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Discussion : Treatment with teriparatide for advanced bisphosphonate-related osteonecrosis of the jaw around dental implants: a case report [2]

Discussion : Treatment with teriparatide for advanced bisphosphonate-related osteonecrosis of the jaw around dental implants: a case report [2]

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

It is therefore important that all patients treated with oral BPs must be given a full explanation of the potential risks of implant failure and BRONJ development in the short and long term. Because the potential role of infection in implant failure and BRONJ occurrence is still debated, great attention should be paid to the long-term oral hygiene and plaque control of implant-prosthetic restorations in patients taking oral BPs.

BPs and other antiresorptives such as denosumab increase apoptosis and inhibit osteoclast differentiation and function, all leading to decreased bone resorption and remodeling [11]. Teriparatide may counteract these mechanisms by stimulating bone remodeling. It has been shown to stimulate the activity and viability of osteoblasts from the alveolar bone of chronic bisphosphonate users [21], while indirectly increasing the metabolic activity and number of osteoclasts by affecting osteoblast function [22]. An increased number of remodeling units and increased bone formation within each unit may promote healing and the removal of damaged bone. Thus, teriparatide may offer therapeutic promise for localized bone defects of the jaw in patients with BRONJ [3, 23–25].

While it has been suggested recently that assertive surgical removal of the sequestrum appears to be effective [26–29], it can sometimes be difficult to distinguish living bone from necrotic bone. Recently, resection of BRONJ-affected tissue produced healing in patients taking oral bisphosphonates more successfully than conservative management [30]. However, bone resection because of surgical treatment may lead to significant oral disability.

Activation of living bone turnover by teriparatide therapy causes progression of the separation of the sequestrum. As a result, teriparatide therapy promotes sequestrum separation followed by normal mucosal coverage of the exposed bone. After 5 months of teriparatide therapy in our patient, sequestrum separation had progressed and thus a sequestrectomy was performed under general anesthesia. After the wound in the affected area had healed, our patient did not report any problems pertaining to her ability to ingest food, despite the presence of the bone defect in the mandible. We treated the patient with teriparatide for 2 years. CT monitoring of the mandible would assist in determining whether teriparatide can allow complete recovery of the bone defect in the mandible in cases of ONJ induced by bisphosphonates.

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