Refers to inflammation of bone and bone marrow. Most commonly occurs due to infections by: Pyogenic bacteria Pyogenic Osteomyelitis

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Infections of bone
Osteomyelitis

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Osteomyelitis
• Refers to inflammation of bone and bone
marrow.
• Most commonly occurs due to infections by:
– Pyogenic bacteria
• Pyogenic Osteomyelitis

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Pyogenic Osteomyelitis
• Usually occurs in children and young adults
• Due to pyogenic infection of bone by:
– Staphylococcus aureus* (most common)
– Escherichia coli & Streptococci - neonates
– Salmonella (common in sickle cell disease)
– Pseudomonas : common in intravenous drug
abusers, diabetics and puncture of foot
through rubber footwear.

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How do these organisms reach the bone?
• Three routes
1. Hematogenous spread (most common)
• Seeding of bone after bacteremia
2. Direct inoculation
3. Spread from an adjacent site of infection.
• Bones affected:
– Infant and children :(long bones)-tibia,
femur, humerus
– Adults: (small bones) - vertebrae, pelvic
bones
• Region of the bone affected
– metaphysis (most vascular part of bone)

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Pathogenesis

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Blood vessel
Organism from Septic focus = boil
Metaphysis of long bone
Acute inflammation
Formation of PUS
Subperiosteal abscess
Soft tissue Surface
Sinus tract
Periosteal elevation
+
Septic thrombosis

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Periosteal elevation
+
Septic thrombosis
Stoppage of blood supply
+
Enzymatic destruction
Involucrum
New bone formation
Sequestrum
Death of part of bone

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Morphology
• Depends upon the stage of Osteomyelitis
• Acute Osteomyelitis:
– Acute inflammation:  cell death and pus
formation.
– Pus may reach the Periosteum 
subperiosteal abscess.
– Rupture of Periosteum  abscess in
surrounding soft tissue  drain to surface
via a draining sinus tract.
– Neutrophils enzymatically destroy the bone.
• Devitalized bone is called sequestrum.

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Morphology
• Chronic disease:
– Is characterized by replacement of acute
inflammatory cells by chronic inflammatory
cells.
– A sleeve of new bone formation may surround
the infected necrotic area
• This reactive new bone is k/a involucrum.

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InvolucrumSequestrum

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Clinical findings
• Rapid onset with C/O feeling ill.
• Most frequent manifestation:
– Fever and severe pain over the
affected area.
– reluctance to use affected extremities.
• On examination:
– Localized area of tenderness
– Erythema and
– Swelling.

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• Investigations:
– Leukocytosis
– Raised ESR
• X ray
– Early stage (10 days) - may be normal.
– Slow periosteal elevation
– Lytic focus of bone destruction with
surrounding sclerosis.
• Radionuclide bone scan:
– Best for detection ( even in early cases)
– Localized increased uptake of traces
• Needle aspiration
• Blood cultures
• Bone biopsy and culture

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Sequestration of bone
In area of destruction

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Bone scan
Gram stain

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Draining sinus
Squamous cell carcinoma

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Complications
• Most important
– Draining Sinus tract to the skin surface
• Danger of Squamous cell carcinoma developing at
orifice of sinus tract.
– Extension of infection to adjacent joint  pyogenic
arthritis.
– Septicemia and infective endocarditis
– Chronic Osteomyelitis
• Others
– Fractures
– Retardation of growth from damage to epiphyseal
cartilage.
– Amyloidosis
– Osteogenic sarcoma (rare).

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Tuberculous Osteomyelitis
• Occurs secondary to tuberculous infection
located elsewhere.
– Active tuberculosis of lung.
– TB of GIT and lymphnodes
• Characteristically occurs in:
– Vertebrae (Pott’s spine or disease)

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Pott’s disease
• Infection begins at the anterior margin of
vertebral body near inter-vertebral disc.
• Complete destruction of inter-vertebral disc
with partial destruction of two adjacent
vertebrae.
• Collapse of vertebral bodies anteriorly.

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• Clinical findings:
– Back pain
– Stiffness,
– Deformity (kyphosis) ,
– Neurological abnormalities (Pott’s
paraplegia)
– Fever, night sweats and weight loss.
• Pathology:
– Granulomas with caseous necrosis on
histology.

