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Decoding the challenging mimickers of osteomyelitis
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Received: ,
Accepted: ,
How to cite this article: Sahu AK, Abrahams SN. Decoding the challenging mimickers of osteomyelitis. Indian J Musculoskelet Radiol. 2026;8:4-15. doi: 10.25259/IJMSR_64_2025
Abstract
Osteomyelitis (OM) is an infection of the bone that can present with a broad spectrum of clinical, laboratory, and radiological findings. Its diagnosis remains a clinical challenge, especially due to a range of non-infectious conditions that can mimic its presentation. These mimickers, both inflammatory and neoplastic, can lead to delayed or inappropriate management if not correctly identified. This review aims to highlight and analyze the key mimickers of OM, elucidate the distinguishing features of each, and provide a framework for clinicians to navigate these diagnostic challenges using an evidence-based, multidisciplinary approach. A comprehensive literature review was performed using different published articles in peer-reviewed journals. Emphasis was placed on recent advances in imaging modalities, including radiograph, computed tomography scan, magnetic resonance imaging, radionuclide scan, and their role in differentiating mimickers. Key mimickers of OM include bone tumors (e.g., Ewing sarcoma, lymphoma, osteoid osteoma), inflammatory arthropathies (e.g., gout, rheumatoid arthritis, chronic recurrent multifocal osteomyelitis [CRMO]), metabolic bone diseases (e.g., Charcot arthropathy), and post-traumatic bone changes. Imaging findings often overlap, such as marrow edema, periosteal reaction, or cortical destruction. However, certain features – like a nidus in osteoid osteoma or diffuse uptake patterns in metabolic bone disease, multifocal manifestation in CRMO can guide the diagnosis. Distinguishing OM from its mimickers is imperative for targeted management and optimal patient outcomes. Accurate diagnosis necessitates a holistic approach combining clinical history, laboratory investigations, advanced imaging, and, where necessary, biopsy. Greater awareness and understanding of these mimicking conditions among radiologists, pathologists, and clinicians can prevent misdiagnosis and facilitate timely intervention.
Keywords
Bone infection
Brodie’s abscess
Ewing’s sarcoma
Osteomyelitis
GRAPHICAL ABSTRACT
INTRODUCTION
Osteomyelitis (OM) is inflammation of the bone and bone marrow with an infectious etiology. The name was coined by the French surgeon Chassaignac in 1852. It results from hematogenous spread, contiguous infection, or direct inoculation due to trauma or surgery. The disease may be acute, subacute, or chronic. In chronicity, it results in the formation of sequestrum (a term coined by Hunter in 1764, describing pockets of dead cortical bone with abscess) and involucrum (another term coined by Totenlade [coffin] in German) which is new bone formed in response to and surrounding the sequestrum. Multiple openings in the involucrum can develop which are called “cloaca” through which pus and sequestrum come out of the bone.[1]
Despite advances in medical imaging and microbiology, OM continues to pose diagnostic challenges. Complicating this landscape is a wide array of disorders – neoplastic, inflammatory, metabolic, and traumatic – that mimic OM both clinically and radiologically.
OM can affect individuals of all ages and may involve any bone. However, common sites include the long bones in children and the vertebrae in adults.[2] Patients typically present with localized pain, swelling, warmth, and sometimes systemic signs such as fever or malaise.
Radiological imaging plays a central role in the assessment of suspected OM. Plain radiographs are often the first step but lack sensitivity in early stages. In both radiograph and computed tomography (CT) scan, loss of soft tissue definition and effusion may be seen in very early disease, advancing to loss of bone trabeculation, regional osteopenia, cortical loss, and even periosteal reaction [Figure 1a]. Magnetic resonance imaging (MRI) is considered the gold standard due to its superior soft tissue contrast and ability to detect early bone marrow changes. In acute OM, MRI will demonstrate marrow edema (lowT1, highT2/short-tau inversion recovery [STIR]), soft tissue involvement, and even abscess formation [Figure 1b and c]. Radiological features of chronic OM, characterized by sequestrum, involucrum, and cloaca, can all be demonstrated on radiography [Figure 2a], CT scan, and MRI [Figure 2b]. Nuclear imaging techniques, including positron emission tomography-CT (PET-CT) and bone scintigraphy, also offer valuable diagnostic information. Nevertheless, overlap in imaging findings between infectious and non-infectious conditions frequently leads to misdiagnosis.
