Transcript Bone & Joint Infections

Pathology of Bone & Joint
Infections
Doç. Dr. Işın Doğan Ekici
• The term osteomyelitis formally
designates inflammation of the bone
and marrow cavity; as commonly used,
however, it almost always implies
infection.
• Osteomyelitis can be a complication of
systemic infection but more frequently
occurs as an isolated focus of disease;
it can be an acute process or a chronic,
debilitating illness.
• Although any microorganism can cause
osteomyelitis, the most common
etiologic agents are pyogenic bacteria
and Mycobacterium tuberculosis.
• Spread to bone by one of
three routes:
– Hematogenous spread
– Direct extension from a
contiguous site of infection
– Direct introduction
• The most serious bone infections are
pyogenic osteomyelitis and tuberculosis
• The clinical course of osteomyelitis depends
on
– the characteristics of the causative organism
– the route of the infection
– the age of the patient
• Osteomyelitis can be occured
as;
• Acute
• Subacute
• Chronic
Acute (Pyogenic) Osteomyelitis
1- Hematogenous Osteomyelitis
2- Osteomyelitis from a Contiguous Infection
3- Osteomyelitis from an Introduced Infection
Hematogenous (Pyogenic) Osteomyelitis
• Acute hematogenous osteomyelitis
• Predominately in children and before
the age of epiphysial closure (<21 y),
• Typically originates in the metaphysis
of long bones:
– the lower end of the femur,
– the upper end of the tibia and
humerus,
– the radius.
• Sometimes results from the bloodborne spread to bone of an
extraskeletal focus of infection.
Etiology of Hematogeneous osteomyelitis
• In children:
– S. aureus (60-90%)
– Group B streptococci and E. Coli (in neonates)
– Salmonella osteomyelitis (Children with sickle cell disease)
• In adults:
– S. aureus (55%)
– Gram-negative bacteria
– Streptococci
Hematogeneous osteomyelitis of children usually begins in the metaphysis of
long bones: The blood-borne bacteria are carried to the marrow space by way
of the nutrient artery
Hematogenous osteomyelitis in adults:
– Vertebrae
– Long bones (rarely)
• The hematogenous spread of infection:
– by way of the nutrient branches of the spinal artery
or
– by flow from the pelvic veins to the lumbar veins
• The vertebral infection is usually secondary to a
primary bacteremia caused by
– genitourinary tract infection
– soft tissue and respiratory infections
– iv drug abusers
• The complications of vertebral osteomyelitis:
– extension of the infection to the adjacent disk
space
– extension to retropharyngeal, mediastinal,
peritoneal, and meningeal sites depending on
the vertebrae involved
Pathology
• Fulminant acute inflammation of the
marrow space
• An exudation of polymorphonuclear
leukocytes
• The presence of an inflammatory
exudate within the rigid limits of the
marrow space causes:
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–
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–
an increase in intramedullary pressure
reduced blood flow
local vascular occlusion
thrombosis
• Local ischemic injury  cell necrosis
(marrow and osseous tissue)
• The bacteria, pus material, and
necrotic debris comprise a septic
focus of purulent inflammation
Exudation of polymorphonuclear leukocytes
• The infection may then spread
rapidly by way of vascular
channels through the medullary
cavity
• The bone cortex which is thin in
the region of the metaphysis and
provides easy access to the
periosteum
• The purulent material may
elevate the periosteum and form
abscesses beneath it or
penetrate the periosteum
(subperiostal abscess)
• Sinus tracts which drain into the
soft tissue or extend to the skin
surface (fistula or cloaca) 
Sinus tracts which drain
into the soft tissue or
extend to the skin surface
(fistula or cloaca)
• Impaired the blood supply
to the cortical and
medullary bone 
ischemic bone tissue 
necrosis
• After several days a
sizeable portion of the
necrotic bone tissue may
separate from the viable
bone as an avascular
bone fragment termed a
sequestrum

– the formation of an
involucrum (coffin)
• With continuation of the bone
infection,
– chronic inflammatory cells
(lymphocytes, histiocytes,
plasma cells),
– proliferating fibroblasts,
– reactive new bone formation
contribute to the microscopic
picture of chronic
osteomyelitis.
