Bone pathology

2nd yr undergraduate
presentation

Topics
Osteomyelitis

Fracture

healing

Osteomyelitis
Inflammation of bone and marrow
Classification
1) The duration - acute, subacute and
chronic
2) Mechanism of infection
exogenous or haematogenous
3) The type of host response to the
infection- pyogenic or non pyogenic

Epidemiology
Most common type of bone
infection, usually seen in children
Decrease in incidence, could be
due to higher standard of living and
improved hygiene.
Bimodal distribution- younger than
2 years, and 8-12 years
More common in males

Routes of spread

Hematogenous spread: most common

cause; usually long tubular bones of
children; usually metaphyseal in children
and adults, although involvement of flat
bones is more common in adults
Direct extension: less common, may be
associated with trauma or rarely
iatrogenic implantation of infectious
material
DM, immunodeficiency, IV Drug abuse .

Pyogenic osteomyelitis

Acute osteomyelitis usually occurs in children

Usually a haematogenous infection from
distant focus
Organisms responsible include:

Staph. aureus
Strep. pyogenes
H. influenzae
Gram-negative organisms

Salmonella infections are often seen in those

with sickle-cell anaemia
Infection usually occurs in metaphysis of long
bones

Bacteria
Staphylococcus

aureus in 80% to

90% of cases
E.coli, Pseudomonas, and Klebsiella
in patients with genitourinary tract
infections and IV drug abusers.
In neonates: Hemophilus influenza
and group B streptococci
In patients with sickle cell disease
Salmonella infection

Organisms once localized in bone

Bacteria proliferate and induce inflammatory reaction and
cause cell death.
Bone undergoes necrosis within first 48 hours
Bacteria and inflammation spread within the shaft of the
bone and may percolate throughout the haversian
systems and reach the periosteum
Subperiosteal abscess
Segmental bone necrosis sequestrum (dead piece

of bone)

Rupture of periosteum leads to an abscess in the

surrounding soft tissue and the formation of draining
sinus.

Pathophysiology

Over time, host response develops

After first week of infection chronic inflammatory
cells become more numerous

Cytokines from leukocytes stimulates osteoclastic

bone resorption ingrowth of fibrous tissue
deposition of reactive bone in the periphery

Reactive woven or lamellar bone which forms

sleeve of living tissue surrounding dead bone is
called as involucrum.

Brodie abscess: is a small

intraosseous abscess that frequently
involves the cortex and is walled off
by reactive bone
Sclerosing osteomyelitis of Garre:
typically develops in jaw and is
associated with extensive new bone
formation

Clinical features

Child usually presents with pain, malaise

and fever
Often unable to weight bear
Early signs of inflammation are often few
Bone is often exquisitely tender with
reduced joint movement
Late infection presents with soft-tissue
swellings or discharging sinus
Diagnosis can be confirmed by aspiration
of pus from abscess or metaphysis
50% of patients have positive blood
cultures

Radiology
X-rays can be normal during first
3 to 5 days
In the second week radiological
signs include:

Periosteal

new bone formation

Patchy rarefaction of metaphysis
Metaphyseal bone destruction

PATHOLOGY

Acute Infiltration of PMNs

Congested or thrombosed vess

Chronic Necrotic bone

Absence of living osteocyt
Mixed inflmmatory cells
predominate
Granulation & fibrous tissu

Osteomyelitis-gross & microscopy

Sequestrum (necrotic
bone)

Involucrum (new bone)

Complications
Pathological

fracture
Secondary amyloidosis
Endocarditis
Sepsis
Dev.of SCC in sinus tract

Chronic Osteomyelitis
Non specific
Develops in 15-30%
Due to lack of treatment, inadequate
antibiotic treatment or incomplete
surgical debridement of necrotic bone
Specific
TB osteomyelitis
Syphilitic osteomyeltis

TB osteomyelitis:

Dissemination of tuberculosis outside

the lungs can lead to the appearance of
skeletal TB:
Skeletal Tuberculosis:
Tuberculous osteomyelitis involves mainly
the thoracic and lumbar vertebrae (known
as Pott disease) followed by knee and hip.
There is extensive necrosis and bony
destruction with compressed fractures
(with kyphosis) and extension to soft
tissues, including psoas "cold" abscess.

Tuberculous osteomyelitis of the bone is secondary

hematogenous spread from a primary source in the lung
or GI tract.
It most commonly occurs in the vertebrae (body) and
long bones.
Once established, the bacilli provoke a chronic
inflammatory reaction.
Small patches of caseous necrosis occur, and these
coalesce to form larger abscesses.
The infection spreads across the epiphysis into the
joints.
The infection may track along soft tissue to appear as a
cold abscess at a distant site (eg: psoas abscess in case
of spinal tuberculosis).

Spinal tuberculosis. Magnetic resonance imaging of the spine

revealing osteomyelitis involving T10 and T11 vertebral bodies
and disc space (A; arrow) and an adjacent multiloculated
paravertebral abscess (B; arrow).

Syphilitic osteomyelitis:
The transplacental spread of
spirochetes from mother to the
fetus results in congenital
syphilis.
Long bones, such as the tibia,
are mainly affected.
Congenital syphilis has 2 forms:
Periosteitis and osteochonditis.

Syphylitic Osteomyelitis

Regarding acquired syphilis, bone lesions are

manifestations of tertiary syphilis.
Gummatous lesions appear as discrete punched-out
radiolucent lesions in medulla or destructive
lesions within the cortex.
The surrounding bone is sclerotic, and no discharge
is present.
Bones frequently affected are those of nose, palate,
skull and extremities, especially the long tubular
bones such as tibia.
Histology : edematous granulation tissue
containing numerous plasma cells and necrotic
bone.

Sabre tibia

Fracture healing

Stage of # healing

Reactive phase

Reactive phase

Reparative phase

Reperative phase

Remodeling phase

Getting back original shape of the

bone .

Mainly done by osteoclastic

activation.