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.