June 15, 2025 • 43 mins
The silent, stealthy nature of osteoporosis makes it one of medicine's most challenging conditions. Patients can lose precious bone mass for years with absolutely no symptoms, only discovering their condition after a devastating, life-altering fracture.
With over a million Australians affected and our population steadily aging, understanding how to identify, investigate and treat this condition couldn't be more crucial. Yet despite its prevalence, osteoporosis remains severely underdiagnosed and undertreated in clinical practice.
In this comprehensive episode, Dr Gavin Nimon ( host and Orthopaedic Surgeon) inteviews Endocrinologist Dr Linn Lee brings about this complex topic. She expertly guides us through interpreting those notoriously confusing DEXA scan reports, breaking down T-scores and Z-scores into practical insights you can immediately apply. You'll discover exactly who needs investigating, when to refer to specialists, and how various risk assessment tools like FRAX and Garvan calculators can quantify fracture risk beyond bone density measurements alone.
Dr Lee demystifies the expansive pharmacological landscape – from bisphosphonates to cutting-edge anabolic agents – with particular attention to selecting the right medication for specific patient profiles. She discusses potential complications like osteonecrosis and atypical femoral fractures with refreshing honesty, providing evidence-based context about their prevalence and management strategies to mitigate risks.
Perhaps most valuable is the practical guidance on monitoring treatment efficacy, managing medication side effects, and navigating challenging clinical scenarios like bisphosphonate "drug holidays" and the complexities of stopping denosumab. The discussion extends beyond medications to emphasize the critical role of calcium, vitamin D, and targeted exercise regimens in comprehensive bone health management.
Whether you're a medical student building your foundational knowledge or an experienced GP managing complex cases, this episode delivers the practical insights you need to provide optimal care for patients with this prevalent but often overlooked condition. Subscribe to Aussie Med Ed for more expert-led, pragmatic discussions on core medical topics.
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:00):
Osteoporosis is often called a silent disease because
it can progress for yearswithout symptoms, only to reveal
itself through a suddendevastating fracture.
It affects more than a millionAustralians and is a major cause
of morbidity in our ageingpopulation.
Yet it's frequentlyunderdiagnosed and undertreated.
General practitioners and alldoctors play a crucial role in
identifying at-risk patients,initiating investigations and
(00:23):
starting early treatment toprevent long-term complications.
So how do we know who to screen, what medications truly make a
difference and how do we knowhow to navigate the risks and
benefits of treatment,especially in elderly or complex
patients?
Welcome back to Aussie Med Ed,a podcast where we take a
pragmatic and relaxed dive intocore medical topics designed
(00:43):
especially for medical studentsand general practitioners.
I'm your host, dr Gavin Lyman,and today we're unpacking the
diagnosis and treatment ofosteoporosis with Dr Lynne Lee
G'day.
And welcome to Aussie Med Ed,the Aussie-style medical podcast
, our pragmatic and relaxedmedical podcast designed for
medical students and generalpractitioners, where we explore
relevant and practical medicaltopics with expert specialists
(01:06):
Hosted by myself, gavin Lyman,an orthopaedic surgeon, this
podcast provides insightfuldiscussions to a hunch of
clinical knowledge withoutunnecessary jargon.
I'd like to start the podcast byacknowledging the Kaurna people
as the traditional custodiansof the land on which this
podcast is produced.
I'd like to pay my respects tothe elders, both past, present
and emerging, and recognisingtheir ongoing connection to land
, waters and culture.
I'd like to pay my respects toelders, both past, present and
emerging, and recognising theirongoing connection to land,
(01:26):
waters and culture.
I'd like to say that thispodcast is for educational
purposes only and does notconstitute medical advice.
Always refer to clinicalguidelines and consult a
qualified healthcareprofessional before making
medical decisions.
In today's episode, we'rediscussing the diagnosis and
treatment of osteoporosis withDr Lynne.
Lee Lynne is a specialistendocrinologist with a
particular interest in bonehealth, reproductive
(01:47):
endocrinology and diabetesmanagement.
After graduating from theUniversity of Adelaide, she
completed her advanced trainingin endocrinology at the Lyme
Acute Hospital and FlindersMedical Centre and is a fellow
of the Royal AustralasianCollege of Physicians.
She practices privately asSouth Australian medical
specialist here in SouthAustralia.
Dr Lee is also undertaking dualtraining in chemical pathology,
(02:08):
giving her a unique depth ofinsight into the biochemical
basis of endocrine conditions.
Welcome, dr Lee.
Thank you very much for comingon board for Aussie Med Ed Lynn,
and it's great to have you herewith us.
Perhaps you can tell me alittle bit about what
osteoporosis actually is andwhat the difference is between
osteoporosis and osteopenia.
Speaker 2 (02:26):
Absolutely so.
Osteoporosis is a conditiondefined by low bone mass and
deterioration in themicroarchitectural quality of
the bone.
It's incredibly common, a hugepublic health concern, and I
guess the easiest way to defineit is purely by the radiological
(02:46):
kind of definition.
So osteopenia is defined by aT-score between minus one and
minus 2.5.
So that's between one to twoand a half standard deviations
below what you'd expect for a30-year-old of the same sex, and
osteoporosis is defined as aT-score of lower than minus 2.5.
So I guess you could sayosteopenia is that sort of
(03:08):
milder form, that sort ofpre-osteoporosis stage before
bone density really gets thatlow.
Speaker 1 (03:14):
So 30-year-olds use as a standard, is it?
Speaker 2 (03:16):
Essentially, yeah.
So when you use a T-score,you're comparing it with
30-year-old bone density of thesame sex.
Speaker 1 (03:23):
Yeah, Okay, how common actually is osteoporosis?
Speaker 2 (03:26):
It's very common.
So it's been estimated that inall Australians over the age of
35 years it's about 2.7% of thatpopulation and that incidence
rises markedly after the age of75 in women, and it's generally
postmenopausal women that havethe highest incidence of
osteoporosis, but pretty commoneven in the 35 to 90-year-old
(03:47):
population.
Yeah, Excellent.
Speaker 1 (03:49):
It's more common in women than men.
Speaker 2 (03:51):
Definitely.
Yeah, it's probably a lot to dowith the fact that women go
through menopause so essentiallyhypogonadal.
They lose that estrogen thatprovides a lot of suppression of
bone turnover and they end updeveloping osteoporosis a lot
easier.
It's a lot less common in men,but certainly happens as well.
Speaker 1 (04:08):
So it's not based purely on the fact that men have
a higher bone load initially.
It's based purely on comparedto the same sex.
Speaker 2 (04:15):
No, that's absolutely a good point.
So we know that having a higherbody mass generally causes more
weight bearing on the bones andleads to achievement of a
higher peak bone mass andtherefore you tend to have a
higher mass to start with.
So you lose less and you'reless likely to develop
osteoporosis.
But I think a big part of whywomen get it more is because of
(04:37):
menopause, and we know thatpostmenopausal women are the
biggest group.
If you compare premenopausalwomen, that's a much smaller
group.
Speaker 1 (04:45):
What are the other risk factors for osteoporosis?
Speaker 2 (04:52):
Yeah, absolutely so.
Lots of risk factors.
Probably the most common onesto consider when assessing a
patient, for example, would bewhether there's a family history
of osteoporosis, particularlyif there's been a family history
of hip fracture in eitherparent.
That's actually used in theFRAX calculation score.
I always ask my patients aboutalcohol intake the less the
better with regards to bonedensity, and we consider other
(05:13):
things like calcium intake aswell, whether that's been
adequate, vitamin D deficiencyand then significant
comorbidities, such as any kindof malabsorption conditions like
celiac disease, malnutrition,low bone density and low weight
bearing states such as peoplethat are confined to wheelchairs
or bed bound.
And there are other conditionslike inflammatory sort of
(05:36):
disorders, like rheumatoidarthritis, glucocorticoid use,
of course, diabetes mellitus,chronic kidney disease.
A lot of these chronicmulti-organ illnesses tend to
raise the risk of osteoporosisas well, but those are probably
the main ones I tend to askabout.
Speaker 1 (05:52):
In my reading I was hearing that obviously smoking
is a factor and then withsmoking and reduced body mass,
it's also a factor.
Is the cause of smoking being afactor on causing osteoporosis
the fact that people who smokemay have a lower body mass
because of the appetitesuppression or the malabsorption
or was it actually a primaryeffect itself?
Speaker 2 (06:12):
yeah, I'm not aware that smoking is a primary risk
factor and directly interfereswith bone metabolism, but
certainly those links that youdescribed, I could absolutely
see that happening.
Lower bone density maybe mightbe associated with lower
nutrition as well, and I do askthat as part of my routine
history, but I don't focus on itso much as a risk factor.
Speaker 1 (06:35):
Yeah, and obviously there's also a lot of
medications, too, that caninterfere as well with it.
Speaker 2 (06:40):
So what are?
Speaker 1 (06:40):
the main ones you would tend to see.
Speaker 2 (06:42):
Yeah, absolutely so.
I already mentionedglucocorticoids.
That's a big one, and we have amuch lower threshold to treat
people with osteoporosis if weknow they're on corticosteroids.
The other ones I see are womenwho use certain
progesterone-only contraceptions, such as the Depo-Provera.
That's the big one, but theImplanon has also been linked to
(07:02):
lower bone density.
So in vulnerable patient groupswe tend to recommend different
ones.
Oestrogen-containing ones wouldbe ideal.
And then the other group ofpatients are the ones that are
on anti-epileptic medications,particularly Valproate.
There's been a clearassociation with low bone mass.
Speaker 1 (07:19):
Right, you've already mentioned the diagnosis looking
at a standard deviation of bonedensity, yep.
That's obviously based on aDEXA score, which I always find
very difficult to interpret.
It's often two or three pagesand there's a bunch of graphs
and things.
What's the easy way for themedical students and young GPs
to try and interpret theseresults?
Speaker 2 (07:37):
Yeah.
So I wanted to start byactually saying that Healthy
Bones Australia has a reallynice two-page PDF.
It's got like a graphicaldiagram of how to go about
interpreting a Dexan.
I thought that was actuallyquite useful, even for myself,
just as something to show people.
But I would always start byfirst of all looking at the age
of the patient.
(07:57):
That plays a huge role indetermining fracture risk.
I then look at the T-scores tostart with and assess whether or
not they have osteopenia orosteoporosis.
The Z-score is useful fordetermining A if the patient has
maybe a secondary cause ofosteoporosis.
Largely speaking, a Z-scoreunder minus two would prompt you
(08:20):
to look for a secondary cause.
And the reason for that is aZ-score is the number of
deviations above or below bonedensity for an age-matched
person.
