Etiology and pathogenesis

Osteomyelitis and septic arthritis. This article talks about the pathogenesis

1. Etiology and Pathogenesis of
Musculoskeletal Infections

2. Etiology
•Commonly occurs in childhood.
•More common in males
•Malnutrition
•History of injury.

3. Pathophysiology
•Adult osteomyelitis
•Pediatric osteomyelitis
•Septic arthritis.

4. Pathophysiology of osteomyelitis
•age of the host
•duration of infection
–< 6 weeks- acute
–> 6 weeks- chronic
•etiology of infection
•type of host response to the infection

5. Routes
•Exogenous- direct inoculation of the bone
from either trauma, surgery, or a contiguous
focus of infection.
•Hematogenous- via the vascular tree into
either osseous or synovial tissue, producing a
localized focus of infection.
•Local tissue compromise or systemic tissue
(i.e., diabetes) compromise associated with an
increased risk.

7. Response
•Pyogenic organisms- rapidly progressive
course of pain, swelling, abscess formation,
and aggressive bone destruction.
•Less aggressive nonpyogenic organisms(eg
AFB) invoke a more insidious granulomatous
reaction.

8. •Age of the host is important in that
differences in bone vascular anatomy
between adults and children slightly alter the
mechanism of hematogenous delivery.
•Children are susceptible to different
organisms depending upon their age.

9. Exogenous osteomyelitis
•clearly identified anatomic site,
•inoculated with pyogenic organisms,
•polymicrobial,
•frequently in association with foreign debris.

10. •Bacteria inoculated into a compromised local
environment,
•Bone and soft tissue disruption providing
ample amounts of necrotic and devascularized
material favorable for bacterial growth.

11. •Tissue devascularization prevents host
response mechanisms from reaching bacterial
colonies, thereby permitting unchecked
proliferation.

12. Host response to injury
•Activation of inflammatory and immunologic
pathways.
•Inflammatory elements serve to destroy
bacteria and remove nonviable material.
•Humoral and cellular immunologic
mechanisms act to recognize specific bacteria
and subsequently confer immunity to prevent
further bacterial dissemination.

13. Inflammatory pathway
•Increases in blood flow
•vascular permeability
•delivery of polymorphonuclear leukocytes
•Mononuclear cells arrive within 24 to 48 hours
and assist in eradication of bacteria and
removal of necrotic bone.
•Pus and abcess formation.

14. •Granulation tissue surrounds the infected area
in an attempt to wall off the infection.
•Reactive bone formation occurs to further
sequester the infection from the host.
•Within the infected region, dead bone is often
prominent, and this is commonly termed the
sequestrum, whereas the reactive bone is
known as the involucrum

15. •This area is isolated from host defense
mechanisms by the avascular fibrous tissue
and can permit the continued proliferation of
bacteria

16. Bacterial adhesions
•Acquiring of a glycoproteinaceous
conditioning film when exposed to a biologic
environment over the tissue- or implant-
derived surfaces.
•This surface is anionic that repels the anionic
covering of the bacteria initially.

17. •However, attractive forces (van der Waals), in
conjunction with hydrophobic molecules on
the exposed substrate and the bacteria,
increase the duration of bacterial
juxtaposition.
•Formation of irreversible cross-links between
bacteria and host surfaces

18. •Proliferation occurs with formation of a
polysaccharide slime layer.
•The biofilm or slime layer is composed of
bacterial extracapsular exo-polysaccharides
that bind to surfaces, thereby promoting cell-
to-cell adhesion, microcolony formation, and
layering of the microorganisms.

19. •Additional species of bacteria may attach to
the surface of the biofilm, resulting in
syntropic interactions between differing
bacteria

22. Properties of biofilm
•Bacterial attachment in production of biofilms
can lead to antibiotic resistance.
•Decreased metabolic rates and phenotypic
changes in surface-adherent bacteria.

23. Pediatric Osteomyelitis
•Hematogenous inoculation.
•Pediatric bones more predisposed due to their
vascular anatomy.
•The nutrient artery of long bones enters
through the cortical bone to divide within the
medullary canal, ending in small arterioles
that ascend toward the physis.

25. •Just beneath the physis, these arterioles bend
away from the physis and empty into venous
lakes within the medullary cavity.
•The acute bend in these arterial loops serve as
points of diminished blood velocity,
promoting sludging of bacteria directly under
the physis.

27. •In addition, phagocytic capability and
reticuloendothelial function may be
depressed in these vascular loops, promoting
the establishment of bacterial colonies.
•Trauma, often associated with the emergence
of osteomyelitis in children, may actually
promote bacterial seating and proliferation in
metaphyseal sites.

29. •This pus can spread in one of three ways:
through the physis, toward the diaphysis, or
through the adjacent bony cortex.
•This purulent material tends to seek the path
of least resistance, through the metaphyseal
cortex, to form a collection of subperiosteal
pus.

31. •Although this is the most common route of
egress, younger children (less than 1 year) with
intact transphyseal vessels may demonstrate
epiphyseal spread with the development of
epiphyseal abscesses.
•In older children, the development of a
subperiosteal abscess results in devascularization
of the bone both from thrombosis of the
endosteal blood supply and from the stripping
away of the overlying periosteum.

32. •The periosteum, which is extremely thick and
loosely adherent in children, is not easily
penetrated; in the devascularization process,
it is lifted off the bone, with the inner
cambium layer producing a layer of new bone.
• In this case, the devascularized bone is
termed the sequestrum, with the reactive
periosteal bone being the involucrum

34. •A cellulitic phase precedes abscess formation,
with medical management alone being
successful to cure the infection.
•Once an abscess forms, surgical debridement
is necessary to remove the nonviable bone,
reduce the bacterial population, and provide
for a vascularized tissue bed for antibiotic
delivery.

35. •Staphylococcus aureus (90%)
•In neonates, the most common organisms
include Staphylococcus aureus, group B
streptococci, and gram-negative organisms

36. Pediatric septic arthritis
•Acute septic arthritis may develop from
hematogenous sources or, more commonly,
from extension of an adjacent foci of
osteomyelitis into the joint.
•Susceptible joints are those in which the
metaphysis is intra-articular, such as seen in
the hip and shoulder where bacteria are
afforded an avenue for dissemination.