- A 13-year-old male with acute osteomyelitis. (a) Radiograph of the right leg shows subtle loss of bone trabecular architecture in the proximal tibia, periosteal reaction, and surrounding soft tissue haziness (white arrows). (b) Post-contrast T1 fat-suppressed coronal and (c) axial images show altered bone marrow signal with peripheral and surrounding soft tissue enhancement.
- (a) A 39-year-old female with chronic osteomyelitis of the right humerus. Lateral radiograph of the right arm shows typical findings in chronic osteomyelitis including sequestrum (white block arrow), involucrum (white slender arrow), and cloaca (white arrow heads). (b) Axial T1-weighted (left image) and short-tau inversion recovery (right image) images of the femur of a 6-year-old child show some features of osteomyelitis in the form of marrow edema (white slender arrows), periosteal reaction (black arrow heads), and surrounding soft tissue collection (black block arrow).
Some of the challenging mimickers of OM can be broadly categorized into neoplastic etiologies, inflammatory conditions, and systemic conditions with skeletal manifestations.
The main neoplastic differentials of OM include Ewing sarcoma, lymphoma, leukemia, metastasis, and osteoid osteoma. Langerhans cell histiocytosis (uncontrolled monoclonal proliferation of Langerhans cells) is more common in the pediatric population with a malignant nature as is also considered to be a close differential for OM.
Regarding inflammatory conditions, the main entities that can mimic OM are gout and psoriatic arthritis.
There are general or systemic conditions with skeletal manifestations that can be a challenge in mimicking OM. Some of these conditions include synovitis, acne, pustulosis, hyperostosis, osteitis (SAPHO) syndrome, chronic recurrent multifocal osteomyelitis (CRMO), and neuropathic joint.
Post-traumatic bone remodeling or stress fractures may produce periosteal reactions or marrow edema on MRI, leading to misinterpretation as infection.
Given the serious implications of missed or delayed diagnosis – ranging from unnecessary prolonged antibiotic therapy to delayed cancer treatment – there is an urgent need to develop a structured approach for evaluating suspected OM. This should integrate patient history, symptom chronology, risk factors (e.g., diabetes, trauma, immunosuppression), laboratory findings, and advanced imaging characteristics. In ambiguous cases, image-guided biopsy remains the gold standard for establishing the definitive diagnosis.
This review aims to decode the diagnostic puzzle posed by OM mimickers. We will discuss the salient clinical and radiological features of common and rare mimicking conditions and propose an evidence-based diagnostic algorithm to aid clinicians in avoiding pitfalls. Greater awareness and interdisciplinary collaboration are a key to improving diagnostic accuracy and patient outcomes.
LITERATURE REVIEW
Multiple studies have addressed the complexity of diagnosing OM, particularly in the face of mimicking conditions. This section synthesizes the current literature on the common mimickers of OM, highlighting their distinguishing features and diagnostic clues.
Ewing’s sarcoma
Ewing’s sarcoma is a malignant small round cell tumor predominantly affecting children and young adults. It clinically manifests with pain, swelling, fever, and elevated inflammatory markers, creating considerable diagnostic overlap with OM.
Radiologically, Ewing’s sarcoma can mimic OM on plain radiographs, typically presenting with a permeative or moth-eaten pattern of bone destruction, periosteal reaction, and soft tissue mass [Figure 3a]. These features are also common in subacute or chronic OM.[3] The classic “onion-skin” periosteal reaction seen in Ewing’s sarcoma may resemble the lamellated or interrupted periosteal elevation found in infectious etiologies.
Both OM and Ewing’s sarcoma can show low signal intensity on T1-weighted images and high signal on T2-weighted images with contrast enhancement on MRI studies, making them indistinguishable.[4] Both entities may also demonstrate cortical disruption and adjacent soft tissue edema or mass, complicating the diagnosis further [Figure 3b and c].
- A 14-year-old male with Ewing sarcoma. (a) Radiograph of the right leg shows a well-defined lytic lesion with a narrow zone of transition in the proximal diaphysis of the tibia (white block arrow). (b) T1-weighted coronal image of the proximal tibia shows the lesion as well-defined hypointense lesion (white arrowhead). (c) Contrast-enhanced T1 fat suppression image shows the lesion to be homogeneously enhancing with cortical breach and soft tissue component (white slender arrow).
Advanced MRI sequences like diffusion imaging and chemical shift imaging also help in differentiating malignancy from OM. While bone scintigraphy and fluorodeoxyglucosePET (FDG-PET) can aid in detecting multifocal disease or metastasis, they are not specific. Increased uptake is common in both malignancy and infection. Importantly, the presence of a large soft tissue mass with relatively minimal cortical destruction on MRI favors Ewing’s sarcoma over infection.
