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Introduction
Normal Anatomy & Histology
Normal anatomy
Parts of a long bones:
diaphysis (shaft),
epiphysis (ends of bone, partially covered by
articular cartilage),
metaphysis (junction of diaphysis and epiphysis,
most common site of primary bone tumors)
Cross section:
periosteum
cortex (composed of cortical or compact bone)
medullary space (composed of cancellous or
spongy bone)
Normal histology
Lamellar Bone ( Mature)
layered bone with concentric parallel lamellae;
gradually replaces woven bone
Cortical
- 80%of skeleton
- 80-90% calcified
- relatively low metabolic activity
Cancellous or trabecular or spongy
- 20% of skeleton
- 5-20% calcified
- relatively high metabolic activity
Woven bone (immature bone)
irregular non-mineralized bone
BONE PATHOLOGY
Classification
Infectious diseases
(Osteomyelitis)
Metabolic diseases
Tumours
Arthritis
BONE PATHOLOGY
Infective - Osteomyelitis
OSTEOMYELITIS
Inflammation of bone (osteo) &
marrow (myelo)
Bacterial osteomyelitis:
Acute suppurative osteomyelitis
Haematogenous / non-haematogenous
Chronic osteomyelitis:
non-specific / specific (TB & Syphilis)
PYOGENIC OSTEOMYELITIS:
is almost always caused by bacteria.
Stapylococcus aureus (80-90%)
E.coli, Klebsiella and Pseudomonas in patients
with GU tract infections / IV drug abusers.
Mixed bacterial infections can be seen in the
setting of direct spread during surgery or open #
In neonatal period, H. influenzae and group B
streptococci are frequent pathogens
Salmonella infections - common in sickle cell
disease patients.
In 50% of the cases no organisms can be isolated.
Sites of involvement:
Influenced by the vascular
circulation, which varies with age.
Neonates: the metaphyseal vessels
penetrate the growth plate, resulting
in frequent infection of the
metaphysis, epiphysis or both.
Children: metaphyseal.
Adults: epiphyses and subchondral
regions.
Pathogenesis
1. Hematogenous spread.
2. Extension from a contiguous site.
3. Direct implantation
Pathogenesis:
Once localized in bone, the bacteria
proliferate and induce an acute
inflammatory reaction
Spread of bacteria and inflammation leads
to suppuration
Pus within bone reaches periosteum & forms
a subperiosteal abscess in 2-3 days.
Within medullary cavity it obstructs the
periosteal & endosteal blood supply causing
bone necrosis in approx. 7 days
Dead pieces of bone are known as the
sequestrum
Microscopy
Inflammation of bone
Acute
osteomyelitis
Clinical Course:
Fever ,chills, malaise & throbbing pain
over the affected region.
Diagnosis:
Sign/symptoms.
X-ray
lytic focus of bone destruction
surrounded by zone of sclerosis
Complications:
Pathologic fracture
Chronic suppurative osteomyelitis: including
sequestrum formation and skin sinus formation
Local Spread of infection: Arthritis / myositis /
neuritis
Systemic Spread of infection - toxaemia,
septicaemia or Endocarditis
Damage to the growth plate causing subsequent
growth deformity
Secondary amyloidosis
Squamous cell carcinoma in longstanding cases
Brodies abscess:
Localised form of acute osteomyelitis
small intraosseus abscess that
frequently involves the cortex and is
walled off reactive bone.
TUBERCULOUS OSTEOMYELITIS
Routes of entry:
Usually blood borne and originate
from a focus of active visceral
disease.
Direct extension (e.g. from a
pulmonary focus into a rib)
spread via draining lymphatics.
Pott disease
presentation of extra-pulmonary tuberculosis that
affects the spine.
lower thoracic and upper lumbar vertebrae are
most often affected
Typically present with pain on motion, localized
tenderness, low-grade fevers, chills, and weight
loss
Paraspinal mass, sometimes a/w numbness,
paraesthesia or muscle weakness of the legs
Potts Disease
Diagnosis
Complications
Vertebral collapse resulting in
kyphosis / Scoliosis
neurologic deficits secondary to
Spinal cord or nerve compression
(Pott paraplegia)
Sinus tract formation
tuberculous arthritis
psoas abscess.