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Hello and welcome to Noon Conference hosted by MRI Online

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Noon Conference connects the global radiology community

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through free live educational webinars that are accessible

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for all and is an opportunity

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to learn alongside top radiologists from around the world.

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You can access the recording of today's conference

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and previous noon conferences

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by creating a free MRI online account.

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Today. We are honored to welcome Dr. Dennis Beki

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for a lecture entitled Introduction to Arthritis.

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Dr. Beki is an academic diagnostic radiologist

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with over 30 years of experience in bone

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and joint radiology.

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He's a senior MSK specialist radiologist at King's College

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Hospital and senior lecturer in imaging

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sciences at King College.

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Dr. Bki is also a member of the Arthritis Subcommittee

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of the ESSA member of the Polish Medical Radiology Society,

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an honorary member of the U Ukrainian Association

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of Radiologists and the editor in chief of Radiology.

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He has published over 50 papers

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and educational exhibits in peer reviewed journals

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and at major radio radiological meetings

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and teaches radiology residents worldwide in the uk, Poland,

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Ukraine, and Israel.

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At the end of the lecture, please join Dr.

1:17

Bki in a q and a session

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where he will address questions you may

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have on today's topic.

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Please remember to use the q

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and a feature to submit your questions so we can get to

1:25

as many as we can before our time is up.

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With that, we are ready to begin today's lecturer, Dr.

1:31

Bki, please take it from here.

1:33

Thank you very much. It's wonderful to be here again

1:37

and to do the last part of this introduction

1:42

to arthritis, which as she said, it can,

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can be found on the website.

1:49

Today we will cover the final group

1:51

of diseases in this lecture series about

1:55

introduction to arthritis.

1:57

Later I will develop a 10 item quiz to help you check

2:01

and reinforce your knowledge.

2:03

Hopefully we'll be able to do

2:05

that sometime later in the year.

2:09

I started to say that uh, the images that I use our

2:14

for educational purposes

2:18

and may be reproduced for educational purposes.

2:21

Otherwise, with due credit given to radio pedia

2:24

and the radiology assistant,

2:28

we will begin today's lecture by discussing calcium

2:31

pyrophosphate dihydrate crystal deposition disease,

2:35

which is my favorite disease.

2:37

The key findings in this disorder are fine chondrocalcinosis

2:42

located at the triangular fiber cartilage complex

2:46

or meniscal tissue in the knee

2:48

or synthesis pubis calcium

2:51

pyrophosphate dihydrate crystal deposition disease is a long

2:55

name for an inflammatory joint disease caused by deposition

3:00

of this crystal in the synovial fluid, synovial lining

3:04

and articular cartilage.

3:07

This disorder is the second most common degenerative disease

3:11

seen in man following osteoarthrosis.

3:15

It causes characteristic degenerative changes in

3:19

specific locations.

3:22

There are several terms that you need to be familiar

3:24

with when talking about CPBD Crystal Deposition Disease

3:30

First Chondrocalcinosis is a descriptive term describing

3:35

fine calcifications in cartilage

3:38

most often used when CPPD is the cause.

3:42

However, CHONDROCALCINOSIS is not an exclusive feature

3:46

of CPPD Crystal Deposition disease

3:49

and can also be seen in severe osteoarthritis

3:54

when it is seen in severe osteoarthritis is a combination

3:58

disorder in in which both diseases exist together.

4:05

Pyrophosphate arthropathy is a distinctive arthropathy

4:08

of CPVD Crystal deposition disease, which is like

4:13

osteoarthritis but has an unusual

4:16

and specific distribution.

4:20

Pseudo gout on the other hand is an acute joint inflammation

4:24

secondary to CPPD crystals.

4:27

It is called pseudo gout

4:29

because clinically it can look like gout in some cases.

4:36

The radiographic findings

4:37

of this disorder using our mnemonic as

4:40

before are there are no erosions present in the

4:45

articular surfaces.

4:47

The bone demonstrates subc chondral cyst formation,

4:50

which is exceedingly common and numerous.

4:54

The cartilage demonstrates joint space narrowing,

4:58

particularly at the radiocarpal joint.

5:02

The distribution is symmetric affecting the radiocarpal

5:06

joint, the carpal metacarpal joints

5:09

and the metacarpophalangeal joint

5:11

of the index and long fingers.

5:15

CPBD arthropathy can also affect the elbow, the hip,

5:19

the synthesis pubis, the knee and the ankle.

5:23

There are no additional findings in this disorder.

5:27

The soft tissue findings

5:29

as we have discussed are chondro calcinosis,

5:32

which when found in hylan cartilage is linear

5:36

as seen in the hip,

5:37

but when found in the triangular fibrocartilage,

5:41

it may occur in patchy fine distribution.

5:45

Let's look at some patients with this disorder.

5:47

Here are two different patients demonstrating classic

5:50

findings of CPPD, crystal deposition disease

5:54

in the left radiograph.

5:56

We see cartilage loss in many joints

5:58

and chondro calcinosis in the carpal metacarpal joint

6:02

of the base of the thumb indicated by a white arrow,

6:06

the metacarpophalangeal joint of the index finger indicated

6:10

by the arrowhead

6:11

and the triangular fibrocartilage complex indicated

6:15

by the asterisk.