So you're really comparing withother people in that age group
and if they've got much lowerbone density than other people
their age, then you think aboutwhether there's celiac disease
or primal hyperparathyroidism orsomething like that.
(08:42):
And the other group that theZ-score is useful for are people
that are under the age of 50,because the FRAX tools and all
our risk calculations they'rereally aimed at people who are
older.
So the Z-score.
You can't really use a T-scorein that population either.
Use the Z-score Then.
The next thing I would look at,particularly for people who are
(09:02):
on treatment.
So when people have alreadybeen on treatment and you're
following them up with a repeatbone density scan, I tend to
look at the percentage changefrom the last scan and we would
consider anything more than 4%in either direction to be a
significant change.
But most bone density centerswill actually tell you whether
(09:22):
or not they feel, according totheir data, whether it's
statistically significant.
Significant, but the sort ofzero to three percent change
that's within what you couldnaturally find between repeat
bone density scans.
It might not be significant andthat helps me to guide
treatment.
So I'll know if there's beendeterioration despite standard
treatment or whether there'sbeen improvement.
Speaker 1 (09:43):
Excellent.
You touched upon the FRAX scoreand I believe there's also a
Garvin score and maybe a fewother scores I'm not aware of,
but these are two I've heard of.
What is the utility of thoseand how do they help us?
Speaker 2 (09:54):
Absolutely.
Those are the two that I knowof as well.
So the FRAX tool is moreinternational and it takes into
account a few other.
It's got a few other questionsas part of.
It looks at glucocorticoid use,inflammatory conditions,
alcohol intake, although I'm notsure to what degree those
actually end up changing theFRAX tool, but they certainly
(10:16):
are part of the questionnaire.
The Garvin I like, particularlyfor people who have a lot of
falls, because it takes intoaccount falls per year and the
frax doesn't.
So if there's someone who has alot of falls the frax may
actually underestimate thatfracture risk because of course
if you're not falling you'remuch less likely to fracture.
(10:37):
The other thing is the Garvinis, I think, australia based, so
I like using that for ourAustralian population.
I tend to go Garvin and thenmaybe might do the FRAX as a
follow-up.
Speaker 1 (10:48):
So you do these routinely on your patients.
Speaker 2 (10:50):
So not routinely.
That's a good point that youraised there.
It's also worth pointing outthat a lot of bone density scan
centers will publishautomatically their calculated
FRAX score based on the bonedensity they've done on that day
, and that's quite helpful.
Generally score based on thebone density they've done on
that day, and that's quitehelpful.
Generally, treatment isrecommended for people who have
(11:13):
a 10-year risk of at least 20%for any osteoporotic site and 3%
for the hip, and if you exceedthat then antiretroviral is
recommended.
So sometimes it's a clear-cutcase someone who's broken their
hip from a minimal trauma event,or a 75-year-old with a t-score
of minus three those are clearindications for treatment.
When it's a bit less clear forexample a 50 year old with no
fracture and a t-score of minus2.5, or maybe a 65 year old with
(11:37):
an osteopenia t-score of minus2.3 those ones that are not
clear cut but maybe have anelevated fracture risk I think
those are where it's useful.
And the other scenario where itmight be useful are anxious
patients who have a low fracturerisk but say a 30 year old with
a t-score of minus 2.5 andthey're worried.
I find that using the fracturecalculator is really useful for
reassuring them that theirfracture risk is really low.
Speaker 1 (12:00):
And in these scenarios, that perhaps these
younger patients particularlywhat would bring them to have a
DEXA scan in the first place.
Speaker 2 (12:06):
I suppose the times that people may consider it is
when there've been significantrisk factors, things like.
I've seen it done for prolongedperiods of untreated
hyperthyroidism or prematuremenopause or what we call
primary ovarian insufficiency.
In the younger population, andI do see it sometimes done in
people who have anorexia nervosa, very low BMIs.
(12:29):
I wouldn't say that it'sappropriate to do it in those
instances, but I can certainlyunderstand why they've been done
.
The thing is that it may bringto light underlying low bone
density.
That doesn't end up having anyclinical consequences because
the risk of fracture is low.
Low bone density is not theonly determinant of fracture
risk but on the other hand onecould argue that it does prompt
(12:51):
patients maybe to make somelifestyle changes.
So get onto their vitamin D andtheir calcium intake and do
more exercise.
So I can see the pros and consof both.
Speaker 1 (12:59):
So over the age of 50 , screening is a tool that's
recommended.
Speaker 2 (13:03):
Absolutely Between the ages of 50 and 65, and
talking about the femalepopulation here, if they have an
additional risk factor forosteoporosis, then screening
with a DEXA scan is recommended,definitely Over the age of 65,
it's recommended that all womenjust get a DEXA scan because
they are long postmenopausal andthe incidence of osteoporosis
(13:25):
is very high in that population.
Speaker 1 (13:28):
Excellent, If we move on to actually further
diagnostic tests.
What's the role of boneturnover markers?
I was actually reading aboutthese and these are blood tests
which I've never heard of untilI prepared for this talk today.
Speaker 2 (13:39):
Yep, absolutely so.
Look, the two main ones that Ithink most people will come
across are the crosslaps, as wecall them.
They've got a much longer name,I think it's C-terminal
telopeptide, and there's alsothe P1NP, and, to put it simply,
crosslaps are an indicator ofbone resorption and P1NP is a
(14:01):
marker of bone formation.
I don't ever really order aP1NP.
It's used a lot in research, ofcourse, and we'll talk a bit
later about the bone buildingagents, and yes, those would be
potentially raised, butpractically we don't really
monitor them.
We just trust that thetreatment's working.
To be honest, crosslaps do havea major role in the management
(14:24):
of osteoporosis.
Crosslaps reduce quite quicklyafter starting anti-resorptive
treatment.
So within one to two weeks ofstarting a bisphosphonate, for
example, cross-lapse will reduceby 50%, and for Prolia
Denosumab, within a few days itwill reduce quite significantly
(14:44):
as well, and it's a really goodindicator of reassuring
ourselves that theanti-resorptive therapy is
working.
And I find that particularlyuseful in a few scenarios.
The main one would be whenyou're treating someone with an
oral bisphosphonate.
Now, oral bisphosphonates arewell known to be not the best
absorbed drug.
It's got a very low oralbioavailability and even in the
(15:06):
best of scenarios, with a bigglass of water, 30 minutes empty
stomach.
It may not be the best absorbeddrug and it's useful to have
cross-laps to do to reassureyourself that it's actually
working and we aim for across-lapse under 400 to tell us
that it's therapeutic.
We'll talk a little bit lateras well about the issues with
prolia and stopping prolia, andwe do use cross-laps as well to
(15:29):
monitor the rebound reduction inbone density that occurs after
the cessation of prolia andstopping prolia.
And we do use cross-laps aswell to monitor the rebound
reduction in bone density thatoccurs after the cessation of
prolia and how that guides uswith managing those patients.
Speaker 1 (15:38):
Yeah, okay, so for the average person?
Obviously most osteoporoticpatients would be treated by
their GP.
We'll talk through thetreatment methods in a minute,
but there'll be occasionalpatients that may have greater
osteoporosis or there may besome concern.
What's the average patient thatwe referred to an
endocrinologist for osteoporosis?
Speaker 2 (15:55):
Yeah, I see patients mainly who may be not satisfied
with the standard treatmentsthat are available
bisphosphonates and or Proliaand they may want to explore
things like hormone replacementtherapy.
They just want to get a secondopinion.
That's pretty common.
We do get a lot of referralsfor failure of treatment or
(16:19):
patients who would benefit fromzoledonic acid because there's
quite a lack of accessibilityfor giving these infusions and I
completely understand gettingreferrals for that.
And with just going back totreatment failure, that's
defined as patients who eitherhave a deterioration in bone
density or a minimal traumafracture despite 12 months of
adequate treatment.
We do now have treatments thatrequire specialist review for
(16:43):
prescription on the PBS and wesee those patients as well quite
a lot, and I suppose anypatient where they have
osteoporosis and too many otherthings going on on CKD is the
big one where we just need maybemore of a bigger picture.
Speaker 1 (16:56):
So balancing the kidney disorders with the
osteoporosis and try tocoordinate the calcium
resorption and reabsorption fromthe kidneys?
Speaker 2 (17:04):
Yeah, absolutely so.
We tend to see those quite abit as well.
Speaker 1 (17:07):
Okay, excellent, we'll move on to the treatment
of osteoporosis.
I understood.
You know, obviously, as a northbig surgeon, about calcium and
taking vitamin d and gettingsunlight very important and
that's about as much as I knew.
I've heard about biphosphonatesin the last few years, but when
you look at it, there's a lotto it.
There's so many different formsof treatment yeah we start off
(17:27):
with the simple things first.
Obviously, obviouslypreventative would be important
reducing alcohol intake anddoing exercise.
Where do you go from there?
Speaker 2 (17:36):
Yeah, and look, I'm glad you brought up exercise.
It's actually really importantto also prescribe the type of
exercise that should be done.
A lot of the patients that youtake a history from will say,
yeah, I walk every day and thewalking's good, but if they've
already had a fall and afracture, we really need to be
looking at what more we can dofor these patients and Healthy
(17:56):
Bones.
Australia actually has a reallynice PDF again about exercise
and they cover exercises forweight bearing and they also
cover resistance training andbalance training.
So these are the three sort ofcategories of exercise, and
balance training is reallyimportant for these patients,
especially the ones who arefalling over just ensuring that
they can write themselves betterif they trip and things like
(18:19):
that and I think exercisephysiology referral is
absolutely reasonable as well.
So with regards to finishing upon the lifestyle things, I guess
I always make sure thatpatients are having adequate
calcium, so the recommendationis at least 1200 milligrams for
a postmenopausal woman per day,and that can look like different
things.
I usually have a little chartof calcium foods and there's
(18:39):
also online calculators thatpeople can use to make sure
they're getting enough calciumand vitamin D.
I think labs quote 60 is thenormal range, but we know that
you need sometimes need up to 80to completely eliminate any
sort of bone resorption.
That's going on, yeah, and mostof us need vitamin D
supplementation.
We're all indoors, so yeah.
So that's the kind of we'vecovered the lifestyle things,
(19:01):
the dietary things, and thenmoving on to pharmacological
management.
So I always split them up intotwo categories the bone, the
antiresorptives, so the onesthat prevent osteoclast action,
and the bone building agents, orthe anabolic agents.
So, in terms of theantiresorptives, you mentioned
(19:21):
the bisphosphonates.
That's the oldest one we have,with the most data comes in oral
form.
Obviously, you've got weeklytablets, monthly tablets.
