Self-consult Program (The Ongoing Relationship)



This section is provided particularly for those patients who have attended one of our self-consult sessions at the DHOC (although we welcome all osteoporosis patients to review the material). We recognize that sometimes important questions arise that cannot be covered during the 2 hour session and many of these questions come up during the years that follow your initial appointment and treatment plan.

Here you will find a list of the most common questions asked by both patients and doctors, regarding osteoporosis care over the longer term. It is important to recognize that medical care is so much more than the listing of medical facts; it is the interpretation of medical science in light of the individual patient. Therefore, it is impossible for a website to give specific medical advice for individual patients (please see our disclaimer for details). However, by providing discussion and examples of the pertinent issues, we believe patients may become better informed of the relevant facts and opinions that may apply to their care. Consultation with your personal health care provider is essential and the DHOC is happy to provide phone support to primary care providers who would like more detailed discussion about specific patients (see our Referral Form).

Finally, it is important to understand that many parts of medicine (osteoporosis care included) are heavily influenced by the physician's interpretation of the relevant science and informed by their own experience with patients over the years. Straightforward and generally agreed-upon medical advice for simple osteoporosis is available at the Osteoporosis Canada website. The questions addressed on the DHOC site below are intended to provide general discussion (from Dr. Kline's perspective) on some of the less definite aspects of osteoporosis care that may be harder to answer from a strictly factual basis.

If you have suggestions for other general questions you'd like to see addressed here, we encourage you to email us at This email address is being protected from spambots. You need JavaScript enabled to view it.. Please note, we are not able to provide any specific medical advice through this email nor can we offer ongoing email discussions; any answered questions will be of a general nature and posted on this section of the website, not through return email to the sender.

pdfView SCP Presentation  pdfSCP_Booklet_My_Osteoporosis_Consultation_and_Plan_Nov_2019.pdf


(Click on Question to Reveal Answer)

1. How do I know if I chose the right thing in my self consult session?

As you probably heard in the self consult session, there really are no absolute "right" or "wrong" decisions when it comes to choosing if or how you want to deal with your bone density or fracture risk. Remember, it is perfectly natural to develop low bone density as you age and so looking at your bone density alone is not really the ideal way to make any such decision. In the self consult session, our focus was on "the big picture" of your whole bone health - considering multiple factors and then ultimately weighing the pros and cons of drug intervention.

KEY POINT: The most important part of the self consult session was the exercise we did to look at your risk of fracture without medications and your risk of fracture with medications. Knowing these two scenarios allows you to make an informed decision.

Here is an example to encourage even more thinking about it:

EXAMPLE: Maria is 67 years old and has a low T-score on Bone Density measurement. Her mother had a hip fracture. Maria is quite thin and remains very active, trying to follow a healthy lifestyle. At the self consult session, her WHO FRAX score showed a 10 year risk of hip fracture of 5% and a 10 year risk of other major osteoporotic fracture of 18%. That means that out of 100 women just like her, approximately 5 of them will break a hip in the next 10 years, by age 77. And approximately 18 out of 100 women just like her will have some other kind of fracture, like a wrist fracture or spinal compression fracture. If she chooses to start anti-fracture drug therapy for at least the next 3 to 5 years, it will probably reduce her risk of hip fracture from 5% to 3% and reduce her risk of other fractures from 18% to around 10%.

Keep in mind these are generalized estimates based on large studies of groups of women - not quite as exact as the numbers on an individual tax calculation!

So, the question is: Will Maria choose to take a medication for 3 to 5 or more years, in order to reduce her risk of fractures from 18% to 10%?

COMMENT: In our experience here at DHOC, some patients will think that a reduction from 18% to 10% is a good value and some people won't. We have met patients who refuse drug therapy no matter how high their fracture risk. And we've also met patients who want drug therapy even though their chance of fracture is really very low. And because there's no such thing as "mandatory" osteoporosis therapy, we're prepared to support all our patients in their decision.

Some patients ask their doctor to make this decision for them - understandable because hopefully the doctor is reasonably good at weighing some of the pros and cons as well. In very general terms and without any patient input, we would generally recommend that if your risk of major fracture is higher than 20%, it's definitely worth thinking about drug therapy. But that's about as much as we can say because it really is such a personal decision. This is discussed further in the questions below.

2. How do I know if my treatment is working?

This is a natural question to ask - you've chosen a medication so it would be nice to know that it's working. The problem is that these medications are not like drugs to lower blood pressure where you can just check your blood pressure to see that it's lower.

KEY POINT: Drugs that reduce your risk of fracture generally work by either maintaining and hardening the bone you have ("anti-resorptives") or building new bone ("anabolics"). All such drugs work very slowly and largely without making you feel any differently. The most important thing is that you stick to your treatment for the whole duration of planned therapy.

Sometimes people will have a repeat bone density while on therapy in an attempt to "check" if the medication is working. This is usually not necessary for most cases but if it is done, have a look at the questions in this section that specifically address the issue of bone density changes.

On rare occasions, there really is a medical concern about whether the drugs are doing what they are supposed to do and in such settings, your doctor may choose to order a blood test called "Beta-CTX crosslaps". This test, done fasting and first thing in the morning, gives your doctor an idea as to the current rate of bone loss - which, if you are taking an anti-resorptive, should be very little. Basically, the higher the BCTX result, the more bone loss is occurring. If the BCTX results are in the normal range, it suggests there is no meaningful bone loss occurring.

EXAMPLE: Surjit is a 72 year old woman with post menopausal low bone density and previous wrist fracture. She attended a self-consult session and chose to be started on an oral bisphosphonate (alendronate) which she has been taking for 1 year now. She has just been diagnosed with celiac disease (a bowel disease causing malabsorption) and her doctor wonders if she has been absorbing the alendronate. A first morning BCTX is measured and is found to be quite high - suggesting that she is losing bone and therefore either not taking or not absorbing the drug properly. Her doctor switches her to the intravenous form of the drug (zoledronic acid) and re-measures the BCTX six months later. It is then found to be low-normal and suggests that the switch has effectively solved the problem and she is not losing bone anymore.

COMMENT: From the example above, BCTX seems like a pretty neat test and some people might wonder why we don't do this kind of test more routinely (and there are some osteoporosis doctors who probably would favour more use of this test too). However, sometimes the test is not as easy to interpret as what it may appear and there are even some debates about whether the test can be truly medically reliable for drug decision making in individual patients. Therefore, this should be viewed as a potentially helpful tool for answering specific questions (like in the example) rather than something that adds to the routine osteoporosis care plan.

3. When should I have another bone density (on therapy)

This is one of the most common questions we get at the osteoporosis centre. It certainly seems like a natural thing to do because both patients and doctors (perhaps especially doctors) have a strong desire to monitor the effects of anything we do for improvement of health. This is usually a very good inclination and we all know that trouble can arise when a treatment situation goes unmonitored for a long period of time. Therefore, it sometimes comes as a surprise when people hear that we actually discourage routine repeat bone density testing while patients are taking anti-fracture drugs.

KEY POINT: Bone density changes (either positive or negative or neutral) tell your doctor very little about the success or failure of your osteoporosis medication. If you have chosen to take an anti-fracture medication to reduce your risk of fracture, the most important thing is to adhere to therapy. If taken properly and regularly, these medications are already known to reduce your risk of fracture, regardless of what repeat bone densities show.

EXAMPLE: Lois is a 64 year old woman with low bone density, low body weight and a strong family history of osteoporosis and fracture. She has opted to be treated with yearly intravenous zoledronic acid (bisphosphonate drug). After 1 year of treatment, she gets a bone density done and in comparison to her pre-treatment bone density, it appears to show no increases. Thus, her bone density is still low and someone tells her that her drug must not be working.

Not true! There are several important facts that must be considered when it comes to interpreting this lack of change in bone density:

  1. Even when bone density does change (either increase or decrease), the amount of change in 1 year is usually so small that the bone density machine will not be able to detect the change as being truly different from before. Therefore, a one year interval is probably much too short to expect to see any real change.
  2. Comparison of two bone density scans is very complicated and depends upon identical positioning on the same machine, along with other factors that can add some degree of error to the results. These types of technical limitations sometimes result in changes (or lack of changes) that are misinterpreted as being medical changes.
  3. There is published evidence that the anti-fracture effect of current osteoporosis medications exert much of their effect by improving the quality and hardness of bone, not necessarily the bone density.
  4. There is published evidence that bone density changes, measured while on therapy, have little or no relationship to whether the patient ultimately has a fracture or not. That even holds true for when the repeat bone density is even a bit lower than the first one.
  5. Anti-resorptive drugs like bisphosphonates do not build new bone, they largely stop bone losses and improve bone quality to reduce fractures. Therefore, it is completely normal and expected to see stable bone density (no increases) while on treatment.
  6. Remember, as a post menopausal woman, it is expected that bone density will decrease naturally over time. Therefore, in this example patient's case, the fact that her bone density did not decrease shows that the drug is doing exactly what it was supposed to do
COMMENT: In years past, it was routine practice to order repeat and sometimes annual bone density scans on patients receiving anti-fracture drug therapy, in order to fulfill our desire to ensure that the drug was working. However, from the aforementioned reasons, it should now be understood that this practice has very little validity and rarely adds much to routine osteoporosis care. In fact, sometimes it causes more harm than good by raising false alarms about possible therapy failure. At the DHOC, we generally recommend against doing routine bone density scans during the years of active drug treatment. Adherence to therapy is always the most important issue, not monitoring.

4. When should I have another bone density (not on therapy)

This question and answer is written specifically for those who have attended a self consult session and have opted not to start anti-fracture drug therapy.

KEY POINT: A general rule of thumb might be to consider repeat bone density testing every 3 to 5 years in post menopausal women who are not taking anti fracture therapy. This will permit the patient to periodically repeat their fracture risk assessment and review their drug treatment decision as they age.

The problem with "rules of thumbs" is that while they probably work in many cases, they are usually over-generalizations and rarely reflect the necessary sophistication for optimal individualized care decisions. We'll go over more details in the example and discussion below.

EXAMPLE: Miriam is a 55 year old woman who dates her menopause from age 52. She had a bone density done just recently which showed slightly low bone density, typical for a woman her size and age. She attended a self consult session and it was calculated that her 10 year risk of hip fracture was 1% and her 10 year risk of other major osteoporotic fractures was 8%. At this low level of fracture risk, she decided not to start any anti-fracture drug therapy. She was happy with her decision but now wonders if she should get a repeat bone density done in a year - and maybe repeat the self consult session as well.

If Miriam gets a repeat bone density done in 1 year, there's a very good chance it will be pretty similar or even exactly the same (see question 3 for a discussion of reasons why short time intervals sometimes show no change in bone density). Does this mean she is not losing bone? Well, not really. As a woman in the first ten years of menopause, she can be virtually certain that she will be losing some bone on an ongoing basis - it is naturally to be expected. The rate of bone loss may be quite variable between different women and it is entirely possible that it may take 2 to 3 years to actually see a measurably different loss of bone density.

So - if the bone density is done and is largely the same, what will the "updated" fracture risk estimate be? Virtually identical to what it was before. And - if she wasn't going to accept drug therapy previously at that level of risk, then she probably won't be any closer to starting drug therapy now either.

What if the 1-year bone density is done and it is actually lower by about 5%? This is also within the realm of normal possibility with natural menopausal bone loss. In that case, we can repeat her fracture risk estimation using the same WHO FRAX online calculator. With all other things being equal, when we input the new, lower bone density, it turns out that her updated 10 year hip fracture risk is now 1.3% and 10 year major osteoporotic fracture risk is 10%. Looking at these figures, Miriam still decides not to have drug therapy.