6:18

It is also important

6:19

to notice the radiocarpal joint face degenerative changes,

6:24

particularly that on the scaphoid side of the joint.

6:28

This is characteristic

6:30

for joint space narrowing in this disorder.

6:34

In the right radiograph,

6:36

we see chondrocalcinosis in the radiocarpal joint

6:40

and triangular fibrocartilage complex indicated

6:44

by the black arrow.

6:46

Scapholunate dissociation is also seen,

6:48

which is a common late finding in this disorder.

6:52

However, scapholunate dissociation may also be seen in

6:56

rheumatoid arthritis or after trauma.

7:02

Here we see two different AP radiographs of the knees.

7:06

Thin calcifications in the cartilage

7:09

and menisci are noted bilaterally on the right side

7:12

indicated by the white arrow as well

7:15

as on the left side indicated by the black arrow.

7:19

Many times this calcification is rather linear

7:23

or clumped as we see here, which is also characteristic

7:27

for CPPD crystal deposition disease.

7:31

These calcifications can be caused by other conditions

7:35

as well such as gout, but this is rarely seen in this case.

7:41

Also note the joint space narrowing

7:43

and mild osteophyte formation.

7:46

CPPD crystal deposition disease has many features like

7:50

osteoarthrosis, however, its

7:53

distribution is completely different

7:59

in these radiographs.

8:00

The right image is a magnification of the left image

8:05

we see well circumscribed coarse calcification adjacent

8:09

to the fourth distal interphalangeal joint.

8:13

This does not look like CPPD crystal deposition

8:16

and scleroderma would be the most likely possibility.

8:20

However, aspiration revealed typical CPPD crystal

8:24

depositions as in other arthropathies atypical

8:29

presentations of CPPD crystal are possible,

8:33

but fortunately are far less common in the future.

8:38

I will do a lecture completely covering CPPD Crystal

8:42

deposition disease.

8:44

Please learn the pattern of distribution which consists

8:47

of moderate to severe degenerative changes

8:50

at the radiocarpal joint.

8:53

Multiple subc chondral cysts in the wrists of usually

8:57

multiple sizes changes at the

9:01

metacarpophalangeal joints of the index

9:03

and long fingers consisting of metacarpal head enlargement

9:08

and beak formation on the thumb side of the metacarpals

9:14

distribution is only seen in two diseases.

9:18

CPPD Crystal deposition disease demonstrates this pathology

9:23

at the index and long finger

9:26

metacarpophalangeal joints while the disease

9:29

hemochromatosis affects all four digits

9:33

and hemochromatosis is more common in men.

9:40

Here we see two radiographic images of the hand

9:43

and wrist taken from radio pedia.

9:45

The beak like osteophytes are noted in both images at the

9:49

metacarpal heads of the index and long fingers.

9:54

Also findings compatible with CPPD include base

9:57

of the thumb degenerative changes,

10:01

mild degenerative changes at the radiocarpal joint

10:04

and scapholunate dissociation

10:07

chondro Calcinosis is not present in this in this case

10:12

and many times it does not have

10:14

to be present if all the other findings exist.

10:23

Now we move on to to a group of different diseases

10:27

that have bone and joint involvement.

10:29

The first disease that we're going

10:31

to discuss is scleroderma.

10:34

Scleroderma, also known as systemic sclerosis,

10:38

is an autoimmune connective tissue disease

10:41

and is characterized by microvascular obliteration

10:46

and sclerosis of the skin and internal organs.

10:50

The key findings radiographically are soft tissue

10:54

calcification and acro osteolysis.

11:01

Soft tissue calcifications in scleroderma are often

11:05

extensive in the distal phalanges.

11:08

Here we see an example of this.

11:10

Notice the calcifications next to the distal alma

11:16

demonstrated by the open arrow.

11:19

There are no signs of cartilage damage.

11:23

The pathophysiology of the calcium deposits,

11:26

it's not well understood in scleroderma.

11:30

It occurs in soft tissues that are under chronic stress such

11:34

as local trauma

11:36

or damage associated

11:38

with an underlying inflammatory process.

11:41

It is usually more abundant in the dominant hand.

11:46

When these findings are present,

11:47

the diagnosis is usually straightforward.

11:53

Here's another patient with scleroderma.

11:56

We see subtle but coarse soft tissue calcification

11:59

at the most distal part of the fingers.

12:03

No acro osteolysis or other signs are present.

12:06

In this case, severe acro

12:11

osteolysis of the fingertips is noted in this patient at the

12:15

distal aspects of the thumb index finger and long fingers.

12:20

Notice the lysis of the soft tissues distally.

12:24

Acro osteolysis is the radiographic finding which refers

12:28

to bone destruction of the distal phlange

12:31

and it occurs in up to 65% of patients

12:36

with scleroderma vascular alterations

12:40

and reduced capillary density.

12:43

Impaired tissue oxygenation

12:45

and the resulting hypoxia may contribute to osteoclast

12:50

ation which causes these changes.

12:55

There's a wide variety of diseases that can cause

12:59

acro osteolysis including psoriatic arthritis, infection,

13:05

reynard's disease and thermal trauma.

