Bisphosphonate treatment and its aetiopathogenic association with aseptic osteonecrosis of the jaw is one of the more prominent public health issues today. The aim of this review is to see into the mechanisms of bisphosphonate effects on bones described in literature (anti-osteoclastic activity, cytotoxicity, antiangiogenesis, genetic factors, and imbalance between osteoclasts and osteoblasts). Bisphosphonate treatment is the dominant cause of jaw necrosis. Epidemiological data show an exclusive incidence of osteonecrosis of the jaw in patients who took one or a combination of nitrogen-containing bisphosphonates. Risk factors vary by the bisphosphonate potency (particularly risky are the highly potent pamidronate and zoledronate, which are given intravenously), dosage, duration of treatment, and the illness. Jaw necrosis is most common in oncology patients, and only 5 % in patients with osteoporosis. From a dental-medical point of view, a good oral health is important because osteonecrosis often appears after a periodontal or oral surgical procedure.