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Official reprint from UpToDate®

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Nonvertebral osteomyelitis in adults: Clinical

manifestations and diagnosis
Authors: Tahaniyat Lalani, MBBS, MHS, Steven K Schmitt, MD, FIDSA
Section Editor: Denis Spelman, MBBS, FRACP, FRCPA, MPH
Deputy Editor: Keri K Hall, MD, MS

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Feb 2023. | This topic last updated: Oct 18, 2022.

INTRODUCTION

Osteomyelitis is an infection involving bone. Osteomyelitis may be classified based on the

mechanism of infection (hematogenous versus nonhematogenous) and the duration of illness
(acute versus chronic) [1].

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 "Nonvertebral osteomyelitis in adults: Treatment".)

Issues related to vertebral osteomyelitis, pelvic and sacral osteomyelitis, and osteomyelitis in
the setting of trauma are discussed in detail separately. (See "Vertebral osteomyelitis and
discitis in adults" and "Pelvic osteomyelitis and other infections of the bony pelvis in adults" and
"Osteomyelitis associated with open fractures 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".)

CLASSIFICATION
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Osteomyelitis may be classified based on the duration of illness (acute versus chronic) and the
mechanism of infection (hematogenous versus nonhematogenous). This approach to
classification was described by Lew and Waldvogel [2-4].

Acute osteomyelitis typically presents with a symptom duration of a few days or weeks.
Sequestra (pieces of necrotic bone that separate from viable bone) are absent.

Chronic osteomyelitis is characterized by long-standing infection over months or years.

Sequestra are usually present; they form as a result of bone ischemia and necrosis in the
context of blood vessel compression due to elevated medullary pressure associated with bone
marrow inflammation. Sequestra can be seen radiographically. The presence of a sinus tract is
pathognomonic of chronic osteomyelitis. (See "Approach to imaging modalities in the setting of
suspected nonvertebral osteomyelitis".)

Nonhematogenous osteomyelitis can occur as a result of contiguous spread of infection to

bone from adjacent soft tissues and joints or via direct inoculation of infection into the bone (as
a result of trauma or surgery).

Hematogenous osteomyelitis is caused by microorganisms that seed the bone in the setting of
bacteremia.

NONHEMATOGENOUS OSTEOMYELITIS

Nonhematogenous osteomyelitis can occur as a result of contiguous spread of infection to

bone from adjacent soft tissues and joints or via direct inoculation of infection into the bone (as
a result of trauma, bite wounds, or surgery).

Epidemiology — Among younger adults, nonhematogenous osteomyelitis occurs most

commonly in the setting of trauma and related surgery. Among older adults,
nonhematogenous osteomyelitis occurs most commonly as a result of contiguous spread of
infection to bone from adjacent soft tissues and joints (such as in the setting of diabetic foot
wounds or decubitus ulcers) [2].

Risk factors for nonhematogenous osteomyelitis include poorly healing soft tissue wounds
(including decubitus ulcers), presence of orthopedic hardware, diabetes, peripheral vascular
disease, and peripheral neuropathy.

Microbiology — Nonhematogenous osteomyelitis may be polymicrobial or monomicrobial.

Staphylococcus aureus (including methicillin-resistant S. aureus), coagulase-negative
staphylococci, and aerobic gram-negative bacilli are the most common organisms. In one study,
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staphylococci were isolated in 53 percent of bone biopsy specimens, enterococci in 8 percent,

streptococci in 12 percent, and anaerobes in 5 percent [5].

Other pathogens including corynebacteria, fungi, and mycobacteria have also been implicated
[4-10].

Clinical manifestations

Signs and symptoms — Acute osteomyelitis typically presents with gradual onset of
symptoms over several days. Patients usually present with dull pain at the involved site, with or
without movement. Local findings (tenderness, warmth, erythema, and swelling) and systemic
symptoms (fever, rigors) may also be present. Patients with osteomyelitis involving the hip,
vertebrae, or pelvis tend to manifest few signs or symptoms other than pain.