13:10

The image labeled A, we see subcutaneous

13:15

and perticular calcifications in the foot of a patient

13:19

with scleroderma.

13:21

There is also a Hal valgus deformity, which is not caused

13:25

by scleroderma in the image labeled B subcutaneous

13:30

calcifications near the elbow are noted in a patient

13:34

with scleroderma.

13:36

These subcutaneous calcifications often form

13:40

at pressure points.

13:44

Now we move on to another systemic disease

13:47

that demonstrates specific radiographic findings.

13:51

Systemic lupus erythema ptosis.

13:55

The key finding in SLE is abnormal joint alignment

14:00

without erosions and with a vascular necrosis.

14:05

Clinically systemic lupus

14:08

erythema ptosis is a generalized autoimmune

14:10

connective tissue disease.

14:13

Essentially, any organ system can be affected

14:16

with systemic findings including muscle weakness, malaise

14:21

and fever mucocutaneous findings demonstrated

14:25

by a typical butterfly rash on the face and renal

14:29

and neurologic symptoms.

14:32

The radiographic findings are that seen in the diagram.

14:37

No joint erosions are noted as the articular findings

14:43

per articular osteoporosis occurs in the bones,

14:48

the cartilage in the joints In a patient with s scleroderma

14:53

and systo, I'm sorry,

14:54

and sys systemic lupus AR erythema ptosis demonstrates

14:59

normal joint spaces.

15:01

The distribution in the hand is as seen in the diagram.

15:05

It affects the base of the thumb.

15:08

All metacarpophalangeal joints at all proximal

15:11

interphalangeal joints,

15:14

the distal interphalangeal joints are not affected.

15:18

The extra findings in this disease include

15:21

avascular necrosis.

15:24

Now, a specific

15:25

and unusual finding in scleroderma

15:29

is the soft tissue.

15:30

C is the, I'm sorry, in SLE,

15:32

I don't know why I'm saying scleroderma in SLE is the soft

15:36

tissue consists of reducible deformities like swan neck

15:41

and BNE deformities.

15:43

When the patient raises their hand,

15:45

the deformities are clearly seen.

15:48

However, when the hand is placed flat on the table,

15:52

the deformity spontaneously reduce soft tissue swelling

15:56

and calcifications in the subcutaneous

15:59

and deep soft tissues may also be seen most

16:03

around small joints.

16:09

In a patient with this disease, we see two AP views

16:12

of the hands Z like thumb deformities and swan.

16:17

Neck fingers are noted in this patient.

16:20

The deformities are thought to be a consequence

16:23

of low grade inflammation of the synovial membrane

16:26

and capsule resulting in ligamentous laxity

16:30

and muscular contracture.

16:32

However, no erosions are found.

16:37

Here's another patient.

16:39

We see another example of swan neck deformity.

16:43

No erosions or signs of cartilage damage are noted

16:49

and yet another patient.

16:51

Here we see swan neck deformities.

16:54

As I mentioned earlier,

16:56

these changes are usually reversible in the early stage

17:00

of the disease and characteristically when the patient

17:04

places their hand on the table or desk.

17:08

The deformity is correct.

17:12

Avascular necrosis is a frequent complication

17:16

and it is seen in up to 15% of patients.

17:20

The femoral head and tibial plateau are the most involved

17:24

sites, but other sites may be infected.

17:29

These patients have bone pain should be suspected

17:32

of having a vascular necrosis.

17:36

A vacu, a vascular necrosis in SLE can occur even in the

17:40

absence of steroid use.

17:42

Here we see subtle increased density in the distal femur in

17:47

a somewhat serpentine pattern

17:50

representing a vascular necrosis in a patient with SLE.

17:57

Moving on, we see radiographs of two different joints

18:01

in the image labeled A.

18:03

We see subluxation of the first

18:06

metacarpophalangeal joint without erosions.

18:09

In a patient with SLE, this is not typical for SLE

18:14

and can be seen in other forms of arthritis.

18:18

In image B, we see SLE of the shoulder.

18:22

This is demonstrated by collapse of the humeral head

18:27

with some loose bony fragments secondary

18:30

to a vascular necrosis.

18:33

Both steroid therapy

18:34

and SLE are associated with an increased risk

18:38

of a vascular necrosis.

18:42

Now we move on to our next disease,

18:44

which is a multisystem disorder of unknown etiology

18:49

characterized by the formation

18:51

of inflammatory non kating granulomas.

18:56

This is sarcoid.

18:59

The key findings in sarcoid are lace like granulomatous

19:03

lesions in the bone.

19:05

Clinically sarcoidosis is a multi-system disorder

19:09

of unknown etiology.

19:12

The musculoskeletal manifestations

19:14

of sarcoidosis occur in about 20% of patients

19:19

with sarcoidosis and include joint involvement, bone lesions

19:23

and muscular disease.

19:27

Primary skeletal involvement without other organ involvement

19:31

is extremely rare.

19:33

Usually arthritis is seen

19:36

early in the course of the disease.

19:39

Chronic disease is rare.

