The document discusses bone infections and tumors. It begins by describing bone anatomy, blood supply, and embryology. It then covers osteomyelitis (bone infection), including classification, epidemiology, risk factors, pathogenesis, microbiology, clinical features, diagnosis, treatment, and complications. It also discusses bone tumors, including classification by tissue type and site. Specific bone tumors discussed include aneurysmal bone cyst and bone metastasis.

1. Bone Infections & Tumors

2. ANATOMY OF THE BONE
• Two epiphyses, diaphysis( intermediate portion)
• Metaphysis( adjoins the epiphysis), epiphyseal plate( growth cartilage
separating the epiphysis from the metaphysis)
• At maturity epiphyseal plate is replaced by bone
• Articular ends of epiphyses are covered with articular cartilage and
the rest of the bone is covered by periosteum
• Microscopic bone classification; woven or lamellar
• Bone cells; osteoblasts, osteocytes, osteoclasts

3. ANATOMY OF THE BONE

4. BLOOD SUPPLY
• Nutrient artery; supply the inner two thirds of the bone
Enters the bone around its middle and divides into 2 branches
• Periosteal vessels; they supply the outer third of the cortex of the
adult bone
• Metaphyseal and epiphyseal vessels; supply the ends of the bone

5. EMBRYOLOGY OF THE BONE
• All long bones with the exception of the clavicle develop from
cartilaginous primordia( enchondral ossification)
• This type of ossification commences in the middle of the shaft(
primary center of ossification) before birth
• The secondary ossification centres( the epiphyses) appear at the ends
of the bone mostly after birth
• The bone grows in length by a continuous growth at the epiphyseal
plate
• The increase in girth of the bone is by subperiosteal new bone
deposition
• At the end of the growth period the epiphysis fuses with the
diaphysis and growth stops
• Fusion of epiphysis has clinical relevance in deciding bone age

6. OSTEOMYELITIS
• Osteomyelitis is an infection involving bone
• It may be classified based on the mechanism of infection (
hematogenous vs nonhematogenous) and the duration of illness ( acute
vs chronic)

7. CLASSIFICATION ( by Lew and Waldvogel)
• Nonhematogenous osteomyelitis-It can occur as a result of
contiguous spread of infection to bone from adjacent soft tissues and
joints or via direct inoculation of infection into the bone eg as a result
of trauma, bite wounds or surgery
• Hematogenous osteomyelitis- is caused by microorganisms that seed
the bone in the setting of bacteremia
• Acute osteomyelitis- presents within few days or weeks and
sequestra are absent
• Chronic osteomyelitis- longstanding infection over months or years
and sequestra is present

8. EPIDEMIOLOGY
• In Uganda, osteomyelitis was diagnosed in 325(3.5%) of the surgical
operations
• In 32% of these operations the patients were children aged btn 10 to
14yrs
• The tibia was the most frequently involved(31%)
• These findings suggest that osteomyelitis disproportionately affects
the young
• Nonhematogenous osteomyelitis in young adults (occurs in the
setting of trauma and surgery) and adults as a result of contiguous
spread of infection to bone from adjacent soft tissue (diabetic foot)
• Hematogenous osteomyelitis occurs mostly in children, in adults
(vertebral osteomyelitis) , more in males, > 50yrs except in injection
drug users (<40yrs)

9. RISK FACTORS
• Poorly healing soft tissue wounds
• Presence of orthopedic hardware
• Diabetes
• Peripheral vascular disease
• Peripheral neuropathy
• Endocarditis
• Presence of indwelling intravascular devices
• Injection drug use
• Hemodialysis
• SCD

10. PATHOGENESIS
• Normal bone is highly resistant to infection
• Osteomyelitis develops when there is a large inoculation of
organisms, presence of bone damage or presence of hardware or
other foreign material
• Important factors virulence of the infecting organisms, the host
immune status and the bone vascularity
• Bacterial adherence- mediated by expression of specific adhesins to
the bone matrix
• Resistance to host defense- persistence of intracellular pathogens
within osteoblasts
• Proteolytic activity

