Osteomyelitis (Acute and Chronic): Causes, Symptoms, and Treatment

What is Osteomyelitis (Acute and Chronic)?

Osteomyelitis is a purulent (pus-forming) infectious process affecting the bones and the bone marrow contained within them. It is a serious condition that, if not promptly diagnosed and treated, can lead to permanent disability, severe structural bone damage, and in some cases, death.

The infection most commonly develops in bones that are rich in spongy (trabecular) tissue and therefore highly vascularized, meaning they receive a greater blood supply. The bones most frequently affected include:

• Long bones (humerus, femur, tibia)
• The vertebral column (spine)
• The mandible (jawbone)

The primary cause is bacterial, with Staphylococcus aureus being the most frequently implicated pathogen. Osteomyelitis caused by viruses, fungi, or parasites is significantly rarer.

Key Symptoms

The main clinical features of osteomyelitis are:

• Localized bone pain
• Fever and generalized malaise
• Limited range of motion in the affected area
• Swelling and redness of the overlying soft tissues

Diagnosis and Treatment Overview

Diagnosis is initially clinical, based on the recognition of signs and symptoms, supported by elevated inflammatory markers in blood tests (white blood cells/leucocytes and C-reactive protein). Imaging studies, particularly MRI, play a critical confirmatory role.

Treatment requires high-dose antibiotics for prolonged periods. Surgical intervention may become necessary in cases of abscess formation or extensive bone destruction.

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Causes

Epidemiology

From an epidemiological standpoint, osteomyelitis has a marked prevalence in younger age groups: the majority of cases occur before the age of 20 (in childhood and adolescence). However, the condition can affect individuals of any age, and a second peak of incidence is observed in older adults. This often occurs in the context of chronic disease, immunosuppression, or orthopaedic interventions.

Causative Pathogens

The most common causative agent is Staphylococcus aureus, a Gram-positive bacterium responsible for the majority of cases across all age groups. Other bacteria capable of causing osteomyelitis include:

• Escherichia coli
• Klebsiella pneumoniae
• Pseudomonas aeruginosa (particularly in intravenous drug users and immunocompromised patients)
• Salmonella spp. (associated with sickle cell disease)
• Mycobacterium tuberculosis (causing tuberculous osteomyelitis, also known as Pott’s disease when affecting the spine)

Osteomyelitis caused by viruses, fungi, or parasites is considerably rarer and typically occurs in the context of significant immunosuppression.

Routes of Infection

The pathogen can reach the bone marrow and establish infection through several distinct pathways:

1. Haematogenous spread (via the bloodstream): This is the most common route, particularly in children. Bacteria circulating in the blood (bacteraemia) seed the highly vascularized metaphyseal regions of growing long bones. This explains why osteomyelitis most frequently affects bones with the richest blood supply.

2. Direct contamination: This occurs when bacteria are introduced directly into bone tissue, most commonly following:

   • Open (compound) fractures, where bone fragments are exposed through a skin wound
   • Penetrating trauma or bite wounds overlying bone

3. Medical or surgical procedures: Iatrogenic (procedure-related) osteomyelitis can result from:

   • Orthopaedic surgical interventions
   • Joint prosthesis implantation (prosthetic joint infection)
   • Internal fixation of fractures (osteosynthesis)
   • Bone biopsies or injections

4. Contiguous spread from adjacent infected tissue: Infection can extend to bone from a neighboring focus in muscle, soft tissue, or skin, as commonly occurs in diabetic foot infections or pressure ulcers.