19:41

The most frequent musculoskeletal manifestation

19:45

of sarcoidosis is an acute arthritis that occurs as part

19:49

of lofgren syndrome characterized by the combination

19:54

of erythema nodosum, bilateral lar adenopathy,

19:59

polyarthritis, and constitutional symptoms.

20:04

If we apply our acronym

20:06

and discuss the radiographic findings, we find that

20:11

the articular changes consist of erosions, sarcoid.

20:16

Bone lesions can be perme or moth, lytic or sclerotic.

20:21

These lesions are very distinctive.

20:24

Joint space narrowing is unusual.

20:28

The distribution typically involves multiple joints

20:32

with symmetric distribution.

20:35

This is an unusual distribution

20:37

as seen in the diagram in the hand.

20:40

Sarcoidosis usually involves the index

20:43

and long finger joints in the skeleton.

20:47

The shoulder and the hip are frequent sites.

20:51

Otherwise, the skeleton, the knee, the ankle

20:54

and the hind foot all may be affected,

20:58

but to a lesser extent,

21:01

there are a wide range of manifestations

21:04

and thereby also many clinical

21:06

and radiographic manifestations.

21:09

The soft tissues demonstrate dactylitis and myopathy.

21:16

Lace like granulomas are associated with sarcoidosis.

21:20

These may be seen in multiple bones as we see here,

21:24

involving the proximal

21:25

and distal interphalangeal joints

21:27

of the index and long finger.

21:30

The osteolytic lesions are quite typical

21:33

and described as having a lace like or trabecular pattern.

21:39

This presence is somewhat of an ant mini

21:42

because once you have seen it,

21:45

you will recognize it when you see it.

21:47

Again, this image shows an

21:52

osteolytic lesion in the distal radius demonstrated

21:56

by the blue arrow with trabecular

21:59

and cortical bone destruction.

22:01

In a patient with sarcoid,

22:03

there is osseous destruction on both sides

22:06

of the interphalangeal joint of the first digit

22:09

with extra osseous extension of granulomatous tissue

22:14

noted by the black arrow.

22:19

Since neuropathic disease affects the joints,

22:22

especially in patients with severe diabetes,

22:25

this is an important topic for you to learn

22:28

and be able to recognize.

22:30

Neuropathic arthropathy, also known as charco arthropathy,

22:35

is a progressive destructive joint disorder in patients

22:39

with peripheral neuropathy with loss of pain, sensation

22:44

and proprioception in the foot, ankle

22:47

and hands seen commonly in diabetes.

22:52

Patients with this disorder may experience fractures

22:55

and dislocations of bones and joints with minimal

22:59

or known known trauma.

23:01

The most common cause, as I said, is diabetes mellitus,

23:06

which typically affects the tarsal

23:08

and tarsal metatarsal joints.

23:12

Arterial wall calcifications are commonly seen

23:16

in these patients.

23:18

Other causes are tertiary syphilis, also known as tbi,

23:23

dorsalis sar, Ringo, Mya leprosy,

23:27

and sometimes CPPD Crystal deposition disease.

23:33

The articulations in neuropathic arthropathy show no

23:37

evidence of erosions.

23:39

In the early phase of neuropathic arthropathy,

23:44

the bones demonstrate inflammation and osteopenia.

23:48

Finally, joint space destruction with presence

23:52

of loose bodies, fragmentation

23:55

and insufficiency fractures occur and are common.

24:00

When charco foot is treated

24:02

and becomes less active, the bone will coalesce

24:06

with formation of osteophytes and bony proliferation.

24:12

The cartilage demonstrates joint space narrowing

24:15

and ankylosis.

24:17

The distribution is primarily in the midfoot

24:20

as seen in the diagram.

24:24

The extra findings include neuropathy and vasculopathy,

24:29

and the soft tissue findings include soft tissue swelling,

24:33

severe joint malalignment leading

24:35

to rocker bottom deformity.

24:39

These radiographs are of two different patients with

24:43

diabetes and neuropathic arthropathy.

24:47

In image A, we see destruction

24:49

of the tarsal metatarsal joint with perticular lucencies

24:54

and soft tissue swelling.

24:56

In image B, we see typical radiologic changes in the foot

25:01

of a diabetic patient.

25:04

There is lateral subluxation

25:06

of the tarsal metatarsal joints, also known

25:10

as the Liz Frank joints.

25:12

The changes in bone

25:13

and joint may mimic severe osteoarthritis,

25:17

severe inflammation or septic arthritis.

25:21

The key in this case is the clinical history

25:25

with the presence of diabetes mellitus

25:28

and diabetic neuropathy.

25:32

Here we see a nice example of rocker bottom deformity.

25:36

This weight-bearing lateral view of the foot

25:39

demonstrates the dislocation in the tarsal metatarsal joints

25:44

and is better visible here than on the AP view.

25:51

Diabetic hand syndrome is another manifestation

25:54

of this disorder

25:56

and these are changes that occur in the hands in patients

25:59

with diabetic neuropathy.

26:02

The diabetic hand syndrome is the inability

26:05

to use the hand due to contractures and stiffness.

26:10

It can occur. It can affect the proximal

26:13

and distal interphalangeal joints

26:15

and metacarpophalangeal joints and is often painless.