Actonel, fosamax are the twomain ones that we tend to
prescribe, and then we've alsogot zoledronic acid, which is an
intravenous infusion that weuse yearly.
Bisphosphonates, like I said,they're very old.
They're very old medications.
(19:42):
We've got lots of data on them.
They work really well.
The main side effect with theoral bisphosphonates are the
gastrointestinal side effectsand, like I mentioned before,
the low bioavailability.
So really emphasizing topatients that the mode of
administration is reallyimportant, sticking to the
advice provided by the pharmacy,and I tend to avoid it in
(20:03):
patients who have had uppergastrointestinal surgeries or
esophageal strictures, anythingwhere that drug might get stuck.
I don't, yeah, I don'trecommend it.
Intravenous bisphosphonates.
So the main one we useobviously is zoledronic acid.
I like that it bypasses thegastrointestinal tracts, are
really good for those that doget reflux and symptoms like
(20:23):
that.
The main side effect isflu-like symptoms.
In some patients it can bepretty severe as well.
They can get this really rundown malaise.
They can get the headaches andbody aches and joint pains and
things and it can be quiteoff-putting.
If they've not expected it, Igenerally tell patients to take
paracetamol three days priorleading up to the infusion and
(20:46):
on the day of as well.
They can take it after as wellif they want, and that's
actually been shown in theliterature to be useful.
I have also seen in clinicalpractice patients who have
really severe reactions.
The next one they might take asmall one-off dose of a
corticosteroids, so 25milligrams of prednisolone or
something like that.
But yeah, those would be themain side effects.
(21:07):
So those are thebisphosphonates.
The other anti-resorptive thatwe see a lot of is Prolia, the
denosumab.
So denosumab is a monoclonalantibody against rank ligand and
it's a very potent inhibitor ofosteoclastic action.
It works extremely well, butthe main downside is that it
(21:27):
only works while it's in thesystem, so it has to be given
every six months pretty strictly, and it also can't be stopped.
So it's meant to be in anindefinite treatment and
cessation is not recommendedunless it's covered by something
else, and even then there arenuances issues with that.
And if it is seized withoutanything to replace it, you can
(21:49):
get a pretty profound bonedensity rebound, bone density
loss.
There's also an increased riskof multiple vertebral fractures
in the spine and actually by twoyears post-cessation it's
almost like you've never been onany prolia at all.
So you actually go back tobeing on essentially similar to
placebo, yeah, yeah.
So quite a profound andsignificant issue there with the
(22:12):
denosumab and I see itprescribed a lot in the younger
population it's such aconvenient drug you inject it
and forget it.
But I am now actually seeingmore and more gps, I think,
being made aware of the issueswith denosumab, and we do get a
lot more referrals now forpeople who have been started on
denosumab either by a differentGP or a specialist or hospital
(22:35):
and they're saying can youplease help us get this patient
off denosumab because they'reway too young to be on it Anyone
over the age of 80 or someonewho's got a lower life
expectancy.
I think very reasonable to beon denosumab.
We've got data going up to 10years for the safety and
efficacy, but we don't have muchbeyond that.
Speaker 1 (22:51):
So in these osteoclastic reduction,
osteoclastic activity they don'tobviously increase the actual
bone density, they just reducethe actual loss.
Is that correct?
Speaker 2 (23:01):
So it yes, it doesn't affect the osteoblast, so it
doesn't actually cause any boneformation.
But by reducing osteoclasticactivity alone that can, I guess
, improve you could say thebalance between the two.
And we do see increases in inbone density.
We do see that particularlywith prolia in the spine.
It's got quite a markedimprovement.
Speaker 1 (23:23):
But we see that with bisphosphonates as well yeah, so
that leads to a change in theirpercentage.
They may move from a lower tvalue or z value, depending on
their age group to a change intheir percentage.
They may move from a lower Tvalue or Z value, depending on
their age group, to a higher Tvalue in that situation I would
be satisfied if they just didn'tlose bone.
Speaker 2 (23:39):
But very often we do see and expect them to gain some
bone as well, right, yep.
Speaker 1 (23:44):
Okay, Moving away from those osteoclastic drugs
are there any other we need tolook at, or is that the main
ones?
Speaker 2 (23:56):
Well, there are the ones that we use less commonly
in women.
So we've got raloxifene, whichis a selective estrogen receptor
modulator and it's an estrogenagonist on bone, but it's an
antagonist on breast and uterinetissue.
It's an oral medication andit's indicated for
postmenopausal women withosteoporosis.
We tend not to use it in peoplewho've had venous
thromboembolisms or people at ahigher clotting risk, because it
(24:20):
can potentially increase therisk of VTE or venous
thromboembolism.
And the last one, just tomention in passing as well, is
tibalone.
So tibalone is a syntheticsteroid that has estrogenic and
progestogenic effects.
It's also an oral medicationand it's also indicated for
postmenopausal osteoporosis andwe tend to choose this one.
(24:40):
For women who also havevasomotor symptoms of menopause
they get a lot of hot flushesbut for whatever reason they
can't have HRT then tibalonemight be something that we can
consider.
And of course, we shouldmention HRT.
Estrogen is a very goodsuppressor of bone resorption.
We don't recommend using it asfirst line treatment in someone
who needs anti-resorptivetreatment, but if they have
(25:03):
troubling vasomotor symptoms ofmenopause and they've got an
increased risk of fracturealthough not a very high risk of
fracture then HRT is a greatoption for those women.
Speaker 1 (25:13):
Excellent.
So there's numerous differentoptions depending on the
scenario.
Obviously, it's not one sizefits all.
What about the osteoblasticdrugs?
Are these newer agents?
Because I've not really heardtoo much about these.
Speaker 2 (25:26):
Yeah, they definitely tend to be ones that
endocrinologists prescribe.
The two that we have on themarket are teriparatide.
So teriparatide is a syntheticPTH analog.
It's been around for ages,although under continuous
parathyroid hormone stimulation,bones tend to become
osteoporotic.
What they've found is that whenyou expose bone to intermittent
(25:49):
PTH stimulation, it actuallyhelps build bones, actually got
an osteoblastic activity.
So that's how teriparatideworks.
It's a daily subcutaneousinjection which, as you can
imagine, brings its ownchallenges with getting patients
to agree to have it, but it'spretty safe.
We've got lots of data,long-term data, on it.
It's safe in a wide range ofkidney functions and it's safe
(26:14):
in people that have a highercardiovascular risk as well.
So it's a really good optionthere as well, and it's given
for 18 to 24 months.
So it's PBS subsidized for 18months, but it's been proven to
be beneficial beyond that, up to24 months.
After 24 months there is a blackbox warning for development of
osteosarcoma.
We always stop at 24.
(26:35):
So the main limitation withprescribing on the PBS is the
fact that you need very severeosteoporosis, so a T-score of
minus 3.0 or less, and you needto have had at least two minimal
trauma fractures, and one hasto be on standard treatment and
lots of barriers there, but wedo see patients who qualify and
(26:55):
I've prescribed it certainly afew times Yep, and but it's
usually well tolerated, usuallyvery well tolerated they
self-administer the injectionsthemselves right yep, so it's
definitely been shown tosignificantly increase bone
density, and both anabolicagents of teriparatide and
romisazumab, which we'll talkabout next, both of these need
to be consolidated.
(27:16):
When we say that, we mean youneed to lock it in with either
Prolia or a bisphosphonate inorder to secure that bone
building and prevent sort ofloss of what was gained.
Speaker 1 (27:28):
So it's used at the same time, or once the first one
stops, you start the second one.
Speaker 2 (27:33):
Classically we stop the anti-resorptive, put on the
anabolic agent, finish thecourse and then consolidate.
But there have been some peoplethat have been looking at using
teriparatide and denosumabtogether and that's been.
There's been some positiveresults there.
Obviously that wouldn't work onthe PBS because you can't be on
(27:53):
an anti-resorptive when you'reon an anabolic.
But if one, if a person, if anindividual was happy to
self-fund one or the other, thentechnically it could be done.
Speaker 1 (28:03):
But apart from teriparatide with denosumab
together, I'm not familiar withany other concurrent treatments
okay, so classically one thanthe other okay, and then one
last drug to go through isthat's it so romisosumab.
Speaker 2 (28:17):
That's the newest one that we have.
It's a fast drug to go through,isn't it?
That's it.
So romisozumab that's thenewest one that we have.
It's a monthly injection.
It's actually two injectionsfor whatever reason, but you
inject them at the same time intwo different sites and it's a
monthly injection for a total of12 months.
And they've never donehead-to-head trials between
(28:39):
teriparatide and romisozumab.
But just looking at numbersalone, it's suggesting that the
romisozumab is probably moreefficacious in increasing bone
density.
The main issue with romisozumabis that there is a small but
theoretical risk of increasedcardiovascular events.
Now, it wasn't found to bestatistically significant.
(29:00):
I think the numbers weresomething like 2.5% in the
romisozumab population versus1.9% in the alendronate.
So it wasn't statisticallysignificant, but it was enough
to make people worried andcertainly enough for the company
to put out a warning that theywouldn't recommend prescribing
this drug in anyone with a heart, a cardioinfarction or a
(29:21):
cerebrovascular event in thelast 12 months, and certainly in
the older, more frail, comorbidpopulation.
I am very hesitant and wouldprobably opt for the
teriparatide instead because ofthat warning.
But apart from that, it is easyto administer.
You just get them to book it inwith their nurse and they
(29:41):
usually tolerate it really well.
I usually just check theircalcium at the six month mark
just to make sure that's notrisen significantly.
But it's a listed thing to lookat but never really seen it be
an issue.
And then after the 12 monthsagain they need to have
consolidation.
The slight difference withromisozumab is that there's
(30:02):
really good evidence thatupfront, first-line romisozumab
so they've never had anyanti-resorptive is actually the
most beneficial and PBS in thelast little while have started
subsidizing romisozumab asfirst-line treatment.
But again there are some strictcriteria, again relating to
very low T-scores and havingspecific symptomatic fractures
(30:25):
within the last 24 months.
But certainly if a patient fitsthat brief, absolutely would
recommend being on romisozumabif they can Brilliant.
Speaker 1 (30:35):
All these drugs are trying to reduce the amount of
bone resorption or increase thebone formation, and they're the
numbers we're looking at, thatwe actually have figures, and
how will they actually preventfractures or reduce the
complications of fractures atall?
Speaker 2 (30:48):
yep, yep, absolutely.
You're absolutely right.
So, at the end of the day, whydo we care about improving bone
density?
It's not just to have a numbergo up, it's actually to reduce
fracture risk.
So I know for a fact thatbisphosphonates have fracture
risk in individuals.
