Sir, denosumab, a human monoclonal antibody that binds and inhibits RANKL, a mediator required for the formation, functioning and survival of osteoclasts, is one of the medications that causes medication related osteonecrosis of the jaw (MRONJ).

A 77-year-old female patient who entered menopause at age 35 with total hysterectomy who had used alendronat and zoledronic acid for five years and one year respectively, attended our outpatient clinic in February 2017. DXA results of the patient were as follows: L1-4:-3.5, L2-4:3.7, Femur neck:-0.9, Femur total:-1.1. The patient was started on denosumab therapy. Three months prior, the patient had full-full dentures, then two months after injection she started to experience pain in the right posterior mandible and therefore consulted an oral, dental and maxillofacial surgeon. Radiological findings were unremarkable according to the bone density measurements made by digital volumetric tomography at first grade of disease, so she was diagnosed with MRONJ clinically and prescribed an antibiotic and mouthwash then directed to our outpatient clinic in June 2017. Denosumab administration to the patient was suspended until the completion of her intraoral treatment. In August 2017, a 1 cm bone fragment in the right mandible broke off, which was found to be compatible with osteonecrosis of the jaw after it was examined pathologically. The patient reported that her pain ended with the rupture of the fragment. A review in September 2017 the region in which the necrosed bone fragment of the patient broke off was observed to have re-epithelised.

As the patient used two different antiresorptive medications the medication that caused MRONJ could not be clarified. The half-life of denosumab is 26 days, whereas that of bisphosphonates (BP) varies between 10-12 years. In contrast to BP, denosumab seems not to accumulate in the bones; therefore, many authors have stated that denosumab-related MRONJ is less aggressive and can be treated with a more conservative therapeutic approach.1

In our case, the rupture of the necrotic bone fragment two months after the observation of necrosed alveolar bone, rapid regression of the symptoms with the rupture of fragment and re-epithelisation of that area within one month led us to believe that the osteonecrosis was related to denosumab. With future technological and medical advancements, we hope to know for sure which drug is the cause of osteonecrosis and whether it is caused by sinergistic effect.