Bisphosphonate-related osteonecrosis of the jaw (BRONJ) is a challenging complication of long-term bisphosphonate treatment. Currently, the drawback in the surgical management of BRONJ is the difficulty distinguishing between viable and necrotic bone. Intraoperative bone fluorescence induced by tetracyclines has been shown to be a valuable aid to overcome this problem. In this technical note we report the finding that viable bone is auto-fluorescent using the VELscope Vx fluorescence lamp. Necrotic bone shows an altered fluorescence pattern (pale or no fluorescence). Thus it is suggested that auto-fluorescence of bone might be of similar use during the surgical therapy of BRONJ.
Bone fluorescence induced by tetracyclines has been shown to enable the demarcation of necrotic and viable bone in different osteonecrosis entities of the jaw. In fact, fluorescence-guided bone resection has been shown to be a very helpful tool, with very good success rates, for standardized and less invasive surgical treatment of bone necrosis induced by bisphosphonates. From our own observations, as well as in consideration of a recent study by Assaf et al. (reporting bone fluorescence after a single administration of tetracycline 1 h preoperatively ), it was assumed that there is an auto-fluorescence of bone (without tetracycline labelling) using an appropriate fluorescence lamp. In this technical note we introduce the auto-fluorescence of bone for the demarcation of viable and necrotic bone.
Materials and methods
All patients included in this study suffered from bisphosphonate-related osteonecrosis of the jaw (BRONJ) stage II, hence surgical therapy was indicated. Four were male prostate cancer patients and four were female breast cancer patients, and all had been treated with zoledronate. Follow-up was carried out at 10 days and at 4 and 16 weeks postoperatively.
Histological work-up of bone samples was performed before and after auto-fluorescence resection using the following standard protocol: the harvested bones were fixed in buffered 4% formaldehyde at 4 °C for 48 h, then separated and decalcified with ethylenediaminetetraacetic acid (EDTA) at 25 °C for 28 days and rinsed with water. After dehydration with ethanol, all samples were degreased in xylene and embedded in paraffin. Sections (4 μm thick) were cut using a microtome (Leica Microsystems, Wetzlar, Germany) and histological staining performed with haematoxylin and eosin. Therapy was considered to be successful when (1) histological work-up verified complete removal of the necrotic bone, (2) the mucosa was closed, and (3) the patient was free of symptoms no later than 4 weeks after the operation.
The surgical treatment was performed according to a standardized protocol under general anaesthesia, as described previously. However, no preoperative tetracycline labelling was performed. In brief, after surgical bone exposure, the VELscope system Vx (LED Dental, White Rock, British Columbia, Canada) was used to induce and visualize auto-fluorescence of the jaw bone. The bone fluorescence showed similar if not identical characteristics to the findings in patients who have received doxycycline preoperatively: viable bone showed a bright greenish auto-fluorescence, while necrotic bone areas showed no or only very pale auto-fluorescence ( Figs 1 and 2 ). Specimens were harvested from the pale bone areas and histopathologically confirmed as necrotic bone in all patients treated. The bone resection was performed until a bright fluorescence of the affected bone was observed, as described in previous studies ( Figs 3 and 4 ). A tension-free wound closure was achieved using mucoperiosteal flaps.