Oral Bisphosphonate-induced Osteonecrosis Research Articles

Oral Bisphosphonate-induced Osteonecrosis of Jaw: A Case Report

Oral Bisphosphonate-induced Osteonecrosis of Jaw: A Case Report

Is rheumatoid arthritis a risk factor for oral bisphosphonate-induced osteonecrosis of the jaws?

Bisphosphonate-related osteonecrosis of the jaws is a relevant side-effect of these drugs that has been generating a great concern through increasing reports, worldwide, of this bone necrosis. Among several BRONJ hypothetical co-factors that could play a role in BRONJ pathogenesis, rheumatoid arthritis (RA) has been included as a relevant risk factor for BRONJ; however, until now the relationship between these diseases has not been fully explained. Thus, the purpose of this paper is to establish hypothetical factors that could link these two diseases, considering mainly inflammatory components and the organism effects of medicines used to treat RA, particularly steroids and methotrexate (MTX).

Dental implant treatment in oral bisphosphonates patients using a drug holiday protocol: a prospective study

Aim Bisphosponates are the most important class of antiresorptive agents commonly used in the management of osteoporosis, Paget’s disease, and tumor-associated osteolysis. Oral bisphosphonateinduced osteonecrosis is a rare but real entity caused by the antiosteoclastic effects of bisphosphonates which inhibit bone turnover. The aim of this work is to determine the extent to which bisphosphonate-associated osteonecrosis occurs after dental implant surgery. We also wanted to determine whether there was any indication that bisphosphonates affected the overall success of the implants. Materials and methods We described 21 patients undergoing dental implants surgery who were taking or had taken oral bisphosphonates. All patients were informed about the risk of osteonecrosis and a written informed consent was obtained from each individual. Results A total of 38 implants were placed in 21 patients who reported having received oral bisphosphonates. None had received intravenous bisphosphonates. There is no evidence of osteonecrosis in any of the patients evaluated. Of the 38 implants, all but 2 fully integrated and met implant success criteria. Conclusion Implant surgery on patients receiving oral bisphosphonates did not result in osteonecrosis. Moreover, oral bisphosphonates did not appear to significantly affect implant success. Nevertheless, sufficient evidence exists to suggest that all patients undergoing implant placement should be questioned about bisphosphonate therapy including the drug taken, the dosage, and length of treatment prior to surgery.

Reconstruction of Defects Caused by Bisphosphonate-Induced Osteonecrosis of the Jaws

Reconstructive surgery of defects for any disease or injury including bisphosphonate-induced osteonecrosis of the jaws requires an understanding of the pathophysiology of the condition. Related to bisphosphonates, it is the apoptosis (programmed cell death) of the osteoclast that inhibits, and in some cases stops, bone renewal/remodeling altogether. Therefore, reconstruction begins with a debridement of resection considering this mechanism. For intravenous bisphosphonate-induced osteonecrosis defects of the mandible, most resections are immediately reconstructed with a rigid titanium plate provided that secondary infection is controlled, there is sufficient soft tissue present, and a resection margin containing variable bone marrow can be achieved. For some similar defects with significant secondary infection, a delayed rigid plate placement after the recipient site has healed and is infection free represents another option. In those defects in which there is a significant soft tissue loss, flap reconstruction may also be necessary. The pectoralis major myocutaneous flap is the most predictable and most commonly used flap, followed by the trapezius myocutaneous flap, and stemocleidomastoid flap. Bone graft reconstructions are rarely needed, and are often not indicated due to minimal benefit for the patient, anesthetic risks, or active cancer at metastatic sites. However, in selected cases, mostly for breast cancer or prostate cancer patients with continuity defects from intravenous bisphosphonate-induced osteonecrosis, standard cancellous marrow grafting with platelet-rich plasma growth factor supplementation has been successful. Maxillary resections are treated with prosthodontic obturators as they are in primary cancer surgery. Reconstruction of oral bisphosphonate-induced osteonecrosis defects usually takes the form of alveolar grafting and/or dental implant placements, and only rarely requires grafting of continuity defects. Standard grafting techniques and dental implant placements can be used if guided by the published serum C-terminal telopeptide (CTX) test. The guidelines are less than 100 pg/mL = high risk, 100 pg/mL to 150 mg/mL = moderate risk, and greater than 150 pg/mL = minimal risk.

Oral Bisphosphonate-Induced Osteonecrosis: Risk Factors, Prediction of Risk Using Serum CTX Testing, Prevention, and Treatment

To assess the risk and time course of oral bisphosphonate-induced osteonecrosis of the jaws. Detailed data from 30 consecutive cases were compared with 116 cases due to intravenous aminobisphosphonates. Results in part noted a higher incidence related to alendronate (Fosamax; Merck, Whitehouse Station, NJ), a 94.7% predilection for the posterior mandible, and a 50% occurrence spontaneously, with the remaining 50% resulting from an oral surgical procedure, mostly tooth removals. Just over 53% of patients were taking their oral bisphosphonate for osteopenia, 33.3% for documented osteoporosis, and 13.4% for steroid-induced osteoporosis related to 4 or more years of prednisone therapy for an autoimmune condition. There was a direct exponential relationship between the size of the exposed bone and the duration of oral bisphosphonate use. There was also a direct correlation between reports of pain and clinical evidence of infection. The morning fasting serum C-terminal telopeptide (CTX) test results were observed to correlate to the duration of oral bisphosphonate use and could indicate a recovery of bone remodeling with increased values if the oral bisphosphonate was discontinued. A stratification of relative risk was seen as CTX values less than 100 pg/mL representing high risk, CTX values between 100 pg/mL and 150 pg/mL representing moderate risk, and CTX values above 150 pg/mL representing minimal risk. The CTX values were noted to increase between 25.9 pg/mL to 26.4 pg/mL for each month of a drug holiday indicating a recovery of bone remodeling and a guideline as to when oral surgical procedures can be accomplished with the least risk. In addition, drug holidays associated with CTX values rising above the 150 pg/mL threshold were observed to correlate to either spontaneous bone healing or a complete healing response after an office-based debridement procedure. Oral bisphosphonate-induced osteonecrosis is a rare but real entity that is less frequent, less severe, more predictable, and more responsive to treatment than intravenous bisphosphonate-induced osteonecrosis. The morning fasting serum C-terminal telopeptide bone suppression marker is a useful tool for the clinician to assess risks and guide treatment decisions.