Chronic osteomyelitis may manifest as pain, erythema, or swelling, sometimes in association

with a draining sinus tract; fever is usually absent. Chronic osteomyelitis may also present with
intermittent flares of pain and swelling. The presence of a sinus tract is pathognomonic of
chronic osteomyelitis.

The diagnosis of chronic osteomyelitis can be particularly challenging when prosthetic material,
extensive skin or soft tissue ulceration, or ischemic changes due to vascular insufficiency are
also present [11]. 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 [11,12]. Chronic osteomyelitis may also present as a nonhealing
fractures.

Patients with diabetes and chronic osteomyelitis may present with atypical findings. Diabetics
who develop cutaneous ulcers often develop osteomyelitis before exposed bone is present on
exam [11]. If a diabetic foot ulcer is larger than 2 cm2 or if exposed bone is present,
osteomyelitis is highly likely [11,13]. (See "Clinical manifestations, diagnosis, and management
of diabetic infections of the lower extremities".)

Osteomyelitis of the foot may develop following nail puncture through a shoe; Pseudomonas
aeruginosa is a typical pathogen in such cases. (See "Infectious complications of puncture
wounds" and "Pseudomonas aeruginosa skin and soft tissue infections", section on 'Infection
following nail puncture'.)

Probing to bone — Probing to bone with a sterile blunt metal tool should be included in the
initial assessment of diabetic patients with infected pedal ulcers. A positive result consists of

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detection of a hard, gritty surface [12-14]. The reliability of the probe-to-bone test may vary by
the ulcer location and the expertise of the clinician performing the test [15,16].

The performance characteristics of the test have been evaluated in the setting of diabetic foot
ulcers. In practice, the test is also used for evaluating nondiabetic ulcers due to peripheral
neuropathy, vasculopathy, or pressure sores, although the performance characteristics have
not been evaluated in these settings.

In a systematic review evaluating the performance of the probe-to-bone test (using bone
histopathology or culture as the reference standard), the pooled sensitivity and specificity for
the test were 87 and 83 percent, respectively [17]. An important limitation was the potential for
selection and verification bias; the studies included in the analysis did not specify whether the
results of the probe-to-bone test influenced pursuit of bone biopsy or culture nor whether
interpreters of the reference standard were blinded to results of the probe-to-bone test.

The probe-to-bone test should be used as a screening tool in conjunction with the patient's
pretest probability for osteomyelitis to determine whether additional tests (such as
radiographic imaging or bone biopsy) are needed for diagnosis of diabetic foot osteomyelitis
[18].

Laboratory tests — Laboratory findings are nonspecific. In the setting of acute osteomyelitis,
leukocytosis and elevated serum inflammatory markers (erythrocyte sedimentation rate [ESR]
and/or C-reactive protein [CRP]) may be observed [19,20]. In the setting of chronic
osteomyelitis, leukocytosis is uncommon; the ESR and/or CRP may be elevated or normal
[21,22].

HEMATOGENOUS OSTEOMYELITIS

Hematogenous osteomyelitis is caused by microorganisms that seed the bone in the setting of
bacteremia.

Epidemiology — Hematogenous osteomyelitis occurs most commonly in children [23]. (See

"Hematogenous osteomyelitis in children: Epidemiology, pathogenesis, and microbiology".)

Vertebral osteomyelitis is the most common form of hematogenous osteomyelitis in adults.

Issues related to vertebral osteomyelitis are discussed separately. (See "Vertebral osteomyelitis
and discitis in adults".)

Among adults, hematogenous osteomyelitis accounts more frequently in males. Most cases
occur in patients >50 years [24], except for injection drug users, most of whom are <40 years of
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age [25].

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 [26].

Microbiology — Hematogenous osteomyelitis occurs following bacteremia. Patients may

present following clearance of bacteremia, so blood cultures are not always positive.

Hematogenous osteomyelitis is usually monomicrobial; S. aureus is by far the most commonly

isolated organism. In some cases, hematogenous osteomyelitis due to S. aureus presents with
multifocal involvement [2,27-29]. Aerobic gram-negative rods are identified in up to 30 percent
of cases.

