Pathophysiology of osteonecrosis of the jaw in patients treated with bisphosphonate.

Apart from the well-known mechanism of bisphosphonates' cellular effect, embryonic development and the specific features of alveolar bone homeostasis have been discussed. The unique ethiopathogenic mechanism which relates osteonecrosis of the jaw and bisphosphonates treatment has not been explained. The emphasis lies on the toxicological effects of bisphosphonates on the physiology of the alveolar bone and on the lasting effect of tooth extraction followed by an infection of the extraction wound and consequent progression into deeper layers of osseous tissue. Epithelial infection includes microbiological findings of Actinomyces species. The risk is pronounced in oncological patients treated with bisphosphonates intravenously in relatively large doses and during a longer period of time, especially with highly potent nitrogen-containing bisphosphonates pamidronate and zoledronate. This review of bisphosphonate-related osteonecrosis of the jaw stresses the significance of some other risk factors (corticosteroids, chemotherapy, tumour tissue etc.) of necrosis development--more precisely of osteomyelitis of the jaw if the microbiological component of the diseases has been taken into account, while the role of the bisphosphonates becomes minor. There is no gold standard for the treatment of jaw osteonecrosis; rather, palliative and minimally invasive treatment is applied, without subsequent oral surgical interventions. Since there is a significant risk of jaw osteonecrosis in oncological patients, the level of oral health is an important factor for the indication of intravenous bisphosphonates treatment.