspects of vertebral bodies
  77. Paraspinal abscess
  78. COMPUTED TOMOGRAPHY ⚫ Demonstrates bone destruction/erosions when x- ray may be normal ⚫ Helps in better anatomic localisation ⚫ Soft tissue findings ‐ Abscess with calcification is diagnostic of spinal TB; CT is excellent modality to visualize soft tissue calcifications ⚫ Evaluates areas such as C-V junction, cervico-dorsal, sacrum providing guidance for biopsy
  79. • On contrast CT • strong rim enhancement around low attenuation collection – “Rind sign”
  80. CT morphology Four patterns of bony destruction is noted:- 1) Fragmentary (most characteristic and most common) 2) Osteolytic. 3) Subperiosteal. 4) Well-defined lytic with sclerotic margins
  81.  CT also demonstrates: ⚫Disc space narrowing ⚫Multilevel involvement ⚫Kyphosis
  82. MRI  Is the imaging modality of choice  Demonstrates early bone marrow involvement/edema , spinal canal and neural involvement  Soft tissue and intraosseous abscess are well demonstrated, but poorly visualizes calcification in abscesses
  83.  T1WI : shows a decreased signal within the affected vertebral marrow along with loss of disc height  Cortical definition of Vertebra is lost  Disc space narrowing is also seen but limited to degree of bone destruction  T2WI : shows an increase in signal intensity within the involved Vertebra and disc
  84.  Enhanced MR studies: show inhomogenous enhancement in the region of marrow infiltration
  85. Sagittal T2W (Images 1-3)and axial T1W (Image 4) High intensity activity in T12 to L3 vertebrae indicative of infection (*) (*). Complete destruction of vertebral bodies with osseous retropulsion into the spinal canal, causing cauda equina (*). On axial view, note destruction of vertebral body with loss of circular shape(*). MRI …
  87. ⚫ Paraspinal soft tissue masses ( seen in 71% of cases) ⚫ T1WI : ⚫ Loss of uniform signal intensity ⚫ Enlargement of affected muscle alteration of paraspinal soft tissue ⚫ T2WI : ⚫ hyperintense ⚫ Post–contrast : ⚫ Thick rim enhancement around intraosseous and paraspinal soft tissue abscess ⚫ Also delineate communication between vertebral and paravertebral components
  88. CORD CHANGES  Plain x-ray or CT: little information  Cord involved by compression or direct extension of disease  MRI : – shows cord edema or myelomalacia in cord as hyperintense signal on T2WI  Indicate irreversible neurological damage
  89. MRI : ⚫Post treatment follow up can be done ideally ⚫progressive increase in signal intensity on T1WI correlates well with resolving symptoms ⚫Reduction in gadolinium enhancement is useful sign of healing ⚫However, increase in soft tissue mass , bone destruction do not indicate failed treatment
  90. NUCLEAR MEDICINE SCINTIGRAPHY ⚫Is economical ,highly sensitive but non- specific ⚫Uptake is increased in osseous tuberculosis ⚫Reveals multiple sites in disseminated disease ⚫Have reported many false-negative bone scans ⚫Seen in disseminated TB, cervical spine regions and neural arch lesions ⚫Limits the use of scintigraphy
  91. Differential diagnosis 1. Pyogenic infection : – Often difficult – Sudden onset with swinging temperature – Rapid bone destruction and rapid disc involvement – Replaced by pronounced new bone formation and sclerosis – However,calcification indicates TB
  92. 2. Degenerative Spondylosis : Clinical findings allow differentiation Disc space is usually not markedly narrowed T2WI : disc dessication is seen as low signal intensity 3.Brucella Spondylitis : H/O undulent fever Lower lumbar vertebra are characterstically involved Erosion of anterior upper or lower margins Step like deformity or rounding-off the corner Extensive sclerosis
  93. 4.Metastatic Deposits : – Collapse of diseased vertebrae but disc remains unaffected – Involvement of other bones and destruction of pedicles suggest metastasis • Other D/D : – Multiple myeloma , chordoma – Primary bone tumors – Lymphomas , sarcoidosis – Bizzare infections :fungal, syphilitic ,
  94. Features:- Tubercular Pyogenic Onset of symptoms Insidious Acute Site of predilection Dorsolumbar Lower lumbar Multifocal involvement common Not common Vertebral body destruction Extensive focal Posterior element May be involved Spared 99 Tubercular spondylitis Vs Pyogenic spondylitis
  95. Features:- Tubercular Pyogenic Disc destruction late early Paraspinal mass large small Calcification in paraspinal mass yes NO Enhancement of paraspinal mass peripheral patchy Spinal deformity common Uncommon Bone sclerosis Absent present 100
  97. MADUROMYCOSIS • Chronic granulomatous fungal disease affecting the feet. • Caused by Nocardia madurae, Nocardia brasiliensis. • Localized swelling , purulentdischarge from sinus tracts. • Osseous lesionsoccur as a direct extension from the soft tissues.