Risk Factors

Certain populations carry a significantly elevated risk of developing osteomyelitis:

• Smokers
• Patients with chronic diseases such as diabetes mellitus or renal insufficiency
• Individuals with compromised immune defences, including:
  • Organ transplant recipients (on immunosuppressive therapy)
  • Patients receiving long-term high-dose corticosteroids
  • Patients undergoing chemotherapy
  • Individuals living with HIV/AIDS
• Intravenous drug users (elevated risk of haematogenous spread with atypical organisms)
• Patients with sickle cell disease (increased susceptibility to Salmonella osteomyelitis)
• Individuals with orthopaedic implants (prosthetic joints, fixation hardware)

Classification

Osteomyelitis is classified primarily according to duration of symptoms:

From Acute to Chronic: The Chronification Process

If the infection is not fully eradicated during the acute phase due to antibiotic resistance, high bacterial virulence, or host immunodeficiency, osteomyelitis becomes chronic. This transition involves significant pathological changes in the affected bone:

• Sequestra form: these are areas of necrotic (dead), devascularized bone tissue that become isolated within a surrounding shell of reactive new bone (the involucrum). Sequestra represent the body’s attempt to contain the infection, but they also serve as a protected niche where bacteria can persist, shielded from antibiotics and immune cells.
• Progressive bone sclerosis (hardening) and structural deformity develop over time.
• The dense, sclerotic bone that characterizes chronic osteomyelitis has poor antibiotic penetration, which is why chronic infections are so difficult to eradicate.

These factors combine to make chronic osteomyelitis one of the most challenging orthopaedic infections to treat, with a high risk of relapse and significant patient morbidity. In the most severe cases, this can even lead to limb amputation.

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Symptoms

Osteomyelitis develops most commonly in bones with abundant spongy tissue and rich vascular supply. The most frequently affected bones are:

• Humerus (upper arm)
• Tibia (lower leg)
• Femur (thigh)
• Mandible (jaw)
• Vertebrae (spine)

Clinical Manifestations

The signs and symptoms of osteomyelitis include:

• Localized bone pain: Often severe, worsening with palpation (tenderness on pressure) and movement
• Swelling and redness of the overlying skin and soft tissues
• Restricted range of motion in the affected limb or spinal segment
• Fever, fatigue, and generalized malaise
• Abscess formation with possible spontaneous drainage of pus through the skin (in more advanced or chronic cases)

In children, osteomyelitis may present more subtly: irritability, refusal to use a limb, or reluctance to bear weight are common early signs in young children who cannot clearly articulate pain.

Serious Complications

In severe or untreated cases, significant complications can develop:

• Sepsis and septic shock: Distant dissemination of the infection through the bloodstream, representing a life-threatening emergency
• Pathological fractures: In areas where infected bone has become structurally weakened
• Bone deformity: Particularly relevant in growing children
• Growth arrest: Damage to growth plates (physes) in children can lead to limb length discrepancy or angular deformity
• Septic arthritis: Spread of infection to an adjacent joint
• Chronic disability and limb amputation in the most severe and refractory cases

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Diagnosis

Clinical and Laboratory Assessment

The diagnosis of osteomyelitis is established primarily on the basis of clinical signs and symptoms, supported by laboratory evidence of systemic inflammation:

• Elevated white blood cell count (leucocytosis)
• Elevated C-reactive protein (CRP)
• Elevated erythrocyte sedimentation rate (ESR)
• Elevated platelet count (thrombocytosis)
• Blood cultures should be obtained before antibiotic therapy to identify the causative organism and guide targeted treatment

Imaging Studies

Plain Radiography (X-ray)

Plain radiography is widely available and useful but has significant limitations in the early stages of osteomyelitis. Radiographic changes (periosteal reaction, bone destruction, sclerosis) typically take at least 2 weeks to become visible, as structural bone changes require time to develop. X-rays are therefore often normal in acute early-stage disease.

Magnetic Resonance Imaging (MRI)

MRI is the gold standard imaging modality for diagnosing osteomyelitis. It can detect early bone marrow edema, abscess formation, and soft tissue involvement within days of symptom onset, making it the preferred first-line imaging investigation when osteomyelitis is clinically suspected. MRI has both high sensitivity and specificity for this diagnosis.

