Version July 2025
INTRODUCTION —
Osteomyelitis is an infection of bone. Osteomyelitis may be classified based on the mechanism of infection (hematogenous, contiguous, direct inoculation), the duration of illness (acute versus chronic), or whether it is associated with an orthopedic device (eg, prosthetic joint) [1].
This topic presents a general approach to diagnosis of native bone osteomyelitis. Issues related to specific osteomyelitis syndromes are discussed in dedicated topics. Examples of such topics include the following:
●(See "Vertebral osteomyelitis in adults: Clinical manifestations and diagnosis".)
●(See "Infectious complications of pressure-induced skin and soft tissue injury".)
●(See "Pelvic osteomyelitis and other infections of the bony pelvis in adults".)
●(See "Osteomyelitis associated with open fractures in adults".)
Issues related to the classification, epidemiology, microbiology, clinical manifestations, and diagnosis of osteomyelitis in adults are presented here. Issues related to treatment of osteomyelitis are discussed separately. (See "Osteomyelitis in the absence of hardware: Approach to treatment in adults".)
Issues related to prosthetic joint infections are discussed separately. (See "Prosthetic joint infection: Epidemiology, microbiology, clinical manifestations, and diagnosis".)
Issues related to osteomyelitis in children are discussed separately. (See "Hematogenous osteomyelitis in children: Evaluation and diagnosis" and "Hematogenous osteomyelitis in children: Management".)
CATEGORIES OF OSTEOMYELITIS
Osteomyelitis can be categorized based on the duration of illness, mechanism of infection, and presence or absence of orthopedic devices [2-4].
●Acute versus chronic osteomyelitis
Acute osteomyelitis typically presents with a symptom duration of a few days or weeks; it can progress to chronic infection.
Chronic osteomyelitis is characterized by long-standing infection over months or years. A hallmark of chronic osteomyelitis is the presence of dead bone (sequestrum). Chronic osteomyelitis may also exhibit involucrum (reactive bony encasement of the sequestrum) and sinus tracts if there is extension through cortical bone. (See "Imaging studies for osteomyelitis", section on 'Pathophysiology'.)
●Mechanism of infection – Infection may occur via the hematogenous route or a nonhematogenous route.
Hematogenous osteomyelitis is caused by pathogens that seed (metastasize) to bone in the setting of bacteremia. In some patients, bacteremia is present at the time of diagnosis of osteomyelitis, but the preceding bacteremia is silent in many patients with hematogenous osteomyelitis.
Nonhematogenous osteomyelitis results from contiguous spread of infection to bone from an adjacent joint or soft tissue infection, or from direct inoculation of infection into bone as a result of trauma, surgery, or injection.
●Native bone infection versus orthopedic device-associated infection
Native bone osteomyelitis is infection of a patient's bone in the absence of hardware.
Orthopedic device infections include infections associated with prosthetic joints, fracture-related infection involving plates, rods, screws, and nails, and spinal implant infections. These infections often have osteomyelitis of the adjacent bone tissue.
Each of the three categories above overlap, but certain types of osteomyelitis have typical profiles. For example, diabetic foot osteomyelitis and pressure ulcer-associated osteomyelitis are usually chronic, contiguous, native bone infections.
EPIDEMIOLOGY
●Hematogenous osteomyelitis – Hematogenous osteomyelitis occurs most commonly in children [5]. (See "Hematogenous osteomyelitis in children: Epidemiology, pathogenesis, and microbiology".)
Vertebral osteomyelitis is the most common form of hematogenous osteomyelitis in adults. Hematogenous osteomyelitis also occurs at other sites, such as the sternal manubrium. Issues related to vertebral osteomyelitis and other types of hematogenous osteomyelitis are discussed separately. (See "Vertebral osteomyelitis in adults: Clinical manifestations and diagnosis" and "Pelvic osteomyelitis and other infections of the bony pelvis in adults".)
Risk factors for hematogenous osteomyelitis include endocarditis, presence of indwelling intravascular devices (eg, vascular catheters, cardiovascular devices) or orthopedic hardware, injection drug use, hemodialysis, and sickle cell disease [6].
●Nonhematologic osteomyelitis – Among younger adults, nonhematogenous osteomyelitis occurs most commonly in the setting of trauma and surgery. Among older adults, nonhematogenous osteomyelitis occurs most commonly as a result of contiguous spread of infection to bone from adjacent soft tissues (such as in the setting of diabetic foot wounds or decubitus ulcers) [2,7].
