subject: Fosamax Onj (osteonecrosis Of The Jaw) [print this page] Fosamax linked to Osteonecrosis of the Jaw:
Fosamax (generic bisphosphonate), a prescription drug used to treat patients with osteoporosis, has been linked to decay of the jawbone when dental procedures such as dental surgeries or gum therapies have been performed. At present, there is no known cure for Fosamax jaw induced injuries. Clearly, Fosamax is behaving differently on different parts of the skeleton. The turnover rate of bone differs regionally and even locally. For example, the spongy bone in the head of the femur may be replaced two or three times a year, whereas the compact bone along the shaft remains largely unchanged. In osteoporosis, not all parts of the skeleton are equally affected. The epiphysis, vertebrae, and the jaws lose more than their share of bone, resulting in fragile limbs, a reduction in height, and the loss of teeth. Insight into the mechanism of Fosamax jaw decay has been provided by a published paper entitled Bisphosphonate-induced exposed bone of the jaws. The author, Dr. Robert Marx, believes that since the jawbone has (i) a large blood supply (compared to other bones); (ii) a faster remodeling rate related to a high activity rate (jaw is used a lot); and (iii) teeth, Fosamax (bisphosphonate) becomes highly concentrated in this area generating brittle bone. When taken orally, Bisphosphonates begin to build up on bone at about the third year of usage. This osteoporotic drug remains in bone for many years given that the half-life of bisphosphonate is around 10 years. Given this half-life, it is not known how long Fosamax jaw problems will remain in patients when they terminate their therapy. In other words, damage continues long after the drug therapy has been stopped.
Studies have demonstrated that there may be a genetic link with Fosamax jaw decay. Researchers have identified a matrix metalloproteinase 2 (MMP2), which is an enzyme (protein encoded by the genome that has mutated) that may be involved with bisphosphonate-induced jawbone decay. These scientists believe that the mutated MMP2 protein is associated with bone abnormalities, which could be related to osteonecrosis of the jaw. Interestingly, bisphosphonates are also associated with atrial fibrillation, and MMP2 is the only known gene to be associated with both bone abnormalities and atrial fibrillation. It seems that cardiovascular disease and bone disease are closely related, suggesting that a single drug such as bisphosphonate, acting on a single mutated gene (MMP2) that is expressed in both tissues could have both bone and cardiovascular side effects different from osteoclast inhibition that is characteristic of bisphosphonate.
Merck is Faced With a Number of Lawsuits:
In 2004, the FDA issued a report on Fosamax and its generics (Zometa, Aredia, Actonel) stating that the package labeling should be revised warning doctors and patients of the potential Fosamax jaw problem. Unfortunately, Merck didnt revise the Fosamax label until almost a year later in 2005. Because Merck didnt change their packaging in a reasonable amount of time and essentially misrepresented the safety issues of Fosamax, lawsuits are being filed against Merck for patients who developed osteonecrosis of the jaw. Patients state that Merck knew of jaw decay problems and kept this from doctors and patients. It has been reported that many orthopedists have stated that aggressive Fosamax marketing over emphasized bone fracture in aging women as a scare tactic essentially promoting Fosamax prescriptions to women who didnt have osteoporosis or were in a low risk category for developing the disease.
If you have experienced a Fosamax jaw decay problem or any other Fosamax side effect, you may be entitled to financial compensation. A Fosamax lawyer can evaluate your potential claim.