Among injection drug users, hematogenous osteomyelitis due to P. aeruginosa and Serratia
marcescens has been described [30]. Among immunosuppressed patients, hematogenous
osteomyelitis due to Aspergillus spp has been described [31].

Hematogenous osteomyelitis due to beta-hemolytic streptococci is relatively rare (<1 percent of

cases) [32]. Other less common pathogens include Mycobacterium tuberculosis [33], Candida spp
[34-36], Bartonella henselae [37], Coccidioides immitis [38,39], and Cutibacterium (formerly
Propionibacterium) acnes [40].

Clinical manifestations

Signs and symptoms — In general, signs and symptoms of hematogenous osteomyelitis may
be indistinguishable from those of nonhematogenous osteomyelitis, discussed above. (See
'Signs and symptoms' above.)

Signs and symptoms referable to specific forms of hematogenous osteomyelitis are discussed
in the following sections.

Forms of disease — Clinical manifestations of hematogenous osteomyelitis mirror those of

nonhematogenous osteomyelitis. (See 'Clinical manifestations' above.)

Clinical presentations that are unique to hematogenous osteomyelitis are discussed in the
following sections. In some cases, adults with hematogenous osteomyelitis may have no local
symptoms referable to bones; soft tissue findings may be more prominent.

● Vertebral osteomyelitis – Vertebral osteomyelitis is the most common form of

hematogenous osteomyelitis in adults. Issues related to vertebral osteomyelitis are

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discussed separately. (See "Vertebral osteomyelitis and discitis in adults".)

● Sternoclavicular and pelvic osteomyelitis – After vertebral osteomyelitis, next most

common sites of hematogenous osteomyelitis in adults are the flat bones of the axial
skeleton (such as the sternoclavicular and pelvic bones). These sites are involved most
frequently among injection drug users; multifocal involvement may be observed in these
patients [41-43].

Specific signs and symptoms of sternoclavicular osteomyelitis include anterior chest wall
swelling, pain, and tenderness. Sternoclavicular osteomyelitis may present as a mass that
is mistaken for a soft tissue abscess or atypical cellulitis. It can also present as infection of
the manubriosternal symphysis (a fibrocartilage union of the manubrium and the body of
the sternum). In addition, sternoclavicular osteomyelitis can develop as a complication of
mediastinitis. Local symptoms include pain, swelling, erythema, and tenderness over the
sternoclavicular joint, and infection can extend into the surrounding soft tissue including
the pectoralis major. (See "Postoperative mediastinitis after cardiac surgery".)

Issues related to pelvic osteomyelitis are described separately. (See "Pelvic osteomyelitis
and other infections of the bony pelvis in adults".)

● Long-bone osteomyelitis – The least common sites of hematogenous osteomyelitis in

adults are the long bones of the appendicular skeleton (in contrast, this is the most
common site of hematogenous osteomyelitis in children) [44]. The clinical presentation is
variable; some present subacutely with low-grade fever and vague pain at the site of
infection, while others present acutely with high fever, sharp pain, and swelling over the
involved site. Long-bone osteomyelitis may be classified based on the degree of bone
involvement as well as host factors ( table 1) [45]. (See "Hematogenous osteomyelitis in
children: Clinical features and complications".)

Long-bone osteomyelitis can also present as septic arthritis of the knee, hip, or shoulder.
This occurs if infection within the metaphysis (the most common site of infection in long-
bone osteomyelitis) breaks through the bone cortex, leading to discharge of pus into the
joint. The clinical manifestations, diagnosis, and management of septic arthritis are
described separately. (See "Septic arthritis in adults".)

• Brodie abscess – A Brodie abscess consists of a region of suppuration and necrosis

encapsulated by granulation tissue within a rim of sclerotic bone. Brodie abscess
occurs in the setting of subacute or chronic osteomyelitis in the metaphysis of long
bones, typically in patients <25 years of age [46]. It is usually of hematogenous origin
but can also occur in the setting of trauma.
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The most common pathogen is S. aureus; other gram-positive and gram-negative

organisms (including P. aeruginosa, Klebsiella spp, and other gram-negative rods) may
be seen. Cultures may be sterile in up to half of cases.