I always tell them.
It doesn't make thembulletproof, though, so they
still need to be really careful.
If you have fractured before,you can fracture again, even
(31:11):
with the best treatment.
But yes, bisphosphonates havefracture risk.
I don't know off the top of myhead the numbers for the other
agents, but they've all beenshown to reduce fractures and
not just improve bone density.
Speaker 1 (31:22):
Excellent.
You've mentioned some of theside effects of the drugs as
we've gone, obviously the onethat a lot of people might've
heard about, the bisphosphonates, the risks of osteonecrosis of
the jaw or unusual femoralfractures as well.
What are your thoughts on those?
Speaker 2 (31:35):
Yeah, yep, so we'll start with the osteonecrosis of
the jaw.
So everyone's really worriedabout it, and that's reasonable.
It can be catastrophic andtreatment can be prolonged and
difficult.
Osteonecrosis of the jaw isactually really uncommon in the
osteoporosis population.
It's better described in theoncology population, where they
(31:57):
get much bigger doses and morefrequent doses of these
medications.
But the incidence in theosteoporotic population is
something between 0.001 to 0.15%.
So it is a pretty unusualcomplication to have and if you
know how to prevent it and whichpopulations are most at risk,
then it's very avoidable.
(32:18):
The biggest risk factors are, ofcourse, being on an
anti-resorptive, but apart fromthat, having poor dentition or
active suppurative dentaldisease.
So periodontal disease andthings like that, those would be
the main risk factors, and alsohaving a recent dental
extraction.
That's one of the biggest riskfactors as well.
So it's always about prevention.
Whenever you're about to startsomeone on treatment, always
(32:40):
have a quick look in their mouth.
If they're happy to get adental review, that would be the
best, but as long as they'venot had any active dental issues
, it's not the end of the world.
I now get most patients just todo a dental review, because you
never know when there'ssomething that's asymptomatic
that gets picked up, they canhave that fixed before they then
go down the route.
Like I said, if they needsomething done emergently, it
(33:02):
can be done.
Now we don't have any good waysof knowing when's the best time
.
I guess it makes sense that youwould aim to do it just before
the next dose for Prolia,because you can't stop it.
You would do it maybe monthfour, so that they've got a
whole month to recover beforetheir next dose With
bisphosphonates.
(33:23):
If they're on an oralbisphosphonate, definitely stop
it.
It's no rebound bone loss, sothat's fine.
And with the zoledronic acid Idon't think there's any hard and
fast rule, but I would maybeaim to do it maybe six months,
at least three to six monthsafter their last dose, before
they have any dental work done.
But if they can have it, alldone before starting, then it
eliminates a lot of issues after.
Speaker 1 (33:44):
So these risks are for all the anti-resorptive
medications is it Essentially.
Speaker 2 (33:48):
Yes, so bisphosphonates and denosumab
equally Okay.
Speaker 1 (33:52):
Right, okay, what about the femoral shaft
fractures?
The proximal subtrochanterictype fractures that we will see
occasionally?
Yes, the proximalsubtrochondriac type fractures
that we will see occasionally?
Speaker 2 (34:00):
Yes, absolutely so.
I'll probably start by justsaying a little bit about
atypical femoral fractures orAFFs.
So AFFs are generally no traumaor minimal trauma fractures
that occur in generally thefemoral shaft.
They have quite specificradiological features that help
us to differentiate it from yourtypical femoral fractures, have
(34:20):
quite specific radiologicalfeatures that help us to
differentiate it from yourtypical femoral fractures.
They tend to start laterally inthe cortex and then move
inwards, either transversely orobliquely.
And you can also get someincomplete ones that just show
as like a little bit of beakingat the side.
That can be quite subtle, butthey are associated with
prolonged bisphosphonate use.
Now the risk of AFFs go up evenwithin the first year of
bisphosphonate use.
Now, the risk of AFFs go upeven within the first year of
(34:40):
bisphosphonate use, but goes upsignificantly after five years.
And in saying that, once youstop bisphosphonates, the risk
of AFF also drops quitesignificantly after cessation.
So that's good to know.
All the antiresorptives areassociated with AFFs, but it
appears that bisphosphonatesmore so than denosumab.
(35:03):
The other thing to note is thatAFFs in general are rare.
They're very rare and they'redifficult to study because
they're so rare.
And the other thing to note isthat patients who have
osteoporosis are also morelikely to have AFFs.
Anyway, you can have AFFswithout being on bisphosphonates
and we do see that happensometimes.
(35:23):
I think this brings us to ournext kind of topic about drug
holidays, because that'ssomething that's discussed a lot
and GPs do ask me a lot ofquestions about drug holidays.
So a drug holiday basicallymeans, after a period of time of
being on a bisphosphonate,taking one to two years off the
bisphosphonate to reduce therisk of AFFs.
Now drug holidays arerecommended in people with a low
(35:45):
to intermediate risk offracture.
If they've, say, had a T-scoreof minus 2.5 and then you
treated them with abisphosphonate and now they're
just osteopenic, they've not hadany fractures you could
definitely consider a drugholiday.
But official guidelinesactually say not to consider it
if they're still at a high riskof fracture, so they've had a
recent fracture or t-scores arestill below minus 2.5.
(36:07):
They actually recommend thatyou keep going because even at
the 10-year mark of being on abisphosphonate for most of the
population, even then the riskof fracture from a from minimal
trauma typical fracture would behigher than the risk of an AFF.
So that's something to be awareof.
Speaker 1 (36:26):
Yeah, I think it's quite commonly known that a
person who breaks their hip hasgot a high risk of mortality in
the first year after that.
Speaker 2 (36:32):
Absolutely, absolutely.
So we'd rather prevent thatthan an incomplete AFF, say.
And the other thing to mentionis that we can be on the lookout
for these.
So if you've got a patientwho's on long-term
bisphosphonates, just alwaysasking them about groin pain,
and if they do mention any groinpain, just doing a bilateral
x-ray, you can then refer themon to our colleagues, like
(36:56):
yourself, and see whether they'dbe suitable for fixation.
Speaker 1 (37:01):
Lynn, once you've got these patients on the
medications treating them, howshould these patients be
monitored, and what are the redflags for treatment failure in
these scenarios too, that youneed to take into account?
Speaker 2 (37:11):
Yep, absolutely.
So.
We touched on brain turnovermarkers.
So cross-laps I would recommenddoing cross-laps at least three
months into treatment just to,particularly with the oral
bisphosphonates, just to makesure that they're doing their
job For the duration oftreatment.
I also do regular, at leastsix-monthly, biochemistry to
check their renal function,because there are limitations on
(37:34):
treatment with bisphosphonates,so you're not meant to use them
, the bisphosphonates,particularly with an EGFR under
30.
I still use oral bisphosphonatesin that CKD population, but
cautiously.
And of course the risk of sideeffects with denosumab goes up
quite a bit.
If you've got CKD you candevelop hypocalcemia which can
(37:55):
send patients to ICU and be verysymptomatic.
So that's something to look outfor as well, always monitoring
the renal function.
I do also monitor their vitaminD, particularly before a
denosumab dose or a zoledronicacid dose, and give them high
dose vitamin D to boost them upquickly, to make sure that we
also reduce that risk ofhypocalcemia after treatment.
And I would also just checktheir calcium just to make sure
(38:16):
they're not hypocalcemic forwhatever reason to start with,
because we would definitely needto manage that before they get
something that could potentiallymake them even more
hypocalcemic.
Speaker 1 (38:27):
And the DEXA scans.
I think you said every coupleof years after you've started
treatment.
Speaker 2 (38:31):
Yes, so if you've just started treatment, you can
get a MBS-rebatable DEXA scanwithin one year.
Otherwise, the other scans aregenerally every two years.
So I'd be happy to do one afterone year of treatment.
Usually, patients are quitekeen to see how their bone
density is doing as well.
So that would be reasonable.
Speaker 1 (38:49):
Excellent, all right.
What's the difference betweentreating a female patient and a
male patient?
Is there any difference youlook into?
Obviously, some of themedications we talked about are
indicated in postmenopausalladies.
That may not be the scenariofor men.
Does that affect how you treatthem?
Speaker 2 (39:04):
So ultimately, the same principles still apply for
treatment.
It's all about whether they'vehad a fracture, how low their
bone density is and what theircalculated fracture risk is
using those tools that wediscussed.
I think the main differencesare actually with regards to
maybe the more nuancedconditions around osteoporosis.
For example, if we look athypogonadism, a common secondary
(39:26):
cause of osteoporosis in men istestosterone deficiency.
Now, men may benefit fromtestosterone replacement for
other reasons energy, libido,things like that but it's
actually not been shown thattestosterone replacement
improves fracture risk, and infact, it's been shown that it
(39:46):
goes the other way around, andwe don't know if that's because
men just get so much energythey're jumping around falling
over, but it does increase bonedensity, but that has not
translated to fracture risk,whereas for women who have had
estrogen deficiency, we knowthat it prevents fractures and
it improves bone density.
So that's probably one of themain things to be aware of.
Speaker 1 (40:06):
Okay, that's an interesting fact to know.
So where do you think thingsare heading for the future in
the treatment of osteoporosis?
I know we focus on calcium as amajor issue.
Where do you think things willbe in the future?
Speaker 2 (40:17):
Yeah, there's lots of things on the horizon, as with,
I'm sure, every field ofmedicine, so we could talk a
little bit about trabecular bonescore.
So trabecular bone score is ameasurement of bone
microarchitecture and it's takenas a measurement of the lumbar
spine, which is obviously it ismainly trabecular bone, and it
(40:37):
just adds more information tohelp the clinician assess
fracture risk.
Most centers don't offer atrabecular bone score, but there
are some that do and that cancertainly be used to help with
decision-making, particularly inintermediate risk patients or
patients who are just on thethreshold of indications for
(40:57):
treatment, and I think as welearn more about how to use it,
it will become a more usefultool.
And then I believe there arealso on the horizon.
There's also the development ofother anabolic treatments,
potentially dual action agentsas well, to address both
osteoclastic activity andosteoplastic activity, and also
(41:17):
looking at different sorts ofbone markers that can help us.
Speaker 1 (41:28):
Excellent.
Speaker 2 (41:28):
Hopefully one day these people, will be
bulletproof and we'll be a lotless work for ourselves in
orthopaedics.
Absolutely absolutely.
Speaker 1 (41:31):
Thank you very much, Lynn.
It's been fantastic having youhere.
Speaker 2 (41:33):
Thank you for having me.
Speaker 1 (41:34):
And it's been really great hearing about these
different agents.
The main thought that camethrough my head, and a lot of
the way through, was thebifosfinates.