Risk factors for nonhematogenous osteomyelitis include poorly healing soft tissue wounds, presence of orthopedic hardware, diabetes, peripheral vascular disease, and peripheral neuropathy.
MICROBIOLOGY —
A broad range of pathogens can cause osteomyelitis depending on the mechanism and source of infection.
Hematogenous osteomyelitis, such as vertebral osteomyelitis, is usually caused by a single pathogen, as bacteremia is usually monomicrobial.
In contrast, nonhematogenous osteomyelitis is often polymicrobial if the contiguous infection tends to be polymicrobial; examples include osteomyelitis associated with diabetic foot infection, pressure ulcer, or trauma. (See "Diabetic foot infection, including osteomyelitis: Clinical manifestations and diagnosis", section on 'Microbiology' and "Infectious complications of pressure-induced skin and soft tissue injury", section on 'Microbiology'.)
Staphylococcus aureus, including methicillin-resistant S. aureus (MRSA), is the most common pathogen, regardless of the type of osteomyelitis; the rate of MRSA varies, largely based on regional rates of resistance (table 1) [7-9]. Numerous other microorganisms cause osteomyelitis as well, including other aerobic gram-positive pathogens, aerobic gram-negative bacilli, anaerobic bacteria, mycobacteria, and fungi.
CLINICAL MANIFESTATIONS
Osteomyelitis typically presents with gradual onset of dull pain at the involved site. However, patients with neurologic compromise (eg, peripheral neuropathy, spinal cord injury) may be unable to feel pain at the site of infection.
Local findings (tenderness, warmth, erythema, and swelling) are often present, particularly in the presence of associated soft tissue infection. Systemic symptoms (fever, rigors) are less frequent, and tend to occur in patients with concurrent soft tissue infection or bacteremia.
The presence of a draining sinus tract on examination is considered by many experts to be pathognomonic for chronic osteomyelitis, though rare cases of sinus tracts associated with soft tissue infection have been reported.
The diagnosis of chronic osteomyelitis can be particularly challenging when prosthetic material, extensive skin or soft tissue ulceration, or ischemia are also present [10]. Deep or extensive ulcers that fail to heal after several weeks of appropriate ulcer care should raise suspicion for chronic osteomyelitis, particularly when such lesions overlie bony prominences [10,11].
DIAGNOSIS
When to suspect osteomyelitis — Osteomyelitis should be suspected based on clinical evaluation:
●Nonhematogenous osteomyelitis should be suspected in the setting of new or worsening musculoskeletal pain, particularly in patients with poorly healing soft tissue adjacent to bony structures, signs of cellulitis overlying previously implanted orthopedic hardware, or traumatic injury (including bite and puncture wounds). It should also be suspected in diabetic patients with ulcers that probe to bone or fail to heal despite appropriate wound care.
●Hematogenous osteomyelitis should be suspected in the setting of new or worsening musculoskeletal pain, especially back pain, particularly in the setting of fever and/or recent bacteremia.
Confirming the diagnosis — Definitive diagnosis of osteomyelitis requires isolation of bacteria or fungus from a sterilely obtained bone specimen with histologic evidence of inflammation and osteonecrosis [11].
A diagnosis of osteomyelitis may be inferred in patients with clinical and radiographic findings typical of osteomyelitis and one of the following:
●Positive blood cultures with a typical pathogen, such as S. aureus; in such cases, bone biopsy is not required but may still be useful.
●Bone histopathology consistent with osteomyelitis in the absence of positive culture data (particularly in the setting of recent antibiotic administration).
●If bone biopsy is not performed, persistently elevated inflammatory markers (eg, erythrocyte sedimentation rate [ESR], C-reactive protein [CRP]) and no suspected alternative diagnosis. This diagnostic approach may lead to overdiagnosis of osteomyelitis, given the nonspecific nature of ESR and CRP.
Specific tests — Besides history and physical examination, available tests for diagnosing osteomyelitis include imaging studies, bone biopsy for culture and histopathology, inflammatory markers (eg, ESR, CRP), and others.
In the absence of bone biopsy, a combination of results of these tests can lead to a presumed diagnosis and empiric therapy. Only a bone biopsy can confirm the diagnosis and allow antibiotic therapy targeted to the proven pathogen(s). (See 'Confirming the diagnosis' above.)