Patients with Brodie abscess typically present with insidious onset of mild to moderate
pain lasting for several weeks to months, with or without fever. If the subacute process
progresses to chronic localized bone abscess, patients present with longstanding dull
pain in the absence of fever [47,48]. The most common site is the distal tibia; other
sites include the femur, fibula, radius, and ulna [49].

Radiography typically demonstrates a single lesion near the metaphysis ( image 1).

• Osteomyelitis in sickle cell disease – Osteomyelitis is a common complication of

sickle cell disease; it occurs in more than 10 percent of patients [1]. This issue is
discussed further separately. (See "Acute and chronic bone complications of sickle cell
disease", section on 'Osteomyelitis and septic arthritis'.)

● Emphysematous osteomyelitis - Emphysematous osteomyelitis is a rare form of

osteomyelitis characterized by intraosseous gas in the extra-axial skeleton (eg, pelvis,
sacrum, femur) or vertebrae [50-53]. It can occur via hematogenous spread or via
contiguous spread from an intra-abdominal source, is usually associated with underlying
comorbidities (eg, diabetes or malignancy), and may be monomicrobial or polymicrobial.
The most commonly associated organisms include Enterobacteriaceae and Fusobacterium
necrophorum.

COMPLICATIONS

Complications of osteomyelitis include both infectious and noninfectious complications.

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 bony deformity or increased risk for bone fracture [54].
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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 [55-
65]. Histopathologic examination of a tissue biopsy can differentiate infection from carcinoma.

DIAGNOSIS

Overview — A clinical presentation of osteomyelitis should be suspected in the following

circumstances:

● Nonhematogenous osteomyelitis should be suspected in the setting of new or worsening

musculoskeletal pain, particularly in patients with poorly healing soft tissue or surgical
wounds adjacent to bony structures, in patients with signs of cellulitis overlying previously
implanted orthopedic hardware, and in patients with traumatic injury (including bite and
puncture wounds). It should also be suspected in diabetic patients with ulcers that probe
to bone.

● Hematogenous osteomyelitis should be suspected in the setting of new or worsening

musculoskeletal pain, particularly in the setting of fever and/or recent bacteremia.

In general, the diagnosis of osteomyelitis is established via culture obtained from biopsy of the
involved bone [12].

A diagnosis of osteomyelitis may be inferred in the following circumstances:

● Clinical and radiographic findings typical of osteomyelitis and positive blood cultures with
a likely pathogen (such as S. aureus); in such cases, bone biopsy is not required but may be
useful, particularly if subsequent therapeutic debridement is needed.

● Bone histopathology consistent with osteomyelitis in the absence of positive culture data
(particularly in the setting of recent antibiotic administration).

● Suggestive clinical and typical radiographic findings and persistently elevated

inflammatory markers in circumstances with no positive culture data and a biopsy is not
feasible.

Issues related to diagnosis of vertebral osteomyelitis are discussed separately. (See "Vertebral
osteomyelitis and discitis in adults".)

Clinical approach — Initial evaluation of patients with suspected osteomyelitis includes history
and physical examination; predisposing factors or events should be elicited (such as underlying

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diabetes, vasculopathy, invasive procedures, or injection drug use). (See 'Epidemiology' above
and 'Epidemiology' above.)

If osteomyelitis is suspected based on clinical history and physical findings, laboratory

evaluation (including erythrocyte sedimentation rate [ESR], C-reactive protein [CRP], white blood
cell count), blood cultures, and radiographic imaging should be obtained. ESR and CRP are
sensitive but not specific for osteomyelitis; if elevated initially, they can be useful for treatment
monitoring. (See "Nonvertebral osteomyelitis in adults: Treatment", section on 'Monitoring
during treatment'.)

