Although the methods of action are not yet completely understood, it is hypothesized that<unk> -associated osteonecrosis of the jaw is<unk>  to a defect in jaw bone healing and remodelling. The inhibition of osteoclast differentiation and function, precipitated by drug therapy, leads to decreased bone resorption and remodelling. Evidence also suggests bisphosphonates induce apoptosis of osteoclasts. Another suggested factor is inhibition of angiogenesis due to bisphosphonates; this effect remains uncertain. Several studies have proposed that bisphosphonates cause excessive reduction of bone turnover, resulting in a higher risk of bone necrosis when repair is needed. It is also thought that bisphosphonates bind to osteoclasts and interfere with the remodeling mechanism in bone. To be more specific, the drug interferes with the cholesterol biosynthesis pathway through the inhibition of farnesyl diphosphate synthase. Over time, the cytoskeleton of the osteoclasts loses its function and the essential border needed for bone resorption does not form. Like aminobisphosphonates, bisphosphonates have shown to have antiangiogenic properties. Therefore, effects include an overall decrease in bone recycling/turnover as well as an increased inhibition of the absorptive bone abilities. Light micrograph of an osteoclast displaying typical distinguishing characteristics: a large cell with multiple nuclei and a "foamy" cytosol. One theory is that because bisphosphonates are preferentially deposited in bone with high turnover, it is possible that the levels of bisphosphonate within the jaw are selectively elevated. To date, there have been no reported cases of bisphosphonate-associated complications within bones outside the craniofacial skeleton.
Medication-related osteonecrosis of the jaw
Osteomyelitis
Metastatic tumor of jaws
Osteoradionecrosis
Osteonecrosis of the jaw
Dysbaric osteonecrosis
Alveolar osteitis
Osteochondritis dissecans