So next, we're going to hear from Sumit Raniga.

He's an academic orthopedic surgeon with a background in molecular medicine and biomechanics.

He specializes in opened and arthroscopic shoulder and elbow reconstruction and joint replacement.

He's head of the upper limb surgery and therapy team at Macquarie.

And he also has established and directs the Macquarie University Translational

Orthopedic Research Program.He's

completed his orthopedic surgical training with the Australasian College

of Surgeons, pursued advanced fellowships in renowned international centers,

including the world-famous Department of Orthopedics and Traumatology in Bern, Switzerland.

He's been awarded the prestigious Charles Nier Award for Research in the Field

of Shoulder Surgery and has been a recipient of the Shoulder and Elbow Society

of Australia's North American Traveling Fellowship.

He'll be speaking about degenerative rotator cuff disease versus osteoarthritis.

Thank you very much, Bernie.

Such a pleasure to be here to share some of our work in this space.

So the topic I was given was the endohemorrhagian osteoarthritis versus rotator cuff tear arthropathy.

It's a fascinating area because in the past, we

couldn't really understand why some people developed osteoarthritis

while other people developed degenerative rotator cuff disease

and then developed cuff tear arthropathy which are

totally different mutually exclusive conditions and with

time with the science that i'll take you through we've now

actually understood that you have a predisposition to

one or the other and you can even predict who's going to go down one path or

the other and how we manage that so the fact that i have a background in basic

sciences i'm going to take you through a talk that's going to give you some

really good understanding of why something happens.

And that's one of the approaches I take to everything.

Why does it happen? So we can work it out and get a better understanding.

And that'll obviously guide management.

So first thing I'd like to do is just thank my mentors, Professor Matthias Junstein,

Bern University Hospital, Des Bocca, who's still with us in our clinic and consults

and he no longer operates and has kindly passed on that baton to me.

And then Professor George Arthwell, who's one of my North American Fellowship mentors.

So the first thing is introduction about the shoulder, a fascinating joint,

the critical shoulder angle, the glenohymalgerone osteoarthritis and rotator cuff tear arthropathy.

So the shoulder is a fascinating joint, and I think all of you usually see shoulder

pain at least maybe a few patients every day.

It's a very common joint that people come through life, and in fact,

if you look at every person's life, they at least have shoulder pain at least

once to maybe even five times based on the data.

It's probably the third most common complaint in the primary care setting,

so something that you need to understand.

These are the two different disease processes. On one side you have osteoarthritis,

on the other side you have a rotator cuff tear arthropathy.

The osteoarthritic pattern is very clear. You have loss of joint space,

you have goat's beard osteophyte, but I'd like you to look at a few more things a little bit carefully.

If you look at the osteoarthritic pattern, you will notice that the glenoid

tilt is slightly inferior.

On the rotator cuff tear arthropathy side, you will see, or the rotator cuff

disease side, the glenoid tilt is not inferior, in fact it's actually slightly inclined.

If you look at the acromion on the right side with the osteoarthritic picture,

sorry, the right side, you can see the acromion is a bit shorter,

so the acromion index is lower.

And on the rotator cuff disease side, you'll see the acromion has a bit more

coverage and has a slightly higher rotator cuff tear index, or a slightly higher acromial index.

Those are not coincidental they're actually highly predictive.

So the shoulder is a fascinating joint. In my mind and my passion for the shoulder,

I can say with a great bias that it's the most unique joint in the human body.

There is no other joint that's as capable as the shoulder.

Think about your shoulder and what it does for you. What differentiates human

beings from the rest of the animal kingdom is the neocortex which gives you

this amazing willpower.

You have this ingenuity that's then produced out by the hand.

Then you have the emotionality and the rationality.

And the shoulder is the crane that provides the ability to be ingenious with

your hand. It places your hand in space.

And that's its role. The shoulder is the crane that allows human beings to be capable of ingenuity.

And the way it's designed is that you've got a scapula that dances on your chest

wall controlled by muscles. The clavicle is purely a strut.

And then you have a golf tee at the end of it and a golf ball sitting on it.

There is absolutely no constraint.

Completely different from the hip joint, which is a ball and socket arrangement.

So in this, you have a very fine balance of a large amount of motor cortex that

modulates the bones, ligaments, tenons, muscles to dance to a rhythm to give

you the symphony of movement that you experience.

And that balance is created by the rotator cuff.

Everyone thinks about the rotator cuff as providing ability to abduct, to adduct.

It's not that. It's actually the combined motion of the four horses in a chariot

that keep that joint centered, that is the most powerful effect of the rotator cuff.