In fact, if Miriam repeated this process every year for the next 5 years, she would see that her 10 year risks of fracture would only increase marginally. If her risk of fracture was 1% and 8% at the self consult session, even five years later, her risks will probably still be so low that drug therapy is not desired - bringing up the question about whether it was worth doing all those bone density scans along the way. This is why there is probably no real value to doing annual bone density scans and hence the 3 to 5 year rule of thumb.

COMMENT: Try this yourself! Anyone can access the online WHO FRAX fracture risk estimation tool for free. Put in all the same values for height, weight, smoking, family history etc that you used in the self-consult session. But, for bone density, put in a T-score that is just a little bit lower than your last bone density (i.e if your T score was -1.3, put in -1.6) in order to get a "preview" of what your fracture risk might look like if repeated in 1 or 2 years. Here's the bottom line (and the most sophisticated way to plan on repeat bone density timing): If you are very close to accepting anti-fracture drug therapy, then it makes sense to repeat your bone density and fracture risk assessment in 1 or 2 years - presumably even small changes might be enough to push you past the "treatment threshold". However, if you are a long ways away from wanting drug therapy (i.e. low risk of fracture), you probably won't be changing your mind for at least another 3 to 5 or even 10 years and so it makes more sense to defer repeat bone density until that time.

5. My DXA bone density is pretty good, does that mean I don't have osteoporosis?

Unfortunately, that is not necessarily true. The only thing that can be said is that you don't have low DXA bone density and may not fit the DXA label of "osteoporosis". But you can still have clinical osteoporosis and be at high fracture risk.

KEY POINT: "Osteoporosis" is a name or label that is intended to convey an understanding that the patient has lost bone in their older years and is now more prone to fracture. DXA bone density scans may be useful to help assess patients' fracture risk but should never be taken to replace a full clinical assessment of risk.

EXAMPLE: Kenneth is an 83 year old man who has become rather thin and frail in the past 10 years after suffering a stroke. He recently slipped off the back step of his porch, fell and broke his hip. After discharge from hospital he follows up with his primary care doctor who decides to order a bone density scan. The scan shows a hip T score of - 1.9 and spine T score of +0.7. Kenneth and his family are uncertain as to whether he has osteoporosis or not.

The answer here is yes, he should be considered to have a clinical diagnosis of osteoporosis. This diagnosis is made by virtue of his age and recent low-trauma fracture. So why is his bone density "so good"? Remember that a DXA bone density is just a special kind of x-ray. There are many things about bone quality that cannot be measured by DXA scanning - and in this case, it is those "unmeasurables" that are most important to his fracture risk. The spine bone density is particularly misleading - many older men (and women) may have extensive degenerative changes in their spines (sometimes associated with osteoarthritis - pain - of the spine). These degenerative changes may cause the DXA bone density to be artificially high - masking the true low bone density. In these cases, the bone density should not be called "normal" or "good", it should be called "not valid for interpretation".

These and other limitations to DXA bone density scans are part of the reason that we do not recommend patients make treatment decisions based on bone density alone - it just doesn't give the full picture. In the self consult session, you will have learned to use a fracture risk prediction tool that includes many risk factors to help give you a more accurate estimate of your fracture risk.

COMMENT: Beware of the "good" bone density, especially in the elderly population. It may mask the true state of the bones and give a false impression that there is no real fracture risk. In the example provided, Kenneth should be considered very high risk for fracture and anti-fracture drug therapy should be offered. It could be a real tragedy for both him and his family if he had another major fracture requiring hospitalization or a move to a full time care facility. In fact, many osteoporosis doctors would say that his hip fracture would be reason enough to consider drug therapy and that a DXA bone density adds little or nothing to his overall assessment. If a DXA bone density were not available or could not be done for some reason, it should not deter his doctor from considering anti-fracture drug therapy.

6. I chose no therapy and my bone density went down. Now what?

If you are a post menopausal woman not taking estrogen or an anti-resorptive drug like bisphosphonate, it is not surprising that your bone density may have decreased. And that's potentially OK.

KEY POINT: Bone loss during post menopausal years (or after age 65 for men) is expected. It does not necessarily mean a disease is present, nor does it necessarily mean that you are suddenly at high risk for fracture if you were low risk for fracture in the recent past.

It might sound like your doctor is uncaring if they say "it's OK to lose bone"! (In fact, we try to word it with a bit more sensitivity) but the reality is that bone loss is an expected part of ageing that does not necessarily mean there will be any changes to your life and abilities. The key is to balance "acceptable changes of ageing" with eventual "increased risk of fracture" and to intervene at the right time. No one wants to take unnecessary or unhelpful drug therapy but no one wants a fragility fracture either and so fracture "risk management" becomes the main focus.

EXAMPLE: Joan is a very healthy 60 year old woman who attends the self consult session and calculates that she is at very low risk of fracture in the next 10 years. She opts not to start any drug therapy but 2 years later, her bone density is reported to be 8% lower. She begins to regret her decision not to take drug therapy as this bone is now "gone for good".

This is a bit of a sad story - we never want patients to have to look back and regret the health decisions they made earlier. Having said that, there are a few key points that Joan should be given to help keep this all in perspective:

  1. As mentioned, bone loss is a natural process with ageing. Bone loss itself does not necessarily guarantee any negative consequences - if everyone lived to age 90 with terribly low bone density but no fractures, we'd conclude that low bone density was irrelevant. And many people are quite fortunate that way - we've all heard the figures stating that 1 in 3 women will have a fragility fracture in her lifetime - while our goal is to reduce that risk, let's not forget the 2 in 3 women who never suffer a fracture…despite having age-associated low bone density.
  2. While it is reasonable to assume that this bone loss is natural, her doctor may want to do some simple blood tests just to make sure she doesn't have another reason for bone loss - examples would be a blood calcium and phosphate level and perhaps a bone enzyme called alkaline phosphatase. In very select cases, other tests may also be useful.
  3. In some ways, it is indeed true that the lost bone is "gone for good" but that doesn't mean that drug therapy, when chosen, will be ineffective. Current drug therapies can significantly improve bone quality and make it less prone to breaking. Although used less often, the anabolic therapies (teriparatide and others in the future) may indeed permit new bone formation.
  4. Her risk of fracture may still be very low. Remember that DXA bone density is just one factor of many that determine fracture risk. An updated WHO FRAX risk score may be done with the new bone density and Joan may be quite pleasantly surprised at her low fracture risk status - so much so that she might still be happy to forego drug therapy.
COMMENT: Bone density is a bit of a double-edged sword; it is certainly useful for predicting fracture risk (especially in those who have other fracture risk factors). On the other hand, it is sometimes used to "monitor" a natural process that occurs in everyone as they age - and it gives both doctors and patients a strange feeling to monitor what looks like "deterioration", while doing nothing about it. Nobody wants to ignore "deteriorating" health!

One of the most common things we hear in clinic is that "I don't want to be like my mother." (For this website, we'll presume that this comment pertains to bone health and risk of stooped posture!) In years past, some people used to argue that we should be much more proactive in osteoporosis and use drug therapy to prevent all osteoporosis. While that certainly sounds good in theory, think about what that would mean: basically every woman would need to begin lifelong drug therapy starting at menopause. All in the hope (theoretical) that at some point 15 to 25 years in the future, there might be a reduced risk of fracture. And, while anti-fracture medications are generally very well tolerated and safe, there are rare and serious side effects that can occur from time to time and it would be a shame to suffer such an effect while taking a drug during a time of life where fracture risk is extremely low.

Bottom line - while there are still some who advocate for early post menopausal use of drug therapy to prevent bone loss, we generally take a more conservative view of such treatment and suggest it may be of more immediate value to those who are actually at a high risk of actual fracture.

7. I chose no therapy but now I have a new risk factor that I didn't have at the Self Consult Session

This is every patient's frustration with doctor visits isn't it? You make the appointment to get help with some symptoms and then the symptoms are gone by the day of the appointment. We recognize that this can also happen in osteoporosis assessments - the situation on the day of the assessment may change and now you have to wait again for another appointment.

KEY POINT: The fracture risk assessment tool that we use at the osteoporosis self-consult session is freely available online and may be repeated and updated by the patient as often as necessary.

EXAMPLE: Gloria is a 62 year old woman who attends an osteoporosis self consult session. She has modestly low bone density, low body weight and is a smoker (trying to quit). Her WHO FRAX fracture risk assessment predicts a 10 year hip fracture risk of 6% and a 10 year major osteoporotic fracture risk of 17%. On the basis of these estimated risks, she decides not to start anti-fracture drug therapy. Two months later, she receives word that her 85 year old mother has fallen and broken her hip (a sure sign of osteoporosis). Gloria remembers from the class that a history of hip fracture in your mother is a major predictor of fracture. Now she begins to doubt her decision made at the class.

First of all, let's not ignore the mother's history. It's important that Gloria review her decision but if possible, her mother should probably have an osteoporosis assessment as well.

It is certainly possible that a patient's osteoporosis risk factors may change with time - beyond just the changes in bone density discussed in the other questions. Parental hip fracture, initiation of steroid therapy, personal fragility fracture, loss of body mass, diagnosis of rheumatoid arthritis are all major risk factors that one may acquire over time. Hopefully nobody actually starts smoking later in life.

Gloria is quite right to think that her osteoporosis decision may now change. She can go to the WHO FRAX website and enter all the same data (height, weight, bone density, etc.) from her self consult assessment form but this time, give herself a "Yes" for parental history of hip fracture. When she does this and pushes the Calculate tab, it shows her updated 10 year hip fracture risk is now 11% and 10 year major ostoporotic fracture risk is 27%. Upon review of these numbers, Gloria decides that drug therapy would be warranted and so she makes an appointment to see her primary care practitioner to discuss her options again.

COMMENT: It is important to remember that fracture risks change over time - generally increasing very slowly with year to year ageing but sometimes abrupt risk factors arise that necessitate re-evaluation of the treatment decision.

8. I chose no therapy but now I've had a fracture. Should I change my decision?

We're sad to hear this - the goal of the osteoporosis self consult session is to help make osteoporosis fracture risk management decisions and ideally, prevent fragility fractures. However, even very low fracture risk patients sometimes have a fracture - there's really no such thing as the "zero fracture risk" and this probably serves as a good time to remember that it's not too late to prevent the next fracture.

KEY POINT: Even very low fracture risk patients can sometimes have a fragility fracture; if that happens, it would be worth re-considering the possibility of starting drug therapy. In osteoporosis research it is well known that "one fracture begets another fracture" i.e. those who actually do fracture are likely the same people who will have multiple fractures and anti-fracture therapy is something to consider.

EXAMPLE: Doris is 59 years old and has a bone density T-score of -1.0 at the hip and -1.4 in the spine. She has no other risk factors for fracture and is not taking any anti-fracture drug therapy. On New Year's Eve, she slips on ice and falls and breaks her wrist. Her primary care practitioner sees her a few weeks later and brings up the question of osteoporosis and possible anti-fracture drug therapy. Doris laughs and says, "I don't need that, I just need to be less clumsy."

There may be a lot of truth in what Doris says - maybe she doesn't "need" drug therapy and perhaps it would be best not to race her grand-daughter across an icy parking lot - but let's look at some of the facts she may want to further consider.

