Osteomyelitis

Osteomyelitis is infection of bone, caused by bacteria, fungi or mycobacteria. Acute and chronic osteomyelitis differ significantly in clinical presentation, microbiology and management, and understanding the pathophysiology, particularly biofilm formation on necrotic bone, is fundamental to effective treatment.

Host and pathogen. The outcome of a bone infection depends on the balance between bacterial virulence and the host immune response. Local factors (vascular supply, foreign material) and systemic factors (diabetes, immunosuppression) determine whether the infection resolves, becomes chronic or disseminates.

Haematogenous spread. Bacteraemia seeds bone during transient episodes, and S. aureus is the most common organism. Different bones have unique vascular patterns that influence their susceptibility:

• Metaphysis of long bones in children - slow sinusoidal blood flow with hairpin loops creates stagnant zones for bacterial seeding
• Vertebral bodies in adults - Batson's valveless venous plexus allows retrograde seeding from pelvic and abdominal infections

Contiguous spread. Infection spreads into bone from a neighbouring focus: after surgery, around hardware and fracture fixation, or from a diabetic foot ulcer. It often involves soft tissue and bone together, and it is polymicrobial in trauma and diabetic cases.

Direct inoculation. The organism is carried in at the time of injury or operation:

• Open fractures - contamination at injury
• Combat injuries - high-energy trauma
• Puncture wounds - a nail through the shoe (Pseudomonas)
• Implant surgery - low-virulence organisms such as Staph epidermidis

From acute to chronic. The infection progresses through three stages, and the sequestrum forms in the second.

View larger

Dead bone and its shell. As infection thromboses the local blood supply, a fragment of bone dies and separates. Cortical bone is supplied by periosteal vessels, so damage to them leads to avascular sequestrum formation. Chronic osteomyelitis is described by the structures that follow:

• Sequestrum - a segment of necrotic, avascular bone, dead and sclerotic, that becomes colonised by bacteria and serves as the nidus for chronic infection
• Involucrum - reactive new bone laid down by the periosteum around the sequestrum as the body attempts to wall off the infection
• Cloaca - an opening in the involucrum through which pus and dead bone escape, often leading to a sinus tract through the soft tissues

View larger

View larger

Biofilm. Biofilm is a structured community of bacteria enclosed in a self-produced polysaccharide matrix, the glycocalyx, and it is the key to chronicity. The bacteria adhere to necrotic bone inside it, and the matrix:

• is a physical barrier against antibiotics
• prevents neutrophil phagocytosis
• allows the bacteria to enter a dormant, metabolically inactive state
• enables quorum sensing between bacteria

Bacteria within biofilm are 1000 times more resistant to antibiotics than planktonic, free-floating bacteria. Initial surface adhesion is followed by matrix-mediated maturation, and dispersion seeds recurrent infection elsewhere.

View larger

Beyond biofilm. Biofilm is only one of several reasons bacteria survive in bone. Chronic osteomyelitis is notorious for relapsing months or even years after apparently successful treatment, and the mechanisms below are why "cure" is better described as long-term remission.

View larger

Staphylococcus aureus causes 80% of osteomyelitis and is the most common organism in all age groups. Beyond it, the clinical scenario predicts the organism.

Cierny-Mader is the gold standard. It combines the anatomic type of the infection (I-IV) with the physiologic status of the host (A-C).

View larger

Confirming it. The diagnosis is confirmed clinically (pain, a draining sinus), on imaging (MRI) and with inflammatory markers (CRP).

Inflammatory markers. CRP is the most sensitive. It rises in 6-12 hours and falls with treatment, and it is better than ESR for monitoring the response. ESR is slower to rise and to fall. The white cell count is often normal in chronic cases and is less useful.

Blood cultures are positive in 50% of acute haematogenous cases and usually negative in chronic osteomyelitis.

Radiographs are first line, and late: changes take 10-14 days to appear, and 30-50% of the bone must be lost before lysis shows. Look for periosteal reaction, lytic lesions, sequestrum and involucrum.

MRI is the investigation of choice, 90% sensitive and 80% specific. It shows marrow oedema (T2 hyperintense), abscess and soft-tissue extension, and it differentiates abscess from cellulitis; gadolinium enhances inflamed tissue.

View larger

View larger

View larger

Nuclear medicine. A bone scan is sensitive but not specific; a labelled white cell scan is more specific for infection.

Microbiology. Tissue culture is the gold standard.

• Take multiple deep samples, not from the sinus tract; a minimum of 3 increases the yield
• Send them for aerobic, anaerobic, fungal and TB culture, and send a specimen for histology
• Hold antibiotics until the cultures are obtained; the exception is the septic patient, who needs empiric therapy

Osteomyelitis is a notorious mimic, and is mimicked by several aggressive lesions. The cardinal rule is that a lytic, painful bone lesion with periosteal reaction must be biopsied before infection is assumed, because Ewing sarcoma and osteosarcoma can look identical.

View larger

The principle. Surgery and antibiotics are synergistic. Debride all necrotic tissue, obtain cultures and manage the dead space, then give approximately 6 weeks of pathogen-directed therapy.

Algorithm

View larger

Chronic osteomyelitis, week by week. The sequence below runs from diagnosis to reconstruction; the deep cultures and histology described under Diagnosis are taken at the first operation.

Choosing the antibiotic. The agents below reflect convergent IDSA, BOA-BOAST, AAOS and EFORT/European practice. The exact agent and dose vary with local resistance patterns and renal function; the principle, narrow, high-bioavailability and pathogen-directed, is universal.

View larger

View larger

Beyond persistent infection, chronic osteomyelitis carries structural and systemic complications that are high-yield in the viva. The pathological femoral fracture in the tumour-mimic figure above is one of them.

Global Epidemiology

• Acute haematogenous osteomyelitis is predominantly a paediatric disease; reported incidence is roughly 1 in 5,000 children per year in high-income settings, higher in low- and middle-income countries where presentation is often delayed.
• Chronic and contiguous osteomyelitis is increasingly an adult disease driven by open fractures, internal fixation, diabetic foot disease and prosthetic joints. Diabetic foot osteomyelitis is rising globally in parallel with the diabetes pandemic.
• Staphylococcus aureus remains the dominant pathogen worldwide across all settings; MRSA prevalence varies markedly by region (high in parts of the Americas and Asia, lower in much of Scandinavia and the Netherlands due to search-and-destroy policies).
• In regions with high tuberculosis burden, skeletal TB (including spinal Pott disease) is an essential differential for subacute/chronic bone infection.

Side-by-Side Society Guidance

Practice Variation: High- vs Limited-Resource Settings

Antibiotic duration. The traditional 6 weeks is dogma more than data. OVIVA standardised 6 weeks but did not test shorter courses, and paediatric RCTs support around 3 weeks. The optimal duration in adults, and whether it differs by Cierny-Mader type, remains unresolved.

Oral or intravenous. OVIVA shifted practice toward early oral switch, but uptake varies, and concerns persist for poorly bioavailable agents, non-adherent patients and certain organisms. Route is now individualised rather than reflexively intravenous.

Single- or two-stage surgery. Single-stage debridement with immediate soft-tissue cover and local antibiotic carriers (e.g. calcium sulphate) challenges the classic staged Lautenbach/bead approach. The outcome data are promising but largely observational.

Diabetic foot osteomyelitis. This is where the surgical rule is contested. Whether forefoot diabetic osteomyelitis needs surgery or can be cured medically is debated; IWGDF accepts antibiotic-only management in selected cases, but recurrence and amputation risk remain high.