Imaging studies — Radiologic imaging is an integral component of the evaluation for suspected osteomyelitis. The optimal radiographic modality depends on specific clinical circumstances and should be tailored accordingly.
Although imaging studies cannot definitively confirm the presence of osteomyelitis, imaging results consistent with osteomyelitis markedly increase the probability of osteomyelitis in patients with compatible clinical findings [12].
We usually obtain a plain x-ray as the initial study if we suspect osteomyelitis (algorithm 1). Plain x-rays have lower sensitivity and specificity than other tests, but they are readily available and are useful for screening for fracture, metallic foreign body, gas in soft tissue, and other alternative or concomitant diagnoses.
For patients who require further imaging, we obtain magnetic resonance imaging (MRI) (algorithm 1). MRI is highly sensitive for osteomyelitis and can detect and delineate associated soft tissue infection. Other imaging options include computed tomography (CT), and nuclear imaging studies (eg, positron emission tomography [PET], bone scan, tagged white blood cell scan).
Detailed discussion of these imaging modalities for osteomyelitis is found separately. (See "Imaging studies for osteomyelitis".)
Cultures
Bone biopsy as gold standard — Bone biopsy is the only definitive way to confirm osteomyelitis. (See 'Confirming the diagnosis' above.)
Indications — In order to confirm the diagnosis of osteomyelitis and guide antibiotic therapy in patients with suspected osteomyelitis, bone biopsy for both histopathology and culture should be obtained when feasible.
Bone biopsy is particularly helpful in the following circumstances [13]:
●Diagnostic uncertainty
●Concern for antibiotic-resistant organism
●Failure of empiric antibiotic therapy
●Suspicion of atypical pathogen (eg, tuberculosis, fungus, Brucella spp)
Bone biopsy is not always routinely available or practical. In such instances, a presumptive diagnosis of osteomyelitis is based on clinical and radiographic assessment. (See 'Confirming the diagnosis' above.)
Results — Bone biopsy is the gold standard for diagnosing osteomyelitis [14]. Furthermore, culture results increase the likelihood that effective and targeted antibiotic therapy is given.
●Histopathology – Histopathology of bone specimens is particularly helpful in cases of diagnostic uncertainty, especially if bone cultures are negative or grow suspected contaminants or if diagnoses other than osteomyelitis are in the differential (eg, malignancy).
A presumptive diagnosis of osteomyelitis can be made based on histopathology, especially if Gram stain or other stains (eg, fungal, mycobacterial) are positive. (See 'Confirming the diagnosis' above.)
Histopathologic features of osteomyelitis include necrotic bone with extensive resorption adjacent to an inflammatory exudate [15].
●Bone culture – Bone cultures provide information to guide antibiotic therapy [16,17]. In studies of the value of bone biopsy, positive bone culture resulted in a change of antibiotics in 59 to 87 percent of patients; most patients underwent narrowing of coverage, but some received broader-spectrum agents after bone culture results [16,18].
Swab cultures, sinus tract cultures, and superficial wound biopsy should not be used, because the correlation between results of bone biopsy and nonbone cultures is poor [8,19-22].
In some cases, bone culture results are discordant with histopathology results [8,17,20,21,23,24]. In patients without osteomyelitis, culture may be positive due to sampling through infected soft tissue. Conversely, patients with osteomyelitis may have negative cultures if they received antibiotics prior to biopsy or if sampling error occurred.
Compared with culture results, advanced molecular tests (eg, 16S rRNA polymerase chain reaction [PCR] or DNA sequencing) may detect more organisms than routine cultures of samples [25]. However, in real-world settings, the yield of advanced molecular tests is lower when done only on culture-negative specimens [26]. Furthermore, the specificity of such advanced molecular testing is likely to be poor, because the tests cannot differentiate true from commensal pathogens [14,22,27-32]. In general, we limit the use of molecular diagnostic testing to culture-negative specimens when organism identification is critical to guide management, and/or in the setting of recurrent or persistent infection despite empiric treatment.
Timing and technique
●Timing – Ideally, bone biopsy is performed before initiation of antibiotic therapy to increase microbiologic yield. However, in many patients, antibiotics have already been administered by the time biopsy is obtained.