It is what provides the pivot point, the centricity, and that's why the rotator cuff is so important.

Yes, it instigates certain motions in certain planes, but the overall effect

is the four horses in a chariot keeping that joint centered.

It is what is the socket of the shoulder, but it's all soft tissue.

And then you've got the deltoid. What does the deltoid do? Every time you move

your shoulder, not even high up here.

In fact, the deltoid moment arms and muscle forces are much lower higher up.

When you're right here and your activity is a day living, it keeps pulling the hemorrhoid head up.

And the rotator cuff is what keeps that joint centered with a transverse force

couple that maintains centricity.

It's the pivoting point to allow biomechanical efficiency of the shoulder.

So the ascending force of the deltoid the compressive

source of the rotator cuff that is the fine balance

that makes the shoulder what it is for you in

terms of function so if you look at this these

x-rays you have the rotator cuff

disease on the one side which is early where they just have a few large tears

and then with time what happens is you get anterior superior migration of the

humeral head why does that happen because now you've got a void in the rotator

cuff and the humerus keeps getting pulled up every time you go to reach out, pick a cup of coffee,

go and reach your mouse because the deltoid keeps pulling that humerus up.

And that's why you get this anterior superior migration and the loss of the

chromium humeral distance, the distance between the top of the head and the

top of the humerus, which then tells you this is high-grade rotatorcafti atheropathy.

The scapula is a fascinating structure. It's a bit like the pelvis in terms of its importance.

And in fact, now we know that it's highly predictive of deciding who's going

to develop osteoarthritis and who's going to develop degenerative rotator cuff disease.

So is there an association between the individual anatomy of the scapula and

the development of rotator cuff tears or osteoarthritis? And the answer is yes.

So, once again, highlighting on the osteoarthritic side, carefully look,

the glenowid is inferiorly inclined, the acromion is short.

On this side, rotator cuff disease, glenowid is upward, acromion is long.

And this is the basis of the concept called the critical shoulder angle.

This is a gentleman called Béat Moore, one of my best friends from Byrne University Hospital.

The very year that I was there, this was discovered, it's called the critical

shoulder angle, where if you draw a line, very simple, in fact,

all of us can do it for our own x-rays, and it does not require accuracy.

Even with a student radiographer doing x-rays, 20 degree rotation,

abnormalities, you can still measure this because it's a two degree angle.

You draw a line from the top of the glenoid to the inferior portion to the lateral

edge, and that is the critical shoulder angle.

If you look at the osteoarthritic again, you can see the critical shoulder angle is small.

Why? Because the angle created by the inferiorly inclined glenoid and the shorter

chromium creates a small critical shoulder angle.

While in the rotator cuff disease, it's a much wider angle because you've got

a superior inclination and a wider chromium.

And we now know, based on the data, that if you have a critical shoulder angle

over 35 degrees, you have an 80% risk of developing degenerative rotator cuff

tears over your lifetime.

And therefore, you also have a risk of developing degenerative rotator cuff tear arthropathy.

While if your critical shoulder angle is less than 30 degrees,

you have a 95 degree percent probability that you're going to belong to the osteoarthritic group.

The fascinating thing is there's only a 5 degree window where you can be sitting safe.

So it tells you subtle differences in scapular morphology have a profound impact

on the biomechanics because it's all about biomechanics, which leads to disease processes.

And there's very clear evidence on that now.

Again, it's because of how the shoulder works. You have an ascending force of

the deltoid, which is balanced by the compressive force of the rotator cuff.

And so what's happening here is that when you have a downward-facing glenoid and a short acromion,

the deltoid has a wrapping effect in the humerus, and it synergistically with

the rotator cuff pulls the humeral head into the joint and that's why you develop osteoarthritis.

While with a rotator cuff disease group, you have an upward facing glenoid and

you have a much wider acromion so the deltoid ripping affects less and the vector

of the deltoid is much more powerful pulling up and therefore with time,

the rotator cuff wears out because it's getting tired of keeping the head down

because it's struggling with the forces.

That is how the critical shoulder angle works.

And there's very clear data. If you have a high CSA, there's almost 30 to 40%,

depending on what study you read, in terms of the forces that the posterior

superior rotator cuff has an effect, is loaded by.

And what are the patterns of tear we see the most? It's the posterior superior

cuff, supraspinatus, infraspinatus.

And this study here in Switzerland showed 44% increase in supraspinatus loading

just with the simplest activities in life.

And therefore every time you use your shoulder and you instigate your cuff to

keep the head down because the humerus is getting pulled up by the deltoid,

you get tear patterns over time.

And we now also know that it requires much more forces for the overall rotator

cuff, not just the supraspinatus, to keep the head down.