I was remembering when theywere just being released.
An old agent shows how old I am.
It's all good fun.
Speaker 2 (41:48):
They've always been in my textbooks.
Speaker 1 (41:49):
Thank you very much for coming on.
Aussie Med Ed.
It's been great to have you,it's been a pleasure, thank you.
Thank you very much.
Thank you, dr Lynn Lee.
I'd like to remind you that allthe information presented today
is just one opinion and thereare numerous ways of treating
all medical conditions.
It's just general advice andmay vary depending upon the
region in which you arepracticing or being treated.
The information may not beappropriate for your situation
(42:10):
or health condition and youshould always seek the advice
from your health professionalsin the area in which you live.
Also, if you have any concernsabout the information raised
today, please speak to your GPor seek assistance from health
organisations such as Lifelinein Australia.
Thanks again for listening tothe podcast and please subscribe
to the podcast for the nextepisode.
Until then, please stay safe.
Osteoporosis is often called a silent disease because
it can progress for yearswithout symptoms, only to reveal
itself through a suddendevastating fracture.
It affects more than a millionAustralians and is a major cause
of morbidity in our ageingpopulation.
Yet it's frequentlyunderdiagnosed and undertreated.
General practitioners and alldoctors play a crucial role in
identifying at-risk patients,initiating investigations and
(00:23):
starting early treatment toprevent long-term complications.
So how do we know who to screen, what medications truly make a
difference and how do we knowhow to navigate the risks and
benefits of treatment,especially in elderly or complex
patients?
Welcome back to Aussie Med Ed,a podcast where we take a
pragmatic and relaxed dive intocore medical topics designed
(00:43):
especially for medical studentsand general practitioners.
I'm your host, dr Gavin Lyman,and today we're unpacking the
diagnosis and treatment ofosteoporosis with Dr Lynne Lee
G'day.
And welcome to Aussie Med Ed,the Aussie-style medical podcast
, our pragmatic and relaxedmedical podcast designed for
medical students and generalpractitioners, where we explore
relevant and practical medicaltopics with expert specialists
(01:06):
Hosted by myself, gavin Lyman,an orthopaedic surgeon, this
podcast provides insightfuldiscussions to a hunch of
clinical knowledge withoutunnecessary jargon.
I'd like to start the podcast byacknowledging the Kaurna people
as the traditional custodiansof the land on which this
podcast is produced.
I'd like to pay my respects tothe elders, both past, present
and emerging, and recognisingtheir ongoing connection to land
, waters and culture.
I'd like to pay my respects toelders, both past, present and
emerging, and recognising theirongoing connection to land,
(01:26):
waters and culture.
I'd like to say that thispodcast is for educational
purposes only and does notconstitute medical advice.
Always refer to clinicalguidelines and consult a
qualified healthcareprofessional before making
medical decisions.
In today's episode, we'rediscussing the diagnosis and
treatment of osteoporosis withDr Lynne.
Lee Lynne is a specialistendocrinologist with a
particular interest in bonehealth, reproductive
(01:47):
endocrinology and diabetesmanagement.
After graduating from theUniversity of Adelaide, she
completed her advanced trainingin endocrinology at the Lyme
Acute Hospital and FlindersMedical Centre and is a fellow
of the Royal AustralasianCollege of Physicians.
She practices privately asSouth Australian medical
specialist here in SouthAustralia.
Dr Lee is also undertaking dualtraining in chemical pathology,
(02:08):
giving her a unique depth ofinsight into the biochemical
basis of endocrine conditions.
Welcome, dr Lee.
Thank you very much for comingon board for Aussie Med Ed Lynn,
and it's great to have you herewith us.
Perhaps you can tell me alittle bit about what
osteoporosis actually is andwhat the difference is between
osteoporosis and osteopenia.
Speaker 2 (02:26):
Absolutely so.
Osteoporosis is a conditiondefined by low bone mass and
deterioration in themicroarchitectural quality of
the bone.
It's incredibly common, a hugepublic health concern, and I
guess the easiest way to defineit is purely by the radiological
(02:46):
kind of definition.
So osteopenia is defined by aT-score between minus one and
minus 2.5.
So that's between one to twoand a half standard deviations
below what you'd expect for a30-year-old of the same sex, and
osteoporosis is defined as aT-score of lower than minus 2.5.
So I guess you could sayosteopenia is that sort of
(03:08):
milder form, that sort ofpre-osteoporosis stage before
bone density really gets thatlow.
Speaker 1 (03:14):
So 30-year-olds use as a standard, is it?
Speaker 2 (03:16):
Essentially, yeah.
So when you use a T-score,you're comparing it with
30-year-old bone density of thesame sex.
Speaker 1 (03:23):
Yeah, Okay, how common actually is osteoporosis?
Speaker 2 (03:26):
It's very common.
So it's been estimated that inall Australians over the age of
35 years it's about 2.7% of thatpopulation and that incidence
rises markedly after the age of75 in women, and it's generally
postmenopausal women that havethe highest incidence of
osteoporosis, but pretty commoneven in the 35 to 90-year-old
(03:47):
population.
Yeah, Excellent.
Speaker 1 (03:49):
It's more common in women than men.
Speaker 2 (03:51):
Definitely.
Yeah, it's probably a lot to dowith the fact that women go
through menopause so essentiallyhypogonadal.
They lose that estrogen thatprovides a lot of suppression of
bone turnover and they end updeveloping osteoporosis a lot
easier.
It's a lot less common in men,but certainly happens as well.
Speaker 1 (04:08):
So it's not based purely on the fact that men have
a higher bone load initially.
It's based purely on comparedto the same sex.
Speaker 2 (04:15):
No, that's absolutely a good point.
So we know that having a higherbody mass generally causes more
weight bearing on the bones andleads to achievement of a
higher peak bone mass andtherefore you tend to have a
higher mass to start with.
So you lose less and you'reless likely to develop
osteoporosis.
But I think a big part of whywomen get it more is because of
(04:37):
menopause, and we know thatpostmenopausal women are the
biggest group.
If you compare premenopausalwomen, that's a much smaller
group.
Speaker 1 (04:45):
What are the other risk factors for osteoporosis?
Speaker 2 (04:52):
Yeah, absolutely so.
Lots of risk factors.
Probably the most common onesto consider when assessing a
patient, for example, would bewhether there's a family history
of osteoporosis, particularlyif there's been a family history
of hip fracture in eitherparent.
That's actually used in theFRAX calculation score.
I always ask my patients aboutalcohol intake the less the
better with regards to bonedensity, and we consider other
(05:13):
things like calcium intake aswell, whether that's been
adequate, vitamin D deficiencyand then significant
comorbidities, such as any kindof malabsorption conditions like
celiac disease, malnutrition,low bone density and low weight
bearing states such as peoplethat are confined to wheelchairs
or bed bound.
And there are other conditionslike inflammatory sort of
(05:36):
disorders, like rheumatoidarthritis, glucocorticoid use,
of course, diabetes mellitus,chronic kidney disease.
A lot of these chronicmulti-organ illnesses tend to
raise the risk of osteoporosisas well, but those are probably
the main ones I tend to askabout.
Speaker 1 (05:52):
In my reading I was hearing that obviously smoking
is a factor and then withsmoking and reduced body mass,
it's also a factor.
Is the cause of smoking being afactor on causing osteoporosis
the fact that people who smokemay have a lower body mass
because of the appetitesuppression or the malabsorption
or was it actually a primaryeffect itself?
Speaker 2 (06:12):
yeah, I'm not aware that smoking is a primary risk
factor and directly interfereswith bone metabolism, but
certainly those links that youdescribed, I could absolutely
see that happening.
Lower bone density maybe mightbe associated with lower
nutrition as well, and I do askthat as part of my routine
history, but I don't focus on itso much as a risk factor.
Speaker 1 (06:35):
Yeah, and obviously there's also a lot of
medications, too, that caninterfere as well with it.
Speaker 2 (06:40):
So what are?
Speaker 1 (06:40):
the main ones you would tend to see.
Speaker 2 (06:42):
Yeah, absolutely so.
I already mentionedglucocorticoids.
That's a big one, and we have amuch lower threshold to treat
people with osteoporosis if weknow they're on corticosteroids.
The other ones I see are womenwho use certain
progesterone-only contraceptions, such as the Depo-Provera.
That's the big one, but theImplanon has also been linked to
(07:02):
lower bone density.
So in vulnerable patient groupswe tend to recommend different
ones.
Oestrogen-containing ones wouldbe ideal.
And then the other group ofpatients are the ones that are
on anti-epileptic medications,particularly Valproate.
There's been a clearassociation with low bone mass.
Speaker 1 (07:19):
Right, you've already mentioned the diagnosis looking
at a standard deviation of bonedensity, yep.
That's obviously based on aDEXA score, which I always find
very difficult to interpret.
It's often two or three pagesand there's a bunch of graphs
and things.
What's the easy way for themedical students and young GPs
to try and interpret theseresults?
Speaker 2 (07:37):
Yeah.
So I wanted to start byactually saying that Healthy
Bones Australia has a reallynice two-page PDF.
It's got like a graphicaldiagram of how to go about
interpreting a Dexan.
I thought that was actuallyquite useful, even for myself,
just as something to show people.
But I would always start byfirst of all looking at the age
of the patient.
(07:57):
That plays a huge role indetermining fracture risk.
I then look at the T-scores tostart with and assess whether or
not they have osteopenia orosteoporosis.
The Z-score is useful fordetermining A if the patient has
maybe a secondary cause ofosteoporosis.
Largely speaking, a Z-scoreunder minus two would prompt you
(08:20):
to look for a secondary cause.
And the reason for that is aZ-score is the number of
deviations above or below bonedensity for an age-matched
person.
So you're really comparing withother people in that age group
and if they've got much lowerbone density than other people
their age, then you think aboutwhether there's celiac disease
or primal hyperparathyroidism orsomething like that.
(08:42):
And the other group that theZ-score is useful for are people
that are under the age of 50,because the FRAX tools and all
our risk calculations they'rereally aimed at people who are
older.
So the Z-score.
You can't really use a T-scorein that population either.
Use the Z-score Then.
The next thing I would look at,particularly for people who are
(09:02):
on treatment.
So when people have alreadybeen on treatment and you're
following them up with a repeatbone density scan, I tend to
look at the percentage changefrom the last scan and we would
consider anything more than 4%in either direction to be a
significant change.
But most bone density centerswill actually tell you whether
(09:22):
or not they feel, according totheir data, whether it's
statistically significant.
Significant, but the sort ofzero to three percent change
that's within what you couldnaturally find between repeat
bone density scans.