  1. The majority of osteoporotic or fragility fractures occur in women whose DXA bone densities are not "osteoporotic". Many people are surprised to hear this. The reason has to do with the pure numbers of women having fragility fractures versus the number of women with "osteoporotic" bone density. It is true that women with "osteoporotic" bone density (a term we are only using to make a point in this case) have a much higher risk of fractures but looking at all the fractures that occur in a population (i.e. the city of Calgary), the majority of fragility fractures actually occur in the large segment of women whose bone density is "not osteoporotic". This is yet another reason why we do not use bone density tests alone to make any treatment decisions.
  2. It can sometimes be difficult to determine what is a "fragility fracture" and what is a "trauma fracture". When we talk about osteoporosis fracture risk, we're really only concerned with low-trauma or fragility fractures. Clearly, if you break your hip during a waterskiing wipeout, that's a trauma. Similarly, if you swing a golf club and get a compression fracture, that's a fragility fracture. But sometimes the mechanism of injury could really go either way. The traditional definition of a fragility fracture is a fracture after a fall from standing height although this is somewhat arbitrary and we've seen lots of patients where it is just hard to classify the fracture and know whether it's of concern or not.
  3. Having said that, there's some interesting research showing that post menopausal women who have traumatic fractures are actually at increased risk of future fragility fractures! So, the differentiation might be less important than we have thought.
  4. A reasonable approach to this problem might be to calculate the 10 year fracture risk both with and without "personal history of fracture" counted as part of the assessment. That way the patient can get an idea of "best case scenario" and "worse case scenario" then make their decisions accordingly.
COMMENT: The example above shows how tricky this fracture assessment can sometimes be. But let's not make this more complicated than it needs to be. As outlined in question #5, a fragility fracture in the menopausal years (or age > 60-65 in men) should be considered as indicative of a clinical diagnosis of "osteoporosis" and usually indicates the patient is at least moderately high risk for another fracture in the near future, sometimes in less than 12 months. Does that mean Doris should automatically choose drug therapy? We won't go so far as to say "automatically" but will say that she should take her doctor's suggestion seriously.

9. I'm on therapy and my BMD didn't get any better. Is my drug failing?

This is a common concern and is partly answered in question #3 which we suggest you read first. Bone density changes are probably a lot less important than one might think. In the example below, we'll discuss what the different drugs actually do to bone and bone density.

KEY POINT: Different anti-fracture drugs have different effects on bone. One might speculate that different effects on bone might mean different overall effectiveness at reducing fractures. However, that has never been convincingly proven and so there is still no scientifically compelling reason to say that one drug is better than another and certainly not on the basis of bone density changes alone.

EXAMPLE: Colleen attended an osteoporosis self consult session and based on her fracture risk, decided to start taking risedronate to reduce her fracture risk. She ended up having a repeat bone density test 3 years later which showed a 1% decrease in her bone density compared to her pre-treatment. She is now doubting her original treatment decision.

Again, see question #3 for a full discussion as to why the repeat bone density test might be viewed with some suspicion. As well, see question #2 for a discussion of a blood test that her doctor could consider using to help reassure that the drug is doing exactly what it's supposed to do.

Explanations aside, sometimes patients feel discouraged in this situation, having hoped that their bone density would "get better". It's understandable why this might be expected - some online resources and education materials can certainly give the impression that improvement in bone density is to be expected. But here are a couple reasons as to why that may not apply to many individual patients:

  1. In clinical trials, patients on bisphosphonates (or other anti-fracture drugs) had a larger increase in bone density than those on placebo. This is a true statement but sometimes people forget that clinical studies report the average bone density changes across the whole treatment group and that individual patients can have a wide range of bone density "responses" and still benefit from being treated. For example, if a clinical trial shows that a drug increases bone density by 6% over 3 years, it's important to realize that some patients in that group will have had 0% increases and some patients may have had 9% increases. Analyses of this kind have subsequently shown that treated patients had fewer fractures almost regardless of whether their bone density was above or below that average.
  2. Remember that many of the anti-fracture drugs, especially bisphosphonates or denosumab do not actually "build" new bone. So, why does bone density increase at all in some patients? The answer lies in the understanding that we are all simultaneously building and removing bone at various rates, all the time. After menopause, the bone losses exceed new bone building (causing a net loss) but the building does not stop altogether (although it may slow significantly with increasing age). When one starts a bisphosphonate drug, the bone losses are slowed or stopped but the bone building continues, inasmuch as is possible, until all of the "active" bone remodelling sites are completed. This may result in a small net bone gain but does not continue indefinitely.
  3. Ultimately, net bone density gain will depend a lot upon the patient's inherent ability to form new bone (such as whether she smokes - a strong inhibitor of new bone formation), along with the degree or rate of bone losses that were occurring at the time of drug initiation.
  4. On occasion a significant decrease in bone density on therapy (i.e. 5% or more) may well raise some concern about possible alternate underlying bone problems and investigation by the health practitioner may be needed to ensure that there is not another diagnosis present. However, in healthy patients, this is quite unusual unless there are other signs and symptoms of a new disease process like anemia or kidney problems. Important and serious bone diagnoses are rarely made on the basis of bone density changes alone.
  5. Either way, if Colleen is adherent to therapy, she can be expected to preserve her bone mass and reduce her fracture risk regardless of her bone density response. She did not choose the wrong drug; she just came to an incorrect conclusion about her bone density tests.
COMMENT: Beware of bone density reports that show no change or minor (1-3%) losses while on therapy and comment that "therapy should be reviewed". That comment may imply lack of effect - which would be incorrect - but perhaps can be a helpful comment if taken as a reminder to ensure ongoing adherence to therapy. Sometimes people use bone density changes (or lack of changes) as reason to switch from one drug therapy to another. There's nothing inherently wrong with doing this - provided the patient understands that there is no proof that doing so necessarily changes anything in terms of fracture risk and that bone density results are not really the goal of therapy anyways. If a bone density is found to be surprisingly and suddenly low (a very, very rare situation), additional investigation should be considered.

10. I'm on therapy and my BMD is still very low, does that mean I'm still at high risk of fracture?

This question tends to come up whenever a person gets a bone density while taking anti-fracture drug therapy. The report will often say something like this, "High risk for osteoporotic fracture", even after several years of drug therapy. That leads some patients to wonder if their medication even worked or whether it was even worth taking in the first place.

KEY POINT: Most DXA bone density scans are read by radiologists who may not know your medical history or whether you have been on therapy or not. Therefore the official interpretation comments may be more appropriate to someone who has never been treated. If you are being adherent to proven therapy, your fracture risk is lessened.

EXAMPLE: Bill is a 78 year old man who developed a rare autoimmune disease 3 years ago. At that time, he needed to be treated with a steroid drug called Prednisone (which is known to be bad for bones, unfortunately). At that time, his doctor had ordered a bone density which showed low bone mass. In light of his bone density, age and prednisone use, his doctor recognized that he was high risk for fracture and started him on alendronate, a bisphosphonate drug. Eventually, Bill was able to stop taking the Prednisone and after 3 years of alendronate treatment, he had a repeat bone density ordered by the doctor. The results showed that his bone density T-score was still low and the radiologist's comment says, "the patient is high risk for fracture." Bill is confused because he understood that alendronate was going to be taken in order to reduce his risk for fracture. Did the therapy fail?

The quick answer here is that the therapy did not fail. The lack of change in bone density is not surprising and is discussed in detail in several of the other FAQ of this section. The question is really whether Bill is still "high risk" despite having taken alendronate for 3 years. Here are a couple of things to consider when answering this question:

  1. The radiologist may not realize that Bill is no longer on prednisone. That being the case, this is one less risk factor to contribute to Bill's overall fracture risk. Sometimes risk factors for fracture change (either for the good or the bad) and that must be taken into account. If someone quit smoking 3 years ago, then they could be at lower risk of fracture than they used to be.
  2. A DXA bone density scan is the most useful when it is being used to determine fracture risk before starting on any drug therapy (the way that we used it in the self consult session). At the session, you would have learned that lower T-scores generally mean higher risks of fracture. However, the relationship between T score and fracture risk changes once you start osteoporosis drug therapy. Therefore, even if the T-score is still low (which it probably will be), it doesn't necessarily mean that the fracture risk is the same as what it was before treatment.
  3. Remember, the whole point of drug therapy is to reduce fracture risk. At the DHOC self consult session, we only discuss therapies that have been proven in large clinical trials to reduce osteoporotic fractures. Therefore, if you have chosen one of these therapies, you can rest assured that with adherence over time, your fracture risk should be lessened….regardless of what radiology reports say.
COMMENT: Remember that the phrases "High fracture risk" or "low fracture risk" are somewhat arbitrary and often applied according to "the eye of the beholder". Some people unfortunately have so many fracture risks that they might always be considered high fracture risk, no matter what they do. However, if a person has chosen to take anti-fracture osteoporosis therapy, the point is that with time, their risk of fracture becomes less than it was and that is the whole purpose of being treated in the first place.

11. I'm on therapy and had a fracture - does that mean my treatment isn't working?

This situation is one of the most common scenarios to prompt a re-referral to the Osteoporosis centre. Depending on the medical complexity of the patient, this may require a fairly comprehensive re-assessment and discussion that would be hard to fully capture in this post. However, there are a few general principles to be considered in all such cases.

KEY POINT: The reality is that even with good anti-fracture therapy, sometimes fractures still happen - just much less than in the absence of therapy. However, nobody wants to be the one this happens to and if a fracture does occur, there are some key questions that the patient and doctor should review together to ensure that the right diagnosis and appropriate therapy is in place.

EXAMPLE: Karen attended the osteoporosis centre where she learned that she was moderately high risk for fracture (WHO FRAX 10 year hip fracture risk of 6% and 10 year major osteoporotic fracture risk of 24%). She opted to start therapy with yearly intravenous zoledronic acid and has now had 2 infusions. Last week, while bending over in the garden, she had the sudden onset of back pain that required an emergency room visit. There, an x-ray showed a new compression fracture of her 12th thoracic vertebra. This wasn't supposed to happen! Should she change her therapy?

It's natural to question the value of therapy at this point and even doctors find themselves wondering if perhaps something somehow could have or should have been done differently in order to have prevented this new compression fracture. Every situation is unique but here are a few key points the doctor will consider when assessing what to do next:

  1. It is entirely possible that there is nothing that needs to be done differently here. Remember that drug therapy reduces the risk of fracture but no drug therapy promises to prevent every possible fracture forever. During the self -consult session, we did an exercise with Karen showing that her 10 year major osteoporotic fracture risk was 24% and that with drug therapy, her 10 year osteoporotic fracture risk would be expected to decline to about 14% on average. That's a useful risk reduction but consider this - even with drug therapy, she still had a 14% of having a fracture. While 14% is not high, it is certainly still possible that a fracture, like the one she had, is still something that could happen. Therefore, even if the drug was doing exactly what it was supposed to, an occasional fracture might still occur.
  2. When starting a new anti-fracture medication, the reduced risk of fracture is not realized immediately. In other words, it takes time for the drug to affect the bone in such a way as to strengthen it and reduce its chance of breaking. Generally speaking, fractures become progressively less common with longer therapy and so Karen should not give up on her current therapy yet. In fact, we often say that fractures occurring within the first year of treatment should probably be considered as independent events - not likely to have been prevented with drug therapy since it just hasn't been taken long enough. This is a good time to point out that drug therapy to reduce fractures is long term therapy - there's really no point to taking these medications for 6 to 12 months and then stopping.
  3. While fracture on therapy is often not a cause for alarm, it does provide a good opportunity for the doctor to review the overall diagnosis. Most healthy older people with osteoporosis only have low bone density on account of menopause or simply getting older in age. However, there are a couple uncommon conditions that can cause bone loss and possible lack of response to medications. Your doctor might check for these conditions by measuring a blood calcium and phosphate level, possibly screening for celiac (malabsorption) disease or checking for a rare blood cancer called myeloma.
COMMENT: So, assuming all blood tests are normal, what should Karen do? Stay the course with the zoledronic acid or switch to another drug? Generally speaking, in this scenario we would advise simply sticking with what she has already chosen. Hopefully, the drug will prevent her from having any more fractures in the future. It's tempting to consider switching to another drug but in a case such as this, there is really no compelling scientific argument for doing so. Many of the osteoporosis medications accomplish largely the same thing albeit in different ways and so switching from one to another is not really proven to change the outcome. The one exception is that in some cases, a doctor may consider switching from an anti-resorptive drug (bisphosphonate, raloxifene, denosumab) to an anabolic (bone building) drug like teriparatide. This sounds theoretically attractive (and some patients do choose to do this) but again, we do not yet have scientific proof that it is necessarily better than just continuing present therapy. It's something to think about but should not be viewed as an automatic choice.