In patients with ≥2 weeks of symptoms, conventional radiography is a reasonable initial

imaging modality for evaluation of suspected osteomyelitis, which is characterized by
osteolysis, periosteal reaction, and bone destruction. In patients with <2 weeks of symptoms,
an advanced imaging modality should be pursued. Advanced imaging is also warranted for
patients with diabetic foot infections, localized symptoms, and/or abnormal laboratory results
whose plain radiographs are normal or suggestive of osteomyelitis without characteristic
features [66].

The optimal radiographic modality may depend upon specific clinical circumstances and should
be tailored accordingly for individual patients, in discussion with radiologist expertise if
necessary. The following concepts may help guide selection of radiographic modality (see
"Approach to imaging modalities in the setting of suspected nonvertebral osteomyelitis"):

● If the patient is diabetic and has symptoms referable to the foot, magnetic resonance
imaging (MRI) is the test of choice.

● If metal hardware precludes MRI or computed tomography (CT), a nuclear study is the test
of choice. The limitations of nuclear studies are discussed separately and should be
considered in interpretation of results.

Findings of osteomyelitis on radiographic imaging should prompt bone biopsy for culture and
histology to confirm the diagnosis and to guide antimicrobial therapy, unless blood cultures are
positive for a likely pathogen (such as S. aureus, a gram-negative enteric rod, or P. aeruginosa).
Osteomyelitis is unlikely in the absence of radiographic evidence on MRI, CT, or nuclear
imaging.

If blood cultures and needle aspirate cultures are negative and the clinical suspicion for
osteomyelitis remains high on the basis of clinical and radiographic findings, repeat bone
biopsy (either percutaneous or open) should be performed. If this specimen is also
nondiagnostic, an empiric antimicrobial regimen should be initiated against common gram-
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positive and gram-negative bacterial pathogens. (See "Nonvertebral osteomyelitis in adults:

Treatment".)

If there is evidence of soft tissue infection over a bony surface without radiographic evidence of
osteomyelitis, an empiric course of therapy for soft tissue infection may be appropriate [12].

Clinical specimens

Blood cultures — The utility of blood cultures is highest in the setting of hematogenous
infection associated with fever or concurrent infective endocarditis [2,67,68]. Blood cultures are
rarely positive in diabetic foot osteomyelitis.

Positive blood cultures may obviate the need for a biopsy if the blood isolate is a pathogen
likely to cause osteomyelitis. (See 'Microbiology' above.)

Bone biopsy — The identification of the causative pathogen(s) is best accomplished by bone
biopsy (open or percutaneous). At least two specimens should be obtained; one should be sent
for Gram stain and culture (including aerobic, anaerobic, mycobacterial, and fungal cultures),
and the other should be sent for histopathology [69]. The microbiologic yield of bone biopsy
(open or percutaneous) is 37 to 87 percent [5,70-73].

Histology is useful if the diagnosis of osteomyelitis is uncertain and, in the setting of

amputation, to assess whether surgical margins are free from infection [5,27,70,71,74]. Stains
for bacteria, mycobacteria, and fungi should be performed on histopathology specimens.
Histopathologic features of osteomyelitis include necrotic bone with extensive resorption
adjacent to an inflammatory exudate [75]. (See "Pathogenesis of osteomyelitis".)

Indications — In general, the diagnosis of osteomyelitis is established via culture

obtained from biopsy of the involved bone.

Bone biopsy for culture is especially important for patients with diabetic foot infection in the
following circumstances:

● Empiric antibiotic therapy has failed.

● There is a concern for antibiotic-resistant organisms requiring targeted antibiotic therapy.
● Presence of a midfoot or hindfoot lesion; these are more difficult to treat, and treatment
failure can result in major amputation.

Bone biopsy may not be needed for patients with positive blood cultures and radiographic
evidence of osteomyelitis, or in cases of relapse if recent prior bone culture data is available. It
may be impractical to obtain a bone biopsy if wound healing is a concern due to advanced

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vascular disease or other comorbidities; in such cases, empiric treatment should be pursued.
(See "Nonvertebral osteomyelitis in adults: Treatment".)

