Like many people—and sadly, that includes many doctors—I had some very wrong ideas about osteoporosis. Weight-bearing exercise, calcium and vitamin D, I figured, are all we really need to keep age-related bone loss in check. Drugs that treat the disease aren’t worth the risk because of hideous side effects (such as a disintegrating jawbone!). Bone density tests are something of a scam, needlessly scaring a lot of people (especially middle-aged women like me) into taking those dreaded drugs. And then there were the dots I somehow failed to connect. For instance, it is no secret that hip fractures are a massive problem for older people, striking more than 300,000 annually in the U.S. alone, half of whom will never walk again without assistance and a quarter of whom will be dead within a year. But somehow I never realized that most of this death and disability can be attributed to the steady skeletal erosion of osteoporosis, a disease that, it turns out, is pretty darn treatable. Unfortunately, false ideas like mine have led us to a perfectly avoidable health crisis. Let me flip the calendar back to 1995, the year when the first drug for osteoporosis, alendronate (brand name: Fosamax), was approved for sale and roughly the time when x-ray-based bone density tests became widely available. Fosamax was the first of several bisphosphonate drugs that work by slowing the turnover of bone cells. Research shows that they cut the risk of fracture by 20 to 50 percent. Doctors embraced the new drugs, and U.S. hip fracture rates began to decline (although you cannot prove cause and effect). Arguably, physicians were a little too enthusiastic. A new diagnosis, “osteopenia”—low bone density that falls short of osteoporosis—was popularized and often treated, particularly in women going through menopause, when bone loss is fastest. “A lot of us were almost evangelical,” concedes endocrinologist Ethel Siris of Columbia University Medical Center. Then, around 2005, came published reports of two rare but terrifying side effects: osteonecrosis of the jaw and a bizarre breaking of the leg bone called atypical femoral fracture (AFF). A chill descended on the field. Use of oral bisphosphonates fell by 50 percent between 2008 and 2012. The U.S. hip fracture rate plateaued, leading to 11,000 more fractures between 2013 and 2015 than predicted, according to a new study by Siris and her colleagues. Yet research shows that both dreaded side effects are, as Siris puts it, “rare, rare, and I’m going to say it three times, rare”—with about one case per 10,000 to 100,000 patients. Clinicians have also learned more about who is vulnerable and, in the case of AFF, how to detect warning signs. Further, new drugs have emerged that do not have the same risks. But since the scare, precious ground has been lost in protecting the most vulnerable group: older patients with fractures. Ideally, all patients over 50 who break a wrist, shoulder, hip or vertebra should be checked for osteoporosis and treated, if warranted. In reality, only about 20 percent are, although 15 years ago 40 percent of hip fracture patients got this kind of workup. Doctors who study and treat osteoporosis are practically apoplectic about the trend. They point to research showing that if you have one “fragility fracture,” you face nearly three times the usual risk of having another one within the year. Nearly half of people who break a hip have previously broken another bone. In short, it’s pretty crazy not to look for and treat osteoporosis with the first fracture. Douglas P. Kiel, a professor at Harvard Medical School, calls it “tantamount to public health malpractice.” Why aren’t testing and treatment happening? Many reasons, on top of the side effect issue. No single specialty owns osteoporosis. Orthopedic surgeons who deal with fractures have no training and little incentive to treat it, nor does Medicare require a bone density evaluation after a bone fracture. Nursing homes, which often manage the care of patients with broken hips, tend to let things lie once the fracture is treated, Siris says. Plus, a flurry of competing recommendations and misconstrued studies have left the average doctor “a little bewildered about who should be getting what treatment and for how long,” says endocrinologist Steven Harris, a clinical professor of medicine at the University of California, San Francisco. Finally, there’s the simple fact that this is a silent disease. We don’t feel our bones degrading; there’s no pain until they crack. But it’s a sad mistake to wait.

And then there were the dots I somehow failed to connect. For instance, it is no secret that hip fractures are a massive problem for older people, striking more than 300,000 annually in the U.S. alone, half of whom will never walk again without assistance and a quarter of whom will be dead within a year. But somehow I never realized that most of this death and disability can be attributed to the steady skeletal erosion of osteoporosis, a disease that, it turns out, is pretty darn treatable.

Unfortunately, false ideas like mine have led us to a perfectly avoidable health crisis. Let me flip the calendar back to 1995, the year when the first drug for osteoporosis, alendronate (brand name: Fosamax), was approved for sale and roughly the time when x-ray-based bone density tests became widely available. Fosamax was the first of several bisphosphonate drugs that work by slowing the turnover of bone cells. Research shows that they cut the risk of fracture by 20 to 50 percent.

Doctors embraced the new drugs, and U.S. hip fracture rates began to decline (although you cannot prove cause and effect). Arguably, physicians were a little too enthusiastic. A new diagnosis, “osteopenia”—low bone density that falls short of osteoporosis—was popularized and often treated, particularly in women going through menopause, when bone loss is fastest. “A lot of us were almost evangelical,” concedes endocrinologist Ethel Siris of Columbia University Medical Center.

Then, around 2005, came published reports of two rare but terrifying side effects: osteonecrosis of the jaw and a bizarre breaking of the leg bone called atypical femoral fracture (AFF). A chill descended on the field. Use of oral bisphosphonates fell by 50 percent between 2008 and 2012. The U.S. hip fracture rate plateaued, leading to 11,000 more fractures between 2013 and 2015 than predicted, according to a new study by Siris and her colleagues.

Yet research shows that both dreaded side effects are, as Siris puts it, “rare, rare, and I’m going to say it three times, rare”—with about one case per 10,000 to 100,000 patients. Clinicians have also learned more about who is vulnerable and, in the case of AFF, how to detect warning signs. Further, new drugs have emerged that do not have the same risks.

But since the scare, precious ground has been lost in protecting the most vulnerable group: older patients with fractures. Ideally, all patients over 50 who break a wrist, shoulder, hip or vertebra should be checked for osteoporosis and treated, if warranted. In reality, only about 20 percent are, although 15 years ago 40 percent of hip fracture patients got this kind of workup.

Doctors who study and treat osteoporosis are practically apoplectic about the trend. They point to research showing that if you have one “fragility fracture,” you face nearly three times the usual risk of having another one within the year. Nearly half of people who break a hip have previously broken another bone. In short, it’s pretty crazy not to look for and treat osteoporosis with the first fracture. Douglas P. Kiel, a professor at Harvard Medical School, calls it “tantamount to public health malpractice.”

Why aren’t testing and treatment happening? Many reasons, on top of the side effect issue. No single specialty owns osteoporosis. Orthopedic surgeons who deal with fractures have no training and little incentive to treat it, nor does Medicare require a bone density evaluation after a bone fracture. Nursing homes, which often manage the care of patients with broken hips, tend to let things lie once the fracture is treated, Siris says. Plus, a flurry of competing recommendations and misconstrued studies have left the average doctor “a little bewildered about who should be getting what treatment and for how long,” says endocrinologist Steven Harris, a clinical professor of medicine at the University of California, San Francisco.

Finally, there’s the simple fact that this is a silent disease. We don’t feel our bones degrading; there’s no pain until they crack. But it’s a sad mistake to wait.