26:21

Prolonged hypo hyperglycemia is thought

26:24

to result in the accumulation

26:26

of advanced glycation end products,

26:29

which cause these changes.

26:32

These glycation end products can break down collagen

26:36

and deposit abnormal amounts

26:38

of collagen in connective tissue

26:41

around the joints resulting in stiffening

26:44

and hardening of the joints in the skin.

26:48

If we look at the images, we see destruction

26:51

of the carpal metacarpal joint at the base of the thumb

26:55

and in all the distal interphalangeal joints.

26:58

We also see erosions

27:00

and bone destruction adjacent to the interphalangeal joint

27:04

of the index finger

27:06

and the distal interphalangeal joints of the long ring

27:10

and fifth fingers and the proximal interphalangeal joints

27:15

of the ring and fifth fingers.

27:18

Subluxations, as we see are also present.

27:22

Notice the extensive vascular calcification noted secondary

27:27

to diabetes mellitus.

27:28

Type two. The hand

27:33

of this patient with neuropathy shows the status

27:36

after removal of the trapezius bone indicated by the arrow.

27:42

Arrow. There is destruction

27:43

of all the distal interphalangeal joints

27:46

and erosions adjacent to the proximal interphalangeal joints

27:50

and metacarpophalangeal joints.

27:53

There are also erosions

27:54

and bone destruction adjacent to the interphalangeal joint

27:58

of the index finger and the distal interphalangeal joint

28:03

and proximal interphalangeal joints as well

28:06

as the metacarpophalangeal joints.

28:10

Subluxations and dislocation is also noted.

28:17

Moving on hemophilia can cause extensive changes

28:22

in the joints that resemble osteoarthrosis,

28:26

but the pattern is unusual.

28:29

Hemophilia is an inherited coa coagulation disorder,

28:34

which is mainly X-linked recessive and

28:38

therefore occurs almost exclusively in male children.

28:43

About 50%

28:44

of hemophilia patients develop hemophilic arthropathy.

28:49

This results from recurrent Hema HESIs,

28:53

which leads to synovial hyperplasia, chronic inflammation,

28:59

fibrosis and hemos.

29:03

It is frequently mono or or oligoarticular.

29:08

Early prophylaxis with coagulation factors

29:12

considerably reduces the musculoskeletal

29:15

complications in the joints.

29:18

In hemophilia, we see erosions

29:20

and eventually joint destruction.

29:24

The bones demonstrate subc chondral cyst formation,

29:28

osteoporosis, which is most peri per articular secondary

29:33

to the hyperemia that's occurring.

29:37

Ankylos may occur also in the late

29:40

stage joints.

29:42

Face narrowing is noted

29:44

and destruction in the late stage of the disease may occur.

29:49

He arthrosis affects the large joints and is frequently mono

29:53

or oligoarticular affecting the wrist, knee,

29:58

anco, and elbow joints less frequently.

30:02

It affects the glenohumeral joint,

30:05

sacroiliac joint and hips.

30:08

Because this is an inherited disorder,

30:10

growth abnormalities may be present as well.

30:14

Soft tissue swelling is also present

30:16

because of joint swelling or extra articular hemorrhage.

30:21

Please remember that when findings look like osteoarthritis

30:25

but are in an odd presentation

30:27

or distribution, think about hemophilia

30:31

especially in a younger patient.

30:36

Here we see radiographs of the knees.

30:38

In a patient with a history of hemophilia

30:41

and repetitive, he arthrosis distension

30:44

of the supra patella.

30:46

Recess of the right knee is noted secondary

30:49

to he arthrosis indicated by the black arrow.

30:53

There is narrowing of the medial joint space caused

30:56

by cartilage destruction

30:58

and secondary osteoarthrosis indicated by the white arrow

31:04

subcon bone cyst formation

31:06

below the intercondylar eminence is also noted

31:10

and no erosions are present.

31:13

As you can see, this picture is like osteoarthrosis,

31:16

so it is important to have clinical history.

31:19

In these cases. The Arnold

31:24

Hillgardner classification is a plain radiograph grading

31:28

system for hemophilia arthropathy of the knee.

31:33

In order to save time, I will not go

31:35

through this chart at this time.

31:39

Here we see AP views of both knees in a patient

31:43

with a history of repeated hemo arthrosis caused

31:46

by a vascular malformation, which is in the soft tissues

31:50

and not visible on this radiograph.

31:53

The image of the right knee shows joint space narrowing,

31:57

subc chondral cyst formation in erosions of the medial

32:01

and lateral tibial plateau.

32:04

A normal left knee joint for a comparison is noted.

32:10

Here's a more typical case in a patient

32:12

with long-term history of repetitive hemo arthrosis.

32:16

Because of hemophilia,

32:18

we see a slightly widened intercondylar notch

32:22

on the left side,

32:24

which can be also found in juvenile rheumatoid

32:27

and tuberculous arthropathy.

32:30

The femoral condyles are bolus

32:33

with flattened condylar surfaces.

32:36

The bone deformity on the left side can also be seen in

32:39

tuber tuber tuber tubercle, I'm sorry,

32:42

tubercle TB arthropathy.