12. I'm on therapy and am having what might be a side effect, what should I do?

Without question, this is the thing that everyone worries about the most - the risk of side effects. It's certainly understandable to be concerned and in the self-consult session, we spoke at length about some of the potential side effects of the drugs for osteoporosis. Because some of the rarest side effects can be quite nasty, patients often struggle to balance the potential benefits of drugs with the fear of side effects. When doctors quote that a certain side effect is thought to affect 1 in 10, 000 patients, many patients say that they expect themselves to be that 1 in 10,000! Statistically speaking of course, a 1 in 10,000 chance of side effect could also be stated as saying that the patient has a 9,999/10,000 chance of NOT getting the side effect. So, do you see a "glass 99.999% full" or "0.0001% empty"?

KEY POINT: We've often heard people say "every drug has side effects." But this is only partially true. It would be more accurate to say that "every drug has POTENTIAL side effects." And, while some of the nastier side effects tend to get a lot of mention in the news (especially if doctors or drug companies try to deny their existence!), the reality is that the drugs used in osteoporosis therapy are safe and effective for the majority of users, when prescribed and taken appropriately.

EXAMPLE: Rami is a man with osteoporosis and high fracture risk related to his age and very low bone density from prostate cancer treatment. His doctor advises him to start taking risedronate (bisphosphonate). Two weeks after taking it he complains of back pain, hip pain and thigh pain. He wonders what to do.

Everyone is different - that's the starting point for all these side effect discussions. Different people have different medical histories and some medical conditions influence your doctor's choice of what medications may be used in any condition. However, even appropriately prescribed medications can have unintended side effects - the key is to figure out what is a legitimate drug-related side effect versus an unrelated symptom that seems to coincide with starting a new drug. Here are a couple general principles:

  1. If the side effect reported is "classic" (i.e. well known to occur with the drug) - it would seem pretty easy to assume a cause and effect, especially if the drug was just started. For example, hot flashes on raloxifene are common enough (7-10%) as is upset tummy or heartburn with bisphosphonates (20-30%).
  2. If the side effect is "atypical", it's much harder to know the source. Are there other explanations? Keep in mind - just because someone on the internet has written about a similar "side effect" - doesn't necessarily confirm it is so.
  3. In many areas of medicine, the usual advice is to avoid stopping a medication until you have discussed with your doctor and this is particularly important with things like heart medications, antibiotics, cancer drugs etc. Anti-fracture medications, generally speaking, are much less of a problem to stop. In many cases, remember that it was optional to start the drug in the first place. Therefore our approach to this problem is as follows:
  4. If the side effect is "classic" and well recognized and either serious or intolerable - we usually advise stopping the drug and choosing a different option if therapy is still desired.
  5. If the side effect is "atypical", we might suggest stopping the drug for a month to see if the symptoms go away. If not - perhaps some other cause should be considered, in which case, the patient may decide to re-start the same osteoporosis medication. On the other hand, if stopping the drug makes the symptoms disappear, we would consider that suspicious for a drug effect - but just to be sure, the patient may consider re-starting the medication to see if the symptoms come back. Doctors call this the "Challenge - Dechallange - Re-challenge" If the symptoms come back with re-challenge, it will probably be concluded that the effect is truly drug related and other treatment options can be considered.

In this case, Rami stopped taking the risedronate drug for a month without any change in his symptoms. He then re-started the medication and the symptoms did not change. Over the next 2 months, the pain seemed to disappear spontaneously despite continuing the medication. It seems like the symptoms were likely unrelated, possibly due to a muscle sprain (his oncologist found no signs of cancer in the bone). It was a good decision not to just quit the medication and go untreated.

COMMENT: Depending on the seriousness of the side effect, if it is determined to be related to the drug therapy, both you and your doctor should consider making a report to Health Canada Adverse Drug Reaction Reporting. Clinical trials do their best to report all side effects discovered but sometimes it is only the long term diligence of patients and doctors in "the real world" who are able to detect rare or unexpected side effects; when enough similar cases are reported to Health Canada, they are able to inform all doctors and patients about this newly discovered possibility.

13. How long should I be on this drug?

One of my favourite sayings is that it is very easy to start a patient on an anti-fracture osteoporosis drug; the hard part is knowing what to do next! Up until a few years ago, this question didn't even exist in osteoporosis circles and now it likely accounts for up to 30% of our new patient referrals. The science behind the answers is far from satisfactory and so this is probably the most controversial issue in osteoporosis care today. Stay tuned for possible opinion changes in the future!

KEY POINT: The question of therapy duration applies to every osteoporosis medication except perhaps raloxifene. Therefore, we recommend that a planned "stop date" be part of the overall osteoporosis treatment plan right from the start. The stop date will depend on the drug used and possibly the risk profile of the patient.

EXAMPLE: Denise attended a self consult session and based on her fracture risk of 3% hip fracture in 10 years with 16% major osteoporotic fracture, she decided to start taking alendronate. Now, after four years treatment, she is wondering if this is something that should be stopped at some point soon.

For those who are comfortable reading scientific papers, the best and most up to date answers to this question might be found be doing a search on Google Scholar using the search term "duration of bisphosphonate therapy" or something similar. If that's not your comfort level, read on and we'll try to summarize very briefly.

  1. Bisphosphonate drugs deposit in bone and may remain there for a long time - up to 2 to 5 years or more after you actually stop taking them. To some extent, they seem to continue to have their intended effect of stopping bone loss, preserving bone density and reducing fracture risk.
  2. The long residence in bone has led scientists to question whether there is a need or benefit to continue taking such drugs long term or beyond a certain target time period.
  3. The clinical trials or patient analyses that have been conducted to answer this question are relatively small and of much less sophistication than we would like; therefore, the results and conclusions are not considered definitive and a lot of debate among experts continues as to the "best" treatment plan.
  4. The value of oral bisphosphonate treatment for up to five years is really not disputed; it's what comes after that which causes controversy.
  5. The value of annual intravenous bisphosphonate treatment for up to 3 years is not disputed.
  6. For both oral and intravenous bisphosphonates, continued treatment beyond 5 or 3 years respectively might be associated with a very small additional reduction in fracture risk compared to people who stop bisphosphonates after that time frame.
  7. The people who might gain this very small additional benefit are probably those people who had the lowest bone densities to start with (i.e. femoral neck T-score less than -2.5).
  8. For the majority of people who discontinue alendronate therapy after 5 years, the bone density may remain stable and fracture risk reduced for up to 5 years off therapy.
  9. For the majority of people who discontinue intravenous zoledronic acid therapy after 3 years, the bone density may remain stable and fracture risk reduced for up to 6 years off therapy.
  10. Risedronate may have less of a "carry-over" effect compared to the other bisphosphonate drugs - perhaps only 1 or 2 years of continued effect after you stop taking the drug.
  11. There is really no data to show that any of these drugs have any benefits when taken for longer than 10 years continuously.
  12. Otherwise rare bisphosphonate side effects such as "osteonecrosis of the jaw" or "atypical femur fractures" seem to become more common among people who take bisphosphonates for longer than 5 years.
COMMENT: As you can see, this is a very technical and tricky area of medicine. It is very difficult for doctors to make blanket recommendations that are meant to apply to all patients. At the DHOC, our general approach would be to recommend 5 years continuous therapy with alendronate or risedronate OR 3 years continuous (annual) therapy with zoledronic acid for most otherwise healthy patients. At the completion of such therapy, patients would be advised to take between 2 to 5 years of "drug holiday" (off drugs). See self consult FAQ #14 for more discussion of what might happen during a "drug holiday". There will always be special cases where longer term bisphosphonate therapy might be considered and balanced against the longer term risks of therapy. These cases likely require individual consultation with your doctor or the osteoporosis centre.

Some people ask about long term denosumab use - unfortunately there is even less known about this situation than we know about bisphosphonates and so in this FAQ we will simply state an opinion using clinical considerations. In many ways, the effect of denosumab on bone is very similar to that of bisphosphonate - which might explain why denosumab has also been associated with the same rare serious side effects like osteonecrosis of the jaw or atypical femur fractures. The difference between denosumab and bisphosphonate is that the effect of denosumab quickly wears off when the drug is stopped. This leads to an interesting paradox in my opinion (Dr. Kline). It might not be advisable to use denosumab on a long term continuous basis (in order to avoid those rare effects), but at the same time, when the drug is stopped, the anti-fracture effect is lost. This would appear to lead to a situation where it is unclear as to how to ever decide on optimal long term management. This differs from bisphosphonates where at least we know the anti-fracture effect persists for at least a few years after you stop taking the medication. At the DHOC, when denosumab is used, we usually feel comfortable with a 3 year treatment course but after that, it will have to be your doctor's decision what to do.

Lastly, we'll briefly mention that teriparatide is typically a two year treatment course. The story behind this two year definition is complicated and originally reflected some uncertainty back when the first large human clinical trial was brought to an end. However, ultimately, it appears as though a two year treatment course probably encompasses the bulk of time in which the drug actually causes new bone formation. Therefore, most osteoporosis doctors are actually medically satisfied that a two year treatment course is likely the most appropriate after all.

14. My doctor said that I should probably come off my bisphosphonate because I've been on it long enough. What do I do about my osteoporosis when I'm off therapy?

This question should be considered a "companion question" to #13 so we suggest you read that one first. The first step is really to decide about whether someone's bisphosphonate therapy should be discontinued. The second (and even more controversial) step is to decide what, if anything, will be done for follow up/treatment of fracture risk once a patient has stopped taking bisphosphonate drugs.

KEY POINT: Bisphosphonate drugs have a "carry over" effect on bone that may last up to 5 years or more, depending on the drug and prior time of use. However, even that carry-over effect will likely come to an end at some point and at some point, most patients who are high fracture risk may well choose to re-start drug therapy again.

EXAMPLE: Thuy is a 65 year old woman who took alendronate for fracture risk reduction since the age of 59. During that time, she did very well and had no fractures. Her doctor reviews her case and recommends that she now take a "drug holiday" by coming off the drug for a while. At just 65 years old, hopefully Thuy will still have a lot of lifetime ahead of her and so she wonders if she will ever need that drug again….and when.

If question #13 was considered controversial for lack of clear evidence, then this question will be even more so. The reality is that we do not have very good evidence to help doctors decide when or if a patient should ever go back on drug therapy again. And so, here are a couple thoughts that might be considered to help make that decision.

