Osteomyelitis is an infection causing inflammation within the bone and its structures. It can affect any bone, but is frequently found in the long bones of the arms and legs in children, and the vertebrae or pelvis in adults. Because bone tissue is not easily penetrated by immune cells or antibiotics, the infection can rapidly compromise the bone’s blood supply. Untreated osteomyelitis can lead to bone necrosis, systemic illness, and long-term disability, meaning prompt medical attention is necessary.
Defining the Infection and Its Entry Points
The infection is most often caused by bacteria, with Staphylococcus aureus being the organism isolated in the majority of cases. These microorganisms reach the bone through one of three pathways.
The first is hematogenous spread, where bacteria travel from a distant infection site, such as a skin infection or pneumonia, through the bloodstream to seed the bone. This route is common in children, where the highly vascularized growth plates of long bones are susceptible to bacterial colonization.
The second pathway is contiguous spread, which occurs when an infection from adjacent soft tissue, like a pressure ulcer or an infected joint, extends directly into the bone structure. The third method is direct inoculation, which happens when bacteria are introduced straight into the bone. This can result from trauma, such as an open fracture, or during surgical procedures involving orthopedic hardware.
The Progression: Understanding the Stages of Osteomyelitis
The disease progression is categorized into three main stages based on the infection’s duration and pathological changes. Acute osteomyelitis represents the initial phase, generally defined as occurring within the first few weeks of infection. During this time, bacteria multiply and trigger a significant inflammatory response, leading to the formation of pus.
This accumulation of pus within the rigid bone marrow cavity causes a rapid increase in intramedullary pressure. The pressure compromises blood flow and can force the pus to rupture through the bone’s outer layer, the cortex, to accumulate under the periosteum. This subperiosteal collection further impairs the bone’s blood supply, leading to localized ischemia and the beginning of bone tissue death.
If the infection is contained or less aggressive, it may enter a transitional period known as Subacute osteomyelitis. This subacute form is characterized by a more indolent course where the body partially walls off the infection, sometimes forming a localized, pus-filled cavity called a Brodie’s abscess. This stage lacks the intense systemic symptoms and rapid destruction seen in the acute phase.
Chronic osteomyelitis is defined by the presence of necrotic, dead bone tissue, which can persist for months or years. The hallmark of this stage is the formation of a sequestrum, a fragment of devitalized, infected bone that has separated from the living tissue. Since the sequestrum is avascular, it acts as a reservoir for bacteria, shielding them from the body’s immune system and circulating antibiotics.
In response to the irritation of the periosteum, the body attempts to contain the infection by forming new bone growth around the area. This new, dense layer of bone is called the involucrum, which creates a shell encasing the dead sequestrum. Often, a channel or sinus tract will form, extending from the infected bone to the skin surface, allowing purulent material to drain intermittently. The presence of both sequestrum and involucrum is the defining pathological feature of chronic disease.
Current Methods for Diagnosis and Treatment
Diagnosis
Identifying osteomyelitis relies on laboratory tests and imaging studies. Initial blood work often reveals generalized markers of inflammation, such as an elevated C-reactive protein (CRP) level and an increased erythrocyte sedimentation rate (ESR). Blood cultures may also be performed to identify the specific causative organism, especially in cases of acute hematogenous spread.
Imaging begins with plain X-rays, though signs of bone destruction may not be apparent until weeks after the onset of acute infection. Magnetic Resonance Imaging (MRI) is the most sensitive imaging modality, providing detailed views of bone marrow edema and soft tissue involvement early in the disease course. For a definitive diagnosis, a bone biopsy is necessary to obtain a tissue sample for both histopathological examination and culture, ensuring the correct pathogen is identified.
Treatment
Treatment involves a dual approach of antibiotics and surgical intervention. Prolonged courses of intravenous (IV) antibiotics, lasting a minimum of four to six weeks, are the standard initial therapy to eradicate the infection. The specific antibiotic is tailored based on the results of the bone culture and sensitivity testing.
In chronic or advanced acute cases, surgery is frequently required. The procedure involves surgical debridement, the removal of all necrotic and infected tissue, including the sequestrum, to eliminate the bacterial sanctuary. Following debridement, the remaining cavity may need management to obliterate the resulting dead space and promote healing.