Lymphoma
Lymphoma, a hematological malignancy, can present with imaging features that closely resemble OM, leading to diagnostic challenges. Both entities may exhibit overlapping clinical symptoms such as localized pain, fever, and elevated inflammatory markers, further complicating differentiation. Radiologically, the primary mimicry arises in MRI and CT, where both conditions can show lytic bone lesions, marrow edema, periosteal reaction, and soft tissue involvement [Figure 4].
- A 33-year-old male with lymphoma. (a) Lateral and (b) anteroposterior radiograph of the right elbow shows a permeative pattern of bone lesion (block white arrows in a) as seen in early osteomyelitis. (c) Sagittal T1, (d,e) sagittal PDFS and (f) sagittal T1 FS post contrast images show multifocal heterogeneously enhancing (block white arrows in f), T1 hypointense (white arrowheads in c), and PDFS hyperintense (white slender arrows in d and e) lesions. PDFS: Proton density fat saturated, T1 FS: T1-weighted fat-saturated sequence
MRI is considered highly sensitive for detecting early bone marrow changes, but not specific for etiology. In OM, MRI typically shows marrow edema, along with contrast enhancement and possible abscess formation.[5] Similarly, primary bone lymphoma and secondary osseous involvement can demonstrate analogous marrow signal alterations, cortical destruction, and soft tissue mass, mimicking infection.[6] Notably, both may present with aggressive features without clear demarcation between tumor and infection [Figure 4].
Increased FDG uptake is seen in PET-CT in both infections and malignancies, and in lymphoma, it may be diffuse and intense, mimicking chronic OM or Brodie’s abscess. In cases of spinal involvement, vertebral lymphoma can be indistinguishable from spondylodiscitis on MRI.
Leukemia
Leukemia, particularly acute lymphoblastic leukemia in children, can mimic OM both clinically and radiologically, posing significant diagnostic challenges. Patients may present with localized bone pain, fever, and elevated inflammatory markers – features also common in acute OM.
On plain radiographs, leukemia may present with metaphyseal lucent bands, periosteal reaction, and lytic lesions, which are also seen in OM.[7] MRI is more sensitive for early changes and often shows bone marrow edema along with cortical disruption and soft tissue swelling – features indistinguishable from OM [Figure 5]. Moreover, both conditions can exhibit periosteal elevation and enhancement after gadolinium contrast administration, further complicating the picture.[8]
- A 6-year-old female with acute lymphoblastic leukemia. (a) Radiograph of left leg in anteroposterior and lateral view shows features mimicking osteomyelitis as permeative bone pattern, wide zone of transition lesion with periosteal reaction (white arrowheads). (b) Axial short-tau inversion recovery (STIR) and (c) coronal STIR images of the distal thigh show increased bone marrow signal (block white arrow in c) and a large circumferential soft tissue component (slender arrows in b and c) mimicking subperiosteal collection.
Both leukemia and OM demonstrate increased metabolic activity with FDG-PET imaging. Infiltration of marrow by leukemic cells can show diffuse or focal FDG uptake, similar to infection or inflammation. Leukemic lesions may also involve multiple sites simultaneously, which could be misinterpreted as multifocal OM, SAPHO syndrome, or CRMO. Key differentiating factors include the distribution and response to antibiotics. Leukemic involvement is often bilateral and symmetrical and does not respond to antimicrobial therapy. In addition, systemic findings such as unexplained anemia, thrombocytopenia, or blast cells in peripheral blood may prompt further hematologic evaluation and bone marrow biopsy.
Osteoid osteoma
Osteoid osteoma, a benign bone-forming tumor, typically occurs in adolescents and young adults. A typical clinical presentation is localized pain – often nocturnal and relieved by non-steroidal anti-inflammatory drugs – similar to the pain in subacute OM.[9]
Radiologically, both conditions may present with a central lucent lesion surrounded by reactive sclerosis. On plain radiographs, osteoid osteoma appears as a small radiolucent nidus often surrounded by dense cortical thickening, whereas Brodie’s abscess may appear as a lytic lesion with sclerotic borders and variable periosteal reaction.[10] These overlapping features often result in misinterpretation, particularly in the metaphyseal regions of long bones.