  1. It is probable that in many patients, prior bisphosphonate therapy effects will likely eventually be lost, given enough time off the drug.
  2. There might be a high degree of variability between patients in the time to loss of effect.
  3. Some doctors might make a recommendation based on simplicity - for example, patients coming off bisphosphonate therapy take a 2 year "drug holiday" and then just re-start in every case. In fact, one could even argue for a standardized 5 year drug holiday just as well. Simple "rules" like this are attractive and easy to implement but probably don't reflect "personalized medicine" - i.e. the idea that we are all different and different people need different medical plans.
  4. Many osteoporosis doctors (including us here at DHOC) don't see much value to regular, repeated bone densities while on therapy (see FAQ above). However, it seems to make practical sense to get a repeat bone density at the very end of therapy - sort of as a new baseline representing the final state at therapy completion.
  5. It would be possible to then repeat the bone density at a later date to determine whether the bone density is decreasing - if so, perhaps one would conclude that there is loss of effect and a reason to re-start treatment. This sounds good in theory but remember, there are a lot of potential problems and difficulties to the interpretation of small changes on repeat bone density. Generally speaking, in some places, the quality of the repeat bone density may not be sufficiently high to permit such confidence, especially if it is the only deciding factor. In these cases of apparent small bone loss, it may be reasonable to wait until two repeat bone density measures have each shown continuous bone loss before concluding loss of prior drug effect.
  6. With dependence upon repeat bone density, it is unknown as to whether such bone densities should be done annually or every two years or less while on drug holiday.
  7. At the DHOC we have the general opinion that a repeat bone density could be done after 3 years off zoledronic acid, after 2 years off alendronate and after 18 months off risedronate. However, these are just educated guesses and your doctor may have a different opinion.
  8. Some doctors may choose to use a second tool, the blood test marker of bone losses (Beta-CTX-crosslaps) as discussed in FAQ #2. This test is theoretically attractive but not all research supports its use and interpretation during a "drug holiday" and so it might be considered somewhat experimental at this stage.
  9. Regardless of when your doctor determines the "drug holiday" to be over, we do recommend that you re-calculate your WHO FRAX risk score before re-starting drug therapy- just to make sure that your fracture risk is sufficiently high to warrant drug therapy - especially if you did not go through this exercise at the first time you were treated.
COMMENT: "Bisphosphonate drug holidays" are probably necessary considerations in most patients and yet the science to direct medical practice is not yet sophisticated enough to permit more definite advice. It is important for doctors practicing in the field of osteoporosis to be sure to stay up to date with the latest data and opinions on this topic. Patients have often asked about the idea that people might go through multiple repeat 5 year sequences of "drug on" and "drug off". This may well be the future of bisphosphonate drug therapy but it highlights the difficulty of practicing medicine over a 40 year period (menopausal years) when the clinical data ends at 10 years. We'll need to encourage governments and pharmaceutical companies to continue to fund even longer term studies to help get better answers.

15. I have a new back pain, does that mean I've had a fracture in my spine?

After wrist fracture, the most common osteoporotic fracture is the vertebral compression fracture - either low trauma or spontaneous collapse of a vertebra in the back which can occasionally involve even 2 or 3 vertebrae. Wrist fractures are easy to spot but vertebral fractures much less so. It's worth being aware of this possibility to help with rapid diagnosis when needed.

KEY POINT: Up to two thirds of vertebral collapse fractures will occur without obvious or severe pain. These sometimes unrecognized fractures are important indicators of osteoporosis and fracture risk and should not be ignored.

EXAMPLE: Henry is a 70 year old smoker with early smoker's lung disease. His doctor ordered a chest x-ray to look for pneumonia. There was no pneumonia but the radiologist commented that three of his thoracic vertebrae show signs of collapse. Both Henry and his doctor are shocked at this report. In retrospect, Henry remembers helping a friend move a desk last summer. While doing so, he had sudden but modest back pain. It didn't stop him from finishing the job but he was sore for about a week thereafter. Because the pain went away on its own, he never mentioned it to his doctor until now

The most important lesson from this example is that Henry should now be given a diagnosis of severe osteoporosis. His doctor may choose to do a bone density scan which may or may not show low bone density. However, at age 70, with a history of long term smoking, he is already at high risk for osteoporosis and the three vertebral collapse fractures simply prove the point.

Not all back pain means fracture however - as most people know, there are all kinds of diagnoses to be considered in the patient who shows up at the doctor's office with back pain. The full list of possibilities is far beyond the scope of this FAQ but we want to make the point that, in the right age group, a vertebral collapse fracture should not be forgotten as a possibility. A simple x-ray will prove the point.

The more difficult part is detecting the more subtle or even painless collapse fractures. At the DHOC, we recommend careful monitoring of patient height as a means to detect such fractures. When measured using an accurate method, a difference in height of more than 2 cm suggests that a vertebral fracture may have occurred and consideration of spine x-ray should follow.

Sometimes, vertebral fractures can be very painful and take a long time to heal - in those cases, the importance is obvious. However, the point of this FAQ topic is to illustrate that detection of subtle or silent vertebral fractures is a very important part of ongoing monitoring for possible fracture risk. The WHO FRAX tool used in class puts a high importance on whether the patient has had prior fracture - and this should include vertebral fracture which may be completely unknown to the patient.

COMMENT: Vertebral fractures are important clues to underlying osteoporosis and high fracture risk. Finding them is sometimes tricky because they may not have obvious symptoms or at least not be recognized as such. In this case, Henry's doctor quite rightly finished an evaluation for osteoporosis. Henry was counselled to quit smoking (again), to increase his vitamin D intake and to start risedronate. Prevention of future vertebral fractures is particularly important in Henry's case in order to avoid developing a sloped spine (kyphosis) which could further impair his lung function.

16. I'm going traveling for a month, must I take my medication with me?

What a hassle. You're heading out somewhere nice for a vacation and wondering whether you need to take your medication with you. This is particularly a nuisance if you're taking teriparatide which is a daily injection.

COMMENT: The stock medical answer is always to take your medication as prescribed and so certainly, if that's easily accomplished then why not. Interestingly, did you know that osteoporosis medication non-adherence might represent one of the biggest wastes of money in all of medical practice? As discussed above, the effects of anti-fracture medication are slow and continued therapy for the full 3 to 5 years is strongly recommended in order to get the anti-fracture benefits to bone. Sadly, studies have shown that up to half of all patients who are prescribed an osteoporosis medication stop taking it in less than 6 months. Therefore, this is a waste of money because the drug will not have any meaningful effect, it will not prevent the fractures (and subsequent costs) and yet the patients have paid for several months' worth of this now unused therapy.

Years ago, at the DHOC we actually used to call patients 6 months after their appointment to find out if they were still taking their prescribed osteoporosis drug. However, we have long since abandoned this "Big Brother" approach in hopes that patients will have more motivation to continue therapy if they are fully involved in every step from risk assessment to fracture estimation and therapy choices.

The flip side to this discussion about adherence is that because these drugs work slowly, there is probably no real effect from missing two to four weeks of therapy in a year. Doctors aren't really supposed to encourage non-adherence (and we're not!) but here we're just trying to be realistic about acknowledging how the drugs work in the context of a patient who is otherwise committed to the full 5 year treatment course. So, if you're headed somewhere wonderful for two weeks of fine dining and recreation and you happen to leave your osteoporosis medication at home… no big deal.

17. I'm on a bisphosphonate and need some dental work. What do I do?

This is one of the most common questions to come in to our pharmacy office. The concern usually pertains to the relationship between "dental procedures" and the risk of bisphosphonate-related osteonecrosis of the jaw (ONJ)

KEY POINT: ONJ is a very, very rare jawbone problem that has been associated with long term or high dose (cancer dose) bisphosphonate therapy. It is extremely unusual to see this in otherwise healthy users of shorter term bisphosphonate therapy for menopausal osteoporosis. ONJ is not related to routine dental work such as cleaning, fillings and root canals.

EXAMPLE: Maureen is taking alendronate for fracture risk reduction and has been on the drug for 3 of a planned 5 year treatment course. Her dentist has informed her that she will need to have 2 teeth pulled. Maureen wonders if she should stop taking her bisphosphonate, and if so, for how long.

ONJ is one of those rare bisphosphonate associated complications that is more recently recognized and publicized. When discussing this issue, the first step is to make sure we know exactly what we are talking about when we say "ONJ".

Bisphosphonate-associated ONJ is defined as an area of exposed bone in the upper or lower jaw that does not heal within 8 weeks after identification by a health care provider. That's pretty specific and note that this does not mean that all general jaw pain, tooth pain, periodontal disease or TMJ dysfunction is necessarily related.

Possible signs and symptoms of ONJ may include persistent jaw pain, new tooth mobility, swelling and redness of the gums on the jawbone or even loss of sensation in one area in the mouth, usually onset following dental surgery such as extractions. However, such symptoms in the absence of exposed bone in the mouth are non-specific and may have other causes. Ultimately, if any such symptoms arise while taking (or recently taking) bisphosphonate, a visit to your dentist is the most appropriate next step to get a proper diagnosis.

Risk factors for development of ONJ include: jaw infection, radiation to the head and neck, chemotherapy, periodontal disease, prednisone use, diabetes, denture use. smoking. Just because a patient has some of these risks does not mean they are destined to get ONJ. On the other hand, this is a good reminder to stop smoking and get regular dental check-ups while on therapy.

In order to prevent ONJ, osteoporosis doctors usually recommend delaying initiation of bisphosphonate therapy until after any planned dental procedures are completed (usually waiting 3 months or until complete healing) along with good oral hygiene.

It is very controversial whether there is any benefit to stopping drug therapy prior to or following dental procedures (like extractions or implants). In theory, short term stoppage of drug therapy probably shouldn't help very much since the bisphosphonate drug is already in the bone and will remain there for a long time to come. However, some dental guidelines still suggest that the drug be stopped prior to any major dental procedure and not re-started until healing is complete. Your dentist will likely have their own advice which you should follow.

Some doctors have occasionally considered doing a blood test called the BCTX Crosslaps (see FAQ#2) to see if bone remodelling is suppressed (as it would be expected to show if taking bisphosphonate therapy). This is theoretically attractive in concept but so far, studies have failed to show that this test really helps with dental management and so it is not recommended.

COMMENT: It is important to remember that in the past 10+ years of public health reporting about ONJ, more than 90% of all cases have occurred in patients receiving high dose bisphosphonates as part of cancer therapy. Denosumab has also been linked to ONJ but since the effect of denosumab wears off quickly six months after the injection, it may be easier to "fit the dental work in" between injections by doing the dental work just prior to the next scheduled denosumab dose. For most people, a risk of 1 in 10,000 to 1 in 100,000 should be considered a very low chance of getting ONJ but it is always best to tell your dentist that you are on this medication and follow their advice.

18. My BMD report says high fracture risk but I don't think I'm high risk, so who is right?

"High Risk" always sounds bad, doesn't it? Terms like "high risk", "moderate risk" and "low risk" often appear on a bone density report and probably play a role in shaping the way both doctors and patients respond to the results.

KEY POINT: "High Risk" is a somewhat emotional term that is really quite arbitrary and depends upon the perspective of the observer. Radiology BMD reports use these terms according to common osteoporosis guidelines but the sophisticated health practitioner will understand that the real importance of any given risk will be determined only through individual consultation with the patient.

