A 65-year-old male patient presented to our clinic with pain, swelling and sensitivity in the left leg. The patient had experienced a trauma to the same leg 12 years ago, but did not develop any impairments in the integrity of the skin. A year after the trauma, he experienced pain, swelling and sinus leakage. Diagnosed with bone infection, the patient had undergone antibiotherapy. Complaints of the patient have increased in the last 6 months with occasionally increasing pain. Chronic sinus orifice, pain, edema and minimal temperature increase were observed in the medial leg at the diaphyseal-metaphyseal junctional region of the tibia during physical examination. No fever was detected.
The patient was a laborer in the low-middle range income level. He was a smoker and had chronic kidney problems. He had received Bacillus Calmette-Guerin (BCG) injections, and his family had no history of tuberculosis. Appearance of a sequelae lesion in the lung radiographs and calcification and pleural thickness in the thorax on the computed tomography (CT) images were observed. Erythrocyte sedimentation rate, C-Reactive protein (CRP) and leukocyte values were 36 mm/h, 7.15 mg/dL and 10.05 x 1000 microL, respectively. The purified protein derivative (PPD) test result was negative.
Intramedullary sclerosis accompanied by cortical thickness and multifocal radiolucent areas were observed in the direct roentgenograms, starting from the tibia, below the diaphyseal region, and extending to the metaphyseal region (Figure 1).
The maximum intensity projection (MIP) method was employed in the examination of the leg with the Multidetector Computed Tomography (MDCT; Aquilion 64; Toshiba Inc., Tokyo, Japan). In the metaphyseal-diaphyseal region, a significant cortex thickness with an irregular contour and an accompanying periosteal reaction were observed. In the intramedullary region, areas surrounded with a sclerotic halo and a high fluid density were detected (Figure 2).
Magnetic resonance imaging (MRI) was performed using the Signa 1.5T HDxt MR system (GE Healthcare, Chicago, IL, USA). On T1-weighted coronal images, a hypointense serpiginous appearance, which is typical for Brodie's abscess, in the metaphyseal-diaphyseal region of the tibia was seen (Figure 3).
On T2-weighted images, a hyperintense intramedullary cavitary lesion, which can be considered as a demonstrative sign for Brodie's abscess, was detected (Figure 4). On contrast-enhanced fat-suppressed images, pre-contrast imaging revealed multifocal hypointense lesions, as post-contrast images showed diffuse peripheral contrast enhancement reminiscent of abscess. The heterogeneous contrast enhancement in the soft tissue was thought to be due to inflammation and edema (Figure 5).
Ziehl-Neelsen staining and Gram staining were performed on the samples taken with injection; however, no pathogen was detected. In addition, no pathogen was isolated from the culture samples. Broad-spectrum antibiotics were started considering pyogenic osteomyelitis. The patient's complaints did not resolve with medical treatment; biopsy was performed followed with curettage and antibiotic cement (Vancomycin; 4 grams added to 40 grams cement package) application.
On histopathological examination, caseating granulomas with Langhans giant cells and a mixed inflammatory cell infiltration were seen. Dead bone fragments (sequestra) were present within the inflamed granulation tissue (Figure 6). Acid-fast bacillus (AFB) staining did not reveal any bacilli. However, M. tuberculosis-specific DNA was detected by real-time polymerase chain reaction (Real-Time PCR; Anyplex  MTB/NTM Real-time Detection Kit, CFX96  Real-Time PCR System; Seegene, Inc., Seoul, South Korea) performed on formalin-fixed paraffin-embedded (FFPE) tissue block (Figure 7). The M. tuberculosis complex was produced from the perioperative samples in the Lowenstein-Jensen medium after 5 weeks. The patient was treated with anti-tuberculosis treatment (Isoniazid 1 x 300 mg, Rifocin (Rifamycin) 1 x 600 mg, Ethambutol 1 x 1500 mg and Pyrazinamide 1 x 1500 mg for 3 months and then Isoniazid 1 x 300 mg and Rifocin 1 x 600 mg for 3 months). At the first year follow-up, the clinical, radiological and laboratory findings were normal.