CT imaging is more definitive in identifying the nidus of osteoid osteoma, often missed on radiographs or misdiagnosed as chronic infection [Figure 6]. The nidus typically measures <1.5 cm and may contain central mineralization, which is not a feature of OM. In contrast, CT may show a cavity with irregular margins in Brodie’s abscess, sometimes with sequestrum or sinus tracts.
- A 15-year-old female with osteoid osteoma presenting with severe bone pain. (a) Coronal T1-weighted and (b) coronal PDFS images of the proximal tibia show features mimicking osteomyelitis in the form of bone marrow changes appearing hypointense on T1 (block white arrow in a) and hyperintense on PDFS (white slender arrows in b), periosteal reaction, and enhancing lesion. (c) Axial computed tomography scan and (d) axial post-contrast T1-weighted images of the proximal tibia show a nidus with cortical thickening the discriminator feature in favor of osteoid osteoma in the form of cortical nidus with cortical thickening (white arrowheads in c and d). PDFS: Proton density fat saturated.
MRI is highly sensitive but less specific in differentiating between the two. Both lesions demonstrate marrow edema. However, MRI may exaggerate the inflammatory response in osteoid osteoma, making it appear like OM with extensive soft tissue involvement [Figure 6].[10]
Radionuclide bone scans show focal increased uptake in both entities, although a “double-density sign” is more characteristic of osteoid osteoma.[11]
Chondroblastoma
Chondroblastoma is a rare benign bone tumor typically arising in the epiphysis or apophysis of long bones in adolescents and young adults. Despite its distinct clinical and histological features, it can radiologically mimic OM, posing diagnostic challenges.
On conventional radiographs, chondroblastoma appears as a lytic, well-defined lesion with a thin sclerotic rim, often associated with peri-lesional edema and joint effusion, particularly when located near articular surfaces [Figure 7]. These findings overlap with subacute or chronic OM, which may present with lytic areas, sclerosis, periosteal reaction, and adjacent soft tissue changes, especially in Brodie’s abscess [Figure 8].[12]
- A 11-year-old boy with chondroblastoma. (a) Radiograph of left ankle joint shows a lucent lesion with surrounding bone sclerosis in the epiphysis of distal tibia (white arrowhead) mimicking a Brodie’s abscess. (b) Coronal T1-weighted and (c) coronal PDFS images of the ankle joint demonstrated the lesion as a fairly well-defined heterogeneous lesion (block white arrow in b) with surrounding bone marrow edema (slender white arrow in c) in the tibia epiphysis and the talus. PDFS: Proton density fat saturated.
- A 10-year-old boy with Brodie’s abscess. (a) Radiograph of the left knee joint shows ill-defined lucency in the distal femoral epiphysis (block white arrow). (b) Coronal T1-weighted image demonstrated the lesion seen in the radiography as a hypointense epiphyseal lesion (white arrowhead) with synovial thickening. (c) Sagittal post-contrast T1 image shows the lesion to be enhancing with cortical breach and intra-articular communication (slender white arrow). There is also enhancing synovium.
MRI further complicates differentiation. Both lesions can exhibit marrow edema, inflammation, and post-contrast enhancement. In chondroblastoma, extensive peritumoral bone marrow and soft tissue edema are frequently seen, resembling the inflammatory changes of OM. Moreover, joint involvement in chondroblastoma can simulate septic arthritis when effusion and synovial enhancement are present.[13]
Advanced imaging features such as internal calcifications, occasionally seen in chondroblastoma, may aid in differentiation but are not definitive. CT can better visualize matrix calcification or subtle bone destruction, although early OM may also lack overt bone changes.[14]
A key distinguishing factor is clinical history; chondroblastoma often presents with long-standing, localized joint pain, while OM may present acutely with systemic signs of infection. Nevertheless, radiologically, overlap is significant, and biopsy remains crucial for definitive diagnosis.
CRMO
CRMO is a rare, non-infectious autoinflammatory bone disorder that primarily affects children and adolescents. It often presents with an insidious onset of bone pain, swelling, and systemic symptoms such as fever.
Radiologically, CRMO mimics OM across several modalities. On plain radiographs, both conditions may show lytic lesions with surrounding sclerosis, periosteal reaction, and cortical thickening. However, in CRMO, lesions are often multifocal and symmetric, commonly affecting the metaphyses of long bones, clavicle, spine, and pelvis.[15] In contrast, acute bacterial OM usually presents as a unifocal lesion with more pronounced cortical destruction.