EXAMPLE: Anita is a 66 year old woman with post menopausal low bone mass. Her T score at the hip is - 2.7 and she is a smoker. Her mother broke her hip at age 75. The report with her bone density lists her 10 year risk of major osteoporotic fracture as 20% and beside it, says "High Risk". Anita is concerned to hear that she is high risk for fracture and wants further discussion with her doctor.

Risk is an interesting concept that consumes a lot of our counselling time in osteoporosis. This is unlike many other medical disorders where the decision to treat may be easy - for example, if you are in the emergency room with heart failure, we don't really spend much time wondering "if" you should be treated. Of course that should be treated!

However, in osteoporosis, the decision to take or not take an anti-fracture medication requires a patient-specific balance between the estimated chance of having a fracture or not, the chance that a medication will reduce that fracture risk and the chance that the medication will have an important side effect. This "balancing" discussion starts with an understanding of the chance that you will have a fracture in the absence of any treatment.

In the self consult session, we spent a lot of time talking about how to estimate your fracture risk and we used a popular tool called WHO FRAX. Some people also use a tool called CAROC which is similar. In both cases, you need to know the health details of the patient in order to correctly enter the data and get an accurate fracture risk estimation. At many radiology clinics, patients will fill out a questionnaire or be asked questions by a technician to help the radiologist use the FRAX tool when writing the bone density report. Obviously, the accuracy of this depends very strongly upon the accurate interpretation of your health information by the questionnaire or interviewer. (If possible, we recommend that you do this exercise with your personal doctor to ensure the information is correct).

Once the radiologist looks at the questionnaire and bone density, they will often make a comment about whether this is a high, moderate or low fracture risk situation.

So - what does high risk mean? In Canada, there are osteoporosis guidelines that have decided to say that any 10 year risk greater than 20% should be considered "high risk". People with a 10 to 20% chance of fracture are called "moderate risk" and people with a less than 10% chance are called "low risk". There's nothing wrong with these guidelines but it's important to remember that the labels of "high, moderate and low" aren't written in stone and simply represent a general view held by the people who wrote the guidelines.

We have often met patients who have a 10 year fracture risk of 30% who refuse drug therapy, sometimes saying things like "I'm happy with my 70% chance of NOT fracturing!" On the other hand, there are some people who have 10 year fracture risks of 8% who are keenly interested in taking fracture risk reduction drugs - they simply want to take a very pro-active approach and are usually not too concerned about possible side effects.

At the DHOC, we believe that the only person who can truly balance their risks is You. We can advise you about what it's like to fracture, what the long term consequences may be and what your chance of fracture will be. We can also provide information about the efficacy and risks of the different drugs available. After that, it's really up to you to decide how you feel about the benefits vs risks. Some people feel comfortable with a 20% "high risk" scenario as being the level at which drug therapy is started and that is fine. But some people feel that 20% is still too low of a risk to justify starting drug therapy. We try to avoid emotional terms like "high risk" and rather just concentrate on the actual risk in order to avoid pushing people to make an emotional decision.

COMMENT: This situation is kind of similar to a mortgage interest rate - a good way of thinking this through. Imagine that you are applying for a mortgage and the bank tells you that the interest rate for a 10 year mortgage is going to be "low". Would you be willing to sign that contract? Of course not - you want to know exactly what the interest rate is going to be. And so, if you ask the banker for that number, let's pretend that they tell you it will be 10%. Is that low? Well, numerically, it's not a high number but in today's market, that would be an incredibly high mortgage rate that no one would take. Do you see the similarity to our osteoporosis conversation? Emotive terms like high, moderate or low can be difficult to apply since they are somewhat arbitrary and depend upon the viewpoint of the person using the term. Therefore, the decision to take or not take drug therapy always lies with the patient, once a full explanation is given. You can certainly ask your doctor's opinion but we don't routinely make drug decisions basely purely on a radiology report.

19. There are a lot of other osteoporosis products advertised on the internet and on my pharmacy store shelf; why didn't we learn about these options in the self consult session?

Some people at our self consult sessions have remarked that our list of treatment options seems to ignore products that are mentioned online or in health magazines and have asked why we don't present these other things as options.

KEY POINT: The whole purpose of drug therapy in osteoporosis is to prevent or reduce the risk of fractures. There may be many treatment options that have interesting effects on bone metabolism, bone loss, bone density etc but if they aren't known to actually reduce fractures, we don't present them as options.

EXAMPLE: Wendy has post menopausal low bone density and, while investigating her options online, comes across a study which seems to show that a certain vitamin supplement is "good for osteoporosis". It looks very safe and seems like a good idea since she wasn't too keen on some of the options she heard at the self consult session. What questions should she ask before starting this other therapy?

As mentioned above, the whole goal of osteoporosis drug therapy is to reduce the risk of fragility fractures. If everyone died at very old age with severe osteoporosis but never having had a fracture, we could argue that osteoporosis would be irrelevant. Remember that bone loss and osteoporosis are painless, natural processes but unfortunately, in concert with age and sometimes frailty, the bone loss makes it easy to fracture. And that is what we're trying to prevent.

Some people worry that some doctors' advice is shaped by what they are told (or sold) by pharmaceutical companies. So, before going any further, we like to point out that the DHOC is not supported by pharmaceutical companies and the staff and physicians are not "in business" with the pharmaceutical industry. Check out our Conflict of Interest Statement for a full discussion. Our decision to focus upon proven therapies has nothing to do with whether we support drug companies or health products, but rather, is intended to ensure we are only offering therapies in which we can have confidence of actual benefit for our patients.

The FDA and Health Canada have taken a similar position. Many years ago, it was possible to bring a new osteoporosis drug to market simply by proving that it maintained or improved bone density. However, today, the bar is much higher: new osteoporosis drugs must be proven to actually prevent fractures in order to be approved for medical use. Therefore, while there may well be other drugs/vitamins/compounds out there that might help bone density - until studies are done proving that they reduce fracture, they simply cannot be recommended for patients whose primary goal is the prevention of fractures.

Why isn't it good enough to just maintain bone density? Remember that bone density is just an X-ray. You want to make sure that any therapy actually has a useful effect on the overall strength and structure (sometimes called micro architecture) of your bone and that cannot be seen through simple X-ray. Several decades ago, it was popular to treat osteoporosis with fluoride - probably because it resulted in a major bone density improvement. However, eventually it was found that fluoride treated patients actually had more fractures than untreated patients which is why we don't use that drug today.

Sometimes the popular news media can make this whole situation extra confusing because of a tendency to report on what are called epidemiological studies related to osteoporosis (and other diseases). Unless you are trained in research, many people are unaware as to what epidemiological studies are and how they differ from clinical trials - and this is a very important distinction because newspapers tend to use the generic phrase "published study" which could apply to either one. Clinical, randomized controlled studies are considered the "purest" and most reliable type of scientific study - this generally involves large groups of patients, some of whom get active drug and some get placebo for several years. At the end of the study, researchers can "count the fractures" in both groups and determine whether the drug was useful and how big was the benefit in preventing fractures. This type of study is what Health Canada requires for new osteoporosis drugs to be approved for use. On the other hand, epidemiological studies often involve questionnaires or surveys of people, looking at various things like smoking, diet, weight etc and simply observing whether are not there are clusters of health problems (like fractures) among various categories of patients. These studies are very popular and much easier for researchers to conduct which is probably why there are so many of them. However, epidemiological studies are simply observations and almost never explain cause-and-effect which is why they are prone to so many errors or assumptions in the results. This is particularly true for epidemiological studies of nutrition and why it seems like the newspapers are constantly reporting conflicting results about different foods or vitamins.

COMMENT: With this in mind, what questions should Wendy ask about this new product she has found online? Here's our suggestions:

  1. Has this product ever been studied in a randomized controlled trial?
  2. Has this product ever been proven in such a trial to reduce fractures?
  3. Have the studies on this product involved large numbers of patients (i.e. more than 500)?
  4. Have the results been reported in a reputable scientific journal? (you can check this at

Wendy may have to do quite a bit of digging around if she wants to get these answers. However, if the answers to any of these 4 questions is "no", we'd advise caution. It doesn't mean that the product in question is necessarily dangerous or ineffective, it just means that nobody really knows about the safety or efficacy of the product.

20. Why doesn't the osteoporosis centre doctor just tell me which drug I should take?

Faced with so many treatment options, some patients would rather just ask for their doctor's advice as to which one they should choose. As doctors, we take these requests very seriously and we understand the huge responsibility that is required to try and choose something on behalf of another person. Having said that, at DHOC, we will always try to give the patient the first and ultimate decision. Why are we so reluctant to just tell people what to do?

KEY POINT: Of the drug treatment options available, we offer only medications that are proven to reduce fracture risk - and that actually means several options. The choice as to which one drug will be used is largely based upon safety, costs and patient preference and no single drug is known to be "the best".

EXAMPLE: Kerry attended an osteoporosis self consult session and took many notes during the discussion of drug options. Each drug had at least one attractive aspect but also seemed to have at least one aspect that made her unsure about her willingness to take it. At the end of the session, she knew she wanted to be treated but just couldn't decide which drug to take and so asked the facilitator for their recommendation.

How do we decide which one is "the best"? I think this question is almost like asking which politician is "the best"! Ask 100 people and you'll get 100 different answers. We all recognize that is because different people have different values and fears and put different levels of importance of those different values. For example, we could mathematically determine which politician is "the best" if we decided that their attendance in the provincial legislature was the most important part of the job. Easy - count up the attendance records and you'll see who is "the best". But what if that person attends every session yet never says a word and never votes? Maybe that person isn't really the best politician. But maybe that person works tirelessly behind the scenes for their constituents so perhaps they are pretty good after all. It depends on what's important to you. And for some politicians, you could listen to an hour of arguments as to why they're "the best" and still never come close to agreeing with them. The same thing goes for osteoporosis drugs - some people will be happy to take a drug that has no side effects except for something really serious that happens to 1 in a million. Other people would rather take a drug where there's a 30% chance of a slightly annoying but non-serious side effect rather than take the 1 in a million chance of something really serious happening. Which one is "the best"? It's impossible to say who is right.

What if we simplify the question and say let's just look at fractures and nothing else. Which drug is "the best" at preventing fractures?

Unfortunately, there is no answer to this question (and if someone tells you otherwise, then they're really just giving an opinion).

Why don't we have an answer to this question? It comes back to the discussion of how we get scientific knowledge that is trustworthy.

It is not good enough to do simple questionnaires with people taking various osteoporosis drugs and then seeing who has the fewest fractures. Such questionnaires (epidemiologic studies) might not be able to detect the various factors that play a part in the fractures. This approach may actually have the opposite effect - it can make really good drugs seem like they're not. For example, if the medical community, through experience, has a hunch that drug A might be the best drug to prevent fractures, the doctors might choose to specifically give drug A to the patients with the worst osteoporosis. And, by having the worst osteoporosis, those patients might still have the most fractures - which would lead the researcher to believe that drug A was ineffective... even if drug A truly was the best drug available.

In order to know which drug is the most effective, researchers would have to do a randomized controlled clinical trial where several hundred (or probably several thousand) similar patients would each get a different drug for 5 years and then at the end, count up to see which group had the fewest fractures. It's a nice idea that could be extremely helpful to medicine but the problem is that it would likely cost tens of millions dollars and thus far nobody has wanted to invest that kind of money into answering this question.

So, for now, we will have to rely upon the fact that each drug we use at DHOC has been proven in a randomized clinical trial to be effective at reducing fractures versus no therapy. We may never know which, if any, of the drug options is "the best."