The effect of antibiotics on bone culture results is unclear. Some studies suggest that antibiotics alter microbiologic yield, whereas other studies have found no effect [7,14,33-36]. The duration of administered antibiotic therapy may matter; one study found that antibiotic administration of fewer than four days did not impact culture-yield [37].
Ultimately, the timing of biopsy relative to antibiotics is dependent on many variables. Patients who have significant soft tissue infection or severe illness should receive antibiotics without delay to prevent spread of infection. For stable patients with minimal soft tissue infection, withholding antibiotics until after biopsy is reasonable; if such patients are already receiving antibiotics, some clinicians discontinue antibiotics for a period of time prior to obtaining biopsy.
The optimal antibiotic-free period prior to biopsy is uncertain. Some experts suggest a two-week antibiotic-free interval. Studies results vary substantially; one study of found that withholding antibiotics for at least four days optimized culture results [7,14,34].
●Biopsy technique – Bone biopsies are obtained either intraoperatively during debridement, or by percutaneous biopsy [38]. If performed percutaneously, sampling through intact uninfected skin under radiographic guidance is preferred.
At least two specimens should be obtained: one for Gram stain and culture (including aerobic and anaerobic culture) and the other for histopathology [39]. During surgical debridement, multiple bone samples may be collected to optimize yield. Fungal and mycobacterial cultures are unnecessary in most cases unless those pathogens are suspected; such cultures may be more helpful for vertebral osteomyelitis [40]. (See "Vertebral osteomyelitis in adults: Clinical manifestations and diagnosis", section on 'Importance of biopsy'.)
Blood cultures — The utility of blood cultures is low in most cases of osteomyelitis. However, in patients with suspected hematogenous infection (eg, vertebral osteomyelitis), signs of systemic toxicity (eg, fever), or severe skin and soft tissue infection, blood cultures are higher yield and should be collected [2,41-43].
Positive blood cultures may obviate the need for a biopsy if the blood isolate is a pathogen likely to cause osteomyelitis. (See 'Confirming the diagnosis' above.)
Other cultures — In patients with contiguous osteomyelitis, superficial swabs of wounds, sinus tract cultures, and tissue aspirates should not be used to establish an osteomyelitis pathogen. Cultures from these specimens often grow organisms that colonize the skin or chronic wounds. Particularly in the setting of diabetic foot osteomyelitis, decubitus ulcers, and postoperative and posttraumatic settings, the correlation between bone biopsy and nonbone culture specimens is poor [8,19-21].
●In patients with osteomyelitis due to contiguous infection, superficial wound swabs or aspiration of adjacent infected tissue are of minimal value. In one study comparing bone culture with swab culture among 76 patients with diabetic foot osteomyelitis who received no antibiotics for at least four weeks prior to culture, the concordance across isolates was low (23 percent overall; 43 percent for S. aureus, 29 percent for gram-negative bacilli, and 26 percent for streptococci) [8]. Similarly, in a study of patients with diabetic foot infection comparing percutaneous bone biopsy with needle aspiration of soft tissue adjacent to the bone, bone biopsy culture correlated with needle aspirate culture in only 32 percent of cases; among patients with a positive bone culture, needle aspirate culture was negative in 38 percent [21].
●Sinus tract cultures may be of some use for prediction of osteomyelitis if S. aureus or Salmonella spp are identified; however, in general, such cultures are not worthwhile because the results do not correlate reliably with the pathogen in the underlying bone [8,19,44-46]. In one report including 40 patients with chronic osteomyelitis, only 44 percent of sinus tract cultures contained the pathogen isolated from a deep surgical specimen [46].
In contrast to contiguous osteomyelitis, in patients with hematogenous osteomyelitis, culture of inflamed soft tissue or abscess adjacent to infected bone may identify causative pathogens with higher sensitivity than bone cultures themselves [34,47,48].
Inflammatory markers (eg, ESR, CRP)
ESR and CRP are often elevated in patients with osteomyelitis [49,50]. White blood cell count may be elevated as well, particularly in patients with acute osteomyelitis [51,52].
ESR and CRP are traditionally thought to have high sensitivity for osteomyelitis; however, a 2022 literature review found sensitivity ranges of 49 to 79 percent for ESR and 45 to 76 percent for CRP [7].