Timing — Ideally, biopsy should be performed before initiation of antibiotic therapy to

increase the microbiologic yield. For patients who are already on antibiotics, the optimal
antibiotic-free period prior to biopsy is uncertain:

● For patients undergoing percutaneous biopsy, some studies have used a two-week
antibiotic-free period to minimize the likelihood of false-negative culture results [72].
However, the potential benefit of more accurate microbiologic data must be weighed
against the risk of progressive infection in the absence of treatment (eg, in patients who
are febrile, bacteremic, septic, critically ill, neutropenic, neurologically compromised, or
experiencing rapid progression of accompanying soft tissue infection).

● For patients undergoing open bone biopsy, cessation of antibiotics 48 to 72 hours is

preferred; however, this may not be necessary for cases in which infections occur in
association with infarction or necrosis, given limited penetration of antibiotics in such
cases.

Technique — For patients who require surgical debridement for definitive management
(such as in the setting of a decubitus ulcer or a wound with compromised vasculature), bone
samples should be obtained at the time of surgical debridement (ie, open biopsy) for histology
and culture [76]. For patients not undergoing debridement, an open biopsy or percutaneous
core bone biopsy should be pursued.

Ideally, percutaneous biopsies should be done with radiographic guidance, to minimize the
likelihood of false-negative results due to sampling error. Needle placement through infected or
ulcerated soft tissue should be avoided to minimize the likelihood of contamination. Two or
three specimens should be obtained; at least one should be sent one for culture and one
should be sent for histology.

Other specimens — Cultures of swabs, sinus tract, tissue aspirates, or superficial wound
biopsy should not be used to establish an osteomyelitis pathogen. In the setting of diabetic foot
osteomyelitis, decubitus ulcers, and postoperative and post-traumatic settings, the correlation
between bone biopsy and non-bone culture specimens is poor [5,70,72,77].

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 [5,77-80]. In one report
including 40 patients with chronic osteomyelitis, only 44 percent of sinus tract cultures
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contained the pathogen isolated from a deep surgical specimen [80]. Isolation of S. aureus from
the sinus tract culture had some predictive value, although the absence of S. aureus in the sinus
tract did not preclude its presence on bone biopsy. Recovery of other organisms in culture is
not predictive for those that will be identified on bone biopsy [80].

Swab culture and tissue aspiration 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) [5]. Similarly, in a study comparing percutaneous bone biopsy with
radiographically guided needle aspiration of tissue adjacent to the periosteum, bone biopsy
culture correlated with needle aspirate culture only in 32 percent of cases; among patients with
a positive bone culture, needle aspirate culture was negative in 38 percent of cases [72].

Sonication of explanted hardware may be useful to detect microorganisms that are highly
adherent to fixation hardware, although this procedure is not routinely available in most
microbiology laboratories [81-83].

Radiography — The general role of radiographic studies in the diagnosis of osteomyelitis is

discussed above. (See 'Clinical approach' above.)

A more detailed discussion of radiographic modalities in the setting of suspected osteomyelitis

is discussed separately. (See "Approach to imaging modalities in the setting of suspected
nonvertebral osteomyelitis".)

DIFFERENTIAL DIAGNOSIS

The differential diagnosis of osteomyelitis includes:

● Soft tissue infection – Soft tissue infection may occur alone or in conjunction with
osteomyelitis. In general, it is prudent to pursue imaging for assessment of bone
involvement in the setting of chronic soft tissue infection that fails to improve with
appropriate antibiotic therapy; this occurs more often in the setting of diabetes. (See
"Clinical manifestations, diagnosis, and management of diabetic infections of the lower
extremities".)

● Charcot arthropathy – Acute Charcot neuroarthropathy may present with localized

erythema and warmth; it can be difficult to determine if such patients have Charcot
arthropathy or osteomyelitis (or both). Furthermore, patients with Charcot arthropathy

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commonly develop skin ulcerations that can in turn lead to secondary osteomyelitis.
Magnetic resonance imaging (MRI; contrast-enhanced) may be diagnostically useful if it
shows a sinus tract, replacement of soft tissue fat, a fluid collection, or extensive marrow
abnormalities. Bone biopsy may be needed for definitive diagnosis. (See "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). Associated osteomyelitis may occur in
patients with 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".)

