Many of my readers ask me about medication for osteoporosis and when it is appropriate. The decision to take osteoporosis medications is a difficult one and one that you should make after carefully weighing out your options.
We know that exercise and nutritional support are very important for optimizing not only the health of our bones but our overall health and wellness. Despite having the knowledge, not all of us are free of co-morbidities (other health issues) that might limit your ability to exercise as hard as you need to or have the financial means of to enjoy a diet rich in fruit, vegetables, healthy fats and proteins.
In December of 2016 one of my clients invited me to attend a teleconference appointment she had with one of Canada’s leading Osteoporosis Specialists, Dr. Jonathan Adachi. The responses to her questions were clear and concise and so I asked Dr. Adachi if he would participate in a similar question and answer session with my readers. I pulled together a range of questions for Dr. Adachi and he kindly responded.
I hope you find this blog helpful when you have your own decision(s) to make regarding your bone health.
Medication for Osteoporosis • Q&A With Dr. Jonathan Adachi
1. How do bisphosphonate medication for osteoporosis (Actonel™, Fosomax™, etc) differ from denosumab (also know as Prolia™)?
Bisphosphonates medication for osteoporosis differ from denosumab (Prolia™) in how they affect the activity of the osteoclast cells. Osteoclast cells are the cleaners of old bone. The newly formed osteoclasts and the mature osteoclasts are the cells whose job it is to break down older bone.
Bisphosphonate medications bind directly to bone at sites of active bone breakdown and are then ingested by osteoclasts, the cells that breakdown bone. When ingested, the osteoclast dies and bone breakdown is prevented.
Denosumab is an immunoglobulin, a glycoprotein that works by binding to the cells that become osteoclasts. When they bind to these cells they lead to the death of the osteoclasts cells and thus stops bone breakdown.
2. Why are so many osteoporosis specialists suggesting to their patients to switch from bisphosphanate medication to Prolia™?
They would suggest switching when patients have side effects to the bisphosphonate, when there are declines in bone mineral density (BMD) or when patients sustain a fracture on bisphosphonates suggesting treatment failure.
In head to head studies of denosumab with each of the bisphosphonates, there are greater increases in bone mineral density (BMD) with denosumab.
3. What is the current recommendation for how long someone should be on denosumab (Prolia™) and are there risks for stopping this osteoporosis pharmaceutical prematurely?
There is evidence that denosumab medication for osteoporosis may be continued for up to ten years with ongoing improvement in spine bone mineral density (BMD). It may be that denosumab may be continued longer however we do not have clinical studies that go beyond ten years.
Stopping denosumab will lead to rapid reversal on bone mineral density (BMD) and may predispose a person to fractures again. If denosumab is to be discontinued then alternate therapy should be considered to prevent the loss of the gains in BMD with denosumab.
(Editor’s note: To learn more about Prolia injections and Prolia side effects, read my blog, How Long Can You Take Prolia.)
4. Could you discuss the concern about denosumab (Prolia™) relative to the impact on the immune system?
There were some concerns expressed when denosumab initially came out. At that time there were some skin infections that occurred in the denosumab treated group and not in the placebo group.
We now have longer term data and data from denosumab treatment in other conditions. The long term ten year data does not suggest that there is a long term risk for infection or malignancy.
In the breast cancer population in whom we treat patients with very high doses of denosumab, there does not appear to be an increase in infection risk and in patients with rheumatoid arthritis who are on immunosuppressive therapy and denosumab we do not see significant increases in infection.
5. How does denusomab (Prolia™) differ from teriparatide (Forteo™)? Please provide the pros and cons of each.
Teriparatide is an anabolic agent, a drug that actually builds bone. Denosumab is an anti-resorptive drug, one that prevents the breakdown of bone.
Teriparatide is used in those who have had multiple fractures with very low bone density. It should not be used in patients who have undergone radiation therapy or who have Paget’s disease.
Denosumab should be used with caution in those who have low calcium levels usually seen in those with malabsorption or severe renal disease.
Both are given by subcutaneous injection with teriparatide given daily for two years and denosumab every six months. The major difference is in price with teriparatide being more expensive than denosumab.
6. Many people are on proton pump inhibitors (PPI’s) for gastroesophageal reflux. There are a few studies that tenuously establish a link between PPI’s such as Nexium and fragility fractures. What do you tell your clients who are on PPI’s? Should they increase their calcium intake?
There is evidence that there may be an association between PPI’s and fractures. This remains controversial. If they are taking the PPI intermittently it is probably less of a concern.
However if they require high doses of their PPI, I suggest that they increase their dietary calcium intake so that they get three to four dairy products a day.
If they do have osteoporosis and are at high risk for fractures or have had fractures, I would recommend treatment with either a bisphosphonate or denosumab.
About Doctor Jonathan Adachi
Dr. Jonathan Adachi shares his time between his rheumatology practice at St. Joseph’s Healthcare in Hamilton, serving as Actavis Chair for Better Bone Health in Rheumatology and teaching for the Department of Medicine at McMaster University.
Dr. Adachi is currently involved in the CIHR funded Canadian Multicentre Osteoporosis Study.
Dr. Adachi’s other area of study involves the use of peripheral quantitative computer tomography (pQCT) and peripheral magnetic resonance imaging (pMRI) for structural analysis of bone and cartilage.
For more information, check out my Osteoporosis Guidelines.