MRI is the modality of choice for evaluating both diseases due to its high sensitivity in detecting bone marrow edema and soft tissue changes. CRMO lesions appear hypointense on T1-weighted images and hyperintense on T2-weighted and STIR sequences, with surrounding soft tissue and periosteal inflammation – findings virtually indistinguishable from those seen in acute or subacute OM.[16] The presence of multifocal bone involvement on whole-body MRI is more suggestive of CRMO [Figure 9].
- A 16-year-old female with chronic recurrent multifocal osteomyelitis (CRMO). (a) Coronal PDFS image of both knee joints and (b) coronal PDFS of bilateral ankle joints show features similar to osteomyelitis, such as marrow edema (white arrows in a and b). However, in CRMO, lesions are often multifocal and symmetric as seen in this case. PDFS: Proton density fat saturated.
CT can demonstrate sclerosis and cortical thickening in CRMO but is generally less useful than MRI in early disease stages. Radionuclide bone scans in CRMO show increased uptake at multiple sites, a pattern that may initially be mistaken for multifocal infectious OM.
Definitive diagnosis often requires exclusion of infection and malignancy through biopsy and microbiological testing. Histologically, CRMO lacks neutrophilic infiltration or abscess formation, typical of bacterial OM.
Neuropathic arthropathy
Neuropathic arthropathy, also known as Charcot joint, is a progressive, degenerative condition resulting from the loss of protective sensation in a joint, commonly associated with diabetes mellitus, spinal cord injury, or syringomyelia. Radiologically, a neuropathic joint can closely mimic OM, especially in its acute phase, leading to diagnostic dilemmas.[17]
On plain radiographs, both neuropathic arthropathy and OM may demonstrate joint space narrowing, periarticular erosions, subchondral sclerosis, and bone fragmentation. In neuropathic joints, these findings are often more extensive and involve disorganization of the joint, known as the “six D’s:” Distension, Density change, Destruction, Dislocation, Debris, and Disorganization [Figure 10].[18]
- A 49-year-old male with Charcot joint presenting with right shoulder swelling, pain, and limited range of movement. (a) Anteroposterior radiograph of the shoulder joint of a patient with diabetes mellitus taken 2 years prior and (b) then at current presentation shows severe remodeling of the humeral head, joint space narrowing, sclerosis of articular margins (block arrow), and soft tissue swelling (white arrow heads). (c) Post-contrast coronal T1-weighted FS re-demonstrates the radiographic findings (white asterisk) and also shows peripherally enhancing subdeltoid collection (white arrow head). Slender arrows show enhancing marrow. FS: Fat-saturated.
MRI, while highly sensitive for early changes, can be particularly problematic in differentiating acute Charcot arthropathy from OM. Both conditions exhibit bone marrow edema, joint effusion, and soft tissue inflammation. In addition, cortical disruption and sinus tract formation may be seen in both entities, especially in diabetic patients [Figure 10]. The presence of a contiguous skin ulcer overlying the area of bone marrow signal change tends to favor OM, although not definitively.
Bone infarction
Bone infarction, or osteonecrosis, results from ischemia-induced death of bone and marrow elements. It is commonly associated with conditions such as sickle cell disease, corticosteroid use, trauma, and coagulopathies. Clinically, bone infarction can present with localized pain, swelling, and elevated inflammatory markers which are features that significantly overlap with OM and make differentiation challenging.[19]
On plain radiographs, early bone infarction may appear normal. As it progresses, it typically shows serpiginous areas of sclerosis with central lucency, especially in metaphyseal or diaphyseal regions. These changes can resemble the sclerosis and lytic patterns seen in subacute or chronic OM. In sickle cell disease, infarcts may show periosteal reaction and cortical irregularities, which mimic infection-related bone changes.[20]
MRI is the most sensitive modality for detecting early bone infarction. Classic findings include a “double line sign” on T2-weighted images – an inner bright line and an outer dark line representing granulation tissue and sclerotic bone, respectively. However, in acute stages, infarction may show diffuse bone marrow edema, similar to that seen in OM [Figure 11]. Both conditions exhibit marrow edema, sometimes with periosteal reaction and soft tissue edema.[20] These overlapping features complicate differentiation, especially in the absence of systemic signs of infection.
- A 31 years old with a bone infarct presenting with left knee pain and limited range of movement. (a) Coronal T1-weighted, (b) coronal PDFS, and (c) sagittal PDFS images of the knee joint show large geographical areas of altered signal intensity involving lateral femoral condyle (block white arrow in a to c), medial femoral condyle and lateral and medial tibial condyles extending into the proximal diaphysis of tibia (slender white arrow in a and b), appearing hyperintense on T1-weighted images and heterogeneously hyperintense on PDFS images. PDFS: Proton density fat saturated.