It might not be significant andthat helps me to guide
treatment.
So I'll know if there's beendeterioration despite standard
treatment or whether there'sbeen improvement.
Speaker 1 (09:43):
Excellent.
You touched upon the FRAX scoreand I believe there's also a
Garvin score and maybe a fewother scores I'm not aware of,
but these are two I've heard of.
What is the utility of thoseand how do they help us?
Speaker 2 (09:54):
Absolutely.
Those are the two that I knowof as well.
So the FRAX tool is moreinternational and it takes into
account a few other.
It's got a few other questionsas part of.
It looks at glucocorticoid use,inflammatory conditions,
alcohol intake, although I'm notsure to what degree those
actually end up changing theFRAX tool, but they certainly
(10:16):
are part of the questionnaire.
The Garvin I like, particularlyfor people who have a lot of
falls, because it takes intoaccount falls per year and the
frax doesn't.
So if there's someone who has alot of falls the frax may
actually underestimate thatfracture risk because of course
if you're not falling you'remuch less likely to fracture.
(10:37):
The other thing is the Garvinis, I think, australia based, so
I like using that for ourAustralian population.
I tend to go Garvin and thenmaybe might do the FRAX as a
follow-up.
Speaker 1 (10:48):
So you do these routinely on your patients.
Speaker 2 (10:50):
So not routinely.
That's a good point that youraised there.
It's also worth pointing outthat a lot of bone density scan
centers will publishautomatically their calculated
FRAX score based on the bonedensity they've done on that day
, and that's quite helpful.
Generally score based on thebone density they've done on
that day, and that's quitehelpful.
Generally, treatment isrecommended for people who have
(11:13):
a 10-year risk of at least 20%for any osteoporotic site and 3%
for the hip, and if you exceedthat then antiretroviral is
recommended.
So sometimes it's a clear-cutcase someone who's broken their
hip from a minimal trauma event,or a 75-year-old with a t-score
of minus three those are clearindications for treatment.
When it's a bit less clear forexample a 50 year old with no
fracture and a t-score of minus2.5, or maybe a 65 year old with
(11:37):
an osteopenia t-score of minus2.3 those ones that are not
clear cut but maybe have anelevated fracture risk I think
those are where it's useful.
And the other scenario where itmight be useful are anxious
patients who have a low fracturerisk but say a 30 year old with
a t-score of minus 2.5 andthey're worried.
I find that using the fracturecalculator is really useful for
reassuring them that theirfracture risk is really low.
Speaker 1 (12:00):
And in these scenarios, that perhaps these
younger patients particularlywhat would bring them to have a
DEXA scan in the first place.
Speaker 2 (12:06):
I suppose the times that people may consider it is
when there've been significantrisk factors, things like.
I've seen it done for prolongedperiods of untreated
hyperthyroidism or prematuremenopause or what we call
primary ovarian insufficiency.
In the younger population, andI do see it sometimes done in
people who have anorexia nervosa, very low BMIs.
(12:29):
I wouldn't say that it'sappropriate to do it in those
instances, but I can certainlyunderstand why they've been done
.
The thing is that it may bringto light underlying low bone
density.
That doesn't end up having anyclinical consequences because
the risk of fracture is low.
Low bone density is not theonly determinant of fracture
risk but on the other hand onecould argue that it does prompt
(12:51):
patients maybe to make somelifestyle changes.
So get onto their vitamin D andtheir calcium intake and do
more exercise.
So I can see the pros and consof both.
Speaker 1 (12:59):
So over the age of 50 , screening is a tool that's
recommended.
Speaker 2 (13:03):
Absolutely Between the ages of 50 and 65, and
talking about the femalepopulation here, if they have an
additional risk factor forosteoporosis, then screening
with a DEXA scan is recommended,definitely Over the age of 65,
it's recommended that all womenjust get a DEXA scan because
they are long postmenopausal andthe incidence of osteoporosis
(13:25):
is very high in that population.
Speaker 1 (13:28):
Excellent, If we move on to actually further
diagnostic tests.
What's the role of boneturnover markers?
I was actually reading aboutthese and these are blood tests
which I've never heard of untilI prepared for this talk today.
Speaker 2 (13:39):
Yep, absolutely so.
Look, the two main ones that Ithink most people will come
across are the crosslaps, as wecall them.
They've got a much longer name,I think it's C-terminal
telopeptide, and there's alsothe P1NP, and, to put it simply,
crosslaps are an indicator ofbone resorption and P1NP is a
(14:01):
marker of bone formation.
I don't ever really order aP1NP.
It's used a lot in research, ofcourse, and we'll talk a bit
later about the bone buildingagents, and yes, those would be
potentially raised, butpractically we don't really
monitor them.
We just trust that thetreatment's working.
To be honest, crosslaps do havea major role in the management
(14:24):
of osteoporosis.
Crosslaps reduce quite quicklyafter starting anti-resorptive
treatment.
So within one to two weeks ofstarting a bisphosphonate, for
example, cross-lapse will reduceby 50%, and for Prolia
Denosumab, within a few days itwill reduce quite significantly
(14:44):
as well, and it's a really goodindicator of reassuring
ourselves that theanti-resorptive therapy is
working.
And I find that particularlyuseful in a few scenarios.
The main one would be whenyou're treating someone with an
oral bisphosphonate.
Now, oral bisphosphonates arewell known to be not the best
absorbed drug.
It's got a very low oralbioavailability and even in the
(15:06):
best of scenarios, with a bigglass of water, 30 minutes empty
stomach.
It may not be the best absorbeddrug and it's useful to have
cross-laps to do to reassureyourself that it's actually
working and we aim for across-lapse under 400 to tell us
that it's therapeutic.
We'll talk a little bit lateras well about the issues with
prolia and stopping prolia, andwe do use cross-laps as well to
(15:29):
monitor the rebound reduction inbone density that occurs after
the cessation of prolia andstopping prolia.
And we do use cross-laps aswell to monitor the rebound
reduction in bone density thatoccurs after the cessation of
prolia and how that guides uswith managing those patients.
Speaker 1 (15:38):
Yeah, okay, so for the average person?
Obviously most osteoporoticpatients would be treated by
their GP.
We'll talk through thetreatment methods in a minute,
but there'll be occasionalpatients that may have greater
osteoporosis or there may besome concern.
What's the average patient thatwe referred to an
endocrinologist for osteoporosis?
Speaker 2 (15:55):
Yeah, I see patients mainly who may be not satisfied
with the standard treatmentsthat are available
bisphosphonates and or Proliaand they may want to explore
things like hormone replacementtherapy.
They just want to get a secondopinion.
That's pretty common.
We do get a lot of referralsfor failure of treatment or
(16:19):
patients who would benefit fromzoledonic acid because there's
quite a lack of accessibilityfor giving these infusions and I
completely understand gettingreferrals for that.
And with just going back totreatment failure, that's
defined as patients who eitherhave a deterioration in bone
density or a minimal traumafracture despite 12 months of
adequate treatment.
We do now have treatments thatrequire specialist review for
(16:43):
prescription on the PBS and wesee those patients as well quite
a lot, and I suppose anypatient where they have
osteoporosis and too many otherthings going on on CKD is the
big one where we just need maybemore of a bigger picture.
Speaker 1 (16:56):
So balancing the kidney disorders with the
osteoporosis and try tocoordinate the calcium
resorption and reabsorption fromthe kidneys?
Speaker 2 (17:04):
Yeah, absolutely so.
We tend to see those quite abit as well.
Speaker 1 (17:07):
Okay, excellent, we'll move on to the treatment
of osteoporosis.
I understood.
You know, obviously, as a northbig surgeon, about calcium and
taking vitamin d and gettingsunlight very important and
that's about as much as I knew.
I've heard about biphosphonatesin the last few years, but when
you look at it, there's a lotto it.
There's so many different formsof treatment yeah we start off
(17:27):
with the simple things first.
Obviously, obviouslypreventative would be important
reducing alcohol intake anddoing exercise.
Where do you go from there?
Speaker 2 (17:36):
Yeah, and look, I'm glad you brought up exercise.
It's actually really importantto also prescribe the type of
exercise that should be done.
A lot of the patients that youtake a history from will say,
yeah, I walk every day and thewalking's good, but if they've
already had a fall and afracture, we really need to be
looking at what more we can dofor these patients and Healthy
(17:56):
Bones.
Australia actually has a reallynice PDF again about exercise
and they cover exercises forweight bearing and they also
cover resistance training andbalance training.
So these are the three sort ofcategories of exercise, and
balance training is reallyimportant for these patients,
especially the ones who arefalling over just ensuring that
they can write themselves betterif they trip and things like
(18:19):
that and I think exercisephysiology referral is
absolutely reasonable as well.
So with regards to finishing upon the lifestyle things, I guess
I always make sure thatpatients are having adequate
calcium, so the recommendationis at least 1200 milligrams for
a postmenopausal woman per day,and that can look like different
things.
I usually have a little chartof calcium foods and there's
(18:39):
also online calculators thatpeople can use to make sure
they're getting enough calciumand vitamin D.
I think labs quote 60 is thenormal range, but we know that
you need sometimes need up to 80to completely eliminate any
sort of bone resorption.
That's going on, yeah, and mostof us need vitamin D
supplementation.
We're all indoors, so yeah.
So that's the kind of we'vecovered the lifestyle things,
(19:01):
the dietary things, and thenmoving on to pharmacological
management.
So I always split them up intotwo categories the bone, the
antiresorptives, so the onesthat prevent osteoclast action,
and the bone building agents, orthe anabolic agents.
So, in terms of theantiresorptives, you mentioned
(19:21):
the bisphosphonates.
That's the oldest one we have,with the most data comes in oral
form.
Obviously, you've got weeklytablets, monthly tablets.
Actonel, fosamax are the twomain ones that we tend to
prescribe, and then we've alsogot zoledronic acid, which is an
intravenous infusion that weuse yearly.
Bisphosphonates, like I said,they're very old.
They're very old medications.
(19:42):
We've got lots of data on them.
They work really well.
The main side effect with theoral bisphosphonates are the
gastrointestinal side effectsand, like I mentioned before,
the low bioavailability.
So really emphasizing topatients that the mode of
administration is reallyimportant, sticking to the
advice provided by the pharmacy,and I tend to avoid it in
(20:03):
patients who have had uppergastrointestinal surgeries or
esophageal strictures, anythingwhere that drug might get stuck.
I don't, yeah, I don'trecommend it.
Intravenous bisphosphonates.
So the main one we useobviously is zoledronic acid.
I like that it bypasses thegastrointestinal tracts, are
really good for those that doget reflux and symptoms like
(20:23):
that.
