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Discussion : Treatment with teriparatide for advanced bisphosphonate-related osteonecrosis of the jaw around dental implants: a case report [1]

Discussion : Treatment with teriparatide for advanced bisphosphonate-related osteonecrosis of the jaw around dental implants: a case report [1]

author: Yusuke Zushi, Kazuki Takaoka, Joji Tamaoka, Miho Ueta, Kazuma Noguchi, Hiromitsu Kishimoto | publisher: drg. Andreas Tjandra, Sp. Perio, FISID

We describe a case of a patient with a 6-year history of alendronate therapy, in which BRONJ developed around her dental implants. In this patient, the dental implants achieved successful osseointegration, and BRONJ occurred after the second surgery. Several factors could have played a role in the development of BRONJ in this patient. Glucocorticoid therapy is associated with an increased risk of BRONJ. This may be a result of multiple factors including inhibition of osteoblast function and increased osteoblast and osteocyte apoptosis. Other effects of glucocorticoids that may contribute to an increased risk of BRONJ include increased bone resorption, immunosuppression, impaired wound healing, and increased risk of local infection [10]. Patient-related local risk factors include dentoalveolar surgery (e.g., tooth extraction) and pre-existing inflammatory dental disease, such as periodontal disease or periapical pathology [11]. Although BPs tend to accumulate in sites of active bone remodeling, such as the jaws, the surgical trauma to the alveolar bone during implant surgery could have further stimulated the postoperative accumulation of the drug in the implant site. The localized interference of BPs on bone turnover may have influenced the peri-implant bone resistance to oral bacteria in the long term, thus increasing the risk of peri-implantitis. Once infection of the implanted bone site is established, BPs further accumulate because of the increased bone turnover; the onsite activation of bisphosphonates will hamper the healing capacity of bone, leading to bone necrosis and sequestration [5].

Nevertheless, the role of the dental implant procedure as a BRONJ pathogenetic factor [12–15] is still unclear. Recently, an increasing number of peri-implant BRONJs have been described [5–9]. Peri-implant BRONJ has been classified into two types: implant surgery-triggered BRONJ, when it develops within 6 months after implant surgery, suggesting that the surgical process may be a contributing factor; and non-implant surgery-triggered BRONJ, if it develops 6 months or more after implant surgery, or when BP administration started after implant placement and osteointegration [8]. Most authors do not consider the surgical procedure of implantation as a trigger factor for MRONJ [7, 8, 14, 16–20].

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