11. pathogenesis
•Organisms reach the bone through the blood
stream from a septic focus elsewhere in the body,
they enter into the bone through the nutrient
artery and finally settle in the metaphyseal region.
•After settling the organisms induce an acute
inflammatory reaction characterized by edema with
inflammatory exudate and pus formation
•The infection may resolve spontaneously because of
good body immunity or Rx

12. • If no intervention is done, pus builds up and may spread
downwards along the length of medulla through
harversian and Volkmann canal causing venous and
arterial thrombosis which results into a wide spread
destruction of bone
• As pus tracks through the canals it goes towards the
surface to lie under the periosteum and forms a sub
periosteal abscess with periosteal stripping from the
bony surface which further compromise the blood
supply to the bone,
• later the abscess may burst into the soft tissues and
eventually reach the surface to form a sinus

13. Ctn….
• The ischemic bone dies and eventually separates from the living bone
as a sequestrum
• New bone is laid down beneath the stripped up periosteum forming
an investing layer known as involucrum
• Infection process rarely crosses the growth plate as it contains no
blood vessels and the periosteum is firmly attached to the plate

14. image

15. MICROBIOLOGY
• Staphylococcus aureus
• Coagulase negative staphylococci
• Aerobic gram negative bacilli
• Corynebacteria
• Fungi eg candida spp
• Mycobacteria
• P aeruginosa – injection drug users
• Serratia marcescens – immunocompromised patients

16. MICROBIOLOGY

17. CLINICAL FEATURES
• acute -Dull Pain at the involved site
• o/e – warmth, erythema, swelling, fever, rigors
• Sinus tract is pathognomic of chronic osteomyelitis
• Chronic –deep or extensive ulcers that fail to heal after several wks
• Others –sequestrum, involucrum (reactive bony encasement of the
sequestrum) , local bone loss
• Subacute osteomyelitis- Brodie abcess ( cavity filled with suppurative
or granulation in a long bone metaphysis surrounded by dense
fibrous tissue and sclerotic bone)

18. ..

19. DIAGNOSIS
1.Clinical
• New or worsening musculoskeletal pain
• Cellulitis overlying previously implanted orthopedic hardware
• Traumatic injuries( bite and puncture wound)
2.Laboratory studies;
• CBC- (leukocytosis, thrombocytosis)
• Biomarkers- raised CRP/ESR
• Cultures- blood and bone biopsy( GS and culture, histopathology)
3.Imaging;
• X-ray
• Ultrasonography
• MRI, CT

20. Radiograph of osteomyelitis
• Plain film radiographs are often performed although have poor
accuracy for osteomyelitis; any visible signs tend to only be visible
from :
• Atleast 2weeks of clinical symptoms
• These include;
• Osteopenia and bone resorption
• Cortical loss
• Bony destruction
• Periosteal reaction
• Soft tissue findings; swelling, loss of fascial planes, ulceration and
soft tissue gas may be observed

21. ..

22. DIFFERENTIAL DIAGNOSIS
• Soft tissue infection
• Charcot arthropathy
• Osteonecrosis
• Gout
• Fracture
• Bursitis
• Bone tumor
• Sickle cell vaso- occlusive pain crisis
• SAPHO ( Synovitis, acne, pustulosis, hyperostosis, osteitis)

23. TREATMENT
• Nonhematogenous osteomyelitis involves;
Surgical debridement
Antimicrobial therapy
• Hematogenous osteomyelitis involves;
Parenteral antibiotics ( vancomycin and 3rd cephalosporin)
Surgical debridement in some cases
• Adjunctive agents; rifampin and fusidic acid

24. ANTIBIOTICS

25. General management principals
• Preoperatively
Patients assesment and clinical staging of the disease full discussion
of all treatment options with potential complications
Diagnostic test for general health
Optimisation of patients & Rx of commorbidities

26. operative
Exposure for multiple, deep bone sampling.
Excision of all non-viable tissue.
IV antibiotics after sampling
•Agents such as co-amoxiclav or ceftriaxone
•Vancomycin (MRSA) and meropenem
(pseudomonas species & other G-Negative
organism)
Bone stabilization
Dead space management
Soft tissue cover which may include plastic surgery

27. Functional rehabilitation.
Continued antimicrobial therapy guided by culture results, with
regular clinical monitoring

28. Acute osteomyelitis
• Its an acute pyogenic inflammation of all parts of the bone viz.
cortex, medulla and the periosteum
• Vertebral column is the commonest site in adults
• In children –long bones are most frequently affected, swelling of the
affected limb
• In young children fever and refusal to bear weight may be the only
clue.