Bone Scintigraphy (Bone Scan)

In chronic osteomyelitis, bone scintigraphy (radionuclide scanning using technetium-99m or labelled white blood cells) can be useful to:

• Identify the extent and distribution of active infection
• Detect multifocal disease
• Monitor treatment response over time

It is particularly valuable when MRI is contraindicated (e.g., patients with certain metallic implants).

Microbiological Confirmation

Whenever possible, and particularly before initiating antibiotic therapy, bone biopsy with microbiological culture should be performed to:

• Confirm the diagnosis histologically
• Identify the causative organism
• Determine antibiotic sensitivity and resistance profiles (essential for guiding treatment, especially in the era of methicillin-resistant S. aureus [MRSA])

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Treatment

Antibiotic Therapy

The cornerstone of osteomyelitis treatment is prompt initiation of antibiotic therapy, which must be:

• Started early: ideally after blood cultures and bone biopsy have been obtained, but without undue delay if the patient is systemically unwell.
• Administered at high doses to achieve adequate drug concentrations within bone tissue.
• Continued for prolonged periods: a minimum of 4 to 6 weeks for acute osteomyelitis is standard. Chronic osteomyelitis may require even longer courses.

Treatment typically begins with intravenous (IV) antibiotics to ensure high bioavailability, followed by a step-down to oral antibiotics once clinical improvement is demonstrated and the causative organism has been identified. The choice of antibiotic is guided by the suspected or confirmed pathogen and local antibiotic susceptibility patterns.

For empirical treatment of community-acquired acute osteomyelitis, agents active against S. aureus (including MRSA coverage when appropriate) are typically selected.

Surgical Treatment

Surgical intervention becomes necessary in several scenarios:

• Abscess drainage: Pus collections (subperiosteal or soft tissue abscesses) must be surgically drained promptly, as antibiotic penetration into abscess cavities is insufficient for eradication.
• Debridement (“surgical toilet”): In cases of extensive bone involvement, surgical debridement (the removal of necrotic bone, sequestra, and infected tissue) is essential to achieve infection control. This may need to be repeated in multiple stages.
• Bone reconstruction: Following debridement, bone defects may require reconstruction using bone grafts, vascularized flaps, or other techniques.
• Implant removal: If osteomyelitis develops around orthopaedic hardware (plates, screws, prostheses), removal of the implant is often necessary to eradicate the infection.
• Amputation: In the most severe, refractory, or life-threatening cases, particularly in patients with extensive bone destruction, compromised vascularity (e.g., diabetic foot), or systemic sepsis unresponsive to other measures, amputation may be the only viable option to save the patient’s life.

Prognosis

The prognosis of osteomyelitis depends critically on:

• Timing of diagnosis and treatment initiation (early treatment dramatically improves outcomes)
• Patient immune status and comorbidities
• Causative organism and antibiotic susceptibility
• Whether the infection becomes chronic

Acute osteomyelitis, when diagnosed promptly and treated aggressively, can be cured in the majority of cases. Chronic osteomyelitis, however, carries a significant risk of relapse and long-term disability, and its management remains one of the most challenging problems in orthopaedic surgery and infectious disease.

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Sources and Bibliography

• NHS – Osteomyelitis
• Manuale di Ortopedia e Traumatologia, AA.VV., Ed. Elsevier
• Lew DP, Waldvogel FA. Osteomyelitis. Lancet. 2004;364(9431):369-379.
• Kaplan SL. Osteomyelitis in children. Infect Dis Clin North Am. 2005;19(4):787-797.
• Zimmerli W. Clinical practice: vertebral osteomyelitis. N Engl J Med. 2010;362(11):1022-1029.
• Berbari EF, Kanj SS, Kowalski TJ, et al. 2015 Infectious Diseases Society of America (IDSA) clinical practice guidelines for the diagnosis and treatment of native vertebral osteomyelitis in adults. Clin Infect Dis. 2015;61(6):e26-46.
• Radiopaedia – Osteomyelitis