COMMENT: Since there is no scientific answer to the question as to which drug is the best at reducing fractures, we cannot make any recommendations on that point. Doctors may certainly have opinions as to which drug might be the best but these are opinions based on experience or theoretical considerations - neither of which are foolproof. At DHOC, we understand that the best drug for any one patient is not just the drug that will be best at reducing fractures but will also have to include the best and most acceptable side effect profile and costs for each person's unique situation. Ask our opinion, that's what we're here for, but don't be surprised if we do not just tell you what to do.

21. Why is my Bone Density lower at my spine than at my hip?

Sometimes in the self consult class, we come across patients (usually women) who have bone density T scores that are quite a bit lower in the spine than in the hip. It makes one wonder if there has been some kind of mistake — shouldn’t the bone density results be the same no matter where they’re measured?

KEY POINT: Bone density measurements in different body locations can sometimes be quite different and still be a “normal” situation. Generally speaking, the risk of any specific fracture is most related to the bone density of that spot. However, use of the hip bone density in the WHO FRAX program is usually reasonably accurate for clinical decision making.

EXAMPLE: Martha wants to calculate her risk of fracture using her most recent bone density results. She notices that her femoral neck T score is -1.3 but her lumbar spine T-score is -3.1. The WHO FRAX programs asks for the femoral neck T score but Martha wonders if she should perhaps use the spine T score.

First of all - why are the T scores different? In most cases it’s because the bone of your spine is different than the bone of your hip. Spine is composed of predominantly trabecular (spongy) bone whereas hip (or forearm) bone is much more cortical (compact) bone. Any condition that causes accelerated bone loss (such as menopause) preferentially affects trabecular-type bone to a much larger degree than cortical bone, especially at the onset of menopause. Therefore, it is quite common to see a low spine T score that seems to be more than expected when compared to the hip T score. By the time you reach your late 70’s, the bone loss at both spine and hip are usually much closer in bone density comparison.

The WHO FRAX program was designed to use the femoral neck bone density and not the spine bone density. Some people have criticized the designers for this but they had pretty good reasons. Femoral neck bone density is the “best” bone density for estimating the chance of hip fractures in particular and hip fracture risk is a major focus of both WHO FRAX and clinical management. It turns out the hip bone density is actually pretty good at predicting all types of osteoporotic fractures in most women so it does make sense to use it in the program. But what if there is a really big discrepancy between hip and spine?

Some studies have looked at this problem. Really large differences between hip and spine bone density (i.e. a bone density difference of more than 1.0 T score level) only affects about 2-3% of women. And, for those women, it does turn out that the WHO FRAX risk estimate probably does underestimate the risk of major osteoporotic fractures (mostly vertebral fractures) by about 3-5% in absolute amounts. This is worth thinking about but may not change many clinical decisions.

Therefore, when Martha calculates her WHO FRAX fracture risk using her hip bone density, it turns out that her 10 year risk of hip fracture is 2.3% and her 10 year risk of major osteoporotic fracture is 9%. Keeping in mind that her spine bone density is more than 1.0 T score levels lower than her hip bone density, it would be reasonable for Martha to assume that her hip fracture risk is the same as what has been stated but her risk for major osteoporotic fractures is probably up to 5% higher than what the WHO FRAX program predicted, perhaps more like 14%. Ultimately, for Martha, 9% vs 14% didn’t make any difference to her opinion about drug therapy.

COMMENT: Note that this kind of “fudge factor” adjustment is really only considered when the spine bone density is more than 1.0 T score levels lower than the hip. In other words, with a spine T score of -2.7 and a hip T score of - 2.3, there is no adjustment needed because the difference is less than 1.0. Note also that this doesn’t work in reverse! If the spine bone density is much higher than the hip bone density, it usually means that the spine has been affected by overlying arthritis which falsely raises the bone density.

22. Why do bone density results get compared to a young person’s bone density for making the T score? It seems unfair to compare an older skeleton to a younger skeleton!

This is probably one of the biggest complaints we get when people are learning how to read their own bone densities! But don’t be mad at us, we didn’t decide this! I’ll explain why it’s done and if you still don’t like it, I’ll include some additional info at the end that you might find more appealing.

KEY POINT: Bone density “T-scores” cause a lot of confusion and concern among both patients and doctors because of how they are calculated and what they are supposed to represent. However, it’s important to remember that the main reason for using a T-score is to help people understand that bone density and fracture risk is a continuum (explained below).

EXAMPLE: Kiko is 72 years old and has a bone density done which reports a T score of -2.4. Her doctor explains that it means her bone density is quite a bit below average for a 22 year old woman. Kiko thinks this sounds crazy — of course her bone density is lower than a 22 year old! But she feels absolutely fine and healthy - maybe more healthy than most women her age — and she wonders why they don’t just compare her results to the average for a 72 year old.

Honestly, I tend to agree with Kiko on this one. However, T scores are not going away so let’s make sure we understand them.

In theory, healthy women should have a “normal” bone density when they’re young and at “peak bone mass” which for most is around age 21-23. Remember of course that it doesn’t mean all women will have the exact same bone density but there will be a range of “normal” readings at age 22 just like there is a range of normal levels for all kinds of blood tests etc.

Now, we don’t send 22 year old women for routine X-ray bone densities just to see what their peak bone mass/bone density is (nor should we— that would be like ordering every possible blood test on all healthy people just to see that they are normal). But by the time a women gets into her menopausal years, we might want to see how much bone she has lost compared to her peak bone mass (or at least that’s how people used to think). However, without that “baseline” result from when she was 22 it’s impossible to know exactly how much bone has been lost since then. Therefore, if we assume that her bone density was “average” when she was young, we can compare her current bone density to the average of all 22 year olds and then again assume that the difference represents how much bone has been lost. Two huge assumptions.

At one time, this kind of reasoning obviously made sense to people so the idea of comparing bone density to young healthy “normals” was born. Today, we don’t really think about bone density this way anymore though. We know that every woman loses bone after the menopause and it really doesn’t matter exactly how much bone was lost compared to her younger self — for clinical decision making, it only matters what her bone density happens to be right now.

And yet, the T scores are still around. Why don’t we get rid of this idea? Well, it’s probably because, to some extent, that would mean throwing away decades of good research (even if it was based on a flawed T-score concept). Like it or not, most of the information we have on fracture risk over time and drug intervention effects was collected using the T-score idea which is why it is still useful for things like WHO FRAX calculations.

There is one other good thing about T-scores that perhaps makes up for the confusion that they cause and that is the idea of “risk continuum”. This is a very complicated concept in some ways but worth thinking about:

Many diseases in medicine are either present or absent. You either have cancer or you don’t (actually not always entirely true but mostly it is). The same thing holds for most medical tests —If the test comes back “in the normal range”, your doctor tells you you’re “normal”. If the test comes back above or below the normal range, your doctor makes a diagnosis of some disease/disorder based on that result.

Bone density doesn’t work that way at all. And the people who came up with the idea of T-scores wanted to make sure that doctors didn’t look at a bone density result and just say “you’re normal” or “you’re diseased” based on the result. That’s because there is no bone density result for which the patient is at ZERO risk of fracture. Even people with “higher-than-average” bone density can still have a fragility fracture — it might be uncommon, but it does happen. Similarly, just because a person has a low bone density doesn’t mean that they are DESTINED to fracture — they might be fairly likely to fracture but some people do get away with no fractures despite very low bone density. This situation exists because the relationship between bone density and fractures is a continuum as opposed to a yes/no situation. Fracture probability increases as the T score decreases from 0 to -4 and every number in between. A person with a T-score of -3.5 has a higher risk of fracture than a person with a T-score of -2.8 who has a higher risk of fracture compared to a person with T-score -1.4 who still has a higher risk of fracture than a person with T-score of -0.2. The closer up towards “0” you go, the lower the risk of fracture but there is no such thing as a T-score where there is no risk whatsoever.

Doctors are not used to reading medical tests this way. We like yes/no answers. We want to know who to worry about and who to reassure. But unfortunately, life is more complicated than that and the T-score ranges were designed to help doctors put their patients’ bone density results in perspective.

For those who are still upset about the comparison to the young people, you might be interested to know that many bone density machines will also report your “Z-score” - or at least, that information is available from the scan, even if not included on the report. The Z-score isn’t talked about much but it is your bone density result compared to a women of your age (or compared to a man if you’re male). Not surprisingly, Z-scores are often much higher than T scores because of the more “fair” comparison. At this point, there are very few uses for Z scores in routine care though - it just hasn’t replaced the T-score.

For the case above, we got Kiko’s bone density Z-score which was +0.5 which means that she was actually above average for a 72 year old woman (anything above 0 is above the average with this kind of calculation). Kiko was happy to know that she was indeed “above average” for her age….but still needs to use the T-score for the FRAX calculation. Sorry!

COMMENT: This is a good spot to put the “osteopenia” and “osteoporosis” terms in perspective. Traditionally, it has been said that a patient has osteopenia (which means “low-ish” bone mass) if the T-score is between -1.0 and -2.4 and “osteoporosis” if the T-score is -2.5 or lower. There is a statistical reasoning behind these numbers, it’s not just random, but unfortunately, this kind of bone density “classifying” has kind of sabotaged the original idea of expressing bone density as a risk continuum. These labels have allowed doctors to go back to the idea of classifying “normal/abnormal” when it comes to bone density rather than recognizing that it is all just a continuous scale for risk estimation, to be used in conjunction with other fracture risk factors. Here at our osteoporosis centre, you will find that we almost never use the term osteopenia because it really has no clinical meaning. And the term osteoporosis is used with reference to the whole fracture risk situation. The calculated risk of fracture is so much more important than the T-score label from the bone density report!

23. After spending so much time talking about predicting fracture risk, why don’t we spend more time talking about predicting side effects risk?

Somebody recently asked us this question in a self consult session. I thought it was brilliant and deserving of a spot on the website.

KEYPOINT: While we are getting better and better at predicting fracture risks for patients, scientists have not yet come up with a program to predict side effects from anti-fracture drugs although it’s a great idea. The best we can do is try to make sure we keep the “risk of side effects” in perspective.

EXAMPLE: In the self consult session, we teach that use of bisphosphonate therapy is thought to be associated with a 1 in 10 000 to 1 in 100 000 risk of osteonecrosis of the jaw (ONJ). Research shows that dental surgical procedures “increases” the risk of ONJ in bisphosphonate users. Up to 20% of people may have gastric upset with bisphosphonates. Which one is more likely and which one is worse?

In the example above, I have deliberately tried to express different risks in different ways that are commonly heard around the clinic. Let’s look at each one. Research shows that using terms like “1 in 10 000” is probably the most accurate way to express a probability when talking about medical decisions. Most people are familiar with this way of speaking - possibly from hearing commercials for lotteries! From a medical research perspective, if I wanted to elaborate on this phrase for maximum clarity, it would be this:

“If I had 100 000 patients in my practice taking a bisphosphonate drug for 5 years or more, I might see 1 of those people develop ONJ during that 5 years.” And of course, that 1 patient could be you….but you might also be one of the 99,999 who doesn’t get ONJ.

The real problem arises when we use imprecise terms like “increase” and “decrease”. Those terms tell you the direction of the risk but not how much.

Obviously, if a dental surgery increased the risk of ONJ from 1 in 100 000 to 1 in 10, that would be a massive risk increase (and the drugs would probably be pulled off the market). However, even if dental surgery “doubled” the risk of ONJ, that still only means 2 out of 100 000 people. In actuality, some research has suggested that dental extractions/surgery may increase the risk of ONJ by up to 600%…which still just means a risk of 6 in 100 000.