  98. • Tarso-metatarsal region is most commonly affected. • Widespread lytic destructive lesions with filiform or undulating deformity. • Fistula formation is common. • Periosteal reaction is minimal. • Sequestrum is characteristically absent.
  99. ⚫In advanced cases, nearlyall bones of the footare involved. ⚫Diffuse intraarticular ankylosis occurs as sequela. ⚫MRI FINDINGS: Generalized low signal intensity of the matrix with lesions of high signal intensity interspersed throughout. ⚫Within these high signal intensity lesions, a low intensity focus can be identified known as DOT IN CIRCLE SIGN. ⚫This sign is highly specific for mycetomaof the foot.
  100. ACTINOMYCOSIS ⚫It is an unusual suppurativebacterial infection. Infective agents- Actinomyces israelii and bovis ⚫2 types- cervicofacial type (m/c) and chest & abdominal varieties ⚫The mandible is the most commonly involved. ⚫Thecharacteristic feature is a lytic destructive lesion at the angle of the mandible with little or no periosteal reaction. ⚫Abscess formation and draining sinuses are associated with mandibular lesions. ⚫Other bones involved are ribs, spineand pelvis.
  101. Osteolytic lesion with periosteal reaction of posterior body and ramus of mandible with the soft tissue infiltrative changes in skin , messator muscle and parotid gland
  102. COCCIDIOIDOMYCOSIS ⚫Caused by Coccidioides immitis ⚫Skeletal involvement is secondary to respiratory infection ⚫Mimics tuberculosis ⚫Bone involvementoccurs in 20% of cases. ⚫Spine, pelvis, ribs and bony prominences such as tibial tuberosity, malleoli, trochanters, acromion, patella & olecranon are involved. ⚫Nocharacteristic radiological criteria. ⚫Bone lesions resemble theappearances of acute and chronicosteomyelitis.
  103. • SPINAL COCCIDIOIDOMYCOSIS: Thoracicand lumbarvertebra Lucent lesions in vertebral body, pedicles & lamina Sparing of discspaces CONTIGUOUS RIB INVOLVEMENT is characteristic Paraspinal mass (abscess formation)
  105. CONGENITAL SYPHILIS ⦿ PHASE1:METAPHYSITIS:P resent at birth or shortly thereafter. ⦿ Spirochaetes are lodged beneath the fetal growth plates producing a metaphysitis.Bone formation in the zone of ossification is decreased creating radiolucent metaphyseal bands
  106. ⦿ These bands lead to metaphyseal irregularity with fragmentation and infarctions referred as sawtoothed appearance. ⦿ WIMBERGERS SIGN:B/L erosive defects on the medial margin of the proximal tibia.
  107. • Phase1 lesions heal without therapywithin 2weeks. • PHASE2:PERIOSTITIS:The periosteum is infiltrated with syphilic granulation tissue creating a diffuse,symemetrical,solid or laminated reaction affecting all long bones.
  108. • PHASE3:OSTEITIS:Infantswho have not received therapycan developosteitis. • Syphylitic granulation tissue can extend from the metaphysis to the diaphysis creating osteolytic lesions surrounded with reactive sclerosis.
  109. ⦿ Anterior bowing of the tibia with Extensive periosteitisand cotical overgrowth givean undulating dense contourto the long bones (SABER SHIN). ⦿ osteolyticdefects can also be seen (GUMMATA).
  110. ADDITIONAL FEATURES • CLUTTON’S JOINTS: B/L painless synovitis of jointsespecially the knee joints. • HUTCHISON’S TEETH : Deformityof the teeth creating peg shaped , hypoplasticand notched teeth.
  111. ACQUIRED SYPHILIS • Fewer than 10% of the patients develop osseous lesions. • Skeletal manifestations are seen in tertiary syphilis • Superficial part of the skeleton which are the skull, tibia and clavicles are usually involved. • There is diffuse proliferative periostitis leading to diffuse thickening of the inner and outer cortices.This periosteal reaction is known as lace like pattern. • Pseudobowing of tibia mayoccur. • Syphilitic osteomyelitis may be localised(gumma) or diffuse(gummatous osteitis). There is sclerosis with irregularity of bone trabeculation.
  112. LEPROSY ⦿ OSTEITIS LEPROSA: Granulomas cause focal cortical and medullary destruction.Small cysts are seen known as OSTEITIS MULTIPLEX CYSTICA LEPROSA. ⦿ Bone loss may occur both longitudinally and circumferentially. • This gives rise toa ‘ LICKED CANDY STICK’ appearance. • Diffuse non specific osteoporosis. • Featuresof superimposed pyogenic osteomyelitis. • Nervecalcification.