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Editor: Tim O'Brien
Profession: Attorney at Law

Category: Fosamax News

I have been interviewed by several news agencies about Fosamax and its relationship to osteonecrosis of the jaw. Time and again, the question is asked: "Why can something which helps prevent bone loss in the hips and thighs cause bone problems in the jaw?" In researching this issue, it is apparent that the same mechanism which makes an oral bisphosphonate like Fosamax an osteoporosis hero, also makes it an ONJ villain. The process by which Fosamax works in preventing osteoporosis is by the inhibition of osteoclasts; by inhibiting osteoclasts, bisphosphonates inhibit bone material from being resorbed (or removed) by osteoclasis.

Normal osteoclasis is vital to bone turnover and the ability of the bone to survive Interruption of this homeostatic cycle by inhibition of bone resorption results in micro fractures of the old mineral matrix and impairs the jawbones' ability to repair themselves. This process also impairs the growth of veins in the jaw bones which in turn inhibits the ability to heal and fight infection.

Marked inhibition of bone remodeling which occurs on bisphosphonate therapy predisposes patients to osteonecrosis, particularly since the jaw has exposed bone and the mouth is never aseptic. Because the jaw bones are the only bones in the human skeleton constantly exposed, (through the teeth), frequent "bone turnover" is imperative to the maintenance of healthy jaw bones. In other words, the jaw bones need constantly to purge the old and bring in the new bone material. Osteoclast inhibition, prevents the purging of the old - - which makes it effective for preventing osteoporosis - - but also doesn't allow the exposed bones in the jaw to bring in the new.

The question presents itself: why does a drug which helps reduce fracture rates in long bones cause such problems in the jaw bones? In his 2005 article, Bisphosphohonate Induced Expose Bone of the Jaws, University of Miami Professor Robert E. Marx answers as follows: "Because the jaws have a greater blood supply than other bones and a faster bone turnover rate related both to their daily activity and the presence of teeth (which mandates daily bone remodeling around the periodontal ligament), bisphosphonates are highly concentrated in the jaws. Coupled with chronic invasive dental diseases and treatments and the thin mucosa over the bone, this anatomic concentration of bisphosphonates causes this condition to be manifested exclusively in the jaws."

Additionally, as a result of the presence of the nitrogen atom on the alendronate chemical chain, Fosamax has a half-life of more than ten years which can result in a massive cumulative dose over the multi-year dosing cycle. Due to this long half-life and the nature of the osteonecrotic process, the progress of the disease occurs even after discontinuation of Fosamax therapy.

Unfortunately for the patient suffering from osteonecrosis, there is no known effective treatment for this drug induced osteonecrosis. Indeed, corrective oral surgery may actually exacerbate the problem. Thus, the need to prevent the disease or catch it in its early stages is apparent.