Introduction
Bone is the third most frequent site of tuberculosis after lung and lymph node, accounting for 10%–20% of all cases of extrapulmonary disease 1 , 2 , 3 . The spine and hip are the most commonly involved sites. Involvement of the small bones of the hand has been described exceedingly rarely, and is usually secondary to pulmonary disease 4 . Because a primary focus is not always found, it can be difficult to make a diagnosis of skeletal tuberculosis. Moreover, because clinical and radiographic features are nonspecific, an early diagnosis will only be made where there is a high degree of suspicion. Isolated osteomyelitis of the scaphoid is uncommon, having previously been reported in association with animal bites and interventions such as radial artery cannulation 5 , 6 . We describe here the unusual occurrence of tubercular osteomyelitis of the scaphoid, a condition which has rarely been reported.
Case report
A 42‐year‐old man presented with complaints of mild pain in the radial aspect of his right wrist and reduced range of motion for the previous 2‐months. There was no history of trauma, recent intervention or drug abuse. Anteroposterior and lateral X‐ray films of the right wrist showed no obvious abnormality (Fig. 1A). The patient was given symptomatic treatment with non‐steroidal anti‐inflammatory drugs. He returned after 4 months complaining of increasingly intense pain and diffuse swelling of the radial aspect of the dorsum of the right wrist. He was in a good general health and had no fever at the time of presentation. A plain radiograph of his wrist showed an osteolytic lesion of the scaphoid (Fig. 1B). CT scan showed an osteolytic lesion with bony sequestra and a mild periosteal reaction (2, 3). Laboratory investigations revealed a total leukocyte count of 9600/mm3 and an erythrocyte sedimentation rate (ESR) of 44 mm in one hour. A fine‐needle biopsy was performed, histopathologic examination of the sample showing epithelioid granulomatous reaction with a focus of caseous material. A plain radiograph of the chest showed no features of current or past tubercular infection. A working diagnosis of primary tubercular osteomyelitis of the scaphoid was made and the patient managed accordingly. Thorough debridement and curettage of the scaphoid was performed and the specimen sent for histopathologic examination and mycobacterial culture and sensitivity. Intensive antituberculosis treatment with four drugs (rifampicin, isoniazid, pyrazinamide and ethambutol) was prescribed for 2 months, followed by continuation phase rifampicin and isoniazid for the next 4 months. The initial diagnosis was confirmed by mycobacterial culture and by histological examination, which showed epithelioid granulomatous reaction and central caseous necrosis. The patient's symptoms improved dramatically during the intensive phase. He has been followed up on a monthly basis. His recovery has so far been uneventful, with complete resolution of his pain and the regaining of normal wrist function and range of movement.
Figure 1.

Anteroposterior radiograph of left wrist. (A) Initial antero‐posterior radiograph of left wrist shows no obvious abnormality. (B) Repeat radiograph after 4 months shows lytic destruction of the scaphoid bone.
Figure 2.

Axial CT scan images through left wrist with (A) bone and (B) soft tissue window settings reveal an osteolytic lesion in the scaphoid bone with central sequestrum formation. Adjacent soft tissue is heterogenous and prominent with evidence of a mild periosteal reaction.
Figure 3.

(A) Coronal CT multiplanar reconstruction through the left wrist shows a lytic lesion with sequestrum formation in the scaphoid bone. (B) Surface shaded display CT image shows the presence of cloaca.
Discussion
Skeletal tuberculosis is not uncommon, accounting for 10–20% of all cases of extrapulmonary disease 1 , 2 , 3 . The spine is the commonest site of skeletal involvement, being affected in 50% of cases. Chronic osteomyelitis of the hand is seen in only 10% of cases. Dactylitis, the most common manifestation of tuberculosis in the bones of the hand, is seen in 70% of such cases and is followed by metacarpal involvement. Isolated tubercular osteomyelitis of a carpal bone is exceedingly rare, only a few cases having been reported 5 . Primary bone involvement in tuberculosis is often diagnosed late because the symptoms are typically minimal and only ⅓ of patients have concomitant active pulmonary disease. The source of infection is usually a primary pulmonary focus, the respiratory system being the primary portal of entry for mycobacteria. Dissemination of infection occurs through lymphatic routes 6 . Precipitating factors, such as trauma, radial artery cannulation, immunosuppression or malnutrition, are commonly identified 5 , 7 .
Skeletal osteomyelitis can manifest with systemic features of fever, night sweats and weight loss in addition to features particular to the local site of involvement, or it may go unrecognized for months due to its indolent course 6 . Isolated osteomyelitis without any concomitant pulmonary or extrapulmonary infection presents as localized inflammatory swelling, pain, decreased range of movement and deformity. Laboratory tests may show leukocytosis, a high ESR and, most importantly, an increased C‐reactive protein concentration. A positive skin tuberculin reaction in association with a high ESR may be seen; however, a normal test does not exclude the diagnosis of tuberculosis. Plain radiographs show bone destruction with sequestrum formation, periosteal reaction and surrounding soft tissue involvement. CT can reveal early bone destruction and periosteal reaction. MRI is more sensitive than CT in accurately identifying early disease; it shows low signal on T1 images and high signal on T2 images 5 .
Because the clinical and radiological features of chronic osteomyelitis are non‐specific, the diagnosis can be confirmed only by histological and bacteriological examination of a biopsy specimen. Tubercular osteomyelitis shows epithelioid granulomatous inflammation with central caseous necrosis. In most cases the causative mycobacteria can be identified by using Ziehl‐Neelsen staining. However, this stain fails to differentiate between tubercular and non‐tubercular mycobacteria 8 . Polymerase chain reaction increases the sensitivity and can exclude non‐tubercular mycobacterial infections 9 . In 10% of cases efforts to identify the causative organism fail; the diagnosis must then rely on the clinical, radiological and histological features 10 . Culture of mycobacteria from a tissue biopsy remains the gold standard for diagnosis 8 .
Antituberculosis chemotherapy is the basis of treatment for chronic mycobacterial osteomyelitis. It includes an initial 2‐month intensive course with rifampicin, isoniazid, pyrazinamide and ethambutol followed by a 6–12 month regimen of rifampicin and isoniazid 8 , 11 . Debridement and curettage is often needed to remove the involved bone and sequestra 5 . Inappropriate antimicrobial therapy and curettage are the main factors associated with recurrence.
Disclosure
The authors have no commercial associations or sources of support that might pose a conflict of interest.
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