Studying the role of microcracks in the pathophysiology of BRONJ

Abstract

There has been a speculation about the potential role of microdamage in the pathophysiology of bisphosphonaterelated osteonecrosis of the jaw (BRONJ) since the condition was first described five years ago. Much of the speculation is fueled by studies showing that treatment with bisphosphonates causes significant reductions in bone turnover and is associated with significant accumulation of microdamage at multiple bone sites [1–6]. In a recent paper, Hoefert et al. [7] report that microdamage exists in just over 50% of bone tissue samples collected from patients with BRONJ and conclude that microdamage “ could be af irst step in the pathogenesis of bisphosphonate-related ONJ.” Given the importance of trying to understand the pathogenesis of BRONJ, Hoefert and colleagues are commended for attempting to study the role of microdamage accumulation in this condition. However, there are several aspects of this study that are important to consider when evaluating the conclusions. Hoefert and colleagues studied bone tissue samples from patients who had been diagnosed with BRONJ, as well as from patients who had various other conditions (radiationinduced osteonecrosis, osteomyelitis, bisphosphonatetreated patients without osteonecrosis of the jaw, and individuals with osteoporosis who were untreated). Bone samples were collected during routine oral surgeries such as extractions, resections, or removal of the sequestra. The evaluation of the tissue was focused on microdamage, which the authors assessed using scanning electron microscopy. They found that 54% of the samples from patients