We are writing regarding the August JADA article by Drs. John Nase and Jon Suzuki, "Osteonecrosis of the Jaw and Oral Bisphosphonate Treatment" (
JADA 2006;137[8]: 1115–9[Abstract/Free Full Text]
). There is no doubt that bisphosphonate-associated osteonecrosis (BON) is a significant concern, with often devastating consequences.
While the more serious problems and greater incidences of complications have been reported following use of intravenous bisphosphonates, cases of BON following tooth extraction in patients with a history of oral bisphosphonate use also have been presented in the literature. The precise role of oral bisphosphonates in the development of BON following various dental therapies is as yet undetermined.
It is for this reason that we are concerned with both the case presented and the conclusions drawn by the authors. In addition to the history of oral bisphosphonate therapy, a number of recognized medical/dental comorbidities were present in the patient Drs. Nase and Suzuki treated. These included poor oral hygiene, periodontitis, dental caries, an abscessed tooth, extension of the caries into the biologic width and a need for endodontic therapy.
Many of these medical/dental comorbidities have been identified by Marx and colleagues1 in their report documenting 119 patients with a history of intravenous and/or oral bisphosphonate therapy who were referred to the University of Miami with refractory bisphosphonate-associated osteonecrosis.
As the patient presented by Drs. Nase and Suzuki was in no discomfort, dental therapy, regardless of the presence or absence of a history of oral bisphosphonate therapy, should have begun with appropriate débridement and plaque control instruction so as to maximize patient home care efforts, remove subgivgival accretions, localize inflammatory infiltrates and obtain some resolution of the periodontal concerns that were present.
The use of an electrosurgical device to remove redundant soft tissues in the presence of inflammation also is ill-founded. Both the need to resolve periodontal inflammation in a site where electrosurgical intervention is planned, and the possible sequelae of electrosurgical therapy in the face of inflammation, including but not limited to bone resorption and bone sequestrum, are well-documented.2–4
Finally, there is no doubt from the radiograph presented by Drs. Nase and Suzuki that the carious lesion that was present impinged on biologic width by approaching to within less than 3 millimeters from the alveolar osseous crest. Placement of a restoration that impinges on biologic width at the time of surgical intervention results in a patient healing response characterized by inflammation and lack of development of an appropriate attachment apparatus.5–6
We are not questioning whether the patient’s history of oral bisphosphonate therapy contributed to the development of osteonecrosis at the treated site. There is no way to determine this, as the medical comorbidities that were present were not appropriately handled, sequencing of therapy was not ideal, electrosurgical therapy was carried out in the presence of inflammation and appropriate biologic width was not established either prior to, or at the time of, placement of the restoration.
Indeed, it would have been surprising if this patient did not develop some type of complication or present with a non ideal treatment result when all these factors are considered. In summary, there is no doubt that a history of bisphosphonate therapy presents a significant concern and challenge to us all as conscientious clinicians. However, such a history should not mask the need for appropriate treatment planning, sequencing of therapy and execution of treatment in every situation.
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