FDG-PET may show increased uptake in both infarction and OM, limiting their specificity. However, infarcts tend to exhibit photopenic (cold) areas in chronic stages due to avascularity, which may aid differentiation from the uniformly increased uptake of active infection.
Given the radiologic similarities, especially in sickle cell patients, a combination of clinical history, laboratory data, and sometimes biopsy is essential for accurate diagnosis.
Stress fractures
Stress fractures are overuse injuries resulting from repetitive mechanical loading, commonly seen in athletes and military recruits. These fractures can mimic OM on radiological imaging due to overlapping features such as bone marrow edema, cortical disruption, and periosteal reaction.
On radiographs, early stress fractures may appear normal or show subtle periosteal reaction, similar to subacute OM.[21] Both conditions may later exhibit cortical lucency, sclerosis, and soft tissue swelling. However, the diagnostic challenge becomes more pronounced on MRI, the modality of choice for both pathologies.
MRI findings in stress fractures typically include a hypointense fracture line on T1-weighted images, surrounding bone marrow edema, and periosteal or soft tissue reaction [Figure 12].[22] These findings can closely resemble acute OM, which also presents with bone marrow edema, cortical destruction, and soft tissue involvement, often with post-contrast enhancement.
- A 16-year-old female with tibial stress fracture. (b) Coronal T1-weighted and (b) post-contrast T1 images of the tibia mimicking features of osteomyelitis as bone marrow edema in the middle third of the tibia, appearing hypointense on T1W (block white arrow in a) and hyperintense on fat-suppressed sequences (slender white arrow in b).
The absence of a fracture line and the presence of a nidus or abscess may favor OM, yet in early stages, these may be absent. Clinical correlation is essential: Stress fractures usually lack systemic signs of infection, while OM may be accompanied by fever, elevated inflammatory markers, and leukocytosis.
CT may delineate fracture lines not visible on MRI, while nuclear imaging can show uptake in both conditions, reducing specificity.[23]
Metastasis
On imaging, metastasis and OM can overlap but have distinguishing features. Metastases typically present as focal or multifocal lesions with marrow replacement, often showing low T1 and variable/high T2 signal on MRI, with enhancing soft-tissue masses, cortical destruction, or pathologic fracture; they commonly involve the axial skeleton and may be multiple, with increased uptake on bone scan or PET. In contrast, OM often demonstrates ill-defined marrow edema, adjacent soft-tissue inflammation, subperiosteal abscess, sinus tracts, or sequestrum, with enhancement that is more diffuse and reactive rather than mass-like; it frequently correlates with clinical signs of infection and elevated inflammatory markers. Distribution, presence of systemic infection, soft-tissue inflammatory changes, and evolution on follow-up imaging help differentiate the two.[24,25]
CONCLUSION
The diagnosis of OM remains a formidable clinical challenge. Neoplastic, inflammatory, metabolic, and post-traumatic disorders often share overlapping clinical signs, laboratory abnormalities, and imaging features with true bone infection. Misinterpretation can result in significant consequences.
Advances in imaging modalities, including MRI, have enhanced the ability to detect early and subtle bone changes but cannot fully eliminate diagnostic uncertainty. Thus, accurate diagnosis requires an integrative approach that synthesizes patient history, risk factor assessment, laboratory parameters, imaging patterns, and, when necessary, histopathological evaluation. In situations where imaging does not solve the query, biopsy of the lesion should be done from the appropriate location and preferably under imaging guidance to come to conclusion.
Ultimately, the key to decoding the challenging mimickers of OM lies in heightened clinical suspicion, adopting a systematic, evidence-based approach, and fostering interdisciplinary collaboration. This not only optimizes patient outcomes but also ensures that management strategies – whether antimicrobial, surgical, or oncologic – are appropriately tailored to the true underlying pathology. An algorithmic approach to suspected cases of OM is shown in graphical abstract.
Ethical approval:
Institutional Review Board approval is not required.
Declaration of patient consent:
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given consent for their images and other clinical information to be reported in the journal. The patient understands that the patient’s names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Conflicts of interest:
Amit Kumar Sahu is on the Editorial Board of the Journal.
Use of artificial intelligence (AI)-assisted technology for manuscript preparation:
The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.
Financial support and sponsorship: Nil.
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