● Gout – Both osteomyelitis and gout can present with joint inflammation; the presentation
of gout is usually more acute than the presentation of osteomyelitis. Gout is distinguished
by presence of uric acid crystals in joint fluid. (See "Clinical manifestations and diagnosis of
gout".)

● Fracture – Osteomyelitis may 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".)

● Bursitis – Both osteomyelitis and bursitis can present with inflammation of the bursa;
osteomyelitis involves infection of the underlying bone whereas bursitis involves infection
that is confined to the bursa. The two are distinguished by clinical history, physical
examination, radiography, and bursa aspiration. (See "Septic bursitis".)

● Bone tumor – Both osteomyelitis and bone tumor may present with bone pain [84,85];
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 may be difficult to distinguish from a vaso-occlusive pain
crisis. Osteomyelitis is more likely to be associated with a prolonged duration of fever and
pain localized to a single site. (See "Acute and chronic bone complications of sickle cell
disease", section on 'Osteomyelitis and septic arthritis'.)

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● 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. Patients with
osteomyelitis lack symptoms of vasomotor instability observed with CRPS. Radiographic
evaluation with MRI can 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

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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
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● Basics topic (see "Patient education: Osteomyelitis in adults (The Basics)")

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SUMMARY AND RECOMMENDATIONS

● Definition and classification – Osteomyelitis is an infection involving bone. Osteomyelitis

may be classified based on the source of infection (hematogenous versus
nonhematogenous) and the duration of illness (acute versus chronic). (See 'Classification'
above.)

● Nonhematogenous osteomyelitis (see 'Nonhematogenous osteomyelitis' above)

• Mechanism of infection – Nonhematogenous infection occurs as a result of

contiguous spread of infection to bone from adjacent soft tissues and joints or via
direct inoculation of infection into the bone (as a result of trauma, bite wounds, or
surgery). (See 'Nonhematogenous osteomyelitis' above.)

• Clinical suspicion – Nonhematogenous infection should be suspected in patients with

new or worsening musculoskeletal pain near soft tissue or surgical wounds, in patients
with signs of cellulitis overlying previously implanted orthopedic hardware, in patients
with traumatic injury (including bite and puncture wounds), and in diabetic patients
with ulcers that probe to bone. (See 'Overview' above.)

● Hematogenous osteomyelitis (see 'Hematogenous osteomyelitis' above)

• Mechanism of infection – Hematogenous infection is caused by microorganisms that

seed the bone in the setting of bacteremia. (See 'Hematogenous osteomyelitis' above.)

• Clinical suspicion – Hematogenous infection should be suspected in the setting of

new or worsening musculoskeletal pain, particularly in the setting of fever and/or
recent bacteremia. Vertebral osteomyelitis is the most common form of hematogenous
osteomyelitis in adults. (See 'Overview' above and "Vertebral osteomyelitis and discitis
in adults".)

● Diagnosis – In general, the diagnosis of osteomyelitis is established via culture obtained

from biopsy of the involved bone. A diagnosis of osteomyelitis may be inferred in the
following circumstances (see 'Overview' above):

• Clinical and radiographic findings typical of osteomyelitis and positive blood cultures
with a likely pathogen (such as Staphylococcus aureus); in such cases, bone biopsy is not
required but may be useful, particularly if subsequent therapeutic debridement is
needed.

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• Bone histopathology consistent with osteomyelitis in the absence of positive culture

data (particularly in the setting of recent antibiotic administration).

• Suggestive clinical and typical radiographic findings and persistently elevated

inflammatory markers in circumstances with no positive culture data or available
biopsy examination.

● Diagnostic evaluation – Patients with suspected osteomyelitis should undergo laboratory

evaluation (including erythrocyte sedimentation rate, C-reactive protein, white blood cell
count), blood cultures, and radiographic imaging.

• Choice of radiographic test

- In patients with ≥2 weeks of symptoms, conventional radiography is a reasonable

initial imaging modality.

