Thank you for your interest in our article. Although stress microfractures may contribute to the development and/or progression of osteonecrosis, this does not adequately account for the development of osteonecrosis in many cases.
Our experience has been that most patients developed osteonecrosis after a surgical insult such as a tooth extraction or placement of an endosseous dental implant. In those cases in which no precipitating event was identified, the lesions developed at sites of mucosal trauma, such as an edentulous alveolar ridge under a poorly fitting prosthesis or on the lingual ridge of the mandible.
With this in mind, it seems that the effect of stress microfractures is less likely to account for the development of osteonecrosis compared with identifiable insults, either surgical or traumatic. To our knowledge, there have been no reports linking excessive masticatory forces with the development of osteonecrosis.
Additionally, if microfractures were a key event in the development of osteonecrosis, one would expect a more diffuse pattern of presentation in the sites of maxillary or mandibular existing bony lesions. Through the same assertion, one would expect the development of more osteonecrosis in other load-bearing bones, such as the lower limbs or vertebrae. Based on the available information, there does not seem to be an advantage to recommending soft diets for all patients with a history of bisphosphonate therapy. However, for those patients at risk of pathological fracture of the mandible as a result of osteonecrosis of the jaw (ONJ), we do recommend soft diets.
Future research to further elucidate the multifactorial process involved in the development of bisphosphonate-associated osteonecrosis is warranted and ongoing. The latter should include investigations into the effects of bisphosphonates in altering bone homeostasis, and it would be interesting to assess the role of physiological forces in this process.
With regard to the prophylactic use of chlorhexidine mouthrinse on patients receiving bisphosphonates, it is unlikely that chlorhexidine mouthrinsing will prevent ONJ or the subsequent bone exposure. The primary benefit of chlorhexidine in the setting of ONJ seems to be in limiting secondary infection of exposed bone. Ideally, a patient’s oral health should be optimized before commencing bisphosphonate therapy.
Similarly, for those patients already receiving bisphosphonates, preventive oral care should be implemented, and we recommend that the treating clinician should make the decision as to whether this regimen includes chlorhexidine mouthrinsing.