29. Dx and mgx
• Early phase(2-3 days) radograph may be normal
• MRI shows bone oedema and periosteal elevation
• 5-7 days;plain radiographs may show subtle abnormality with
osteopenia and periosteal new bone formation
• ESR and CRP are often abnormal

30. management
• ABC 4-6 weeks (2wksiv then 4wks oral)
• Analgesics
• Rehydration
• Bed rest
• Surgical options-limb deterioration on Rx, or imaging with evidence
of disease progression

31. Chronic osteomyelitis
• 2 factors are responsible for the chronicity of the disease.
• Sequestrum which can’t be absorbed
• The intraosseus abscess which can not be absorbed because of its
rigid bony walls.

32. Clinical features
• Purulent discharge from a sinus over the affected bone
• Pain is predominant in some cases
• Discharge of pus may be continuous or intermittent & may contain
bone chips
Examination
Bone is palpably thickened & there are nearly always a number of
overlying scars or sinuses

33. image

34. investigation
• X-Rays
• Thickening and irregularity of the cortices
• Sequestrum ; seen as a dense loose fragment with irregular but
sharply demarcated edges lying within a cavity in the bone.

35. Complications of osteomyelitis
• Septic shock
• Metastatic infections
• Cellulitis, arthritis
• Bone deformities
• Pathological fractures
• Amputation
• Discharging sinuses
• Brodie’s abscess
• TB osteomyelitis-potts disease

36. management
• Cierny and Mader classification is used to define features of bone
infection and relate it with the patient’s general condition

37. CIERNY AND MADER CLASSIFICATION OF
BONE INFECTION AND ITS MANAGEMENT
STAGE 1 (MEDULLARY)
• Only cancellous bone is involved.
• Excision of the dead bone can be carried out by intramedullary reaming
or by windowing the cortex.
• The resulting defect may be filled with antibiotic-loaded cement beads
or absorbable pellets. Structural
• stability is rarely affected
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38. STAGE 2(SUPERFICIAL)
• Only the cortical bone is involved and this requires excision.
• It often follows skin ulceration and there may be large skin defects
which require complete excision and local or free muscle flaps.
• If more than one-third of the cortical circumference is excised,
splintage is essential, usually with external fixation to prevent
fracture.
• Secondary bone grafting may be needed.
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39. STAGE 3 (LOCALISED)
• There is a limited area of dead cortical bone with medullary infection.
• Radical excision is required, and filling the defect and providing soft-
tissue cover may be a challenge.
• Staged reconstruction may be necessary with cancellous bone
grafting
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40. STAGE 4(DIFUSE)
• Involves the entire circumference of the bone and surrounding soft
tissue
• All infected non-unions
• Resection must be segmental and stabilisation in an external fixator
will be required.
• Reconstruction will involve the introduction of new bone and
healthy soft tissue forexample the Ilizarov method.
• Antibiotic therapy for 6-12 weeks following surgery
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41. OTHER FORMS OF OSTEOMYELITIS
Diabetic foot
• Foot infection in diabetic patients has an annual incidence of foot
complications of 1–2% per year, due to the combined influence of
macro- and micro vascular insufficiency,
 mechanical disruption
 peripheral and autonomic neuropathy
 immune defects and impaired tissue healing.
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42. DIABETIC FOOT CONT..
• Ulceration most common on calcaneum and bones of fore foot most
especially great toe and first metatarsal head leading to osteomyelitis
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43. MANAGEMENT
•Etiological agents for diabetic foot infection are the
same as bone infection in non diabetic individual
•Empirical therapy with addition of metronidazole to
cover for anaerobes
•Surgical debridement
•Optimizing glycemic control
•Relieving pressure with appropriate foot wear
•Improving vascular supply
•amputation