Specificity of inflammatory markers is suboptimal; conditions besides osteomyelitis that cause elevated markers include soft tissue infection, inflammatory arthritis, myositis, trauma, malignancy (eg, sarcoma), and other inflammatory disorders.
Inflammatory markers do not provide additional diagnostic information in patients who have had other more sensitive and more specific studies (eg, MRI) [7]. Furthermore, the value of following inflammatory markers to assess response to therapy is doubtful as observational data are not able to predict clinical failure any better than a clinician's examination. Of note, ESR decreases at a slower rate than CRP due to its physiology, sometimes continuing to rise for several weeks during treatment in patients who are ultimately cured [53].
Other inflammatory markers, such as procalcitonin, have not been shown to have better accuracy in the limited studies available [7].
"Probe-to-bone" test — In patients with diabetic foot ulcers, the ability to probe to bone with a sterile blunt metal tool has been shown to correlate with the presence of osteomyelitis [11,54-59]. (See "Diabetic foot infection, including osteomyelitis: Clinical manifestations and diagnosis", section on '"Probe-to-bone" test'.)
In practice, this test has been used for evaluating nondiabetic ulcers due to peripheral neuropathy, vasculopathy, or pressure ulcers. However, the performance characteristics have not been evaluated in these settings. Furthermore, the reliability of the probe-to-bone test may vary by the ulcer location and the expertise of the clinician performing the test [56,57]. The authors recommend against using a positive probe-to-bone test for confirmation of osteomyelitis outside of the diabetic foot.
COMPLICATIONS —
Complications of osteomyelitis include both infectious and noninfectious conditions.
Infectious complications — Infectious complications generally occur as a consequence of spread from the bone to adjacent tissues or elsewhere in the body, and include the following:
●Sinus tract formation
●Contiguous soft tissue infection
●Abscess
●Septic arthritis
●Systemic infection
Noninfectious complications — Osteomyelitis can lead to permanent bone damage that may result in bone deformity or increased risk for bone fracture [60].
Rare cases of carcinoma, including squamous cell carcinoma and sarcoma, at the site of chronic osteomyelitis have been reported, mostly in individuals with osteomyelitis of an extremity [61-71]. Histopathologic examination of a tissue biopsy can differentiate infection from carcinoma.
DIFFERENTIAL DIAGNOSIS —
The differential diagnosis of osteomyelitis includes:
●Soft tissue infection – Clinical features of soft tissue infection are similar to those of osteomyelitis (eg, focal tenderness, erythema). Furthermore, many patients with osteomyelitis also have soft tissue infection. A clue to underlying osteomyelitis may be failure of soft tissue infection to resolve with antibiotic therapy. Imaging may be necessary to differentiate these infections. (See 'Imaging studies' above.)
●Charcot arthropathy – Charcot neuroarthropathy occurs in patients with diabetes, and often presents with localized erythema and warmth. It can be difficult to determine if such patients have Charcot arthropathy or osteomyelitis (or both). Certain imaging studies may be able to differentiate these conditions, but imaging may not be definitive. Bone biopsy may be necessary for definitive diagnosis. (See 'Imaging studies' above and "Diabetic neuroarthropathy".)
●Osteonecrosis – Osteonecrosis (avascular necrosis of bone) is usually relatively easy to distinguish from osteomyelitis since a precipitating cause is usually present (such as steroids, radiation, or bisphosphonate use). However, osteomyelitis may complicate pre-existing osteonecrosis, including in patients with sickle cell disease and mandibular osteonecrosis. (See "Risks of therapy with bone antiresorptive agents in patients with advanced malignancy", section on 'Osteonecrosis of the jaw' and "Treatment of nontraumatic hip osteonecrosis (avascular necrosis of the femoral head) in adults".)
●Fracture – Osteomyelitis can mimic the appearance of fracture on radiographic imaging. Fracture is typically associated with antecedent trauma. In some cases, bone biopsy may be required to distinguish these two entities, particularly in the absence of healing following suspected fracture. (See "General principles of fracture management: Early and late complications".)
●Bone tumor – Both osteomyelitis and bone tumor can present with bone pain [72,73]. Bone tumor is generally distinguished by radiographic imaging and bone biopsy. (See "Bone tumors: Diagnosis and biopsy techniques".)
