Osteomyelitis

Osteomyelitis is an infection of bone that can be caused by bacteria, fungi, or mycobacteria. The clinical presentation, microbiology, and management differ significantly between acute and chronic forms. Understanding the pathophysiology—particularly biofilm formation on necrotic bone—is fundamental to effective treatment.

Key Definitions:

• Sequestrum: Segment of necrotic, avascular bone that becomes colonized by bacteria and serves as a nidus for chronic infection
• Involucrum: Reactive new bone that forms around a sequestrum as the body attempts to wall off the infection
• Cloaca: Opening in the involucrum through which pus drains, often leading to a sinus tract

The fundamental principle is that chronic osteomyelitis cannot be cured with antibiotics alone—surgical debridement is mandatory because biofilm-coated sequestrum prevents antibiotic penetration.

Biofilm Formation - The Key to Chronicity

Biofilm is a structured community of bacteria enclosed in a self-produced polysaccharide matrix (glycocalyx). This matrix:

• Provides physical barrier against antibiotics
• Prevents neutrophil phagocytosis
• Allows bacteria to enter a dormant, metabolically inactive state
• Enables quorum sensing between bacteria

Bacteria within biofilm are 1000x more resistant to antibiotics than planktonic (free-floating) bacteria. This is the fundamental reason why surgical debridement—not antibiotics—is the cornerstone of chronic osteomyelitis treatment.

Vascular Anatomy and Susceptibility

Different bones have unique vascular patterns that influence infection susceptibility:

• Metaphysis of long bones: Sinusoidal blood flow with hairpin loops creates stagnant zones for bacterial seeding
• Vertebral bodies: Batson's valveless venous plexus allows retrograde seeding from pelvic/abdominal infections
• Cortical bone: Supplied by periosteal vessels—damage leads to avascular sequestrum formation

Host-Pathogen Interaction

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

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 explanation lies in distinct mechanisms of bacterial persistence beyond the glycocalyx. These are the cellular reasons why "cure" is better described as long-term remission, and why agents with intracellular activity matter.

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Routes of Infection

Stages of Infection

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Differential Diagnosis

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 assuming infection, because Ewing sarcoma and osteosarcoma can look identical.

Algorithm

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Pathogen-Directed Antibiotic Selection (Global Reference)

These agents reflect convergent IDSA, BOA-BOAST, AAOS and EFORT/European practice. Exact agent and dose vary with local resistance patterns and renal function; the principle (narrow, high-bioavailability, pathogen-directed) is universal.

Beyond persistent infection, chronic osteomyelitis carries a set of structural and systemic complications that are high-yield in the viva. The pathological fracture shown earlier in this topic is one example; the others below complete the picture.

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.

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Practice Variation: High- vs Limited-Resource Settings

Osteomyelitis is bacterial bone infection with Staphylococcus aureus responsible for 80% of cases. The key to chronicity is biofilm formation—bacteria adhere to necrotic bone within a glycocalyx matrix that prevents antibiotic and immune cell penetration. A sequestrum (necrotic bone fragment) acts as a nidus for persistent infection, while the involucrum (new bone shell) forms around the infected segment. The Cierny-Mader classification combines anatomic type (I-IV: medullary, superficial, localized, diffuse) with host status (A-C). MRI is the investigation of choice (90% sensitivity) showing marrow edema and abscess; plain X-ray changes take 10-14 days to appear. Treatment requires surgery plus antibiotics—debride all necrotic tissue, then a pathogen-directed course of roughly 6 weeks (antistaphylococcal penicillin or cefazolin first-line for MSSA). The landmark OVIVA RCT (N=1054) established that oral antibiotics are non-inferior to intravenous therapy once the patient is clinically stable. CRP is superior to ESR for monitoring response.