So if we took an x-ray of every single person in this room right now and we

measured the critical shoulder angle, you could actually tell yourself what

will happen with time. So it's very predictive.

Next thing is, it's a prognostic factor. So I had a young rugby player.

Critical shoulder angle of 45 degrees will a full thickness isolated super tear

from a traumatic injury.

What do we do for those patients? Well, you can actually change the natural

history and these data support that now.

So I do a lateral acrimoplasty in those very high ones to see if I can bring

the critical shoulder angle closer to normal to reduce the risk of load in the

rotator cuff that I've just repaired.

A bit like what Mike does with a tibial osteotomy in terms of correction when

he repairs his meniscus. Similar concept.

Furthermore, we also know in terms of failures that if you have a patient group

that has a very high critical shoulder angle and a patient group that has a

lower critical shoulder angle, when they have rotator cuff repair,

they've got a high risk of failure.

Because we know smoking diabetes has an effect, but when you control for those,

why do some people fail and others don't? And now we're getting an understanding of that.

There, that's the paper from the American Journal of Sports Medicine.

Furthermore, in terms of anatomic total shoulder arthroplasty,

one of the modes of failure of

the anatomic total shoulder arthroplasty is that the rotator cuff fails.

And we now know that if you don't preoperatively planned and then you leave

an increase in critical shoulder angle before to compare to what they had before,

those patients also have a high risk of failure of the arthroplasty.

So it has an impact on that too. So you have to account for that in planning.

So in terms of physiotherapy, it has a role too.

And I tell my physio colleagues that don't just generically start strengthening

the delto in these patients because that's counterproductive.

If it's not working empirically within six weeks, get an x-ray and measure the

angle and change the way you approach these patients for non-operative management.

Isometric adduction is a lot more powerful in this setting if you have a high

critical shoulder angle, which is likely with a degenerative rotator cuff disease patient.

But this is just the tip of the iceberg. In our lab, we're looking at lots of

other morphological factors that can have a huge predictive outcome and change

how we manage these patients.

Next thing I'm going to move on to is the glenohumeral joint, osteoarthritis.

This is a fascinating area. So what we know is that a lot of you think that

osteoarthritis is just where of that cartilage, where of the joint,

and it's the end of the story.

It's a lot more than that. This is actually a really interesting syndrome in

the shoulder, and I'll take you through that journey.

This is Professor Nier, who basically first described that what he noticed,

that people actually had a very eccentric wear pattern in the shoulder,

where they'd actually posteriorly subluxed, and they had created a historic

glenoid, which they'd left alone, and they were now articulating in the back

in what we call the neoglenoid.

They created a new glenoid within the glenoid. And that was purely because the

humeral head was subluxed back.

And then we had a classification that described that.

And furthermore, a new classification came out where, wow, not only was the

glenoid retroverted, the humeral head was pushed back, but it was actually wearing

with time and becoming concentric.

So you'd see the B3 pattern on an x-ray and you think, oh, it's just a normal

concentric arthritis, but it's not.

It's completely worn and it's created a new environment for itself,

which completely unbalances the shoulder.

So these are some papers that described how these evolve. And this is x-ray of a patient who's 45.

You can see how they're wearing with time. And then they become like that.

Why is that important? Well, it is very important because it's completely disrupted

the balance of the shoulder, and these patients now have a very high risk of

failure after an anatomic total shoulder replacement.

In fact, much higher failure rates than anyone else because they're still posterior sublux backed.

They have eccentric wear. You put an anatomic total shoulder replacement,

and it wears abnormally, and they fail.

So there's been a lot of work, which we've been part of as well,

with several papers that have now studied this.

So until 2019, when we published this paper, all we knew is that the glenoid

was retroverted, the humerus was posteriorly subluxed, there was an eccentric

wear pattern. That's all we knew.

And I thought to myself, you know what? If you look at the hip and its development,

hip dysplasia is very much related to the femur.

The humerus has to be involved. You can't just have an isolated disease, takes two hands to clap.

So then I studied the humerus of these patients, and what do we find?

Look at these fascinating data.

In a normal patient who has no osteoarthritis, the male has a humeral torsion

of 39 degrees, so they face back by 39 degrees, retro-torted. Female, 32.

When you have a simpler, milder form of arthritis, the Walsh type A,

their humerus is relatively anti-torted.

It's only 22 degrees. Look at the Walsh type B.

The humerus is almost facing forward.

It's 14 degrees and that's with a p-value of 0.001 regardless of sex.

So what that tells you is that it's not just on the glenoid side.