Osteomyelitis from a Contiguous Infection
• The adjoining sites of microbial
infection that may spread to bone:
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Burns
Sinus disease
Periodontal infections of jaws
Soft tissue infection
Skin ulcers caused by peripheral vascular
disease
• Arteriosclerosis
• Diabetes
• Vasculitis
• The pathological and radiological
changes are similar to those seen in
chronic hematogenous osteomyelitis
• The treatment usually requires surgical
intervention (debridement of necrotic
tissue, drainage of abscesses, etc.)
combined with bacteriological cultures
and appropriate antimicrobial therapy
• Blood cultures are positive in about
10% of cases.
Osteomyelitis from an Introduced Infection
• Penetrating wounds
• Compound fractures
• Simple fractures treated surgically with open
reduction and internal fixation
• Prosthetic joint replacements
• Other orthopedic appliances (plates, nails,
screws, pins)
The pathological changes in the involved
bone (as occur in hematogenous
osteomyelitis):
• suppurative inflammation
• ischemic necrosis
• fibrosis
• reactive new-bone formation
Subacute osteomyelitis
Subacute osteomyelitis
(Brodie abscess)
• A Brodie abscess is a subacute
osteomyelitis with a predilection for
the ends of long bones and the
carpals and tarsals
– may mimic various benign and
malignant conditions, resulting in
delayed diagnosis and treatment
• Infectious agents:
Etiology
– Subacute osteomyelitis is one of the many
clinical presentations of hematogenous
osteomyelitis
– The causative organism usually is
Staphylococci (30-60%)
• Others:Streptococcus, Pseudomonas,
Haemophilus influenzae, coagulasenegative Staphylococcus, and Kingella
kingae (a gram-negative
coccobacillus).
– The organisms reach the bone from a
disrupted site
• skin pustule
• furuncles
• impetigo
• infected blisters and burns
– Infection has even been suggested to be
the outcome of common events such as
normally harmless daily teeth brushing.
• Site of infection
– The lower limb is affected
much more often than the
upper limb.
• tibia is affected relatively more
often than is the femur
– Involve the epiphysis and
metaphysis
• Radiographic findings:
• a localized destructive lesion of
bone
• with a surrounding sclerosis in the
metaphysis
• and a variable degree of periosteal
new-bone formation
Histologic Findings
• The surrounding bone is usually
sclerotic
• Granulation tissue lines the
abscess cavity
• Fibroblastic response, remnant of
necrotic bone, and new bone
formation
• Pus is a rare finding
• Inflammatory infiltration consisting
of polymorphonuclears,
lymphocytes and plasma cells
(mixed)
Chronic
osteomyelitis
• Garrè’s sclerosing osteomyelitis
• Chronic suppurative osteomyelitis
• Chronic recurrent multifocal
osteomyelitis
• Specific forms of chronic
osteomyelitis (Tbc,Syph)
• SAPHO syndrome (synovitis, acne,
pustulosis, hyperostosis, osteitis)
• The disease may result from
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(1) inadequately treated acute osteomyelitis
(2) a hematogenous type of osteomyelitis
(3) trauma
(4) iatrogenic causes such as joint
replacements and the internal fixation of
fractures
– (5) compound fractures
– (6) infection with organisms, such as
Mycobacterium tuberculosis and Treponema
species (syphilis)
– (7) contiguous spread from soft tissues, as in
diabetic ulcers or ulcers in peripheral
vascular disease
Infective process
• Chronic osteomyelitis results when
the inflammatory process continues
over time, leading to bone sclerosis
and deformity
• The ends of long bones are the most
common locus of infection, and
Staphylococcus aureus is the most
common infective organism involved
( chronic suppurative
osteomyelitis)
• Remember
Infection  increase of intramedullary
pressure (due to inflammatory exudate)
 strips the periosteum  leading to
vascular thrombosis  bone necrosis
 formation of sequestra
• These sequestra with
infected material are
surrounded by sclerotic bone
that is relatively avascular.