32:44

There we go. As a note,

32:47

this is stage five Arnold Hilde Gartner classification

32:51

of hemophilic arthropathy.

32:53

This is demonstrates severe joint space narrowing,

32:58

subc chondral cyst formation and erosive destruction.

33:04

This image is of the shoulder in a patient with hemophilia

33:08

and re requirement he arthrosis of the shoulder joint.

33:12

It looks amazingly like osteoarthrosis.

33:16

There are features of secondary osteoarthritis

33:20

with subc chondral sclerosis

33:22

and osteophyte formation at both sides

33:25

of the glenohumeral joint superior and inferior.

33:30

In general, hemophilic arthropathy has similarities

33:33

with osteoarthritis.

33:35

As we stated earlier,

33:37

however, the presence of aver erosions,

33:41

extensive subc chondral bone cyst formation

33:44

and the history of recurrent hemo arthrosis

33:48

are distinguishing factors in favor of

33:51

hemophiliac arthropathy

33:56

in this radiograph of the ankle on the left

33:59

and a magnified view of the same ankle on the right

34:03

of a patient with hemophilia.

34:05

The findings include extensive symmetrical joint space

34:09

narrowing, subc chondral, bons formation,

34:13

and erosive changes.

34:18

Here's a nice representation

34:20

of end stage hemophilic arthropathy.

34:23

In this AP and lateral view of the elbow,

34:26

we see symmetric joint space narrowing, joint effusion,

34:31

subc chondral cyst formation,

34:33

and secondary osteoarthrosis with osteophyte formation.

34:39

Although the finding themselves are not that specific,

34:43

you can see the similarities in all the above cases

34:46

that I've shown you today.

34:50

Moving on to chronic recurrent multifocal osteomyelitis

34:55

is an unusual condition which demonstrates multifocal areas

35:00

of sterile bone inflammation.

35:03

Clinically, this is an uncommon autoimmune inflammatory

35:08

disorder of the bones in children

35:10

and young adults that is characterized

35:13

by non bacterial osteomyelitis.

35:18

Patients present with episodic mul multifocal bone pain

35:23

secondary to sterile osseous inflammation.

35:27

The disease has a relapsing and remitting course.

35:31

The cause of this disorder is unclear.

35:35

The diagnosis is made by exclusion

35:38

and the main causes

35:40

to be excluded are neoplasms and infections.

35:45

It is sometimes diagnosed along

35:47

with inflammatory bowel disease or psoriasis

35:51

and there seems to be a genetic component.

35:56

If we look at the diagram, the findings are rather unusual.

36:00

The mandible and clavicle are frequently affected

36:04

as are the elbows, knees, and ankles.

36:08

The pisiform joint is affected in the wrist.

36:11

No other joints are affected in the hand

36:14

and there is no foot involvement.

36:17

There are no definitive articular findings in this disorder.

36:23

First, the bones demonstrate lytic lesions

36:26

and then bone edema later progressively sclerotic lesions

36:31

develop in the metaphysis along

36:34

with thick peros titis.

36:38

The cartilage demonstrates no abnormal findings.

36:42

The distribution is as seen in the illustration,

36:46

often symmetrical and multifocal.

36:49

Typically, the medial clavicles and the tibia are involved.

36:54

Other common sites are ribs, the mandible, the pelvis

36:59

and vertebrae bodies.

37:01

Extra findings occur in children

37:03

and adolescents with an average age of onset of seven

37:07

to 14 years and the female

37:09

to male ratio is approximately two to one.

37:14

Soft tissues demonstrate edema

37:16

around the regions of inflammation.

37:21

If you look carefully, we see here cortical thickening

37:26

sclerosis and bone enlargement of the diaphysis

37:29

and metaphysis of the right clavicle

37:34

and metaphysis of the left clavicle.

37:40

A spectacular SPECT CT

37:42

and bone scintigraphy in the same patient

37:46

demonstrate abnormal radionuclide uptake in the

37:49

corresponding areas reflecting increased bone turnover.

37:56

This patient demonstrated pain on the left side of the hip.

38:01

There is subc chondral osteolysis lateral

38:03

to the proximal femoral femur

38:06

demonstrated by the blue arrow.

38:08

The MRI study belows including axi

38:11

and coronal T one TSE FS sequences

38:17

with contrast shows a region of bone

38:20

and soft tissue enhancement about the left hip.

38:25

This was found to be due to non-infectious osteomyelitis

38:29

with extra osseous extension.

38:34

Our final disorder in this lecture series is SFO syndrome.

38:39

This is a syndrome that consists of synovitis, acne,

38:44

osis of the hands and soles of the feet, hyperos, ptosis

38:49

and osteo osteitis,

38:51

and it's an uncommon inflammatory disorder

38:55

of bone joints and skin.

38:58

The pathogenesis of SFO syndrome is not well understood.

39:02

It is sometimes described as an autoinflammatory disorder.

39:08

If we look at the radiographic findings

39:11

and apply our mnemonic,

39:13

the articular findings include joint, joint erosions

39:17

and erosion of the vertebral body contours.

39:21

The bones demonstrate osteitis, which is bone inflammation

39:25

and demonstrated as sclerosis of the medullary cavity

39:29

and bone marrow edema.