It's the humerus that is probably driving this deformity. And in fact,

it could be that we could measure humeral torsion in young people and know who's

going to develop this repetitive arthritis.

So now we know the glenoid is retro-taughted, humerus is posteriorly subluxed,

eccentric wear, and the humerus,

is facing relatively forward, completely different from normal anatomy.

Then we published the next paper in 2021, two years later, we said,

okay, if the bones are doing that, are the muscles driving this?

Is there imbalance in the muscles in these shoulders? Is that why they go down this path?

And fascinatingly, we found that when we 3D segmented all the muscles in these

shoulders, the muscles were balanced, but the infraspinatus in the back had

more fat in it and it was actually dysfunctional.

It was not doing its best bit to push the head back. The head kept on going back.

So now we know Glenwood is retroverted, eccentric wear, humerus faces forward,

and the muscles in the back are much weaker.

That's why the head keeps going forward and you get this pattern of arthritis.

Then we said, okay, what about the vectors. And how do we correct these?

So when we do these replacements, we need to know how to correct the bone to get the balance right.

And so then we were the first group in the world to publish that in order to

balance the shoulder, we had

to correct so that the retroversion of the glenoid was only seven degrees.

Until then, there was no data in the literature that was guiding surgeons as

to how to correct and how much to correct.

And so now we know that as soon as you bring it to seven degrees,

the whole rotator cuff, which is the key, becomes in balance.

Because if you do not, the imbalance is still there and the head will kill going back.

And that's why you get early failures after osteoarthritis.

So the key thing, takeaway point there, it's not that simple.

And you need to plan. Because if you do not plan, you are going to get failures.

What about full thickness tears? This is really important. This is a space that

has changed dramatically in the last 12 years.

Full thickness tears, the rotator cuff tear in a young patient are not benign lesions.

One of the things we see in the joint registry is a steep rise in reverse total

shoulder replacements. And we've been wondering, why is that?

One reason is some people feel it's an easy operation, so they do that more than the anatomic.

But the major reason is because all these patients, just like the meniscectomy,

had these rotator cuff tears when they were young plumbers, fitters,

turners, and they were told this is benign, you're going to be fine.

They are okay for a little while, but they're now all coming back. Why?

Because they progress and they become unrepairable. And the only solution we

have is a reverse total shoulder replacement. Let me show you the data.

50% of full thickness rotator cuff tears in a young patient progress within four years.

It's a coin toss. They progress.

Full stop and they become irreparable by nine years which is a huge factor for

a young patient especially physiologically young high demand patient if you

look at how people how long people live in australia it's it's neglect if you

don't if you don't treat them appropriately,

repeat mri is indicated at 12 months follow-up for full thickness rotator cuff

tear because we know they progress.

And 50% definitely progress based on most of the literature by 45 months.

So if you have a full thickness tear in a young patient, it is our duty to educate

that patient about the natural history of that disease.

Here are all the studies. And if you look at overall, it's 50% by 45 months.

What is irreparable? Number one, when you examine them, they basically have some lag signs.

So first is that they basically cannot lift their arm up.

They struggle. It's pseudoparalysis because the nerves are working,

but they just do not have the transverse force couple and the rotator cuff to provide balance.

Secondly, you place the arm in this position, you externally rotate, it falls.

And the last, the hornblower sign, it falls. So that's the clinical evaluation,

a lag sign. Second, the x-ray. I showed you before.

The humeral head has migrated up and now the acromion has become an acetabulum.

That's a problem. Those are irreparable.

Next is the rotator cuff tendon retracts towards the glenoid.

Sometimes you can still bring it back. But the most powerful thing is if you

measure the tendon length and it's less than 15 millimeters, boom, it's done.

92% risk of failure. It's unethical to offer these people surgery.

Last but most important is the amount of fat in the muscle.

As soon as you start having the same amount of muscle and fat in the rotator

cuff muscle, it has become unrepairable. It is unethical to offer surgery.

Based on this slide alone, it is unethical to offer surgery for rotator cuff

to a patient without an MRI. Full stop.

Because there is no way you can get a fully informed consent in a patient with

an ultrasound because you do not have any of the prognostic elements.

And I say this in international stage as well, and so do a lot of my colleagues.

But there are still people who do that, and I think it's not appropriate.

Because you can't inform the patient. What are you operating on?

What if it's irreparable?

What are the prognostic factors? What are you going to tell the patient?

How can they be fully informed?

Risk factors for progression? Full thickness tears, definitely.

Medium to large size tears. This is a very important point. Rotator cable disruption.

So the rotator cuff inserts into the bone like that.