44. MEGGITT’S CLASSIFICATION OF DIABETIC FOOT
Grade 0: Foot symptoms like pain, only
 Grade 1: Superficial ulcers
 Grade 2: Deep ulcers
 Grade 3: Ulcer with bone involvement
 Grade 4: Forefoot gangrene
 Grade 5: Full foot gangrene
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45. Brodie’s abscess
• There is a localized abscess within a bone or near a bone
• A deep boring pain (worsen at night) is the predominant symptom &
the common sites upper end of tibia & lower end of femur
• Rx is operative surgical evacuation and curettage is performed and
antibiotics cover given
• The residual cavity is filled with cancellous bone chips

47. Complications of osteomyelitis
• Septic shock
• Metastatic infections
• Cellulitis, arthritis
• Bone deformities
• Pathological fractures
• Amputation
• Discharging sinuses
• Brodie’s abscess
• TB osteomyelitis-potts disease

48. COMPLICATIONS
• Infectious complications
Sinus tract formation
Contiguous soft tissue infection
Abcess
Septic arthritis
Systemic infection
• Non infectious complications
Bony deformity
Bone fracture
Carcinoma
Sarcoma

49. BONE TUMORS
• Bone tumors can be divided
into primary and secondary (metastatic) tumors.
• Primary tumors arise from cells which constitute the bone and
can divided into benign and malignant types

50. Primary Bone Tumors
Bone-Forming tumors
• Osteoma
• Osteoid osteoma
• Osteoblastoma
• Osteosarcoma
Cartilage-Forming tumors
• Chondroma
(Enchondroma)
• Osteochondroma
• Chondrosarcoma
Miscellaneous tumors
− Ewing’s sarcoma
• Giant cell tumor of bone

51. CLASSIFICATION OF BONE TUMOURS BY SITE
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59. 7/25/2023 59

60. aneurysmal bone cyst
• It is a benign cystic lesion of bone consisting of blood-filled spaces
separated by fibrous septa.
• The lesion is more aggressive than a simple bone cyst and often
presents with pain and swelling.
• Plain radiographs commonly show aggressive features with eccentric
expansion of the cortex and an open physis
• Scans always show multiple fluid levels
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61. 7/25/2023 61

62. Sclerotic bone metastasis on plain film radiograph (arrows), secondary to
metastatic prostate cancer.

63. Primary Bone Tumours
• Primary bone tumors can be either benign or malignant;

64. Tissue Type Benign Malignant
Bone forming
Osteoid osteoma
Osteoblastoma
Osteosarcoma
Cartilage forming
Osteochondroma
Chondroblastoma
Chondrosarcoma
Fibrous tissue
Fibroma
Fibromatosis
Fibrosarcoma
Giant-cell tumours Benign osteoclastomas
Malignant
osteoclastoma
Marrow tumours
Ewing’s tumour
Myeloma

65. Risk Factors
• There are certain well documented risk factors for developing a
primary bone cancer:
• Genetic association
• RB1(familial retinoblastoma) and p53 (Li Fraumeni syndrome) are
associated with an increased risk of osteosarcomas
• Mutations to TSC1 andTSC2 mutation (tuberous sclerosis) are associated
with an increased risk of chordomas during childhood
• Previous exposure to radiation or alkylating agents in
chemotherapy
• Benign bone conditions, such as Paget’s disease and fibrous
dysplasia (both increase the risk of osteosarcoma)

66. Clinical Features
• The main symptom of a (primary) bone tumor is pain.
• This is typically not associated with movement and is worse at
night (often deemed a ‘red flag’ symptom).
• As the tumor enlarges, a mass may be palpable. If the patient
presents with a fracture without a history of trauma
(pathological fracture), a bone tumor may be suspected

67. Differential Diagnosis
• Patient presenting with ongoing bone pain can have a wide variety of
conditions, including;
1. osteomyelitis,
2. multiple myeloma,
3. metabolic bone disease (e.g. renal osteodystrophy),
4. pathological fracture.