“Gastric upset is seen in 20%”. What does that mean? If we convert that number to a similar expression as above, we could say that gastric upset develops in 20 000 out of 100 000 bisphosphonate users. Notice the huge difference vs the ONJ figures!

So, when it comes to predicting and assessing the risk of side effects, there are two things to consider: the frequency of the side effect and the seriousness of the side effect:

A minor side effect that affects 1 in 100 000 probably isn’t worth mentioning. A minor side effect that affects 20 000 in 100 000 should be mentioned because it happens often enough that the patient should be aware. A major side effect that affects 1 in 100 000 should still be discussed because it is serious and patients need to know about all serious possibilities, even if rare. A major side effect that affects 20 000 in 100 000 people will probably result in the drug being banished unless it happens to cure a lethal cancer or some other severe disease.

To keep side effects in perspective though, you must also consider the benefits. In the case of bisphosphonate use in a person with a 20% chance of fracture, we could say that 8 000 fractures could be prevented if 100 000 patients took the drug.

So, this boils down to a 1 in 12 chance of preventing a fracture vs a 1 in 5 chance of having tummy upset with 1 in 100 000 chance of ONJ. Now, those numbers are easier to balance.

Ideally, scientists should come up with more complicated ways to predict adverse effects in specific patients rather than relying upon estimates in large groups….a very good research idea.

COMMENT: Some statistics quote the chance of death due to an accident while on a hike may be around 6 in 100 000 per year so it looks like even fun and “safe” things sometimes are more risky than the serious side effects of bisphosphonates. But it’s still up to you to weigh these pros and cons.

24. In the self consult program you talked about the “side benefit” of raloxifene in reducing the risk of some breast cancers. I’d like more details on this.

It’s not very often that we talk about a drug’s side benefit but in the case of raloxifene, it is actually something to think about. Originally marketed as trademarked “Evista”, raloxifene has been available as a generic medication since 2014. When a drug goes generic, you usually see that advertising disappears, both in medical journals and public (US) media. As the drug has come to the end of its patent, so too have the large scale clinical trials. Therefore, there really hasn’t been much discussion of this drug among physicians in recent years and many doctors don’t even know that it exists. However, it’s my impression that when we present this option as a treatment for osteoporosis, there seems to be a lot of interest from patients so here are a few more details about it.

KEYPOINT: Raloxifene has been in use for the reduction of fracture risk for a long time and continues to be recommended as a potential “First-line agent” for use in osteoporosis patients, according to the Osteoporosis Canada guidelines. Every drug has its pros and cons but this drug is quite different than some of the other options.

EXAMPLE: IMarnie is 57 years old and has a lumbar spine T-score of -2.8 with femoral neck T score -2.0. She has been menopausal for 6 years. She had a wrist fracture last year and her WHO FRAX risk of hip fracture is estimated at 1.8% and risk of major osteoporotic fracture is 17% over the next 10 years. Her mother had a history of breast cancer and Marnie is wondering if raloxifene might be a good choice for her own treatment.

Raloxifene is a drug that belongs to a class known as “SERMs” — which stands for “Selective Estrogen Receptor Modulators”. Other drugs in this class include Tamoxifen (which is still used to treat and prevent breast cancer). These drugs behave similarly to estrogen in some parts of your body (like bone) but interestingly, they behave like estrogen-blockers in other parts, like breast tissue. Therefore, raloxifene was studied for osteoporosis because it was hoped that it would treat osteoporosis just like estrogen but without the (small) breast cancer risk that may be linked to longer term post menopausal estrogen use.

A study called the MORE study, published in 1999 and updated in 2005 was the first to show that raloxifene reduced the risk of spine fractures by about 30%-40% on average. Follow up studies confirmed that the drug was effective at maintaining bone density over a longer period of time (up to 8 years).

This drug is very different from bisphosphonates as it does not deposit in bone and has no long term effect once it is stopped. Therefore, women using raloxifene do not generally have a “drug holiday” the way that they would if taking bisphosphonate. Once the raloxifene is stopped, bone loss begins again very soon. There is technically no “stop date” for raloxifene users.

One of the other differences between bisphosphonates and raloxifene is often stated as follows: “raloxifene has not been shown to prevent hip fractures”. This is a tricky statement to interpret.

It is certainly true that the MORE study and follow up reports did not provide any proof that raloxifene specifically prevented hip fractures (unlike the clinical trials with bisphosphonates). There are a couple possible reasons for that and each one has its own possible conclusion.

One possibility is that raloxifene, as a drug, is simply unable to prevent hip fractures, perhaps because it is not “strong” enough at stopping bone loss or some other inherent property of the drug. If that was true, we might think that raloxifene may not be the best choice for someone in whom hip fracture prevention was the biggest goal of treatment (i.e. someone with a particularly high risk of hip fracture).

However, the other possibility is that the MORE study involved women who tended to be younger and healthier than those in the bisphosphonate trials. Younger, healthy post menopausal women, as a group, tend to have very few hip fractures in the short term, even when untreated. Therefore, it’s hard to prove that a drug prevents hip fractures when the people taking it aren’t even the type to have hip fractures in the first place. If this was true, we might think that raloxifene may well be able to prevent hip fractures (much like estrogen), when studied in people who are actually at high risk of having hip fractures. Lack of observed effect in the clinical trial might just be related to the kind of women that were being studied. In this case, perhaps raloxifene is still useful for preventing hip fractures in those who take it - or at least, possibly more effective than no treatment at all.

Now, the “side benefit” part. In the MORE study, women were followed for an average of 40 months. Out of 5129 women taking the drug, 13 cases of breast cancer were found. Out of 2576 women taking a placebo pill, there were 27 cases of breast cancer. When you do the math, this equates to 70% fewer breast cancers with raloxifene — which sounds great but keep in mind that we are still talking about a very few number of women overall. The authors of the study stated the findings in a different way that is very helpful — out of every 126 women who take raloxifene, there will be 1 less breast cancer (over 3 years). The effects might be even better with longer use - the 4 year follow up raloxifene study showed that for every 94 women who take raloxifene for 4 years, there will be one less breast cancer.

The final results of the STAR trial reported in 2012 showed that raloxifene was useful for reducing the risk of breast cancer although perhaps just a little bit less effective than tamoxifen and so raloxifene continues to be used mostly in the osteoporosis clinic rather than the breast cancer clinic. If a woman is concerned about her risk for breast cancer, we recommend discussing with your family doctor regarding any necessary screening or testing.

COMMENT: In the self consult program, the primary focus is on preventing osteoporotic fractures and so that is where we put our attention; note that the full side effect profile of raloxifene is discussed in more detail in the session. However, for those who like the idea of raloxifene for fracture risk reduction, it is interesting to note this additional reduced risk of breast cancer which may be particularly useful for a small subset of women who take it.

25. I heard that I should not stop denosumab (PROLIA®) or delay a scheduled injection without a discussion with my health care provider. Why not?

This is a very new issue in the field of osteoporosis management which was not really known prior to 2017 and so many people may not yet have heard of this point.

Key Point: Although it may be quite uncommon, there is some concern that patients who abruptly stop denosumab or are very delayed in getting their scheduled injection (i.e. delayed by more than several months) may have a sudden increase in risk for low trauma vertebral compression fractures.  Patients are advised not to stop denosumab treatment until they have discussed with their physician.

Denosumab is an “anti-resorptive” drug designed to inhibit the cells that would otherwise remove bone (osteoclasts).  In this way, it is similar to the bisphosphonate type of drug (alendronate, risedronate, zoledronic acid).  However, there is at least one major difference: the bisphosphonate drugs remain in bone for a long time after the patient stops taking it (hence the whole discussion about “bisphosphonate drug holidays”, see question #14) whereas the effect of denosumab is quickly lost when the drug is stopped (or even just delayed in administration of sequential doses).  This may be associated with a “rebound effect” whereby the osteoclasts quickly start their work once more.  The consequence is that there may be a rapid increase in risk of fracture, particularly vertebral compression fractures.  There have now been a number of reported cases where women coming off denosumab (or missing injections) have sustained multiple low-trauma vertebral compression fractures which may be related to this “rebound” effect.  This is probably very uncommon and there is still some debate as to the exact nature of the “rebound effect” and its link to such fractures but it is an issue that is thought to be sufficiently important to bring to the attention of patients and their health care providers.

Providers who have not yet heard of this issue may wish to read more in this recent review in the Canadian Medical Association Journal (April 23, 2018).

Example:  Cheuk is a 72 year old woman who has been taking injections of denosumab every 6 months for the past 4 years.  She hasn’t discussed her therapy with her doctor in quite some time and has begun to wonder whether it’s necessary to continue.  She decides to skip her next injection and makes a mental note to bring it up with her physician at her next annual visit next year. Fortunately, her pharmacist notices that she is a few weeks late for her denosumab injection and advises Martha to get the injection now and ensure that her physician visit takes place well before the next scheduled dose.

How should a physician manage the discontinuation of denosumab in a patient who wants to stop taking it?  This is still an area of debate and a lot more study is needed in order to give the best advice.  Generally, some experts have recommended that patients coming off of denosumab should be transitioned to a bisphosphonate type drug and this seems reasonable for most.  Whether that should be an oral or intravenous bisphosphonate is not really known but our general preference at the Osteoporosis Centre would be to use an oral bisphosphonate.  The subsequent duration of “transition bisphosphonate therapy” is also unknown but many osteoporosis physicians will probably look at using this for at least one to two years.  Individual treatment plans will vary of course.

A related question that often comes up with this discussion: why are we just hearing about this now?  Well, a reality of medical science is that sometimes rare and serious side effects of a drug are just too uncommon to be detected in the course of a clinical trial prior to bringing the drug to market.  Even though clinical trials may include thousands of patients over several years, they still might not be able to detect a very rare problem.  For example, if a clinical trial has 4000 patients, half of whom get the experimental drug and the other half get a placebo pill, it might just so happen that the investigators see one serious problem in the 2000 actively treated patients and none of such problems in the placebo group.  With just one single occurrence, (especially if it’s something unusual or unexpected), the investigators would have no idea as to whether that one patient suffered as a consequence of the drug or just through random occurrence.  Or, maybe it happened because they had some other kind of medical problem. Either way, it would be impossible to say that this now means the new drug causes that particular problem.  Only after the medication is available on the open market can researchers begin to notice very rare serious events once tens of thousands of patients have used it over several years.  Health Canada actively encourages health care providers and consumers to report adverse reactions to health products and this is part of the way that our society can eventually “detect” these less common side effects that may be linked to certain drugs.

Comment: It’s always distressing to both physicians and the public when “new” information comes out showing that a widely prescribed medication may be associated with side effects not previously known.  In such situations, there is always potential for some pseudo-medical internet sites to exaggerate the risks and/or severity of the problem, often by highlighting particularly awful sounding stories of harm.  Additionally, this type of “news reporting” may subtly (or not-so-subtly) imply that the medical or pharmaceutical establishment is guilty of “suppressing” this knowledge in the interest of profits over patient well-being.  While we recognize that such situations are theoretically possible we would encourage our patients to seek out the facts and discuss them with a trusted and qualified health professional if concerned.  The vast, vast majority of health care providers (and scientists/drug developers) are truly interested in doing what is best for individual patients which is why you should always include your health care provider in all these kind of decisions.