This is the most common pattern of tear, where you get a charisenteric shape,

These are the pillars of the rotator cuff, just like the root of the meniscus in your talk.

And if one of them comes off, there's a very high risk that tear is going to

progress. Even if it's a small tear, those patients are very symptomatic.

And the test that tells you the rotator cable has gone in the front is the Whipples

test. Very different from the Jobes test. The Jobes test is up here.

Empty can is what we call it. And we push up. The Whipples is in the forearm

pronator neutral position in front of you, pulling up. If they hurt there,

there's a good chance that cable is gone, and those have a very high risk of

progression. Dominant side makes sense.

Ongoing pain makes sense. Smoking, 60 years of age.

And the fact that they have a high risk of progression to full thickness tears

is related to all these elements as well.

So rotator cuff tears are not benign lesions. All high-functioning physiologically

young individuals should have a surgical opinion because they have a risk of

developing rotator cuff tear arthropathy where the only solution is a reverse

total shoulder replacement.

So what about the older patients who have rotator cuff tears?

I'm not saying all of them need surgery because now we can understand from the

base and the pattern of tear who's going to do fine with surgery and who's not.

And what we've learned is that if you only have two tendon tears,

they do fine. If you have three tendon tears, they have a higher risk of developing pseudoparalysis.

And those are the patients that usually need surgery.

One more thing about another adjunctive treatment. Not everyone with a massive

rotator cuff tear needs to have a reverse total shoulder replacement.

So if you have a patient who has a massive tear, they can lift their arm but

it hurts and the biceps is there.

If you actually do a biceps tenotomy, they can lift without pain.

The only time a reverse is indicated is when they cannot lift their arm.

Reverse is designed to restore elevation. It doesn't need to be done when you

can elevate, you can do other things. And that's important to understand.

And the reverse total shoulder arthroplasty is an incredible operation.

It's made a huge difference to patients' lives.

Survivability is well over 90% at 15 years. And in fact, in certain areas,

the survivability is better than an atomic.

So it's a very powerful tool, but it needs to be well-executed, well-planned.

Every single reverse total shoulder replacement, just look at that,

you can see, has different designs and therefore it has different biomechanics.

In our lab, we test lots of prosthesis to understand the biomechanical personality

of each so we can guide surgeons to do these operations better with planning.

Planning is absolutely clear because if you do not plan your operations,

it's very hard to execute because if you carefully look at the glenoid,

all you're seeing is a golf tee.

We don't see anything behind that. You have no idea where the good bone is,

where the bad bone is, where you should be fixing components,

and how accurate you can be. The exposure just isn't there.

And therefore, it's very important that not only do you plan,

but execute to the best of your ability, and there are tools to allow you to do that.

And there's patient-specific instrumentation, robotics is coming into play,

and now computer navigation. In my case, I use PSI guides, patient-specific

instrumentation for the humerus, and I use computer navigation for the Glenwood side.

Just to give you a peek into the future, these are the PSI guides we currently use.

This is the navigation system that's right here. We can play with that if you're

interested at the end. And this is robotic surgery.

This is my North American Traveling Fellowship, University of Columbia, New York.

Just pay attention to that young lady at the back.

She's like going hard trying to keep everything out of the way.

So the robotics is at its very early stage.

Okay it's got great promise but you

can imagine not only is that girl hurting but if

that robot comes in a different line you could get a significant

traction injury of the shoulder as well so even though

robotics is coming it is still something that's been worked out in terms of

how we're going to execute it and how it's not easy i've never seen anyone traction

a shoulder this much while i was watching this my nerves were twitching that

it's gonna my nerves are dying What's the patient's nerves doing?

So still very early stages.

And this is a guided reaming where the robot is guiding how it reams.

So that's coming, but it's a long way away.

Preoperative planning is absolute key. And I just want to, before I finish off,

just to give you a quick idea of what preoperative planning looks like in the

shoulder, if I'm allowed.

Go through the process of segmenting the bones.

That data is then used to essentially create 3D models of the bones.

We perform the operation six weeks in advance, place components in the best

possible positions we can.

This is like, for example, the humerus.

And we have parameters that tell us what size it'll be, how it's put in,

what version. The same is done for the glenoid.

In my case, I do bio-RSA and so my graft is also planned so that I can execute

my graft and get it perfect in theater.

And then screw positions, length, everything is guided so we can actually get

the lengths as perfect as possible so that we can actually give the patient

the best chance to get the best recovery and then we use tools intraoperatively to execute that plan.

So planning is key because the pathology is not simple and there's a lot to

it than just an osteoarthritis and a cuffed arthropathy.

It's about putting it all together. Thank you very much.