• Antibiotics cannot penetrate
these relatively avascular
tissues and are hence
ineffective in clearing the
infection.
Chronic
osteomyelitis
Sclerosing osteomyelitis of Garré – Mandible: a
sclerotic nonpurulent form of osteomyelitis
Complications of Chronic Osteomyelitis
 (1) arthritis
 (2) skeletal deformations
 (3) malignant transformation (eg,
Marjolin ulcer [squamous cell
carcinoma], SCC of the sinus tract)
 (4) secondary amyloidosis
 (5) pathologic fractures
Specific forms of chronic osteomyelitis
• Tuberculous osteomyelitis
• Syphilis (congenital and acquired)
• Actinomycotic osteomyelitis
Tuberculous osteomyelitis
• Bone Tuberculosis
• Hematogenous spread of organisms from an
active focus of tuberculosis :
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lung (common)
mediastinal or aortic lymph nodes
kidney
bowel
• Most common in children&youngs
• The vertebrae and the long bones of the
extremities are most frequently involved
• In many cases the infection also spreads to
contiguous joints such as the hip, knee, and
intervertebral joints
Pathology
• The onset of tuberculous osteomyelitis is usually
insidious.
• The infection is unrelenting, necrotizing, and
destructive of bone, cartilage, and soft tissue.
• The tuberculous exudation and the inflammatory
necrosis may extend through the medullary and
cortical bone, penetrate through the periosteum,
and progress through the epiphysial and articular
cartilage.
• Tunneling sinuses may extend into the adjoining
soft tissue and drain to the skin surface.
• Sequestration and the formation of an involucrum
are uncommon.
Tuberculosis of the spine (Pott's disease)**
• The thoracic and lumbar vertebrae
• The infection often begins in the
anterior part of the vertebral body
and extends into the intervertebral
disc:
- Destruction and collapse of the
vertebral bodies and discs
– Kyphosis
– Kyphoscoliosis
Pott's disease
The tuberculous exudate:
• may spread through sinuses in the
soft tissue
• dissect along fascial planes and
muscle sheaths
• present at a more remote site as a
"cold" abscess.
– In this way, tuberculous exudation from
the thoracolumbar spine may spread
along paravertebral muscles and the
psoas muscle sheath and localize in the
inguinal region (psoas abscess).
• Microscopically, tuberculosis
of bone and joint is
characterized, as are all
tuberculous lesions, by the
presence of
– epithelioid granulomas
(tubercles)
– with central caseous necrosis
and
– Langhans' multinucleate giant
cells
Epithelioid granulomas & Langhans' multinucleate giant cells
Bone Syphilis
• Syphilitic infection may be acquired inutero (congenital syphilis) or postnatally
(acquired syphilis)
• Hematogenous spread of Treponema
pallidum
• In congenital syphilis, the infection is
spread to the fetus by way of the
placenta
– The spirochetes localize at active sites of
endochondral ossification in the metaphysis
of long tubular bones
• The two chief bone lesions of
congenital syphilis are:
• osteochondritis
• periostitis
Actinomycotic osteomyelitis
• Actinomyces israelii : Actinomycosis is a
chronic granulomatous disease
• Two-thirds of all cases occur in the
cervicofacial region
• Microorganisms occur as normal flora of
the oral cavity,
• Remain localized in the soft tissues or
invade the jaw bones.
• The patient exhibits swelling, pain, fever
and trismus.
• If the lesion progresses slowly, little
suppuration takes place; however
• If it breaks down, abscesses are formed
that discharge pus containing yellow
granules (nicknamed sulfur granules)
through multiple sinuses
• The more aggressive lesion resembles
chronic suppurative osteomyelitis
Arthritis (Synovitis)
Changes in synovial fluid in diseases of joints
S. aureus (common), S.pyogenes,
S.pneumoniae, N.gonorrhoeae, and
H. influenzae.; Leukocytosis.
------------------------------------------------Knee, hip, or wrist:
- culture of joint fluid
- examination of a synovial biopsy
specimen