The main side effect isflu-like symptoms.
In some patients it can bepretty severe as well.
They can get this really rundown malaise.
They can get the headaches andbody aches and joint pains and
things and it can be quiteoff-putting.
If they've not expected it, Igenerally tell patients to take
paracetamol three days priorleading up to the infusion and
(20:46):
on the day of as well.
They can take it after as wellif they want, and that's
actually been shown in theliterature to be useful.
I have also seen in clinicalpractice patients who have
really severe reactions.
The next one they might take asmall one-off dose of a
corticosteroids, so 25milligrams of prednisolone or
something like that.
But yeah, those would be themain side effects.
(21:07):
So those are thebisphosphonates.
The other anti-resorptive thatwe see a lot of is Prolia, the
denosumab.
So denosumab is a monoclonalantibody against rank ligand and
it's a very potent inhibitor ofosteoclastic action.
It works extremely well, butthe main downside is that it
(21:27):
only works while it's in thesystem, so it has to be given
every six months pretty strictly, and it also can't be stopped.
So it's meant to be in anindefinite treatment and
cessation is not recommendedunless it's covered by something
else, and even then there arenuances issues with that.
And if it is seized withoutanything to replace it, you can
(21:49):
get a pretty profound bonedensity rebound, bone density
loss.
There's also an increased riskof multiple vertebral fractures
in the spine and actually by twoyears post-cessation it's
almost like you've never been onany prolia at all.
So you actually go back tobeing on essentially similar to
placebo, yeah, yeah.
So quite a profound andsignificant issue there with the
(22:12):
denosumab and I see itprescribed a lot in the younger
population it's such aconvenient drug you inject it
and forget it.
But I am now actually seeingmore and more gps, I think,
being made aware of the issueswith denosumab, and we do get a
lot more referrals now forpeople who have been started on
denosumab either by a differentGP or a specialist or hospital
(22:35):
and they're saying can youplease help us get this patient
off denosumab because they'reway too young to be on it Anyone
over the age of 80 or someonewho's got a lower life
expectancy.
I think very reasonable to beon denosumab.
We've got data going up to 10years for the safety and
efficacy, but we don't have muchbeyond that.
Speaker 1 (22:51):
So in these osteoclastic reduction,
osteoclastic activity they don'tobviously increase the actual
bone density, they just reducethe actual loss.
Is that correct?
Speaker 2 (23:01):
So it yes, it doesn't affect the osteoblast, so it
doesn't actually cause any boneformation.
But by reducing osteoclasticactivity alone that can, I guess
, improve you could say thebalance between the two.
And we do see increases in inbone density.
We do see that particularlywith prolia in the spine.
It's got quite a markedimprovement.
Speaker 1 (23:23):
But we see that with bisphosphonates as well yeah, so
that leads to a change in theirpercentage.
They may move from a lower tvalue or z value, depending on
their age group to a change intheir percentage.
They may move from a lower Tvalue or Z value, depending on
their age group, to a higher Tvalue in that situation I would
be satisfied if they just didn'tlose bone.
Speaker 2 (23:39):
But very often we do see and expect them to gain some
bone as well, right, yep.
Speaker 1 (23:44):
Okay, Moving away from those osteoclastic drugs
are there any other we need tolook at, or is that the main
ones?
Speaker 2 (23:56):
Well, there are the ones that we use less commonly
in women.
So we've got raloxifene, whichis a selective estrogen receptor
modulator and it's an estrogenagonist on bone, but it's an
antagonist on breast and uterinetissue.
It's an oral medication andit's indicated for
postmenopausal women withosteoporosis.
We tend not to use it in peoplewho've had venous
thromboembolisms or people at ahigher clotting risk, because it
(24:20):
can potentially increase therisk of VTE or venous
thromboembolism.
And the last one, just tomention in passing as well, is
tibalone.
So tibalone is a syntheticsteroid that has estrogenic and
progestogenic effects.
It's also an oral medicationand it's also indicated for
postmenopausal osteoporosis andwe tend to choose this one.
(24:40):
For women who also havevasomotor symptoms of menopause
they get a lot of hot flushesbut for whatever reason they
can't have HRT then tibalonemight be something that we can
consider.
And of course, we shouldmention HRT.
Estrogen is a very goodsuppressor of bone resorption.
We don't recommend using it asfirst line treatment in someone
who needs anti-resorptivetreatment, but if they have
(25:03):
troubling vasomotor symptoms ofmenopause and they've got an
increased risk of fracturealthough not a very high risk of
fracture then HRT is a greatoption for those women.
Speaker 1 (25:13):
Excellent.
So there's numerous differentoptions depending on the
scenario.
Obviously, it's not one sizefits all.
What about the osteoblasticdrugs?
Are these newer agents?
Because I've not really heardtoo much about these.
Speaker 2 (25:26):
Yeah, they definitely tend to be ones that
endocrinologists prescribe.
The two that we have on themarket are teriparatide.
So teriparatide is a syntheticPTH analog.
It's been around for ages,although under continuous
parathyroid hormone stimulation,bones tend to become
osteoporotic.
What they've found is that whenyou expose bone to intermittent
(25:49):
PTH stimulation, it actuallyhelps build bones, actually got
an osteoblastic activity.
So that's how teriparatideworks.
It's a daily subcutaneousinjection which, as you can
imagine, brings its ownchallenges with getting patients
to agree to have it, but it'spretty safe.
We've got lots of data,long-term data, on it.
It's safe in a wide range ofkidney functions and it's safe
(26:14):
in people that have a highercardiovascular risk as well.
So it's a really good optionthere as well, and it's given
for 18 to 24 months.
So it's PBS subsidized for 18months, but it's been proven to
be beneficial beyond that, up to24 months.
After 24 months there is a blackbox warning for development of
osteosarcoma.
We always stop at 24.
(26:35):
So the main limitation withprescribing on the PBS is the
fact that you need very severeosteoporosis, so a T-score of
minus 3.0 or less, and you needto have had at least two minimal
trauma fractures, and one hasto be on standard treatment and
lots of barriers there, but wedo see patients who qualify and
(26:55):
I've prescribed it certainly afew times Yep, and but it's
usually well tolerated, usuallyvery well tolerated they
self-administer the injectionsthemselves right yep, so it's
definitely been shown tosignificantly increase bone
density, and both anabolicagents of teriparatide and
romisazumab, which we'll talkabout next, both of these need
to be consolidated.
(27:16):
When we say that, we mean youneed to lock it in with either
Prolia or a bisphosphonate inorder to secure that bone
building and prevent sort ofloss of what was gained.
Speaker 1 (27:28):
So it's used at the same time, or once the first one
stops, you start the second one.
Speaker 2 (27:33):
Classically we stop the anti-resorptive, put on the
anabolic agent, finish thecourse and then consolidate.
But there have been some peoplethat have been looking at using
teriparatide and denosumabtogether and that's been.
There's been some positiveresults there.
Obviously that wouldn't work onthe PBS because you can't be on
(27:53):
an anti-resorptive when you'reon an anabolic.
But if one, if a person, if anindividual was happy to
self-fund one or the other, thentechnically it could be done.
Speaker 1 (28:03):
But apart from teriparatide with denosumab
together, I'm not familiar withany other concurrent treatments
okay, so classically one thanthe other okay, and then one
last drug to go through isthat's it so romisosumab.
Speaker 2 (28:17):
That's the newest one that we have.
It's a fast drug to go through,isn't it?
That's it.
So romisozumab that's thenewest one that we have.
It's a monthly injection.
It's actually two injectionsfor whatever reason, but you
inject them at the same time intwo different sites and it's a
monthly injection for a total of12 months.
And they've never donehead-to-head trials between
(28:39):
teriparatide and romisozumab.
But just looking at numbersalone, it's suggesting that the
romisozumab is probably moreefficacious in increasing bone
density.
The main issue with romisozumabis that there is a small but
theoretical risk of increasedcardiovascular events.
Now, it wasn't found to bestatistically significant.
(29:00):
I think the numbers weresomething like 2.5% in the
romisozumab population versus1.9% in the alendronate.
So it wasn't statisticallysignificant, but it was enough
to make people worried andcertainly enough for the company
to put out a warning that theywouldn't recommend prescribing
this drug in anyone with a heart, a cardioinfarction or a
(29:21):
cerebrovascular event in thelast 12 months, and certainly in
the older, more frail, comorbidpopulation.
I am very hesitant and wouldprobably opt for the
teriparatide instead because ofthat warning.
But apart from that, it is easyto administer.
You just get them to book it inwith their nurse and they
(29:41):
usually tolerate it really well.
I usually just check theircalcium at the six month mark
just to make sure that's notrisen significantly.
But it's a listed thing to lookat but never really seen it be
an issue.
And then after the 12 monthsagain they need to have
consolidation.
The slight difference withromisozumab is that there's
(30:02):
really good evidence thatupfront, first-line romisozumab
so they've never had anyanti-resorptive is actually the
most beneficial and PBS in thelast little while have started
subsidizing romisozumab asfirst-line treatment.
But again there are some strictcriteria, again relating to
very low T-scores and havingspecific symptomatic fractures
(30:25):
within the last 24 months.
But certainly if a patient fitsthat brief, absolutely would
recommend being on romisozumabif they can Brilliant.
Speaker 1 (30:35):
All these drugs are trying to reduce the amount of
bone resorption or increase thebone formation, and they're the
numbers we're looking at, thatwe actually have figures, and
how will they actually preventfractures or reduce the
complications of fractures atall?
Speaker 2 (30:48):
yep, yep, absolutely.
You're absolutely right.
So, at the end of the day, whydo we care about improving bone
density?
It's not just to have a numbergo up, it's actually to reduce
fracture risk.
So I know for a fact thatbisphosphonates have fracture
risk in individuals.
I always tell them.
It doesn't make thembulletproof, though, so they
still need to be really careful.
If you have fractured before,you can fracture again, even
(31:11):
with the best treatment.
But yes, bisphosphonates havefracture risk.
I don't know off the top of myhead the numbers for the other
agents, but they've all beenshown to reduce fractures and
not just improve bone density.
Speaker 1 (31:22):
Excellent.
You've mentioned some of theside effects of the drugs as
we've gone, obviously the onethat a lot of people might've
heard about, the bisphosphonates, the risks of osteonecrosis of
the jaw or unusual femoralfractures as well.
What are your thoughts on those?
Speaker 2 (31:35):
Yeah, yep, so we'll start with the osteonecrosis of
the jaw.
So everyone's really worriedabout it, and that's reasonable.
It can be catastrophic andtreatment can be prolonged and
difficult.
Osteonecrosis of the jaw isactually really uncommon in the
osteoporosis population.