39:32

Hyper osis is also seen as cortical thickening formation

39:37

of osteophytes, paravertebral ossification

39:41

and ankylos osteo

39:44

osteolysis is also a common finding

39:47

and may lead to vertebral body collapse.

39:50

The cartilaginous changes include joint space narrowing.

39:55

This distribution is asymmetric including the anterior chest

40:00

wall, which is the most common site of involvement,

40:05

then the men mandible and spine

40:08

and less frequently the cer cervical spine

40:11

and sacroiliac joints.

40:15

The extra findings for this disorder is

40:17

that it is seen in an average age of 30 to 50 years of age

40:22

with a female predominance.

40:25

Soft tissue changes include acne

40:28

and pustulosis of the palms and soles of the feet.

40:33

Although skin and osteoarticular manifestations do not

40:37

necessarily coexist.

40:40

An important point in this disorder is that the degree

40:43

of inflammation determines the type of bone abnormalities.

40:48

Osteolysis will occur when there is extensive inflammation.

40:54

Increase of bone activity

40:55

and sclerosis will occur when there is less inflammation.

41:03

Here we see three different images of the same patient.

41:07

Notice on the sagittal CT on the left

41:10

that there is osteitis of the sternum indicated

41:14

by the yellow arrow

41:18

with sclerotic thoracic vertebral bodies

41:21

and some nplate erosions

41:23

and paravertebral CDEs fight formation indicated

41:26

by the blue arrow.

41:29

The middle image is a lateral view from a

41:32

nuclear medicine bone scan.

41:35

Increased activity can be seen in the sternum indicated

41:38

by the black arrow and then

41:41

and in the mid thoracic spine indicated

41:44

by the yellow arrow head.

41:47

The right image is an axial CT of this patient demonstrating

41:52

sclerosis in the manubrium stern eye.

41:58

Here is a good example of hyperos osteos in sfo.

42:03

This patient has extensive hyperos osteos of the medial side

42:07

of the CVIC clavicles bilaterally.

42:11

In the CT of the same patient,

42:14

we see extensive hyperos ptosis of the medial side

42:18

of the clavicle and the sternum ankylos

42:23

of the sternoclavicular joints and of the first

42:26

and second sternal costal joints is also noted.

42:32

We have come to the end of the arthritis lecture series.

42:36

On this slide, you will find comp a comprehensive table

42:40

demonstrating all the findings seen in all the diseases

42:44

we have discussed.

42:46

It might be helpful for you to photograph this

42:48

and keep it in your telephone for reference.

42:51

You'll be able to find it on the

42:55

modality website under noon conferences.

43:00

Virtually everything I talked about is in this table

43:04

and as I said, this lecture will be available on the

43:07

modality website along with the two

43:10

previous lectures under noon conference.

43:13

Thank you so much for your attention

43:15

and I hope you found this enjoyable.

43:19

Thank you so much Dr.

43:20

Beki, and at this time we will open the floor

43:23

for any questions from our audience.

43:25

You may submit your questions through the q

43:26

and a feature below.

43:29

Uh, it looks like we have a couple

43:31

of questions in here already that I'll read to you,

43:33

Dr. Beki, if you're ready.

43:36

I'm ready. Alright.

43:37

Uh, will dual energy CT show CPPD deposition

43:42

not seen on plane radiographs,

43:47

Dual energy CT Might,

43:49

but once again, I'm a playing film expert

43:52

and I don't work so much with sec sectional imaging,

43:55

so I can't tell you the answer to

43:57

that question definitively,

43:59

but it would make sense that it might do so.

44:03

All Right, and that's really all

44:05

I can say on that topic.

44:07

Excellent. Uh, this next question, uh,

44:10

I will AP apologize in advance, uh, to everyone

44:13

for my mispronunciation of words.

44:16

Uh, so how will you differentiate, differentiate between,

44:21

uh, this might be a typo actually, so arthritis

44:26

and neuropath and syndrome

44:30

PS psoriatic arthritis and neuropathic arthritis?

44:34

Yes, There's a big difference.

44:37

There's a big difference.

44:39

Neuropathic, as we talked about, is regional,

44:42

usually in the foot and sometimes in the hand.

44:48

It, it occurs

44:51

and involves all the joints of the midfoot

44:56

and all the joints of the hand when we see it.

44:59

Psoriatic has a rate like distribution.

45:04

It has discreet erosions which have

45:08

behind them bony proliferation.

45:13

This bony proliferation is not osteophytosis,

45:17

but rather the body's response to the erosive changes.

45:23

Psoriatic is a slower disease when compared

45:27

to rheumatoid arthritis,

45:30

which causes an ero which cause erosions with an

45:33

with a vengeance,

45:35

and the body doesn't have time to build up a repair response

45:39

as it does in psoriatic arthritis.

45:42

So they're really, they're really two different entities.

45:47

Okay, great.

45:50

Let's see if there are any in the chat for you.

45:56

Uh, any role of USG and arthritis?

46:01

Do they help in differentiation?

46:05

Everybody likes ultrasound. I am not an ultrasound doctor.

46:10

I read him when I was in training.