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Spinal TB - Potts Disease

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Caseous necrosis

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Langhans Giant cell
Caseous necrosis

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Osteomyelitis: Note
• MC organism : Staphylococcus aureus
• In patient’s with:
– Sickle cell anemia Salmonella paratyphi*
– Genitourinary tract infections
• E coli, Pseudomonas, Klebsiella
– IVDA pseudomonas.
– Dog and cat bites Pasteurella multocida (a gram
negative rod)
– Nail puncture through rubber footwear
pseudomonas*.
– AIDS: ??**

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Fracture (#) of bones

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Fracture (#)
• Is a complete break in the continuity of bone
or
– it may be an incomplete break or crack.
• CLASSIFICATION:
– Closed and open fractures
• Closed or simple fracture: no
communication between site of fracture
and exterior of body.
• Open or compound fracture: direct
communication between the skin surface
and the fracture site through the skin
wound.

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Closed # Open #

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Open or compound fracture

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Classification: According to etiology
• Fractures caused solely by sudden injury
– Most common ; Caused by :
– Direct violence, Indirect violence
• Fatigue or stress fracture:
– Due to oft-repeated stress
– Risk group:
• Athletes, New military recruits
• Bone : metatarsal
• Pathological fracture
– Fracture through a bone already weakened
by disease.
– Cause of # :Trivial trauma

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Patterns of fracture
1. Transverse fracture
2. Oblique fracture
3. Spiral fracture
4. Comminuted fracture (more than two
fragments)
– The bone is broken into several pieces
5. Greenstick fracture (incomplete break)
– The bone is cracked, but not broken
into two pieces. "Incomplete" fracture.
6. Compression or crush fracture

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Healing of fractures
• Process divided into 4 stages
1. Hematoma formation and Inflammation
2. Formation of soft callus or procallus
3. Formation of Hard callus or bony callus
4. Bone Remodeling

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Stage 1 – Hematoma & Inflammation
• Fracture causes
hemorrhage and tissue
destruction ; blood clot
(hematoma) forms
(hours).
• Swelling and
inflammation around the
fracture site.

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Stage 2- Soft Callus
• Fibrin mesh of hematoma: Acts as a
framework.
– inflammatory cells (neutrophils and
macrophages) move in ; phagocytize
debris.
– Fibroblasts and capillary grow into blood
clot forming granulation tissue.
• Cartilage is formed ( from primitive
mesenchymal cells)
• Granulation tissue + cartilage = soft tissue
callus or procallus (provisional callus)
• Soft callus bridges the fractured bone.

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Stage 3 - Hard Callus
• Osteoblasts proliferate
• Form new bone
• New bone is mineralized
• Soft callus converted into bony
callus (or osseus callus.)
• This spans across the fracture and
fills in the space between broken
bone ends.
• The fracture is now stable.

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• Portions of callus that are not
under physical stress are resorbed.
• continual reduction in the size of
callus
• Restoration of marrow cavity.
• Strengthening of bone along the
lines of stress.
Stage 4 - Bone Remodeling

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Factors which affect # healing
• Age
• Type of fracture (Simple Vs. Compound/
comminuted/spiral etc.)
• Favorable factors:
– Good blood supply
– Immobility
• Factors that hinder union:
– Impaired blood supply
– Movement between the fragments
– Infection
– Interposition of soft tissue
– Systemic disorders : DM , vitamin deficiency

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Fracture healing: Complications
– delayed union
– nonunion
– pseudoarthrosis (false joint)

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Important fractures
• Femoral neck #:
– Bleeds into capsule
– Compromises Medial femoral circumflex artery 
avascular necrosis of femoral head.
• Scaphoid bone #:
– MC # of carpal bones
– Susceptible to avascular necrosis and nonunion
• Colles’ #:
– Person falls on outstretched hand
– # distal end of radius  dinner fork deformity
• Supracondylar #:
– Distal # of humerus
– Compromises brachial artery with danger of
Volkmann’s ischemic contracture of forearm muscles

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# femoral neck

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Miscellaneous bone disorders
Myositis ossificans

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Myositis ossificans
• Is characterized by
development of bony tissue
in:
– Skeletal muscle or soft
tissue
– Following a blunt trauma.
• Favored Locations:
– Quadriceps or brachialis
muscle
• Pathogenesis:
– Soft tissue trauma 
hematoma formation 
bone formation.
• Differential diagnosis:
– Bone sarcomas (
osteosarcoma)