It's better described in theoncology population, where they
(31:57):
get much bigger doses and morefrequent doses of these
medications.
But the incidence in theosteoporotic population is
something between 0.001 to 0.15%.
So it is a pretty unusualcomplication to have and if you
know how to prevent it and whichpopulations are most at risk,
then it's very avoidable.
(32:18):
The biggest risk factors are, ofcourse, being on an
anti-resorptive, but apart fromthat, having poor dentition or
active suppurative dentaldisease.
So periodontal disease andthings like that, those would be
the main risk factors, and alsohaving a recent dental
extraction.
That's one of the biggest riskfactors as well.
So it's always about prevention.
Whenever you're about to startsomeone on treatment, always
(32:40):
have a quick look in their mouth.
If they're happy to get adental review, that would be the
best, but as long as they'venot had any active dental issues
, it's not the end of the world.
I now get most patients just todo a dental review, because you
never know when there'ssomething that's asymptomatic
that gets picked up, they canhave that fixed before they then
go down the route.
Like I said, if they needsomething done emergently, it
(33:02):
can be done.
Now we don't have any good waysof knowing when's the best time
.
I guess it makes sense that youwould aim to do it just before
the next dose for Prolia,because you can't stop it.
You would do it maybe monthfour, so that they've got a
whole month to recover beforetheir next dose With
bisphosphonates.
(33:23):
If they're on an oralbisphosphonate, definitely stop
it.
It's no rebound bone loss, sothat's fine.
And with the zoledronic acid Idon't think there's any hard and
fast rule, but I would maybeaim to do it maybe six months,
at least three to six monthsafter their last dose, before
they have any dental work done.
But if they can have it, alldone before starting, then it
eliminates a lot of issues after.
Speaker 1 (33:44):
So these risks are for all the anti-resorptive
medications is it Essentially.
Speaker 2 (33:48):
Yes, so bisphosphonates and denosumab
equally Okay.
Speaker 1 (33:52):
Right, okay, what about the femoral shaft
fractures?
The proximal subtrochanterictype fractures that we will see
occasionally?
Yes, the proximalsubtrochondriac type fractures
that we will see occasionally?
Speaker 2 (34:00):
Yes, absolutely so.
I'll probably start by justsaying a little bit about
atypical femoral fractures orAFFs.
So AFFs are generally no traumaor minimal trauma fractures
that occur in generally thefemoral shaft.
They have quite specificradiological features that help
us to differentiate it from yourtypical femoral fractures, have
(34:20):
quite specific radiologicalfeatures that help us to
differentiate it from yourtypical femoral fractures.
They tend to start laterally inthe cortex and then move
inwards, either transversely orobliquely.
And you can also get someincomplete ones that just show
as like a little bit of beakingat the side.
That can be quite subtle, butthey are associated with
prolonged bisphosphonate use.
Now the risk of AFFs go up evenwithin the first year of
bisphosphonate use.
Now, the risk of AFFs go upeven within the first year of
(34:40):
bisphosphonate use, but goes upsignificantly after five years.
And in saying that, once youstop bisphosphonates, the risk
of AFF also drops quitesignificantly after cessation.
So that's good to know.
All the antiresorptives areassociated with AFFs, but it
appears that bisphosphonatesmore so than denosumab.
(35:03):
The other thing to note is thatAFFs in general are rare.
They're very rare and they'redifficult to study because
they're so rare.
And the other thing to note isthat patients who have
osteoporosis are also morelikely to have AFFs.
Anyway, you can have AFFswithout being on bisphosphonates
and we do see that happensometimes.
(35:23):
I think this brings us to ournext kind of topic about drug
holidays, because that'ssomething that's discussed a lot
and GPs do ask me a lot ofquestions about drug holidays.
So a drug holiday basicallymeans, after a period of time of
being on a bisphosphonate,taking one to two years off the
bisphosphonate to reduce therisk of AFFs.
Now drug holidays arerecommended in people with a low
(35:45):
to intermediate risk offracture.
If they've, say, had a T-scoreof minus 2.5 and then you
treated them with abisphosphonate and now they're
just osteopenic, they've not hadany fractures you could
definitely consider a drugholiday.
But official guidelinesactually say not to consider it
if they're still at a high riskof fracture, so they've had a
recent fracture or t-scores arestill below minus 2.5.
(36:07):
They actually recommend thatyou keep going because even at
the 10-year mark of being on abisphosphonate for most of the
population, even then the riskof fracture from a from minimal
trauma typical fracture would behigher than the risk of an AFF.
So that's something to be awareof.
Speaker 1 (36:26):
Yeah, I think it's quite commonly known that a
person who breaks their hip hasgot a high risk of mortality in
the first year after that.
Speaker 2 (36:32):
Absolutely, absolutely.
So we'd rather prevent thatthan an incomplete AFF, say.
And the other thing to mentionis that we can be on the lookout
for these.
So if you've got a patientwho's on long-term
bisphosphonates, just alwaysasking them about groin pain,
and if they do mention any groinpain, just doing a bilateral
x-ray, you can then refer themon to our colleagues, like
(36:56):
yourself, and see whether they'dbe suitable for fixation.
Speaker 1 (37:01):
Lynn, once you've got these patients on the
medications treating them, howshould these patients be
monitored, and what are the redflags for treatment failure in
these scenarios too, that youneed to take into account?
Speaker 2 (37:11):
Yep, absolutely.
So.
We touched on brain turnovermarkers.
So cross-laps I would recommenddoing cross-laps at least three
months into treatment just to,particularly with the oral
bisphosphonates, just to makesure that they're doing their
job For the duration oftreatment.
I also do regular, at leastsix-monthly, biochemistry to
check their renal function,because there are limitations on
(37:34):
treatment with bisphosphonates,so you're not meant to use them
, the bisphosphonates,particularly with an EGFR under
30.
I still use oral bisphosphonatesin that CKD population, but
cautiously.
And of course the risk of sideeffects with denosumab goes up
quite a bit.
If you've got CKD you candevelop hypocalcemia which can
(37:55):
send patients to ICU and be verysymptomatic.
So that's something to look outfor as well, always monitoring
the renal function.
I do also monitor their vitaminD, particularly before a
denosumab dose or a zoledronicacid dose, and give them high
dose vitamin D to boost them upquickly, to make sure that we
also reduce that risk ofhypocalcemia after treatment.
And I would also just checktheir calcium just to make sure
(38:16):
they're not hypocalcemic forwhatever reason to start with,
because we would definitely needto manage that before they get
something that could potentiallymake them even more
hypocalcemic.
Speaker 1 (38:27):
And the DEXA scans.
I think you said every coupleof years after you've started
treatment.
Speaker 2 (38:31):
Yes, so if you've just started treatment, you can
get a MBS-rebatable DEXA scanwithin one year.
Otherwise, the other scans aregenerally every two years.
So I'd be happy to do one afterone year of treatment.
Usually, patients are quitekeen to see how their bone
density is doing as well.
So that would be reasonable.
Speaker 1 (38:49):
Excellent, all right.
What's the difference betweentreating a female patient and a
male patient?
Is there any difference youlook into?
Obviously, some of themedications we talked about are
indicated in postmenopausalladies.
That may not be the scenariofor men.
Does that affect how you treatthem?
Speaker 2 (39:04):
So ultimately, the same principles still apply for
treatment.
It's all about whether they'vehad a fracture, how low their
bone density is and what theircalculated fracture risk is
using those tools that wediscussed.
I think the main differencesare actually with regards to
maybe the more nuancedconditions around osteoporosis.
For example, if we look athypogonadism, a common secondary
(39:26):
cause of osteoporosis in men istestosterone deficiency.
Now, men may benefit fromtestosterone replacement for
other reasons energy, libido,things like that but it's
actually not been shown thattestosterone replacement
improves fracture risk, and infact, it's been shown that it
(39:46):
goes the other way around, andwe don't know if that's because
men just get so much energythey're jumping around falling
over, but it does increase bonedensity, but that has not
translated to fracture risk,whereas for women who have had
estrogen deficiency, we knowthat it prevents fractures and
it improves bone density.
So that's probably one of themain things to be aware of.
Speaker 1 (40:06):
Okay, that's an interesting fact to know.
So where do you think thingsare heading for the future in
the treatment of osteoporosis?
I know we focus on calcium as amajor issue.
Where do you think things willbe in the future?
Speaker 2 (40:17):
Yeah, there's lots of things on the horizon, as with,
I'm sure, every field ofmedicine, so we could talk a
little bit about trabecular bonescore.
So trabecular bone score is ameasurement of bone
microarchitecture and it's takenas a measurement of the lumbar
spine, which is obviously it ismainly trabecular bone, and it
(40:37):
just adds more information tohelp the clinician assess
fracture risk.
Most centers don't offer atrabecular bone score, but there
are some that do and that cancertainly be used to help with
decision-making, particularly inintermediate risk patients or
patients who are just on thethreshold of indications for
(40:57):
treatment, and I think as welearn more about how to use it,
it will become a more usefultool.
And then I believe there arealso on the horizon.
There's also the development ofother anabolic treatments,
potentially dual action agentsas well, to address both
osteoclastic activity andosteoplastic activity, and also
(41:17):
looking at different sorts ofbone markers that can help us.
Speaker 1 (41:28):
Excellent.
Speaker 2 (41:28):
Hopefully one day these people, will be
bulletproof and we'll be a lotless work for ourselves in
orthopaedics.
Absolutely absolutely.
Speaker 1 (41:31):
Thank you very much, Lynn.
It's been fantastic having youhere.
Speaker 2 (41:33):
Thank you for having me.
Speaker 1 (41:34):
And it's been really great hearing about these
different agents.
The main thought that camethrough my head, and a lot of
the way through, was thebifosfinates.
I was remembering when theywere just being released.
An old agent shows how old I am.
It's all good fun.
Speaker 2 (41:48):
They've always been in my textbooks.
Speaker 1 (41:49):
Thank you very much for coming on.
Aussie Med Ed.
It's been great to have you,it's been a pleasure, thank you.
Thank you very much.
Thank you, dr Lynn Lee.
I'd like to remind you that allthe information presented today
is just one opinion and thereare numerous ways of treating
all medical conditions.
It's just general advice andmay vary depending upon the
region in which you arepracticing or being treated.
The information may not beappropriate for your situation
(42:10):
or health condition and youshould always seek the advice
from your health professionalsin the area in which you live.
Also, if you have any concernsabout the information raised
today, please speak to your GPor seek assistance from health
organisations such as Lifelinein Australia.
Thanks again for listening tothe podcast and please subscribe
to the podcast for the nextepisode.
Until then, please stay safe.
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