give information about general osteomyelitis

1. Osteomyelitis

2. Osteomyelitis
 Inflammation of bone and marrow
 Types
 Pyogenic osteomyelitis
 Tuberculous osteomyelitis

3. Pyogenic
Osteomyelitis

4. Pyogenic osteomyelitis
 Always caused by bacteria
 Routes of infection
 Hematogenous spread
 Extension from a contiguous site
 Direct implantation

6.  Causes
 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

7.  Morphology
 Acute
 Subacute
 Chronic

8. 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.

9.  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.

10.  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

13. PATHOLOGY
Acute Infiltration of PMNs
Congested or thrombosed vessels
Chronic  Necrotic bone
Absence of living osteocyte
Mixed inflmmatory cells
predominate
Granulation & fibrous tissue

14. Osteomyelitis-gross & microscopy

15. Sequestrum (necrotic bone)

16. Involucrum (new bone)

17. 
Osteomyelitis of the tibia of a
young child. Numerous
abscesses in the bone show
as radiolucency.

18. HEMATOGENOUS OSTEOMYELITIS
Clinical manifestation
Classic presentation: Sudden onset
High fever, Night sweats
Fatigue, Anorexia, Weight loss
Restriction of movement
Local edema, Erythema, & Tenderrness

19. Clenched fist
osteomyelitis

22. HEMATOGENOUS OSTEOMYELITIS
Diagnosis & work-up
Lab study:
WBC  May be elevated, Usually normal
C-Reactive Protein (CRP)
Erythrocyte Sedimentation Rate
(Usually is elevated at presentation
Falls with successful therapy)
Blood culture
( Acute osteomyelitis + ve > 50% )
{

23. HEMATOGENOUS OSTEOMYELITIS
Diagnosis & work-up
Imaging
Radiology:
Normal
Soft tissue swelling
Periosteal elevation
Lytic change
Sclerotic change

24. Complications of chronic osteomyelitis:
1) Deformities of bones:
2) Pathological fractures.
3) Systemic effects such as chronic fever & fatigue.
4) Amyloidosis of the AA type (secondary
amyloidosis).This can get further deposited in the
kidney, liver & blood vessels.
5) Squamous cell carcinoma of the skin: The skin at
the edges of the draining sinus tracts may undergo
malignant transformation over time.
6) Sepsis
7) Rarely sarcoma in the infected bone

25. Specific forms of chronic osteomyelitis
 Forms of chronic osteomyelitis include:
 Brodie abscess,
 Tuberculous osteomyelitis,
 Osteomyelitis of congenital syphilis, and
 Osteomyelitis of acquired syphilis.

26. 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.

27.  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).

28. 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).

29. Psoas abscess: Computed tomographic scan of the
abdomen showing a left iliopsoas abscess (arrow) that
likely originated from tuberculous osteomyelitis involving
the T12, L1, and L2 vertebrae.

30. 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.

31.  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.

32. “Sabre” tibia
