Osteoporosis: 5 New Drugs That Can Challenge Bone Loss

Our expert explains the math behind bone loss and gain

Middle-aged couple

Osteoporosis specialists are researching new ways to curb the bone loss that affects many women and men as they age.

In osteoporosis, the bones lose their structural integrity. They grow fragile and fracture easily. The spine often curves forward into what is commonly called a dowager’s hump.

A matter of math

“The fundamental cause of osteoporosis is bone breakdown that exceeds bone formation,” explains Chad Deal, MD, Director of the Center for Osteoporosis and Metabolic Bone Diseases in Cleveland Clinic’s Department of Rheumatic and Immunologic Diseases.

The body is continually adding bone tissue and losing it. Up until about age 30, we add more bone than we lose. After about age 35, we start to lose more bone than we add. This process gathers momentum as we age, and accelerates at the start of menopause.

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Dietary supplements, weight-bearing exercise such as walking, and hormone therapy help to prevent osteoporosis when bone density declines.

The ‘gold standard’

A class of drugs called bisphosphonates is the gold standard treatment for low bone density– so far. Bisphosphonates slow the body’s breakdown of bone tissue. They trigger natural cell death among bone tissue-dissolving cells — which is good. But they also cause the cells that build bone tissue to slow down or stop adding new tissue — which is bad.

So researchers have been hard at work coming up with new osteoporosis drugs that can stop bone loss without disrupting the natural growth of new bone. Dr. Deal, Head of the Center for Osteoporosis and Metabolic Bone Diseases, keeps a close eye on these emerging drug therapies.

Five promising new approaches include:

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  1. Cathepsin K inhibitors. Unlike bisphosphonates, these drugs don’t trigger the death of bone-dissolving cells and may not inhibit bone formation to the same extent as bisphosphonates. Instead, they block a substance produced by these cells – cathepsin K — to slow osteoporosis without disrupting the body’s natural bone loss-bone gain balance.
  1. Glucagon-like peptide 2 (GLP-2). This drug is a digestive hormone that tricks the body into thinking that it is going to bed with a full meal. It seems that most bone loss takes place at night and may be linked to food intake. Researchers report that treatment with GLP-2 at bedtime significantly reduces overnight bone loss — but not bone formation.
  1. Nitrates. These inexpensive drugs deliver small increases in bone mass and reduce fractures. One study showed that applying a nitroglycerine ointment once a day reduced hip fractures by 15 percent. Bone mass increased in the lumbar spine (in the small of the back), upper thigh bone and hip. Also, bone loss declined and bone formation increased. All good — but more studies are needed.
  1. Anabolic agents. These bone and tissue builders improve the quality and strength of bone. Only one anabolic agent — teriparatide, or recombinant human PTH1-34 — is currently available in the United States. Another agent, recombinant human PTH1-84, is available in Europe. More anabolic treatments for osteoporosis are needed, says Dr. Deal.
  1. Wnt signaling antibodies. Wnt proteins are part of a family of key proteins involved in bone formation. Certain substances can keep these proteins from signaling and decrease bone formation. Researchers have injected antibodies to those substances into postmenopausal women. They found that bone density increased in the lumbar spine. Clinical trials are ongoing for postmenopausal osteoporosis and fracture healing, says Dr. Deal.

Prevention: What you can do

If you have a family history of osteoporosis, smoke, have a low body weight (< 127 pounds) or have had fragility fractures after age 50, you are at increased risk of osteoporosis. Being on prednisone for medical conditions such as asthma, rheumatoid arthritis and inflammatory bowel disease also ups your risk.

Discuss preventive measures with your primary care physician. These include taking calcium and vitamin D supplements, exercising and smoking cessation, and bone density testing when appropriate. “In some cases, prescription medication is required,” Dr. Deal notes.

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  • Jim

    I believe the “gold standard” for men is NOT bisphosonates but rather testosterone teamed up with calcitonin.  A testosterone deficiency is always somewhere at the bottom of male osteoporosis.  Calcitonin is a hormone that naturally enhances bone density.  Bisphosponates at the very least are corrosive and it takes a woman’s superior tolerance of pain to live with that and its other side effects.  Of course, we must not forget calcium supplements.  I truly don’t understand why osteoporosis isn’t relabeled as male osteoporosis and female osteoporosis because the two are diagnosed and treated differently. 

  • Jim

    Since you don’t seem to be taking comments on your other entry about testicular cancer, let me just put in my two cents worth here.  You say: Testicular cancer is a highly treatable cancer with more than 90 percent of cases being labeled as cured following therapy. Even better, the cure rate is nearly 98 percent when the cancer is detected early. 
    So, the question becomes, why don’t we do like we do with women and female breast cancer.  That is, recommend testicular ultrasounds for boys and men in the at risk age range, at least once a year.  I bet then the cure rate might reach 100 percent.  Ah, but that would cost money and we don’t spend money on men’s health if we can help it (it’s called the Titanic model of healthcare).  Add this to my earlier suggestion: a home pregnancy test when taken by a man can register a positive result if he has a testicular tumor.  Why not promote that too? 

    • Health Hub Team

      We practice evidence-base medicine, and no scientific studies support screening for testis cancer — the tumor is so rare it would not be cost effective to do this. We do recommend monthly self-exams (just like for breast cancer screening) for men in the appropriate group. — Eric A. Klein, MD, Chairman, Glickman Urological and Kidney Institute