68. Benign
a.) Osteoid Osteoma
• Osteoid osteomas arise from osteoblasts, often around
the second decade of life (10-20yrs), and are more common in
males. They are typically small tumours (<2cm), located usually
around the metaphysis of long bones (e.g. proximal femur or
tibia).
• They present with a localised progressive pain, worse at night,
and typically made better with NSAIDS. There may be
associated localised swelling, tenderness, or limping.
• Radiologically they show a small mass, comprised of a radiolucent
nidus with a rim of reactive bone.
• Most can be managed conservatively through serial radiological
imaging every 4-6 months, however those with severe pain may
warrant surgical resection.
• Overall they have a good prognosis, with most resolving
spontaneously

69. Osteoid osteoma at the lesser trochanter, on plain film radiograph and subsequent MRI
scan

71. osteodosteoma

72. Osteochondroma
• Osteochondromas (also known as exostoses) are benign bony
tumours, forming as an outgrowth from the metaphysis of long
bones covered with a cartilaginous cap.
• They develop most commonly in the second decade of life (10-
20yrs) and are more common in males.
• Most are detected incidentally, as usually
are asymptomatic and slow growing, although can cause
deformities or impinge on nerves if they grow large enough.
• On plain film radiograph, they show as a pedunculated bony
outgrowth from metaphysis pointing away from the joint.
• Most can be managed conservatively through serial radiological
imaging every 4-6 months, however those with significant
deformity or neurological symptoms may warrant surgical
resection.

73. Multiple osteochondromas as seen on plain film radiograph affecting the left knee

74. Chondroma
• Chondromas arise from chondroblasts within the medullary
cavity of the bones (termed enchondromas) or from the cortical
surface.
• They present in patients 20-50 years old, most commonly
affecting the long bones of the hands, femur, and humerus.
• Most are asymptomatic, however they can present as
a pathological fracture.
• On plain film radiograph, they appear as a well circumscribed
oval lucency with intact cortex.
• Chondromas should be managed depending upon
the size and clinical features.
• Most asymptomatic and small chondromas can be observed,
however large or symptomatic chondromas may require removal
with curettage and bone grafting.
• There is a small risk of transformation into
chondrosarcomas (malignant).

75. Giant Cell Tumours
• Giant cell tumours, also called osteoclastomas, arise from
the multinucleated giant cells and stromal cells.
• They occur in patients 20-30 years old, usually affecting
the epiphysis of long bones (most commonly the distal femur,
proximal tibia, and distal radius).
• Patients will typically present with pain, swelling, or a limitation
of joint movement.
• On plain film radiograph, giant cell tumours show an eccentric
lytic area, giving a “soap bubble” appearance.
• Surgical resection is the treatment of choice, potentially
requiring bone grafting or reconstruction.

76. Malignant
Osteosarcoma
• Osteosarcomas are the most common malignant primary bone
tumours.
• They have a bimodal age of onset, either at 13 to 16
years(coincide with adolescent growth spurt) or in those >65yrs
(typically in those with Paget’s disease), and most commonly
found at the metaphysis of the distal femur or proximal
tibia (most common).
• More common in males than females
• Risk factors include; radiation and chemotherapy, pagets dse,
genetics, retinoblastoma

77. CONTD……
• Patients present with localised constant pain and a tender soft tissue
mass may be palpable.
• Plain film radiographs will show medullary and cortical bone
destruction, with significant periosteal reactions (termed “Codman’s
triangle” or as a “sunburst pattern”).
• Tissue biopsy is required for diagnosis and typically
warrants aggressive surgical resection with systemic chemotherapy.
Osteosarcoma are predisposed to metastasize to the lung and bone.

79. osteosarcoma
• Multiple sites may be noted over a period longer than 6 months
(metachronous osteosarcoma) this is very rare but when it occurs ,
tends to be in patients less than 10years
• A number of variants of osteosarcoma exist including:
1. conventional types(osteoblastic, chondroblastic and fibroblastic)
2. telengiectatic
3. Parosteal
4. periosteal

80. Etiology
• Exact cause is not known.
• However a number of risk factors have been identified.
• Genetic predisposition plays a role
Bone dysplasia including Paget's disease, fibrous dysplasia,
enchondromatosis and hereditary multiple exotoses and
retinoblatoma are risk factors
• Environmental factors like exposure to radiations is an important
risk factor.