●Sickle cell vaso-occlusive pain crisis – In patients with sickle cell disease, the clinical presentation of osteomyelitis can be difficult to distinguish from a vaso-occlusive pain crisis. Osteomyelitis is more likely to be associated with a prolonged duration of pain localized to a single site and may be associated with fever. (See "Acute and chronic bone complications of sickle cell disease", section on 'Osteomyelitis and septic arthritis'.)
●Synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO) – SAPHO syndrome consists of a wide spectrum of neutrophilic dermatoses associated with aseptic osteoarticular lesions. It can mimic osteomyelitis in patients who lack the characteristic findings of pustulosis and synovitis. The diagnosis is established via clinical manifestations; bone culture is sterile in the setting of osteitis. (See "SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome" and "Major causes of musculoskeletal chest pain in adults", section on 'Sternocostoclavicular hyperostosis (SAPHO syndrome)'.)
●Complex regional pain syndrome (CRPS) – CRPS is characterized by pain, swelling, limited range of motion, skin changes, and patchy bone demineralization, usually of the distal limbs. It frequently begins following a fracture, soft tissue injury, or surgery and is associated with vasomotor instability. MRI can usually differentiate between osteomyelitis and CRPS. (See "Complex regional pain syndrome in adults: Pathogenesis, clinical manifestations, and diagnosis".)
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Osteomyelitis and prosthetic joint infection in adults".)
INFORMATION FOR PATIENTS —
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Osteomyelitis in adults (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Overview – This topic presents a general approach to the diagnosis of native bone osteomyelitis. Issues related to specific osteomyelitis syndromes are discussed in dedicated topics. (See 'Introduction' above.)
Examples of such topics include the following:
•(See "Vertebral osteomyelitis in adults: Clinical manifestations and diagnosis".)
•(See "Infectious complications of pressure-induced skin and soft tissue injury".)
•(See "Pelvic osteomyelitis and other infections of the bony pelvis in adults".)
•(See "Osteomyelitis associated with open fractures in adults".)
●Classification – Osteomyelitis can be categorized based on the duration of illness, mechanism of infection, and presence or absence of orthopedic devices. (See 'Categories of osteomyelitis' above.)
●Risk factors – (See 'Epidemiology' above.)
•Hematogenous osteomyelitis (eg, vertebral osteomyelitis) – Risk factors include endocarditis, presence of indwelling intravascular devices (eg, vascular catheters, cardiovascular devices) or orthopedic hardware, injection drug use, hemodialysis, and sickle cell disease.
•Nonhematogenous osteomyelitis (ie, contiguous) – Risk factors include poorly healing soft tissue wounds, presence of orthopedic hardware, diabetes, peripheral vascular disease, and peripheral neuropathy.
●Microbiology – Staphylococcus aureus, including methicillin-resistant S. aureus (MRSA), is the most common pathogen, regardless of the type of osteomyelitis. Other causes include aerobic gram-positive pathogens other than S. aureus, aerobic gram-negative bacilli, anaerobic bacteria, mycobacteria, and fungi. (See 'Microbiology' above.)
●Clinical manifestations – Osteomyelitis typically presents with gradual onset of dull pain at the involved site. Local findings (tenderness, warmth, erythema, and swelling) are often present. (See 'Clinical manifestations' above.)
●Diagnosis – Definitive diagnosis of osteomyelitis requires isolation of bacteria or fungus from a sterilely obtained bone specimen with histologic evidence of inflammation and osteonecrosis. (See 'Confirming the diagnosis' above.)
The diagnosis may be presumed in patients with clinical and radiographic findings typical of osteomyelitis and one of the following:
•Positive blood cultures with a typical pathogen, such as S. aureus; in such cases, bone biopsy is not required but may still be useful.
•Bone histopathology consistent with osteomyelitis in the absence of positive culture data (particularly in the setting of recent antibiotic administration).
•If bone biopsy is not performed, persistently elevated inflammatory markers (eg, erythrocyte sedimentation rate [ESR], C-reactive protein [CRP]) and no suspected alternative diagnosis. This diagnostic approach may lead to overdiagnosis.
●Imaging – We usually obtain a plain x-ray as the initial study if we suspect osteomyelitis. For patients who require further imaging, we obtain an MRI (algorithm 1). (See 'Imaging studies' above.)
●Differential diagnosis – Soft tissue infection without underlying osteomyelitis is in the differential, as well as fractures and numerous bone disorders. (See 'Differential diagnosis' above.)