- In patients with <2 weeks of symptoms, an advanced imaging modality (magnetic

resonance imaging, computed tomography, or nuclear imaging) should be
pursued. Advanced imaging is also warranted for patients with diabetes, localized
symptoms, and/or abnormal laboratory results whose plain radiographs are
normal or suggestive of osteomyelitis without characteristic features.
Osteomyelitis is unlikely in the absence of radiographic evidence on advanced
imaging. (See 'Clinical approach' above.)

• Role of bone biopsy – Findings of osteomyelitis on radiographic imaging should

prompt bone biopsy for culture and histology to confirm the diagnosis and to guide
antimicrobial therapy, unless blood cultures are positive for a likely pathogen (such as
S. aureus, a gram-negative enteric rod, or Pseudomonas aeruginosa). (See 'Clinical
approach' above.)

Use of UpToDate is subject to the Terms of Use.

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Topic 7668 Version 36.0

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GRAPHICS

Cierny-Mader staging system for long-bone osteomyelitis

Anatomic type
Stage 1: Medullary osteomyelitis

Medullary osteomyelitis denotes infection confined to the intramedullary surfaces of the bone.
Hematogenous osteomyelitis and infected intramedullary rods are examples of this anatomic type.

Stage 2: Superficial osteomyelitis

Superficial osteomyelitis is a true contiguous focus infection of bone; it occurs when an exposed
infected necrotic surface of bone lies at the base of a soft-tissue wound.

Stage 3: Localized osteomyelitis

Localized osteomyelitis is usually characterized by a full thickness, cortical sequestration, which can
be removed surgically without compromising bony stability.

Stage 4: Diffuse osteomyelitis

Diffuse osteomyelitis is a through-and-through process that usually requires an intercalary resection

of the bone to arrest the disease process. Diffuse osteomyelitis includes those infections with a loss of
bony stability either before or after debridement surgery.

Physiologic class of host*

Class A denotes a normal host

Class B denotes a host with systemic compromise, local compromise, or both

Class C denotes a host for whom the morbidity of treatment is worse than that imposed by the
disease itself

Factors affecting immune surveillance, metabolism, and local vascularity

Systemic factors Local factors

Malnutrition Chronic lymphedema

Renal or hepatic failure Venous stasis

Diabetes mellitus Major vessel compromise

Chronic hypoxia Arteritis

Immune disease Small vessel disease

Malignancy Extensive scarring

Extremes of age Radiation fibrosis

Immunosuppression or immune deficiency Neuropathy

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Tobacco abuse (≥2 packs per day)

* Host factors are important for prognosticating containment of infection. A systemically and/or
locally compromised host cannot isolate an infectious focus as well as a normal host, so treatment
of osteomyelitis is more difficult in such patients.

Adapted from: Cierny G, Mader JT, Pennick JJ. A clinical staging system for adult osteomyelitis. Contemp Orthop 1985; 10:17.

Graphic 64015 Version 5.0

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Brodie abscess radiograph

Lateral (A) and frontal (B) radiographs of the right lower extremity demonstrate an
ovoid lucent lesion in the medullary cavity of the proximal metadiaphysis of the tibia
(arrows) with associated periosteal reaction (arrowheads). The lateral radiograph (A)
also demonstrates irregular cortical lucency anteriorly suggesting an area of focal
cortical disruption (dashed arrow).

Reproduced with permission from: Abdulhadi MA, White AM, Pollock AN. Brodie abscess. Pediatr Emerg
Care 2012; 28:1249. Copyright © 2012 Lippincott Williams & Wilkins.

Graphic 87102 Version 5.0

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Contributor Disclosures
Tahaniyat Lalani, MBBS, MHS No relevant financial relationship(s) with ineligible companies to
disclose. Steven K Schmitt, MD, FIDSA No relevant financial relationship(s) with ineligible companies to
disclose. Denis Spelman, MBBS, FRACP, FRCPA, MPH No relevant financial relationship(s) with ineligible
companies to disclose. Keri K Hall, MD, MS No relevant financial relationship(s) with ineligible companies
to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
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