46:13

Remember, I'm American trained.

46:15

I work in Europe, but I'm American trained

46:18

and those scans are done by technologists in,

46:21

in the hospitals in the United States,

46:23

and they're most frequently interpreted

46:28

by technologists.

46:30

The me, the MSK

46:35

ultrasound examinations are done by specific physicians.

46:40

Not every one of us does ultrasound you.

46:43

I'll give you a reference.

46:44

John A. Jacobson, who is a brilliant, brilliant man,

46:49

writes a lot about it,

46:50

and he is, he's been doing that for 20 years

46:54

and he can tell you more about that.

46:56

You can actually search Google for him and for his works.

47:01

All right. Um, this looks like difference between

47:07

CPPD and hemochromatosis

47:12

for Tri mm-Hmm.

47:13

Angular fibro cartridge.

47:16

Okay. Once again, rarely do we see

47:21

chondrocalcinosis and hemochromatosis.

47:25

Hemochromatosis causes beaking of the heads of

47:30

the metacarpals.

47:32

All four of them save the thumb.

47:36

CPPD causes beaking of the first

47:40

and second metacarpal heads.

47:43

Also, hemochromatosis is a disease of men,

47:49

whereas CPPD is a disease of everybody

47:52

and we'll all probably get it as we get older

47:55

because it's quite ubiquitous

47:59

after probably 50 years of age

48:02

and it's presentation is seen in 100% of patients

48:07

by the time they reach 100 years of age.

48:12

Okay. Uh, is it always possible to distinguish

48:16

subc chondral cyst and erosion?

48:21

That's a difficult question. It's difficult.

48:25

It's very difficult sometimes

48:27

because if the cyst opens into the joint,

48:32

then it'll look like an erosion,

48:35

but the erosions that we see in rheumatoid tend to be

48:40

marginal no matter whether they're in the wrist

48:43

or in the digits.

48:45

Whereas the subc chondral cysts

48:50

seen in CPPD commonly are more centrally

48:54

located in the bone.

48:55

It's a very fine differentiation,

48:58

and if you look at a a lot of these cases,

49:00

you will see the difference.

49:02

Mm-Hmm.

49:04

Uh, then we have, uh,

49:08

I'm not sure if this is supposed to be disuse

49:10

or discuss osteopenia versus complex pain

49:14

regional syndrome on X-ray differences.

49:19

Oh, yo, yo, yo yo. That I can't do.

49:21

That's out of my, out of the scope

49:23

of this lecture at this point.

49:27

Uh, all right. We will, let's see, what's this one?

49:32

Uh, I'll just read this whole thing. Thank you very much.

49:35

Once again, Dr. Blei

49:36

and the moderator, please serve

49:38

for a resident going for exams.

49:40

A lot of these can be listed as differentials, differentials

49:44

of each other, not directly, but somehow.

49:46

So Dr. Beki, please.

49:48

Any tips on stratifying, orthopathy

49:52

and arthritis differentials something less extensive than

49:56

the table at the end of the presentation?

49:59

Okay. What you need to do is you need

50:03

to learn the target area approach,

50:05

which this lecture is based upon.

50:09

You can learn it through practice.

50:11

The best presentation of the target area approach

50:15

for the hand risk

50:17

and foot is in the new Resnick book

50:21

that just came out two months ago, the fourth edition

50:25

of Bone and Joint Imaging,

50:29

and that has a detailed explanation.

50:32

You basically have to just look at a lot of cases

50:36

and you have to put together the findings in your head

50:41

relative to the way the, the, the diagrams are,

50:45

because the diagrams are well known to be accurate

50:49

and using those, and over time you'll learn it

50:52

and then the differentials become very, very clear to you.

50:56

It's, there's not lists of them,

50:57

but the things that are different

50:59

and the things that are similar become clear.

51:04

I, I started using this uh, method many, many years ago

51:09

as a, after I did a fellowship with Dr.

51:12

Resnick and it really does work.

51:13

It takes time, but it really does work

51:17

and you become brilliant

51:18

and instantaneous at diagnosing these disorders.

51:22

You're really good at it after a while

51:25

because some of them actually have very specific findings

51:30

and these findings are, you know,

51:32

and the ones that have very specific findings,

51:34

many of them are common.

51:37

So it's the rarer disorders

51:38

that have the non-specific findings in General.

51:44

General. Alright, well that's, those are the questions Dr.

51:49

Bki. So thank you so much Super

51:51

For lecture

51:52

And then taking the time to answer everyone's questions.

51:56

No problem, no problem.

51:58

Yes. Thank you so much and thank you to everyone

52:00

for participating in our noon conference

52:02

and asking great questions Today.

52:04

You can access the recording of today's conference

52:06

and all our previous noon conferences

52:08

by creating a free MRI online account.

52:11

We'll also email out a link to the replay later today.

52:15

Be sure to join us next week on Thursday,

52:17

July 25th at 12:00 PM Eastern,

52:19

where Dr. Laura Avery will deliver a lecture entitled

52:22

Abdominal Trauma.

52:24

You can register for, uh, mri online.com

52:27

and follow us on social media

52:28

for updates on future noon conferences.

52:30

Thanks again and have a great day.