Pathogenesis and morphological changes
The development of osteomyelitis goes through several regular stages. Initially, bacterial contamination causes local inflammation with increased vascular permeability and edema. The accumulation of purulent exudate increases the pressure inside the medullary canal. This inevitably leads to ischemia and subsequent necrosis of the bone tissue. Pus can break through under the periosteum, forming a subperiosteal abscess (sub-periosteal abscess).
Key morphological elements of the chronic form:
- Sequestrum (sequestrum) is a piece of dead, infected bone that has separated from healthy tissue.
- Involucrum (involucrum) is a capsule of newly formed bone tissue that surrounds the focus of infection and the sequestrum in an attempt to isolate it.
Vascular anatomy directly influences localization. In children, infection frequently settles in the metaphyses of long tubular bones. This is because narrow capillaries make a sharp hairpin-like bend there, slowing down blood flow and allowing bacteria to enter the tissue. In infants under 18 months of age, these capillaries pierce the growth plate entirely, allowing the infection to easily penetrate the joint, causing septic arthritis (septic arthritis).
Clinical presentation and diagnostics
Unlike the acute phase, chronic osteomyelitis in children and adults presents without fever and pronounced symptoms of systemic intoxication. The patient may look entirely healthy. The main symptom is sharply localized pain that worsens with physical activity and subsides at rest. Locally, moderate tenderness on palpation and mild edema are noted.
Diagnostic algorithm:
- Laboratory markers: Normal ESR and CRP levels help to reliably rule out the diagnosis. Meanwhile, the leukocyte count may remain normal even during an active process. CRP is well suited for monitoring treatment response.
- Diagnostic imaging: Plain radiography allows visualization of sclerotic areas (sequestra) and exclusion of other pathologies (fractures, metastases). However, the gold standard and imaging modality of choice is MRI, which clearly visualizes intramedullary edema.
- Bone biopsy: A critically important step. It not only confirms the diagnosis but also allows precise identification of the pathogen to select antibiotics (e.g., detecting typical Staphylococcus aureus or Salmonella in sickle cell anemia).
Principles of surgical treatment
Chronic osteomyelitis cannot be cured conservatively because systemic antibiotics do not penetrate avascular necrotic bone. The mainstay of treatment is radical surgical debridement (surgical debridement).
During the surgery, the physician exposes the focus, completely excises the infected tissue, removes all sequestra and any previously left metal implants. Local antibiotic carriers are placed into the resulting bone defect (trough):
- Calcium sulfate: a biodegradable material that is absorbed on its own.
- Polymethyl methacrylate (PMMA): bone cement that provides structural support but requires a repeat operation for removal.
If the infection has developed around a joint prosthesis, two-stage revision arthroplasty is used: removal of the old joint, control of the infection, and only then implantation of a new one.
Complications and prognosis
Even with adequate surgical and medical treatment, pathogen eradication is not always achieved (failures occur in approximately 25% of cases).
The chronic course threatens serious orthopedic problems:
- Impaired bone healing or non-union of fractures (nonunion).
- Bone deformity due to malunion (malunion).
- Formation of sinus tracts (sinus tract), which in rare cases may undergo malignant transformation.
- Spread of the purulent process to adjacent joints and soft tissues.
In advanced cases with irreversible vascular changes or total bone destruction, the only option remains amputation.
Briefly: answers to topical questions
What microorganisms are typical causative agents of chronic osteomyelitis?
Typical causative agents of chronic osteomyelitis include bacteria, fungi, and mycobacteria. Staphylococci play a leading role.
- Staphylococci are the main pathogen, detected in 60–80% of cases; they are frequently found in association with other microorganisms, including asporogenous anaerobes.
- Staphylococcus aureus is the most common pathogen in patients without comorbidities.
- Salmonella is the most common pathogen in individuals with sickle cell anemia.
- Pseudomonas aeruginosa in association with staphylococcus causes severe intoxication and extensive destructive processes.
- Streptococci, Klebsiella, mycobacteria, and pathogenic fungi, including Candida, may also occur.
In post-typhoid osteomyelitis, the causative agent is usually ordinary pyogenic microflora with reduced virulence.
What radiographic features are characteristic of chronic osteomyelitis?
Chronic osteomyelitis is characterized by a combination of bone destruction processes and new bone formation. The main radiological signs include:
- Sequestrum (sequestrum) — a focus of increased density (opacity) representing an area of dead bone tissue.
- Involucrum (involucrum) — a capsule of newly formed bone tissue surrounding the sequestrum.
- Osteosclerosis — marked thickening of the bone structure.
- Periostitis — inflammatory changes of the periosteum.
- Osteomyelitic cavities — areas of destruction alternating with zones of osteoporosis.
What anatomical and physiological classifications of chronic osteomyelitis exist?
The anatomical classification of osteomyelitis is represented by the Cierny-Mader system, which distinguishes four stages of involvement:
- Stage 1 — infection is limited to the medullary cavity (medullary cavity).
- Stage 2 — superficial infection involving the bone cortex (cortex).
- Stage 3 — involvement of the cortex and medullary substance without loss of structural stability.
- Stage 4 — involvement is accompanied by loss of structural stability.
The physiological part of this classification further subdivides patients depending on the host's health status (presence of diabetes mellitus, vascular insufficiency, neuropathy, and other factors).
What primary chronic (atypical) forms of osteomyelitis exist?
Primary chronic (atypical) forms of osteomyelitis include diseases that proceed sluggishly or subacutely from the very beginning, without a pronounced acute stage. The following forms are distinguished:
- Brodie's abscess (Brodie's abscess) — an intraosseous purulent process forming an isolated cavity with a sclerotic rim, usually without sequestra.
- Garré's sclerosing osteomyelitis (Garré's sclerosing osteomyelitis) — a non-purulent form with markedly pronounced sclerosis, fusiform thickening of the diaphysis, and narrowing of the medullary canal.
- Ollier's albuminous osteomyelitis — a form in which, instead of pus, serous fluid rich in proteins or mucin accumulates.
- Tumor-like osteomyelitis — a rare form simulating a bone neoplasm with the presence of a soft tissue infiltrate.
To understand the structure of the lesion, remember the SIN acronym: Sequestrum (dead center), Involucrum (new living shell around it), Necrosis (the core process inside).
Class and exam questions
Can chronic osteomyelitis be cured with pills or IV infusions alone?
No. Due to sequestration and impaired blood supply within the lesion, antibiotics simply cannot reach the bacteria. Without surgical removal of the dead tissue, treatment is ineffective.
How to differentiate osteomyelitis from a bone tumor (e.g., Ewing's sarcoma)?
In orthopedics, there is a rule: what looks like a tumor may be an infection. Ewing's sarcoma can also cause pain and fever. A biopsy is the only way to definitively differentiate them.
Why can osteomyelitis not be ruled out when leukocyte counts are normal?
White blood cell (WBC) count is a non-specific marker and often remains within normal limits in chronic disease. Normal ESR and CRP values are used to rule out the diagnosis.
What else to study on this topic
- Cierny-Mader classification of osteomyelitis (anatomical stages 1–4).
- Differential diagnosis with Charcot neuroarthropathy in diabetic neuropathy.
- Features of empirical and targeted antibiotic therapy in children and adults.
- Radiological signs of fracture nonunion in the setting of infection.
- Clinical features of infection in intravenous drug users (vertebral osteomyelitis).
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