81. Epidemiology
• In the US the incidence is 3.1 per million(4.4 per million population
less than 25years)
• The incidence is slightly higher in blacks than in the whites
• Incidence of osteosarcoma is slightly higher in men than
females(1.22:1)
• Osteosarcoma is very rare in young children(0.5cases per year in
children less than 5 years) however incidence increases with
adolescent spurt
• 5-9 years 2.6cases per million per year
• 10-14years 8.3 cases per million per year
• 15-19years 8.9 cases per million per year
• A second peak of incidence exists in individuals older than 60years

82. Clinical manifestation
Symptoms
• Pain particulary with activity
• There may history of swelling
• Pathological fractures
• Fever and night sweats
• Respiratory symptoms
Physical examination
Mass may or may not be present
Decreased range of motion
Lymphadenopathy
Respiratory findings

83. Investigations.
• Laboratory studies
• LDH
• ALP
• CBC
• LFTs
• RFTs
• Electrolytes
• Urinalysis
• LDH and ALP have prognostic significance, pts with elevated ALP
are likely to have pulmonary metastases. Pts without metastase
those with elevated LDH are less likely to do well than those with
normal LDH
• Histology lesion classically presence of osteoid cells

84. IMAGING STUDIES
• Plain radiography ((PA), Lateral chest views is helpful, plain films of
the suspected lesion should be obtained in two views.
Codman triangle(elevation of the periosteum), sunburst appearance
(extension of tumor through the periosteum)
Bone scanning with technetium 99 is important for evaluating
presence of metastatic or multi focal disease
CT scan of the primary lesion and chest
MRI of the primary lesion, best method for assessing the
intramedullary disease as well as associated soft tissue masses

85. TREATMENT
chemotherapy is given
pre-op for 8-12 weeks.
wide resection is carried
out.
If the tumor responds to
chemotherapy, the
treatment is continued
for another 6-12 months.

86. Ewing’s Sarcoma
• Ewing’s sarcomas are pediatric malignancies,
• more common in males, and arise from primitive poorly differentiated
neuroectodermal cells. They commonly affect the diaphysis of long
bones.
• Patients present with a painful and enlarging
mass with tenderness and warmth (often initially mistaken as
osteomyelitis).
• Plain film radiographs demonstrate lytic lesion with periosteal
reactions, producing layers of reactive bone leading to characteristic
“onion skin” appearance.
• Management is via neoadjuvant chemotherapy followed by surgical
excision. Radiation may be considered for local control in patients with
unresectable primary tumours.

87. Ewing Sarcoma affecting a tibia

88. Chondrosarcomas
• Chondrosarcomas are malignant tumours of the cartilage,
commonly arising as primary lesions but can appear as malignant
transformation from benign chondromas.
• For primary chondrosarcomas, the age of onset is 40-60 years,
typically affecting the axial skeleton.
• Patients typically present with a painful and enlarging mass.
• Plain film radiographs demonstrate lytic lesions with
calcification, cortical remodeling, and endosteal scalloping.
• Low grade lesions can be treated using intralesional curettage,
whilst wide en-bloc local excision is the preferred for
intermediate- and high-grade lesions.
• Prognosis depends on the grade and location; axial skeleton and
high grade tumours have a worse prognosis.

89. Chondrosarcomas affecting the femur on plain film;
red arrow = normal bone,
yellow arrow = chondrosarcomas

90. Investigations
• Investigations for a suspected bone tumor vary depending
on suspected tumor type. Most will obtain initial plain film
radiographs, however all suspected cases should be discussed in
an appropriate multidisciplinary team (MDT) meeting before
further investigations are arranged.

91. Radiological Features of Bone Tumours
• Features from a plain film radiographs can help in determining
whether a suspected bone tumor is either benign or malignant:
1. Benign lesions are often sharp and well-defined, lacking soft
tissue involvement and no cortical destruction
2. Malignant lesions are often poorly defined with rough
borders, involving soft tissues and have cortical destruction
3. If there is any degree of suspicion or uncertainty, additional
imaging for further assessment should be sought.

92. investigations
• Most suspected cases will need
I. MRI imaging to assess the lesion, as well as evidence for soft
tissue involvement.
II. CT imaging can be useful in determining cortical involvement.
III. bone biopsy may be required for definitive diagnosis.

93. Management
• Management of bone tumours depends on patient
factors and disease factors.
• most benign bone tumours are managed with observation.
• surgical treatment is the mainstay for malignant tumours.

94. Marrow tumors
Begnin
• none
malignant
• Ewing’s tumor
• Multiple myeloma

95. Multiple myeloma
• Arise from the plasma cells in the
bone marrow.
• Solitary condition is called
plasmacytoma.
• should be considered in all
patients with back pain over 65
years of age.
• Back pain with an ESR > 100 mm
h–1 is multiple myeloma until
proved otherwise.

96. EWING'S SARCOMA
Malignant round cell tumor
Affect patients in the 5-20 age group.
Arises from endothelial cells in the bon
e marrow.
May be misdiagnosed as infection beca
use of warm swelling.
Moth eaten and may show an onion ski
n periosteal reaction.

97. EWINGS SARCOMA
Symptoms
• Pain –throbbing in nature
• Localized swelling
• Pyrexia
Rx-radiotherapy, chemotherapy and surgery though prognosis is
always poor
With the 3 combination of treatment patient has a 5 year survival rate.

99. TREATMENT
Chemotherapy
is the mainstay
of treatment.
The prognosis
is poor.

100. METASTATIC BONE T
UMOURS

101. METASTATIC BONE DISEASE
• Most tumors which metastasize to bone are carcinomas
• Most common sources of metastasis are breast,
prostate, lung, kidney and thyroid.
• Most common sites of bone metastases are
the spine, proximal, femur and proximal humerus.
• Metastasis is usually by hematogenous spread and direct
spread is rear.
• Tumor cells metastasise to the spine,-valve less Batson’s v
enous plexus.
• Bone metastases can be lytic, sclerotic or mixed

102. STAGING OF PRIMARY BONE TUMORS
ENNECKING STAGING SYSTEM FOR BENIGN TUMOURS
A. Latent e.g. osteochondroma. usually asymptomatic and incidently
discovered
B. Active e.g. osteoid osteoma; Presents with mild symptoms and
continue to grow
C. Aggressive eg giant cell tumor; tend grow rapidly and destroy the
bone
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103. ENNECKING STAGING FOR MALIGNANT
TUMORS
The compartment is the bone in which the tumor arises
7/25/2023 103

104. EVALUATION AND INVESTIGATION OF THE
PATIENT WITH SUSPECTED BONE TUMOR
History and physical examination.
Pain history
Non mechanical night pain in children
Relief of pain on NSAID eg in osteoid osteoma
Patient with a history of malignancy presenting with back pain-
considered to have metastatic disease
other symptoms per presentation of each tumor
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105. INVESTIGATIONS
LOCAL INVESTIGATIONS
ultrasound scan
 plain radiographs of the whole affected bone or soft tissue lesion
MRI of the whole affected bone or soft tissue mass
 CT scan may be helpful in addition to or instead of MRI scan.
DISTANT INVESTIGATIONS
blood tests;
Complete blood count
ESR
 urea and electrolytes
 bone profile
protein electrophoresis
7/25/2023 105

106. ctn..
plain radiographs or CT scan of the chest. more sensitive
whole body isotope bone scan for suspected primary or metastatic
bone tumors
ultrasound or CT scan of abdomen if renal metastasis
Biopsy, only when staging investigations have been completed
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107. PRINCIPLES OF TREATMENT
Treatment of benign tumors
Conservative approach for simple bone cysts, injection with steroids
if cysts persist
Most latent & active benign lesions can be treated by intralesional
curettage
CT-guided thermo coagulation is used for osteoid osteoma
 Large or more rapidly growing benign tumors may require excision
and reconstruction
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108. Cont..
Treatment of malignant tumors
Multidisciplinary(chemotherapy, radiotherapy and
surgery).
Osteosarcomas and Ewing’s sarcoma require
neoadjuvant chemotherapy and surgery
Chondrosarcomas are insensitive to radiotherapy
or chemotherapy Rx is surgical excision
Most malignant tumors can be treated with limb
salvage
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109. Treatment of metastatic bone disease
• Resuscitation for electrolyte imbalance, anemia, cardiorespiratory
problems
• Surgical Rx is usually palliative
• Spine may need stabilization or cord decompression
• Radiotherapy relives pain.

110. REFERENCES
Bailey and love’s short practice of surgery, 27th
edition.
UPTODATE 2023